Perspectives on Modern Orthopaedics

Magnetic Resonance Imaging of

Articular Cartilage of the Knee

Thomas R. McCauley, MD, and David G. Disler, MD

Abstract

Recently developed magnetic resonance (MR) imaging techniques allow accu- gradient technology, which have
rate detection of moderate- and high-grade articular cartilage defects. There has improved image quality, spatial re-
been increased interest in MR imaging of articular cartilage in part because it is solution, and speed of imaging. 4
useful in identifying patients who may benefit from new articular cartilage These improvements have resulted
replacement therapies, including chondrocyte transplantation, improved tech- in the ability to use MR imaging to
niques for osteochondral transplantation, chondroprotective agents, and carti- detect moderate- and high-grade
lage growth stimulation factors. The modality also has the potential to play an articular cartilage abnormalities
important role in the follow-up of patients during and after treatment. with a high degree of accuracy.
Detection of articular cartilage defects is beneficial for patients undergoing
arthroscopy for other injuries, such as meniscal tears, because the presence of
articular cartilage injury worsens prognosis and may modify therapy options. Cartilage Structure and
J Am Acad Orthop Surg 2001;9:2-8 Function

The structure of hyaline cartilage is

Interest in cartilage imaging has
increased recently for many rea-
sons. As the mean age of the popu-
lation has risen, the incidence of os-
teoarthritis has increased. Articular
cartilage abnormalities are common,
with nearly 75% of persons over age
75 years having osteoarthritis.1 The
advent of arthroscopy has brought a
greater demand for accurate preop-
erative evaluation. Identification of
isolated articular cartilage injuries
with magnetic resonance (MR)
imaging prior to arthroscopy is im-
portant because articular cartilage
injuries can clinically mimic menis-
cal tears.2 In addition, prearthro-
scopic evaluation of articular carti-
lage allows better prediction of
prognosis for planned interventions
because of the association of articu-
lar cartilage defects with a less satis-
factory clinical outcome.3
The most important reason for
the increased interest in accurate
imaging evaluation of articular car-
tilage is the development of carti-
lage replacement therapies. Detec-
tion of articular cartilage defects is
necessary to identify patients for
whom such therapies are appropri-
ate. Magnetic resonance imaging
allows surgeons to evaluate treat-
ment options on the basis of knowl-
edge of the size and location of artic-
ular cartilage derangements before
arthroscopy or surgery. Further-
more, MR imaging offers the poten-
tial for follow-up of patients in trials
of these new cartilage replacement
therapies. A noninvasive alternative
for articular cartilage evaluation is
important because these patients are
often unwilling to undergo follow-
up arthroscopy to determine success
of treatment.
The ability to visualize articular
cartilage with MR imaging has
advanced with the development of
new sequences, receiver coils, and
critical to its function. Understand-
ing this structure helps explain the
imaging appearance of normal and
abnormal cartilage and has been
essential to the development of new
imaging techniques.
Normal articular cartilage is
composed of hyaline cartilage.
Chondrocytes account for 1% of
Dr. McCauley is Associate Professor of
Diagnostic Radiology and Chief of MRI, Yale
University School of Medicine, New Haven,
Conn. Dr. Disler is Associate Clinical Pro-
fessor of Radiology, Virginia Commonwealth
University, Richmond, and is in private prac-
tice with Commonwealth Radiology, Richmond.
Reprint requests: Dr. McCauley, Diagnostic
Radiology, Yale University School of Medicine,
Box 208042, 333 Cedar Street, New Haven, CT
06520-8042.
Copyright 2001 by the American Academy of
Orthopaedic Surgeons.

2 Journal of the American Academy of Orthopaedic Surgeons


hyaline cartilage volume; a hydro-
philic matrix, which is 80% water,
constitutes the remaining 99% of
cartilage volume. The matrix serves
three major functions: providing a
nearly frictionless surface, distrib-
uting forces to underlying sub-
chondral bone with little deforma-
tion, and transporting nutrients to
the chondrocytes.5 After water, the
two largest constituents of the hya-
line cartilage matrix are collagen
(which makes up 60% of the dry
weight of cartilage) and proteogly-
can aggregates (30% of the dry
weight). 5 Collagen provides the
structural framework, tensional
stability, and covering surface of
cartilage. Proteoglycan aggregates
are extremely large macromole-
cules that contain many hydroxyl
and negatively charged moieties.
These attract water and cations,
thereby creating osmotic, ionic, and
Donnan forces that result in a swell-
ing pressure in the collagen frame-
work, which resists compression.6
There is a highly ordered struc-
ture to the collagen in cartilage,
which is critical to its biomechani-
cal function. This structure can be
divided into four zones, or laminae,
on the basis of the collagen orien-
tation seen microscopically.7 The
most superficial portion of the car-
tilage is the tangential zone, which
contains collagen fibers oriented
parallel to the articular surface.
The second, or transitional, zone
contains fibers oriented oblique to
the cartilage surface. In the third,
or radial, zone, the fibers are ori-
ented perpendicular to the cartilage
surface and are thicker than in the
more superficial zones. The fourth
zone, the zone of calcified cartilage,
is present at the interface of the car-
tilage with the underlying bone.
The arcadelike configuration of the
collagen fibers provides even dis-
tribution of forces to underlying
bone and resists shearing forces.
The swelling pressure created by
the proteoglycans provides the
Vol 9, No 1, January/February 2001
Thomas R. McCauley, MD, and David G. Disler, MD
main resistance to compressive
loads.6 The biomechanical proper-
ties of cartilage are lost when there
is damage to this highly ordered
structure.
Cartilage Damage and
Repair
Osteoarthritis and trauma are the
most common causes of cartilage
damage. Inflammatory arthritis is
less common.
There are three stages of osteo-
arthritis.8 In the first stage, there is
disruption of the collagen frame-
work with softening associated
with decreased proteoglycan con-
tent and increased water content.
In the second stage, there is repair
with proliferation of chondrocytes
and increased anabolic activity.
Thickening of cartilage may occur
in this stage; however, the thickened
cartilage has abnormal mechanical
properties. In the third stage, the
repair mechanisms can no longer be
sustained, and decreased cellular
proliferation and anabolic activity
of the chondrocytes occurs, result-
ing in articular cartilage loss, fibril-
lation, erosion, and cracking.8
When articular cartilage defects
form due to osteoarthritis or trauma,
there may be repair; however, nor-
mal hyaline cartilage does not re-
generate. Repair generally does
not occur when there are partial-
thickness cartilage defects, as the
repair response is usually initiated
only with damage extending to
subchondral bone, as occurs in full-
thickness defects.6 Full-thickness
defects initiate repair by filling
with fibrin clot and inflammatory
cells, which release growth factors
and other proteins that stimulate
repair. Unfortunately, fibrocarti-
lage usually only partially fills the
defects in the articular cartilage
surface. The fibrocartilage does not
have the same mechanical proper-
ties as normal hyaline cartilage
because of abnormal collagen
structure and because of produc-
tion of smaller chain lengths and
smaller amounts of proteoglycan
aggregates, which decreases the
attraction for water. The fibrocarti-
lage usually begins to degenerate
within a year after formation be-
cause of its abnormal biomechanical
properties.6
Pain is not directly caused by
cartilage damage because articular
cartilage is aneural. Cartilage ab-
normalities and associated bone
abnormalities likely cause forces
that act on the subchondral bone,
joint capsule, menisci, and other
supporting structures of the joint,
resulting in pain.9
MR Imaging of Articular
Cartilage
The accuracy of articular cartilage
assessment with MR imaging has
greatly improved with the recent
development of imaging sequences
designed specifically for hyaline
cartilage. The two most widely
used imaging techniques are the T1-
weighted fat-suppressed three-
dimensional spoiled gradient-echo
technique and the T2-weighted fast
spin-echo technique. Cartilage is
well visualized with these tech-
niques due to the differences in T1
and T2 between articular cartilage
and fluid. Cartilage is higher in sig-
nal intensity than fluid on T1-
weighted images and is lower in
signal intensity than fluid on T2-
weighted images.
Magnetic resonance arthrogra-
phy with injection of contrast mate-
rial into the joint is not generally
necessary for articular cartilage
evaluation. The accuracy of MR
arthrography has not been found to
be higher than that of imaging
techniques that do not entail con-
trast injection.10,11 However, MR
arthrography is useful in a subset
of patients for whom assessment of
3
MR Imaging of Articular Cartilage of the Knee

cartilage integrity over osteochon-

dral defects 12 or identification of
loose bodies is necessary.13
The fat-suppressed three-dimen-
sional spoiled gradient-echo se-
quence provides high accuracy,
with a sensitivity of 86%, specificity
of 97%, and accuracy of 91% for
detection of cartilage lesions in the
knee (data are for detection of carti-
lage lesions excluding softening
without cartilage loss)2 (Figs. 1–3).
T2-weighted fast spin-echo tech-
niques, both without and with fat
suppression, have recently been
shown to result in similarly high
accuracy, with a sensitivity of 87%,
specificity of 94%, and accuracy of A B
92%14,15 (Fig. 2). As with other MR
techniques, accuracy is highest in
the patellofemoral joint, likely due
to the thickness of the patellar car-
tilage.2 In addition, high-grade ab-
normalities with thinning or focal
defects in cartilage are detected with
greater accuracy than low-grade
cartilage abnormalities, in which
there is little or no loss of cartilage
thickness.2
The two imaging techniques C D
have different advantages and dis-
advantages. The T2-weighted fast Figure 1 Full-thickness traumatic articular cartilage defect in the knee of a 14-year-old
spin-echo technique is less suscep- soccer player seen on fat-suppressed three-dimensional spoiled gradient-echo images.
Cartilage appears as high signal intensity; fluid and other tissues appear as low signal
tible to metal artifacts, which can be intensity. A, Sagittal image (repetition time [TR] = 60 msec; echo time [TE] = 5 msec)
an advantage when imaging patients shows articular cartilage defect in the lateral femoral condyle at the trochlear groove (solid
after surgery. The fat-suppressed arrow). Note low-signal lamina due to truncation artifact in adjacent normal cartilage
(open arrow). B, Sagittal image (TR/TE = 60/5) obtained lateral to A shows cartilage frag-
three-dimensional spoiled gradient- ment in suprapatellar recess (arrow). C, Surface rendering of the defect from an anterior
echo sequence provides thinner sec- perspective, created from the three-dimensional image set. D, Arthroscopic image of
tions, which has been found advan- trochlear groove as seen from below confirms the presence of the articular cartilage defect
seen with MR imaging. (Part A reproduced with permission from Disler DG, McCauley
tageous in identifying morphologic TR, Wirth CR, Fuchs MD: Detection of knee hyaline cartilage defects using fat-suppressed
defects. T2-weighted sequences can three-dimensional spoiled gradient-echo MR imaging: Comparison with standard MR
better visualize signal abnormalities imaging and correlation with arthroscopy. AJR Am J Roentgenol 1995;165:377-382. Parts C
and D reproduced with permission from McCauley TR, Disler DG: MR imaging of articu-
within cartilage and thus may allow lar cartilage. Radiology 1998;209:629-640.)
detection of lower grades of carti-
lage abnormality, especially in the
patellar cartilage (Fig. 4). These two
techniques for detection of defects Both the fat-suppressed three- available at those field strengths,16
have not yet been directly com- dimensional spoiled gradient-echo along with decreased reliability or
pared. Neither has the ability of technique and the T2-weighted fast unavailability of fat suppression.
these techniques to accurately mea- spin-echo technique have been val- No direct comparison has been per-
sure the area of defects, which can idated in patients at 1.5 T. 2,14,15 formed at different field strengths;
influence selection of cartilage re- Lower accuracies would be expected however, in a recent study, 17 the
placement therapies, been investi- at lower field strengths because accuracy of evaluation of cadaveric
gated. of the lower signal-to-noise ratio patellar articular cartilage at 0.2 T

4 Journal of the American Academy of Orthopaedic Surgeons

 Thomas R. McCauley, MD, and David G. Disler, MD

tation of the cartilage with respect to

the magnetic field. The latter varia-
tion is due to the anisotropy of the
collagen fibers in the various layers
of the cartilage.19 Experienced read-
ers can recognize normal variation
in the laminar appearance and there-
fore are not hindered in the detec-
tion of cartilage damage.

Clinical Importance of
A B Cartilage Imaging
Figure 2 Images depicting a near-full-thickness articular cartilage defect in the medial The ability to accurately evaluate
femoral condyle in a 28-year-old man with chronic knee pain. No other abnormality was articular cartilage with MR imaging
found in the knee at arthroscopy. A, Sagittal fat-suppressed three-dimensional spoiled
gradient-echo image (TR/TE = 40/6) shows a defect (arrow) containing fluid, which can provide more complete infor-
appears as low signal intensity. B, Coronal T2-weighted fast spin-echo image (TR/TE = mation with which to make thera-
4,000/96) shows the same defect (arrow) containing fluid, which appears as high signal peutic decisions. Articular cartilage
intensity.
injury in the knee is common; in
one study,2 it was visualized on MR
images of 32 (67%) of 48 patients
was lower than that obtained in pede visualization of cartilage de- who subsequently underwent ar-
evaluation of patellar cartilage with fects; it can even be helpful in de- throscopy of the knee. In that study,
1.5-T magnets.2 In addition to high- termining the depth of the defects. two thirds of the patients with artic-
quality equipment, the appropriate High-resolution T2-weighted MR ular cartilage defects had concur-
pulse sequences and imaging pa- imaging can demonstrate a nonarti- rent meniscal tears or ligament
rameters must be used (Table 1). In factual laminar signal-intensity pat- injuries; however, one third had
our experience, radiologists are tern in cartilage, predominantly due isolated articular cartilage injuries.
better able to identify articular car- to the laminar structure of the colla- Detection of articular cartilage
tilage injuries with increased expe- gen fiber orientation.19,20 The size defects with MR imaging can ex-
rience, including feedback based and signal intensity of the laminae plain symptoms in patients with
on arthroscopic findings from re- can vary with changes in imaging isolated articular cartilage injuries
ferring orthopaedic surgeons. variables and with changes in orien- that might otherwise have eluded
A number of factors may influ-
ence the appearance of articular
cartilage at MR imaging. Articular
cartilage has uniform high signal
intensity on fat-suppressed three-
dimensional spoiled gradient-echo
images2; however, artifactual low-
signal laminae may be visualized in
the center of cartilage due to trun-
cation artifact18 (Fig. 1). This arti-
fact occurs due to undersampling of
signal from small objects with high
contrast. The location and appear-
ance of truncation artifact is pre- A B
dictable. Truncation artifact can be Figure 3 Sagittal fat-suppressed three-dimensional spoiled gradient-echo images (TR/TE
decreased by increasing the in- = 40/6) of a 17-year-old girl 1 year after osteochondral transplantation to repair a femoral
plane resolution; however, increas- articular cartilage defect. A, Image obtained at the site of osteochondral plug placement
(arrow) shows slight depression of the articular surface. B, Image obtained at the donor
ing resolution typically increases site along the lateral margin of the intercondylar notch depicts filling with intermediate-
imaging time. This artifact is usually signal-intensity tissue, likely representing repair tissue in the osteochondral defect (arrow).
easily recognized and does not im-

Vol 9, No 1, January/February 2001 5

MR Imaging of Articular Cartilage of the Knee

group has used short-echo-time ac-

quisitions to obtain proton spectra in
articular cartilage, which has the
potential to provide more detailed
analysis of biochemical information.23
Second, imaging techniques are
being developed that use magneti-
zation transfer contrast. Magnetiza-
tion transfer contrast is dependent
predominantly on collagen integrity
in cartilage.24 Unfortunately, these
techniques have not yet been found
A B to be superior to other routinely
Figure 4 Images of a patellar cartilage abnormality due to osteoarthritis in a 46-year-old available MR imaging techniques.
man. A, Fat-suppressed three-dimensional spoiled gradient-echo image (TR/TE = 40/6) Third, ionic gadolinium contrast
shows cartilage abnormality as decreased signal intensity in the normally high-signal- material is being used for detection
intensity cartilage with associated surface irregularity (arrows). B, Abnormality is more
clearly seen on T2-weighted axial image (TR/TE = 2,000/80) of patella, where it is depicted of early biochemical changes with
as increased internal signal within the normally low-signal-intensity cartilage (arrows). cartilage degeneration.25 The con-
(Reproduced with permission from McCauley TR, Disler DG: MR imaging of articular car- trast medium is introduced into the
tilage. Radiology 1998;209:629-640.)
joint by either direct or intravenous
injection. In normal cartilage, the
negative charges of proteoglycan
detection. Identification of articular tistically significant higher accu- aggregates exclude the negatively
cartilage injury with MR imaging in racy than that obtained with a fat- charged gadolinium chelate. Be-
patients with intact menisci is espe- suppressed three-dimensional spoiled cause proteoglycans are lost early
cially useful because symptoms due gradient-echo technique in a study of in cartilage degeneration, increased
to isolated cartilage defects often 10 human cadaveric patellae. The amounts of the negatively charged
mimic those due to meniscal tears.2 authors hypothesized that the high gadolinium can gain entry into de-
Identification of cartilage damage is sensitivity of this technique was due generating cartilage, with resulting
important in patients with associ- to signal changes related to disorgani- signal enhancement. A study of
ated injuries because the presence zation of collagen fibers. Another cadaveric patellar cartilage found
of defects can worsen the prognosis
after arthroscopic surgery.3 Iden-
tification of defects also facilitates Table 1
preoperative planning for articular Suggested Protocols for Articular Cartilage Imaging2,4,14,15*
cartilage replacement therapies.
Fat-Suppressed
Three-Dimensional
Future Developments Technique Spoiled Gradient-Echo Fast (Turbo) Spin-Echo

Currently available techniques allow Pulse sequence TR = 30-50 msec; TE = TR = 3,500-5,000 msec;
detection of morphologic defects in <10 msec (minimum TE = 30-54 msec; echo
articular cartilage with high accuracy. full echo); 40° flip angle train length = 8-10
However, low-grade injuries with Tissue contrast Fat suppression or Fat suppression pref-
internal cartilage damage without water excitation erable
morphologic change are not accurate- Field of view, cm 14 12-14
ly visualized.21 A number of MR Acquisition matrix 160 × 256 256-512 × 256-384
techniques for detection of cartilage Section description 1.5-mm sections, 3.5- to 4.0-mm sections;
damage at early stages are being 60 locations gap = 0 to 1 mm
developed. First, Brossmann et al22
Number of excitations 0.75 or 1 2
reported that a technique utilizing
ultra-short echo times resulted in * Sagittal and axial planes are most useful. Three-dimensional images can be reformatted
100% sensitivity and specificity for to obtain high-quality axial images.
detection of cartilage defects with sta-

6 Journal of the American Academy of Orthopaedic Surgeons


that use of gadolinium allowed de-
tection of loss of proteoglycans
from mechanically intact articular
cartilage, while changes in T2 in
cartilage could be used to detect
mechanical damage.26
Fourth, MR imaging of sodium
rather than hydrogen has been
investigated as a potential method
for evaluation of proteoglycan con-
tent in articular cartilage.27 Imaging
techniques that detect early bio-
chemical changes can facilitate iden-
tification of cartilage abnormalities
before morphologic abnormalities
occur, which may allow chondro-
protective interventions before loss
of the morphologic integrity of carti-
lage occurs.
Another area of ongoing devel-
opment takes advantage of the
three-dimensional information avail-
able with MR imaging of articular
cartilage. Surface models of articular
cartilage can be created from MR
imaging data sets (Fig. 1, C). Measure-
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Thomas R. McCauley, MD, and David G. Disler, MD
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 The Musculoskeletal Effects of Smoking

Scott E. Porter, MD, and Edward N. Hanley, Jr, MD

Abstract

Currently, there are more than 50 million smokers in this country, and approxi- crease microvascular prostacyclin
mately 800 billion cigarettes are smoked each year. Smoking is now the leading levels, and inhibit the function of
avoidable cause of morbidity and mortality in the United States. According to fibroblasts, red blood cells, and
one report, over 500,000 deaths per year in the United States alone can be attrib- macrophages.6,7 Carbon monoxide
uted to smoking. For years, orthopaedic surgeons have known about the rela- has a stronger affinity for hemoglo-
tionships that putatively exist between smoking and an array of orthopaedic con- bin than oxygen, resulting in the
ditions and complications. It has been shown to adversely affect bone mineral displacement of oxygen from the
density, lumbar disk disease, the rate of hip fractures, and the dynamics of bone hemoglobin and a lower oxygen
and wound healing. Although scientific and clinical information on smoking tension in tissues.8
and its consequences suggests differing degrees of correlation between smoking For years, orthopaedic sur-
and orthopaedic conditions, most available data do suggest a real and repro- geons have known about the rela-
ducible relationship. In the past, there have been many individual reports that tionships that putatively exist
deal with these relationships separately but very few published comprehensive between smoking and an array of
reviews. This summary of the current literature regarding the relationship orthopaedic conditions and com-
between smoking and musculoskeletal diseases and their treatment provides plications. In the past, there have
information that can be used clinically by both the practitioner and the patient. been many reports that deal with
J Am Acad Orthop Surg 2001;9:9-17 these relationships as separate
entities but very few published
comprehensive reviews. This arti-
cle will summarize the currently
Cigarette smoking has come under Cigarette smoke has two phases: available literature regarding the
increasing attack by a number of a volatile phase and a particulate relationships between smoking
different groups both within the phase. The volatile phase is the and musculoskeletal diseases, as
United States and worldwide. This longer phase and accounts for 95% well as the effect on the treatment
has been fueled, in part, by recog- of the cigarette smoke. Nearly 500 of those diseases, to provide infor-
nition of the increasing number of different gases are released during mation that can be used clinically
diseases with which smoking has the volatile phase, including nitro- by both the practitioner and the
been directly or indirectly associated. gen, carbon monoxide, carbon di- patient.
Currently, there are more than 50 oxide, ammonia, hydrogen cyanide,
million smokers in this country, and benzene. The roughly 3,500
and approximately 800 billion ciga- different chemicals released in the
Dr. Porter is Harry Winkler, Jr, Orthopaedic
rettes are smoked each year.1 The particulate phase include nicotine,
Surgery Research Fellow, Department of
adverse effects of smoking on the nornicotine, anatabine, and anaba- Orthopaedic Surgery, Carolinas Medical
cardiovascular system are common sine.5 Stripped of water, the partic- Center, Charlotte, NC. Dr. Hanley is Chair-
knowledge.2,3 Smoking is implicated ulate matter that remains, or “tar,” man, Department of Orthopaedic Surgery,
in the etiology of a multitude of contains the majority of the car- Carolinas Medical Center.
cancers as well.2,4 Smoking is now cinogens of cigarette smoke.6 Nico-
Reprint requests: Dr. Porter, Department of
the leading avoidable cause of mor- tine, which is considered the addic-
Orthopaedic Surgery, Carolinas Medical
bidity and mortality in the United tive component of cigarette smoke, Center, PO Box 32861, Charlotte, NC 28232.
States. According to one report, has been implicated in the patho-
more than 500,000 deaths per year genesis of a variety of diseases. 6 Copyright 2001 by the American Academy of
in the United States alone can be at- Nicotine has been shown to in- Orthopaedic Surgeons.
tributed to smoking.2 crease platelet aggregation, de-

Vol 9, No 1, January/February 2001 9

Musculoskeletal Effects of Smoking
Osteoporosis
Osteoporosis is a common finding
in postmenopausal women and
elderly men. It is a complex disor-
der that occurs earlier in life and
more often in women than in men.
Osteoporosis is characterized by a
decrease in bone mass with a resul-
tant increased risk of fractures of the
radii, femoral necks, and vertebral
bodies.9,10 Honkanen et al11 have
warned against generic compar-
isons of studies that deal with osteo-
porotic fractures. They emphasize
that the relationships between the
risk factors associated with pre-
menopausal, perimenopausal, and
postmenopausal fractures differ by
fracture type, which precludes their
general comparability.
In an early study by Daniell, 12
fractures of the weight-bearing spine
occurred more frequently in os-
teoporotic postmenopausal women
who smoked than in women of
similar age who did not smoke. He
determined that smokers had an ap-
parent cortical bone loss of roughly
1.02% per postmenopausal year,
compared with only 0.69% for non-
smokers (P<0.001). This rate in-
creased to 1.19% for nonobese osteo-
porotic women who smoked.12 A
later study by Stevenson et al13 sup-
ported the findings of Daniell by
also documenting that the vertebrae
of women who smoke have appre-
ciably less bone mass.
Many authors believe that this
increase in the rate of osteoporosis
observed in women who smoke is
mediated by the complex and often
inhibitory interaction between
smoking and estrogen. 14-18 The
effects of this interaction include
unfavorable lipid profiles, a reduc-
tion in the rate of endometrial can-
cer, earlier menopause, and reduced
rates of estrogen receptor–positive
breast cancers.16,17,19-21
Williams et al 14 showed that
smoking adversely affected women
who were not users of exogenous
10
estrogen. In their study, they dem-
onstrated an increase in the rates
of hip and forearm fractures in
postmenopausal women smokers.
However, this increase was statisti-
cally significant only for the subset
of thin women who smoked and
were not estrogen users.
In a recent prospective study of
more than 115,000 nurses, Cornuz
et al 17 demonstrated a small in-
crease (1.3%) in the risk of sustain-
ing a hip fracture in smokers and a
greater increase (1.6%) in this risk
for women who smoked more than
25 cigarettes per day. This risk
decreased to a level below that of
control subjects after smoking ces-
sation, but only after a mean of 10
years. The authors concluded that
their observed results might be
attributable to the inhibitory effects
smoking has on circulating estro-
gen. This inhibition would decrease
the protective effects of estrogen on
bone mass.
La Vecchia et al19 showed simi-
lar results in their study of over 200
women. They demonstrated that
women smokers had a 1.6% in-
crease in the relative risk of sus-
taining a hip fracture compared
with age-matched controls. This
risk increased to 2.8% for the women
who smoked more than 25 ciga-
rettes per day. A smaller subset of
women who were actively taking
hormone replacement therapy
(HRT) had a nonsignificant de-
crease in their relative risk to 0.4;
however, the authors conjectured
that the small numbers in this sub-
set may have prevented the dem-
onstration of statistical significance.
Melhus et al15 postulate that it is
the increase in reactive oxygen
intermediates, or free radicals,
found in the circulation of smokers
that is directly antagonizing to
estrogen. They were able to dem-
onstrate a nearly fivefold increase
in the relative risk of hip fractures
in smokers with a low intake of the
antioxidant vitamins C and E when
Journal of the American Academy of Orthopaedic Surgeons
compared with a control group,
after adjustment for other major
osteoporosis risk factors.
Jensen and Christiansen18 stud-
ied oral and percutaneous HRT and
the effects of smoking on these
modalities. Oral HRT resulted in a
decrease in the rate of bone loss for
nonsmokers, but this beneficial re-
sponse to oral HRT was significantly
lessened for smokers (P<0.01). In-
cidentally, they also reported that
smoking is antagonistic to the effect
of the favorable lipid profile shared
by women as a result of HRT.
Osteoporosis afflicts men as well.
Recent estimates based on bone den-
sitometry studies suggest that be-
tween 250,000 and 2,000,000 white
men have osteoporosis of the femoral
neck.22 The prevalence is roughly 1%
in white men over the age of 80.10
Grisso et al10 and Kanis et al23
have shown that many of the risk
factors for hip fractures in women
also apply to men. Specifically,
lean body mass, the absence of
physical activity, and smoking were
all associated with an increased risk
of hip fracture. The authors of the
National Health and Nutrition
Examination Survey study exam-
ined the possible risk factors for hip
fracture in more than 2,500 white
men. 22 Although the differences
failed to reach statistical signifi-
cance, the results did demonstrate
an increase in the number of hip
fractures sustained by men who
smoke. Forsén et al24 also demon-
strated increases in the relative risk
of hip fractures for smokers in their
study of 35,000 men and women
(5.0 and 1.9, respectively). Further-
more, they reported that this in-
creased risk persisted in their
subjects even if they had stopped
smoking within 5 years of the in-
ception of the study.
De Vernejoul et al25 suggest that
at the root of a decrease in bone
mineral content is a defect in os-
teoblast function that is caused by
smoking. They demonstrated a

statistically significant decrease in
trabecular volume and thickness
(P<0.05) and mean wall thickness
(P<0.001) of iliac-crest biopsy sam-
ples from smokers compared with
samples from nonsmokers. The
bone resorptive properties of these
individuals were normal. The ability
to form bone, however, was mark-
edly decreased, and this uncoupled
resorption could result in osteo-
porosis.
Galvin et al26 demonstrated this
same relationship experimentally in
a study of the effects of smokeless
tobacco. Tibias from chick embryos
were cultured in nicotine and smoke-
less tobacco extracts, and the effects
on bone glucose metabolism and col-
lagen synthesis were measured. The
authors concluded that tobacco
extracts, in concentrations found in
saliva, resulted in a nearly 25% de-
crease in oxygen consumption and
an 88% reduction in collagen synthe-
sis. This relationship between smok-
ing and osteoblast function could
explain the relationships between
smoking, osteoporosis, and altered
bone healing that many investigators
have shown.9,12,18,25,27-29
In contrast to these findings,
many other studies have not demon-
strated a relationship between smok-
ing and the risk of osteoporotic frac-
tures.9,16,24,30-33 In a recent study,
Christensen et al34 were unable to
support the conclusions drawn by de
Vernejoul et al25 implicating osteo-
blasts that have been rendered defec-
tive by nicotine as a cause of osteo-
porosis. Admittedly, the cohorts and
purposes of the two studies differed.
Nevertheless, Christensen et al found
no differences in the function of
osteoblasts harvested during postero-
lateral fusion procedures in smokers
and nonsmokers.
In the Framingham Study,33 the
authors were unable to demonstrate
a relationship between smoking and
hip fractures in either men or
women. They reexamined this rela-
tionship in a follow-up study be-
Vol 9, No 1, January/February 2001
Scott E. Porter, MD, and Edward N. Hanley, Jr, MD
cause of the large amount of data
that suggested some type of an
association.9,10,12,13,16,17 They specifi-
cally focused their efforts on women
and were once again unable to
prove a statistically significant dif-
ference between smokers and non-
smokers who were not receiving
oral HRT. This was true regardless
of the number of cigarettes smoked.
There was a trend toward increased
fracture rate in the heavy (>20 ciga-
rettes per day) smokers, but this did
not reach statistical significance.
When they stratified the smokers
and nonsmokers by their HRT histo-
ry, however, the women who had
used HRT and were currently smok-
ing had a substantially greater risk
of sustaining a hip fracture com-
pared with women who had never
smoked (adjusted odds ratio, 3.44).16
This, too, could be explained by the
adverse effects of nicotine on estrogen.
Hemenway et al32 examined the
data on 96,000 women in a prospec-
tive study and found no difference in
the rates of hip and forearm fractures
in smokers and nonsmokers. The
authors postulated that the relatively
young age of the subjects, which
ranged from 35 to 59 years, might
have influenced the results. In sepa-
rate studies, Hemenway et al30,31 also
looked at the rates of hip and wrist
fractures in men. The researchers
were unable to find a correlation
between smoking and an increase in
the rates of these fractures. Again,
the authors noted that the subjects in
this study were young, with ages
ranging between 44 and 75 years.
Most of the 50,000 men who partici-
pated were less than 70 years of age.
Furthermore, very few (<3%) of the
subjects in one study were heavy
smokers.30
Low Back Pain
Causal Link
Low back pain is a very com-
mon complaint that can be costly in
time, money, and resources for the
patient, the physician, and society
as a whole. Studies indicate that in
the Western world, 60% to 80% of
the population will have an epi-
sode of incapacitating low back
pain at some point during their
lives. Fortunately, 80% to 90% of
these persons will return to being
functional within a period of 4 to 8
weeks and will not experience
long-term disability. However, in
some individuals, the condition
will progress to become chronic
low back pain. 35-38 A study con-
ducted in The Netherlands demon-
strated that as much as 1.5% of the
Gross National Product was spent
on patients with low back pain.
Surprisingly, only 3% of that cost
was actually medically related; the
remainder of the costs were for
such work-related events as leaves
of absence, early retirements, and
job changes.39
In the recent era of antismoking
campaigns waged by health advo-
cates and lobbying groups, smok-
ing has come under fire from the
orthopaedic community as being a
possible cause of low back pain.
There has been scientific evidence
to both support and refute this
notion.
The findings from several epi-
demiologic studies have suggested
an association between smoking
and low back pain.35,36,40-52 Using
questionnaires, Frymoyer et al49,52
determined that low-back-pain
sufferers were likely to be cigarette
smokers (P<0.001), particularly
when smoking was accompanied
by a chronic cough (P<0.001). The
authors postulated that the chronic
cough of smokers might adversely
affect intradiskal pressure, causing
the symptom of low back pain. Al-
ternatively, smoking or one of the
ingredients within cigarette smoke
may directly and unfavorably af-
fect the spine. Later studies by
Symmons et al51 and Kelsey et al,53
however, were unable to support a
11
Musculoskeletal Effects of Smoking
link between chronic cough and
low back pain.
Svensson et al54 determined that
there was a weak relationship be-
tween smoking and low back pain,
but found other variables with a
stronger relationship to low back
pain, such as calf pain on exertion,
the degree of physical activity at
work, and worry or tension. With
the exception of the latter, all of
these findings are common to other
smoking-related diseases, such as
heart disease and peripheral vascu-
lar disease.2,3
Smoking may simply be an indi-
cation of poor health and lifestyle
more than a direct cause of low
back pain. Biering-Sørensen and
Thomsen55 felt that although there
is an apparent causal relationship
between cigarette smoking and low
back pain, it is not as strong as ini-
tially suggested. In nearly 1,000
subjects, they found that the contri-
bution of smoking to the develop-
ment of low back pain was statisti-
cally significant (P<0.05), but that it
had no significance as a risk factor
for recurrent or persistent low back
pain. Moreover, they postulated
that it might not necessarily be
smoking that contributes to low
back pain, but rather poor general
health.
In a study by Cox and Trier,41 it
was found that smokers were much
more likely to have low back pain
and were more likely to exclude
exercise from their daily routine.
This finding was echoed by Deyo
and Bass, 42 who suggested that
smoking might be indicative of a
complex interaction of personal and
social traits that together are associ-
ated with the increased risk of low
back pain purported to occur in
smokers.
The complex etiology of low
back pain is supported by the work
of Heliövaara et al.50 In their study
of over 5,500 subjects, they demon-
strated a weak relationship between
smoking and low back pain and
12
proposed that the risk of low back
pain seems to be better determined
by the overall quality of one’s work,
lifestyle, and health behavior.
Notably, they showed differences in
the association between smoking
and low back pain in groups gener-
ated by sex, age, and quantity of
cigarettes smoked. The relationship
was strong in men aged 50 to 64
who smoked 20 cigarettes a day or
more (odds ratio, 1.9). Interestingly,
in women aged 30 to 49, there was
no association with any quantity of
cigarettes smoked (odds ratio, 1.0).
Moreover, this apparent dichotomy
was reversed for women aged 50 to
64 years. In this age group, the
women who smoked more than 20
cigarettes a day had an odds ratio
for the development of low back
pain of 2.7. 50 This suggests that
there may be some type of protection
conferred on younger women. This
protection can also be appreciated in
relation to cardiovascular disease.2
Boshuizen et al44 suggest that the
link between smoking and low back
pain may never be fully elucidated.
Leboeuf-Yde and co-workers con-
ducted several studies to evaluate
the relationship between smoking
and low back pain. 46-48,56 Their
most recent study surveyed a popu-
lation of 29,424 twins and found an
association between smoking and
low back pain (odds ratio, 2).47 The
odds ratio increased to 3 for the
group of subjects with long-standing
(>30 days) complaints of low back
pain. Furthermore, the cessation of
smoking did not reverse these find-
ings. More important were the find-
ings in a large group of monozygotic
twins who were discordant in their
smoking histories (264 pairs of iden-
tical twins composed of a smoking
and a nonsmoking sibling). There
was no difference in the prevalence
of low back pain in the chronic-
smoker group compared with their
siblings in the nonsmoker group.
This supports earlier work by Battié
et al57 on a much smaller sample of
Journal of the American Academy of Orthopaedic Surgeons
identical twins. The large popula-
tion size in the study by Leboeuf-
Yde et al47 also allowed a critical look
at the possibility of a dose response
between total cigarette consumption
and degree of low back pain. It was
obvious from their data that this rela-
tionship did not exist. This contra-
dicts the earlier work by Frymoyer
et al,49 Heliövaara et al,50 and Kelsey
et al.53
Although these findings may
appear to refute any biologic or
causal link between smoking and
low back pain, there is still a wealth
of epidemiologic, circumstantial,
and anecdotal evidence supporting
the earlier claims that smoking has
adverse effects on the lumbar spine.
Furthermore, some cases of low
back pain have recognizable etio-
logic factors that may be linked to
smoking.50,57-59
Disk Disease
Lumbar disk disease and hernia-
tion has become a popular diagno-
sis in cases of low back pain, in part
because a potential cure can be
sought with surgical intervention.58
Some authors believe that smoking
adversely affects the intervertebral
disks, predisposing patients to disk
disease and low back pain. 45,53,60
Ernst45 believes that the interverte-
bral disks are “malnourished” due
to many of the vascular and hema-
tologic changes that result from
long-term smoking. He postulates
that tissues such as the vertebrae
and vertebral disks have a tenuous
blood supply and are not able to
compensate for the decrease in
blood flow that occurs in the micro-
vasculature of chronic smokers.
Over time, the diffusion capacity for
the delivery of oxygen and nutrients
becomes insufficient, leaving the in-
tervertebral disks more vulnerable
to insults.45
Kelsey et al 53 determined in
their epidemiologic study that ciga-
rette smoking in the year prior to a
patient’s presentation to a physi-

cian increased the risk of having a
prolapsed disk (odds ratio, 1.7).
Furthermore, they discerned a
weak dose response for smoking
and the subsequent risk of disk pro-
lapse; for every 10 cigarettes that
were smoked per day, the risk of
having a prolapsed disk increased
by 20%.
Hanley and Shapiro 61 deter-
mined that a smoking history
longer than 15 years was an impor-
tant factor in determining the post-
operative success of lumbar diskec-
tomies performed to treat severe
radiculopathies. They postulate
that the persistent back pain after
the procedure may be a manifesta-
tion of the vascular effects of nico-
tine. Furthermore, the metabolic
changes within the disk may render
it more susceptible to mechanical
problems.61
Battié et al 57 examined differ-
ences in magnetic resonance (MR)
imaging studies of the lumbar
spines of identical twins who were
highly discordant in their smoking
histories. They found no differences
in the reported rate of occurrence of
low back pain between the smok-
ing and nonsmoking groups but
did demonstrate a difference in the
disk degeneration scores (based on
MR imaging criteria) used to evalu-
ate the intervertebral regions of the
two groups.
Stronger evidence comes from
An et al.60 In their study, the rates
of smoking in a population of pa-
tients with surgically confirmed cer-
vical or lumbar disk disease were
examined. The relative risk values
for lumbar and cervical disk disease
for smokers were 2.2 (P = 0.00029)
and 2.9 (P = 0.0025), respectively.
When the authors excluded those
patients who had recently quit
smoking from the “smokers” group,
the relative risks increased to 3.0
and 3.9, respectively. They demon-
strated that the association between
cigarette smoking and documented
disk disease, not just the subjective
Vol 9, No 1, January/February 2001
Scott E. Porter, MD, and Edward N. Hanley, Jr, MD
complaint of low back pain, is quite
significant. Continued smoking in
light of these problems could actually
worsen the diskogenic or radicular
symptoms that accompany disk
disease.
So how does smoking exert these
changes in the intervertebral disks
that render them more susceptible
to disease? As stated earlier, Ernst45
believes that the macrovascular and
microvascular changes that occur in
smoking may affect the blood sup-
ply around intervertebral disks.
The decreased blood flow renders
the disks susceptible to pathologic
changes.
The study by Battié et al57 sup-
ports this notion. In that study, the
authors used MR imaging to evalu-
ate disk integrity in pairs of identi-
cal twins discordant in their smok-
ing histories. Although there was
no difference in complaints of low
back pain, the mean score for lum-
bar spine disk degeneration was
18% higher for the smokers (P =
0.015). Furthermore, because their
results demonstrated involvement
of the entire lumbar spine, the au-
thors postulated that the mecha-
nism of action must be systemic.
In a recent article, Newby et al3
showed that smoking has dramatic
adverse effects on the endogenous
fibrinolytic capacity of the vascular
endothelium of smokers, leading to
a systemic increase in the risk of
atherothrombotic disease or micro-
vascular occlusive disease. Jayson
and co-workers62-64 have performed
several studies demonstrating that
a decrease in fibrinolytic activity is
common in many chronic back pain
syndromes. It is feasible that this
mechanism is active in a large num-
ber of patients who smoke and
have low back pain. It is also feasi-
ble that this is a mechanism that
results in the local hypoperfusion of
the lumbar spine, as well as the
alterations in disk metabolism that
some authors believe occur in
smokers.3,45,60-64
Wound Healing
The effects of cigarette smoking on
soft-tissue wound healing, skin
physiology, and the complex vari-
ables that control these entities
have been studied by several groups
of researchers. In a review by
Leow and Maibach, 8 most of the
studies analyzed showed a de-
crease in cutaneous blood flow in
subjects exposed to nicotine or cig-
arette smoke. Jensen et al65 noted
an acute decrease in the subcuta-
neous tissue oxygen tension in the
forearms of subjects after smoking
cigarettes. The authors attributed
these effects to the pharmacologic
actions of nicotine.
In 1977, Mosely and Finseth 66
were among the first to demonstrate
that smoking impairs wound heal-
ing in the soft tissues of the hand.
They postulated that the vasocon-
striction and moderate blood levels
of carbon monoxide secondary to
smoking could retard proper wound
healing, especially in the extremi-
ties. It was noted that severe digital
vasoconstriction can occur after
smoking a single cigarette. The fol-
lowing year, they demonstrated that
systemic nicotine given to rabbits re-
sulted in decreased wound healing
in an established rabbit-ear injury
model.67
Several authors have noted
changes in the blood flow and oxy-
gen tension of the cutaneous and
subcutaneous tissues that can be
related to smoking.8,65-67 Forrest et
al68 specifically examined the skin
hemodynamics of random-pattern
skin flaps from rats that had been
given either low-dose or high-dose
subcutaneous nicotine for the 24
weeks prior to a surgical procedure.
The capillary blood flow and distal
perfusion were lessened in these
animals, resulting in flaps with a
much smaller area of viability.
When the nicotine was withheld
during the 2 weeks before surgery,
the hemodynamics of the skin flaps
13
Musculoskeletal Effects of Smoking
returned to near-control levels.
Nolan et al69 and Lawrence et al,70
in separate studies, also showed
that the survival of skin flaps in rats
exposed to a cigarette smoke–filled
environment was appreciably less
than the survival of skin flaps in
control rats.
Abidi et al71 demonstrated a dif-
ference in wound healing after open
reduction and internal fixation of
calcaneal fractures in smokers who
either were or were not allowed to
smoke perioperatively. A major
complication associated with this
surgery is poor healing of the lateral
surgical wound; although the differ-
ence was not statistically significant,
the authors noted that those who
continued to smoke perioperatively
had prolonged wound healing times.
Nicotine has been shown to me-
diate many other actions within the
body. In their review, Sherwin and
Gastwirth1 note that the prolifera-
tion of cells within the extracellular
matrix and the process of epithelial
regeneration are decreased by the
damaging effects of nicotine and
carbon monoxide. In a prospective
human trial, Jorgensen et al7 showed
that collagen synthesis was hin-
dered in the wounds of those sub-
jects who smoked more than a pack
per day compared with the matched
nonsmoking group. Mature colla-
gen is the main determinant of the
tensile strength in a healing wound,
and its assembly is dependent on
sufficient perfusion and oxygena-
tion. The authors concluded that
wound healing is definitely impeded
by smoking.
It is believed by many that this
interference with the natural process
of wound healing may lead to higher
rates of postoperative wound infec-
tions in smokers. Calderone et al72
determined that the additional costs
involved in treating deep postopera-
tive spinal infections could increase
the total cost of caring for a patient by
more than four times. Capen et al73
included smoking as a preoperative
14
risk factor for postoperative wound
infections after lumbar fusion.
Thalgott et al 74 retrospectively
reviewed the cases of 32 patients in
order to develop a classification
scheme for identifying populations
at risk for postoperative spinal
wound infections and for guiding
therapy. In their classification
scheme, cigarette smokers, patients
with systemic diseases, and immu-
nocompromised patients are con-
sidered to be at high risk for post-
operative wound infections. In the
group of patients who sustained an
infection after elective spinal fusion
and instrumentation, 90% were cig-
arette smokers. Furthermore, the
only patients to have a superficial
or deep infection worsen to an in-
fection that included myonecrosis
were heavy smokers. The findings
of these authors led them to con-
clude that patient smoking is a con-
trollable variable that should be
stopped in the perioperative period.
Fracture Healing
In addition to its effects on the soft
tissues and vasculature of the body, it
is believed that cigarette smoking
also retards the healing of bone.
Silcox et al75 reported that union did
not occur in the lumbar spines of rab-
bits after a single-level lumbar fusion
with use of autologous iliac-crest
bone graft if the rabbits were subse-
quently exposed to systemic nicotine.
Cobb et al76 evaluated the rela-
tive risk of nonunion in smokers
versus nonsmokers in a case-control
study. Although they had a rela-
tively small study group, and their
results only approached statistical
significance, they demonstrated that
the relative risk of progression to a
nonunion after ankle arthrodesis
was 16 times greater for smokers
than for nonsmokers.
Brown et al77 reported that the
pseudarthrosis rate for lumbar ar-
throdesis in 50 of their patients
Journal of the American Academy of Orthopaedic Surgeons
approached 40%. The rate for the 50
nonsmokers in that study was only
8%. Carpenter et al78 furthered the
work presented by Brown et al and
reported that the outcomes of repeat
procedures for pseudarthrosis that
developed after an attempted local
arthrodesis of the lumbar spine
were significantly more favorable
for nonsmokers (P = 0.02). Patients
who stopped smoking also had a
better mean outcome score and
were more likely to return to work
than those who continued to smoke.
These findings have led several inves-
tigators to recommend periopera-
tive cessation of smoking as a gener-
al measure to improve the outcome
of surgical procedures.1,7,71,79,80
De Vernejoul et al25 have identi-
fied a possible explanation for these
findings. They demonstrated that
smoking impairs osteoblast func-
tion in osteoporotic individuals.
The quantity of bone resorbed re-
mained normal, but the rate of bone
formation was decreased. This
could result in the defective healing
response demonstrated clinically in
the previously mentioned studies.
Campanile et al80 suggest that the
effects of smoking are mediated by
the vasoconstrictive and platelet-
activating properties of nicotine, the
hypoxia-promoting effects of car-
bon monoxide, and the inhibition of
oxidative metabolism at the cellular
level by hydrogen cyanide.
There are no conclusive studies
that have generated definite guide-
lines about perioperative cessation
of smoking. Campanile et al80 note
that suggestions range from 1 day
to 3 weeks preoperatively and from
5 days to 4 weeks postoperatively.
Sherwin recommends that smoking
be stopped at least 12 hours before
surgery because it takes the body
roughly this amount of time to clear
the carbon monoxide.1 Abidi et al71
noted that cessation of smoking 5
days before surgical procedures had
a favorable outcome on subsequent
wound healing. Lind et al81 recom-

mend 1 week of cessation, on the
basis of the pharmacokinetics of free
radicals and thrombotic compo-
nents. Mosely et al67 demonstrated
that healing was impaired for a
period of 4 to 10 days after wound
creation in rabbits. After 12 days, the
wounds of rabbits either exposed or
not exposed to nicotine contracted at
nearly the same rate.
Whitesides based his recommen-
dations concerning perioperative
smoking on studies showing that a
nonsmoker can make 1 cm of bone
in 2 months, but that it takes a smok-
er an average of 3 months to make
the same amount of bone. 82 He,
therefore, feels that it is not prudent
to perform elective spinal surgery on
smokers unless they demonstrate
abstinence from smoking for a period
of 60 days. In contrast, Hanley of-
fers the argument that many of the
effects of chronic smoking are irre-
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17
 Displaced Acetabular Fractures: Indications for
Operative and Nonoperative Management

Paul Tornetta III, MD

Abstract

Displaced acetabular fractures are a challenging problem. In contradistinction atic nerve is damaged in as many
to most conditions in which surgery is based on specific operative indications, as 20% of acetabular fractures
displaced acetabular fractures should be considered an operative problem unless affecting the posterior wall or col-
specific criteria for nonoperative management are met. These include a congru- umn, 1-3 the motor and sensory
ent hip joint on the anteroposterior and oblique (Judet) radiographs, an intact function of the extremity must be
weight-bearing surface (as defined by roof arc and subchondral arc measure- carefully documented. In particu-
ments on computed tomographic scans), and a stable joint. The final decision lar, because the peroneal division is
about the treatment method must also consider the patient’s functional most at risk, foot dorsiflexion and
demands, expectations, and physical condition and the physician’s experience eversion must be tested.
and institutional support for dealing with this type of injury. Displaced both- Closed soft-tissue injuries may
column fractures with secondary congruence may have better results than other occur about the hip region, especial-
displaced fractures. In older patients, nonoperative management may be effec- ly over the trochanter. A closed
tively utilized. Understanding the current criteria for effective use of nonopera- degloving injury is referred to as a
tive treatment will help the surgeon make these difficult decisions. “Morel-Lavallee lesion.” The sero-
J Am Acad Orthop Surg 2001;9:18-28 sanguineous fluid collections that
develop in these cavities are culture-
positive in as many as 31% of cases.4
If this injury pattern is discovered,
Displaced acetabular fractures are experience. As with all surgical pro- irrigation and debridement of these
among the most complex injuries cedures, the potential benefits of areas should be performed, and
that the orthopaedic surgeon has to surgery must be weighed against internal fixation should be delayed
manage. This is in part because their risks. until the area is clean.4
they are uncommon; a surgeon may Plain-radiographic assessment
encounter only one or two such inju- of a patient with an acetabular in-
ries per year. In cases of polytrauma, Evaluation jury begins with the five standard
associated musculoskeletal, neuro-
logic, and soft-tissue injuries may After the emergent resuscitation of
complicate evaluation and treat- the trauma patient who potentially
ment. The anatomic complexity of has an acetabular fracture, the ortho- Dr. Tornetta is Associate Professor and Vice
the acetabulum and pelvis, along paedic surgeon is generally con- Chairman, Department of Orthopaedic Sur-
gery, Boston University School of Medicine,
with the difficulty of accurately sulted. Initial assessment includes Boston, Mass; and Director of Orthopaedic
defining and classifying the fracture a careful physical examination and Trauma, Department of Orthopaedics, Boston
pattern, makes treatment decisions review of relevant radiographs. A Medical Center.
even more challenging. physical examination focusing on
The decision between surgical the acetabular injury should in- Reprint requests: Dr. Tornetta, Department of
and nonsurgical management is clude a well-documented, complete Orthopaedics, Boston Medical Center, Dowling
2 North, 818 Harrison Avenue, Boston, MA
often not a black-and-white issue. neurologic assessment of the pelvis 02118.
Many factors must be considered, and lower extremity, evaluation of
including the fracture pattern, indi- the soft tissues in the trochanteric Copyright 2001 by the American Academy of
vidual patient factors, institutional and gluteal regions, and the resting Orthopaedic Surgeons.
facilities and support, and surgeon position of the leg. Because the sci-

18 Journal of the American Academy of Orthopaedic Surgeons


views of the pelvis: anteroposte-
rior (AP), iliac oblique, obturator
oblique, inlet, and outlet. These
views will delineate associated
pelvic fractures, femoral head in-
jury, and hip dislocations. The
standard AP radiograph is usually
sufficient for recognition and clas-
sification of an acetabular fracture.
However, the 45-degree oblique
(Judet) views are needed to fully
characterize the fracture and to
determine whether there is sublux-
ation of the hip joint, which may
not be visible on the AP view. The
obturator oblique view is taken
with the affected side of the patient
rotated 45 degrees forward. This
allows clear visualization of the
anterior column in the region of the
hip, the posterior wall, and any
posterior subluxation of the hip.
The iliac oblique view is taken with
the unaffected side of the patient
rolled 45 degrees forward. This
view profiles the posterior column
from the notch to the ischium and
the anterior wall, which is curvilin-
ear and shallower than the posterior
wall. The inlet and outlet pelvic
radiographs may depict pelvic in-
juries that would affect the man-
agement of the acetabular fracture.
Occasionally, anterior sacroiliac
joint widening is present with
transverse and both-column ace-
tabular fractures, which may be
difficult to appreciate on the stan-
dard AP view.
A computed tomographic (CT)
study with 1.5- or 2-mm sections
through the affected area of the
acetabulum allows more precise def-
inition of the fracture than is possi-
ble with plain radiography. Two-
dimensional and three-dimensional
reconstructions of the fracture often
help in understanding the rotational
deformities of the displaced frac-
tures but are not necessary for deci-
sion making or operative planning.
In fact, volume-averaging, along
with the reconstructive technique,
may mask fractures that are not
Vol 9, No 1, January/February 2001
markedly displaced. The informa-
tion commonly available from the
standard radiographic series allows
classification of the fracture and
definition of many associated vari-
ables affecting outcome.
The classification of acetabular
fractures was standardized by
Letournel.5 He described five ele-
mental and five complex (associated)
fracture patterns (Fig. 1). The frac-
ture pattern has relevance to treat-
ment alternatives and prognosis.
Determinants of Outcome
Clinical outcome after treatment of
an acetabular fracture is related to
many factors. Some of these fac-
tors, such as comorbidities and
bone quality, are present before
injury. Others, such as the fracture
pattern, injury to the cartilage sur-
face of the acetabulum or the fe-
moral head, vascularity of the head,
and neurologic impairment, are
determined at the time of injury.
Still others, such as the accuracy of
final reduction of the roof of the
acetabulum and the stability of the
hip, are established at the time of
treatment. In addition, surgical
complications may have a profound
effect on outcome.
Fracture Location
More than 30 years ago, Rowe
and Lowell6 recognized the prog-
nostic importance of displaced frac-
tures affecting the roof of the ace-
tabulum. As the art of acetabular
fixation became more advanced
and fracture classification became
standardized, the guidelines for
assessment and determination of
which fractures may benefit from
surgery were developed.
Matta began this process with the
description of roof arc measurements
that describe the location of the
main-column fracture lines in rela-
tion to the roof of the acetabulum.7
These measurements are relevant
Paul Tornetta III, MD
only if there is no subluxation of the
hip. Three roof arc measurements
are made, one each from the AP,
obturator oblique, and iliac oblique
radiographs of the acetabulum. Each
arc is generated by measuring the
angle between a vertical line from
the center of the nonsubluxated
femoral head and a line from the
center of the head to the point where
the fracture enters the joint. If the
fracture does not enter the joint on
one of the views, the angle cannot be
measured, and the joint in that view
is considered intact. With larger
arcs, the fracture is farther away
from the roof of the acetabulum. For
example, in the case of a transverse
fracture, a roof arc of 10 degrees
measured on the AP radiograph
places the fracture almost directly
above the femoral head; a 90-degree
arc indicates that the fracture is low
and does not affect the roof. Dis-
placed fractures that affect the roof,
or weight-bearing surface, of the
acetabulum, do not have outcomes
comparable to those that do not
affect this area. However, the precise
area of the acetabulum that must
remain intact to allow a good func-
tional result with nonoperative treat-
ment of a displaced acetabular frac-
ture remains unknown.
The use of roof arc measurements
as a means to decide between opera-
tive and nonoperative management
has evolved since their original
description. The minimum roof arc
that is required to consider nonoper-
ative management has varied be-
tween 20 degrees and 45 degrees,
but the value currently considered
most appropriate is 45 degrees.
In subsequent work, Olson and
Matta8 described the CT correlate of
having 45-degree roof arc measure-
ments on all three views of the
acetabulum. This is called the CT
subchondral arc and is defined as
the subchondral ring of the acetabu-
lum 10 mm inferior to the subchon-
dral bone of the roof. By mathemat-
ical derivation, it was determined
19
Displaced Acetabular Fractures

A B C D E

F G H I J

Figure 1 The Letournel classification of acetabular fractures. A, Posterior-wall fracture. B, Posterior-column fracture. C, Anterior-wall
fracture. D, Anterior-column fracture. E, Transverse fracture. F, Associated posterior-column and posterior-wall fractures. G, Associated
transverse and posterior-wall fractures. H, T-shaped fracture. I, Associated anterior-column and posterior hemitransverse fractures.
J, Both-column fracture. (Adapted with permission from Matta J: Surgical treatment of acetabulum fractures, in Browner B, Jupiter J,
Levine A, Trafton P [eds]: Skeletal Trauma. Philadelphia: WB Saunders, 1992, pp 899-922.)

that if the fracture of the acetabulum
does not break this ring, then the
roof arcs must be greater than 45
degrees as measured on the three
standard views (Fig. 2). Olson and
Matta reported that early onset of
radiographic evidence of arthritis
and poor clinical results correlate
with (1) displacement present at the
time of union within the weight-
bearing dome, (2) any roof arc mea-
surement less than 45 degrees, or (3)
a broken CT subchondral arc of the
acetabulum. The subchondral CT
arc should be used only in conjunc-
tion with the standard radiographic
views, as fractures in the plane of
the CT scan may be missed if CT is
the only modality utilized.
Hip Stability
In addition to the location of the
fracture, the stability of the hip joint
affects outcome. A fracture pattern
that results in subluxation of the hip
joint increases the stress on the artic-
ular cartilage in the area adjacent
to the fracture.9 Radiographically,
subluxation manifests itself as an
incongruity between the head and
the roof, which is described as a lack
of parallelism.5 Good or excellent
clinical results are obtained after
treatment of fewer than 50% of frac-
tures in which the head is not con-
gruent with the roof after surgery,
and more than 60% of these hips
will develop arthritis.5 Subluxation
is most often manifested by a lack of
congruence of the femoral head
with the roof, but it can also take the
form of dynamic instability. In par-
ticular, certain posterior wall frac-
tures may allow dynamic hip sub-
luxation, leading to femoral-head
wear and joint degeneration.
Posterior-wall fractures cannot
be assessed by using roof arc mea-
surements, as they are outside the
planes of measurement. Radiographic
assessment is best performed with
CT, which demonstrates not only
the portion of the posterior wall
affected but also the degree of mar-
ginal impaction that is associated
with the injury10,11 (Fig. 3). Several
authors have sought to describe the
amount of the posterior wall that is
necessary to maintain hip stability,
and a number of measurement tech-
niques have been employed, in-
cluding the use of radians and lin-
ear measurements.12-14 The easiest
method for measuring the amount
of posterior wall affected is to di-
vide the length of the intact articu-
lar surface on the affected side by
that of the normal side on a CT sec-
tion obtained at the same level to

20 Journal of the American Academy of Orthopaedic Surgeons


determine a ratio. Areas of mar-
ginal impaction are considered to
be displaced. These measurements
are not necessary if any subluxa-
tion is visible on the CT scan, as
clinical instability has then already
been demonstrated. As a general
rule, dynamic clinical instability
exists in fractures affecting more
than 40% of the posterior wall,
while those affecting less than 20%
of the wall are stable. 12-14 How-
ever, instability has been reported
when as little as 15% of the wall is
affected.15
In those patients with fractures
affecting less than 40% of the poste-
rior wall, including marginal im-
paction, 15,16 a fluoroscopic stress
view of the hip can be obtained.
With the patient supine on the table
and under general or regional anes-
thesia, the hip is viewed fluoro-
scopically while it is brought into
flexion. The relationship of the
head to the roof is observed. Any
widening of the joint space indi-
cates instability in the AP view. If
the hip is stable in flexion, a posteri-
orly directed stress is applied that is
2 cm
45°
Figure 2 Having roof arc measurements
of 45 degrees on all three views of the
acetabulum is equal to having an intact CT
subchondral ring located 10 mm below the
subchondral bone of the acetabular roof.
(Adapted with permission from Olson SA,
Matta JM: The computerized tomography
subchondral arc: A new method of assess-
ing acetabular articular continuity after
fracture [a preliminary report]. J Orthop
Trauma 1993;7:402-413.)
Vol 9, No 1, January/February 2001
of sufficient force to rock the pelvis.
Again, the relationship of the head
to the roof is analyzed. The stress
view may be saved on the screen
and compared with the normal side
if there is any question about insta-
bility. This is repeated in the obtu-
rator oblique projection. Even if the
hip is stable, fractures that affect
only 33% of the wall have been
shown to increase the contact stress
in the roof of the acetabulum,
which may lead to posttraumatic
arthritis in the long term.9
Other Factors
The clinical outcome of patients
with acetabular fractures is affected
by many factors other than the frac-
ture pattern and hip stability. These
include neurologic injury, cartilage
injury, and osteonecrosis. Regard-
less of the treatment method, any of
these factors may result in a poor
clinical outcome. Neurologic injury
as a consequence of the accident may
be permanent, especially if there is a
complete injury. 17 Sciatic nerve
palsies most commonly result in a
foot-drop. Although the peroneal
division is most frequently injured, a
dense (complete) palsy may occur.
Direct cartilage injury may affect
either the acetabulum or the fe-
moral head. At this time, there is
no effective treatment for cartilage
lesions. The degree of cartilage in-
jury may affect the clinical outcome
even if there is an anatomic reduc-
tion. 5,18-25 Matta 21 demonstrated
that cartilage injury to the femoral
head visible on gross visual inspec-
tion is a risk factor for arthritis even
with an excellent reduction.
Osteonecrosis of the femoral
head may occur after hip disloca-
tion or fracture-dislocation. Al-
though immediate reduction of the
hip may decrease the rate of osteo-
necrosis, the patient is at risk for as
long as 5 years after injury.16 Dam-
age to the blood supply of the fem-
oral head may also occur during
surgery, increasing the risk of osteo-
Paul Tornetta III, MD
Figure 3 CT section of a nondisplaced
transverse and posterior-wall fracture
demonstrates that the femoral head is sub-
luxated and clarifies the area of impaction
(arrows). No articular surface of the poste-
rior wall remains intact.
necrosis. The degree of femoral
head involvement is quite variable,
and the effect on patient outcome
correlates with the size of the avas-
cular segment and its location. Os-
teonecrosis may also affect acetabu-
lar fragments, particularly small
posterior wall fragments without
soft-tissue attachments.5 This may
lead to loss of stability, followed by
femoral-head wear and joint degen-
eration.
Surgical Treatment
Surgical management of acetabular
fractures is technically demanding
and has many potential complica-
tions. The goal of surgery is to ac-
curately restore the anatomic con-
figuration of the joint surface, as
well as congruence and stability of
the hip joint, while avoiding com-
plications. The results after surgery
correlate most closely with the
quality of the reduction.7,21,23,26 At
an average of 6 years after injury,
the clinical results in patients with
fractures reduced to less than 1 mm
of displacement are superior to
21
Displaced Acetabular Fractures
those in patients with 1 to 3 mm of
displacement.21 A review of a num-
ber of series showed that even in
the most experienced hands, reduc-
tions to within 1 mm of the normal
anatomic relationship are obtained
in only 55% to 75% of cases.5,7,11,20-27
In the same series, reductions with
less than 3 mm of fracture displace-
ment and a congruent hip joint were
obtained in nearly 90% of cases. It
should be noted, however, that there
has been no study that evaluated the
precision or accuracy of these preop-
erative and postoperative measure-
ments made on plain films.
Factors Affecting Surgical
Reduction
Many factors affect the quality of
a surgical reduction, with the experi-
ence of the surgeon being one of the
most important. This is a difficult
factor to examine because the excel-
lent results reported in the large
series of operatively treated acetabu-
lar fractures come from surgeons
with significant experience. One re-
port, however, describes the results
in 49 patients treated by nine sur-
geons over a 10-year period.28 At an
average of 38 months, poor radio-
graphic results were present in 40%
of the hips, and poor clinical results
in 38%. In the largest reported
series, Letournel described his learn-
ing curve by 4-year intervals. For
acute fractures, the rate of imperfect
reductions fell from 32% to only 10%
as his experience increased.5
The timing of surgery also has a
bearing on the surgeon’s ability to
obtain an accurate reduction. The
mobility of the fracture decreases
with time from injury. Brueton29
reported that the average time to
surgery for fractures with an ac-
ceptable reduction was 11 days,
whereas for unacceptable reduc-
tions the time to surgery was 17
days. 10 Likewise, Letournel re-
ported an anatomic reduction rate
of only 52% in fractures that were
operated on more than 21 days from
22
the time of injury, despite the fact
that almost half of the fractures
were the posterior-wall type.5 Fur-
thermore, he reported that 40% of
fractures seen more than 4 months
after injury were not reconstructible.
The ability to achieve an anatomic
reduction is also affected by the
fracture pattern. The more complex
the pattern, the more difficult it is
to reduce the fracture. The degree
of comminution and the classifica-
tion affect the surgeon’s ability to
reduce a given fracture. In a series
of 262 patients, Matta 21 reported
that 96% of elemental fractures
were anatomically reduced, com-
pared with only 64% of complex
types. In Letournel’s series, ana-
tomic reductions were obtained in
94% of posterior-wall fractures but
only 61% of both-column fractures.5
The worst outcomes, as judged
by accuracy of reduction, are seen
in those patients who require a re-
vision after the initial surgical pro-
cedure resulted in a malreduction.
In one series of 64 patients, only
29% of fractures seen after 3 months
could be anatomically reduced, and
significant chondral injury of the
femoral head was present in 44%.23
Risks
Potential complications must be
carefully considered when contem-
plating surgical treatment. It must
also be borne in mind that the risks
of surgery vary inversely with the
level of experience of the surgeon.28
Injury to the sciatic nerve occurs
most commonly when fractures
are fixed through a posterior ap-
proach.1-3,28 The peroneal division
is most at risk. Careful attention to
intraoperative sensory and motor
pathway monitoring may provide
an early warning that the nerve is
under tension, and thereby de-
crease the incidence of permanent
iatrogenic injury.1,2 However, sev-
eral experienced surgeons have re-
ported iatrogenic nerve injuries in
only 2% of cases without the use of
Journal of the American Academy of Orthopaedic Surgeons
monitoring3; this rate is as low as
the reported rates when nerve mon-
itoring is used. Thus, monitoring
may be useful for less experienced
surgeons, but may not be as neces-
sary for more experienced surgeons.
Range of motion of the hip may
be diminished postoperatively if
heterotopic ossification develops.
The occurrence of heterotopic ossifi-
cation has been reported in as many
as 80% of patients with acetabular
fractures fixed through a posterior
approach. 28,30 Factors that have
been associated with the formation
of heterotopic ossification include
male gender, the use of an extensile
approach or trochanteric osteotomy,
or the presence of extensive cartilage
injury, T-shaped fracture, or con-
comitant abdominal, chest, or head
injury.31,32 In most cases, the devel-
opment of heterotopic ossification
does not markedly restrict hip mo-
tion. Indomethacin and low-dose
radiation therapy have both been
shown to be effective in reducing the
incidence of clinically important het-
erotopic ossification.30-33 Most sur-
geons now use some form of pro-
phylaxis when performing internal
fixation through a posterior or exten-
sile approach. Despite this, clinically
significant heterotopic ossification
may develop in as many as 5% of pa-
tients; some may require additional
surgery to regain hip motion.28,31
Infection after acetabular surgery
has been reported to occur in 2% to
5% of patients.5,7,11,22,25,26,28,34 How-
ever, Kaempffe et al28 reported an
infection rate of 12% in a multisur-
geon series in which each surgeon
performed only a few cases. The
presence of soft-tissue injury, such
as a Morel-Lavallee lesion, increases
the risk of infection.4,5 Infection may
be intra-articular or extra-articular,
depending on the approach used.
Extra-articular infections occur after
indirect reduction of the joint, most
commonly after an ilioinguinal
approach. Intra-articular infections
may destroy the articular surface of

the joint and make salvage difficult,
whereas extra-articular infections
usually allow preservation of the
joint.
The complications of infection,
heterotopic ossification, and neuro-
logic injury are emphasized because
of their potentially catastrophic effect
on outcome. The most common com-
plication after surgical treatment of
acetabular fractures, however, is ar-
thritis. Arthritis is a radiographic
diagnosis and is present in 15% to
45% of acetabular fractures followed
for more than 5 years.5 Matta21 re-
ported that with anatomic reduc-
tions, arthritis developed in only
16% of patients, as opposed to 45%
in those not reduced anatomically.
Likewise, Letournel reported a 10%
rate after perfect reductions and 36%
after imperfect reductions.5 The diag-
nosis of arthritis was made 10 years
or less after surgery in 80% of pa-
tients who had imperfect reductions,
but more than 10 years after surgery
in 50% of those who had a perfect
reduction. Of note, Letournel ques-
tioned the inclusion of arthritis as a
complication of surgery in those
with late presentation.
Outcome
The outcome after surgical treat-
ment of an acetabular fracture corre-
lates with the quality of the reduc-
tion and the occurrence or avoidance
of complications. In several large
series of acetabular fractures, the
overall clinical results (based on a
modified D’Abinge score) were good
or excellent in 75% to 85% of patients
with a good reduction.5,21,22,26,27,34 If
there was residual displacement of 3
mm, this dropped to 50% to 68%.
The overall clinical results in several
recent series are given in Table 1.
Decision Making
Fracture Pattern
Many factors must be taken into
consideration when deciding whether
Vol 9, No 1, January/February 2001
to treat an acetabular fracture oper-
atively or nonoperatively. Individ-
ual patient factors, institutional
circumstances, and the fracture pat-
tern should be considered (Fig. 4).
Regardless of the treatment chosen,
part of the plan must be early mo-
bilization of the patient to avoid
the risks of prolonged recumbency.
To justify surgery, the result after
surgery must be better than the
expected natural history of a non-
operatively treated fracture. Un-
like other fractures for which crite-
ria are applied to determine whether
surgery is indicated, displaced ace-
tabular fractures should be consid-
ered an operative problem unless
specific criteria for nonoperative
management are met. Patients with
fractures that meet criteria for non-
operative management can be mobi-
lized early with the expectation that
the outcome will be satisfactory.8,15
Olson and Matta8 reported the
use of a CT subchondral arc in com-
bination with other criteria in de-
ciding which acetabular fractures
may be treated without surgery.
Their criteria include an intact 10-
mm CT subchondral arc, intact 45-
degree roof arc measurements on
plain radiographs, at least 50% of
the articular surface of the posterior
wall intact on all CT sections, and a
femoral head congruent with the
acetabular roof on the AP, obtura-
Table 1
Results in Recent Series of Acetabular Fractures Treated Operatively
No. of
Author(s) (year) Fractures
Matta21 (1996) 262
Mayo22 (1994) 163
Ruesch et al24 (1994) 53
Alonso et al34 (1994)* 59
Cole et al27 (1994)† 55
Wright et al25 (1994) 87
* Only extended approaches used.
† Only modified Stoppa approach used.
Paul Tornetta III, MD
tor oblique, and iliac oblique views.
In a study of patients with dis-
placed acetabular fractures treated
without surgery,8 9 (82%) of 11 frac-
tures meeting these criteria had a
good or excellent result at 1 year,
compared with only 5 (42%) of 12
fractures not meeting these criteria.
The results in the patients who met
these criteria and were treated non-
operatively were equal to those in
patients treated operatively over
the same time period. The authors
concluded that there is no advan-
tage to operative management in
this patient population.
The use of fluoroscopic stress
views has been recommended to
augment these criteria.15 In a series
of 41 patients who met the Olson-
Matta criteria, 3 had fluoroscopically
demonstrable hip instability. Two
had posterior-wall fractures affect-
ing 15% and 35% of the posterior
wall, and 1 had a transverse fracture
(Fig. 5). The remaining patients who
had fractures that met the criteria for
nonoperative management and who
had fluoroscopically demonstrated
stable hips were treated nonsurgically
with early mobilization (20-lb toe-
touch for 10 to 12 weeks). Good or
excellent results were obtained in 32
(91%) of 35 patients followed up for
an average of 2.7 years (Fig. 6). On
the basis of these studies, if criteria
for nonoperative treatment are met
Acceptable Good or Excellent
Reductions, % Clinical Results, %
90 76
81 75
81 81
100 71
89 89
85 45
23
Displaced Acetabular Fractures

Displaced acetabular fracture (except both-column fracture)

Is femoral head congruent with acetabular roof on AP and Judet views?

Yes No
Consider patient factors:
• Age >60?
• Serious comorbidities?
Evaluate radiologic factors: Evaluate whether • Increased surgical risk?
• Intact 45° roof arc? fracture pattern can • Preexisting hip arthritis?
• 10-mm CT subchondral be improved with ORIF • Very low-demand patient?
ring intact? • Demented patient?
• >50% of posterior wall • Patient refuses transfusion?
intact on all CT sections? Yes

No

Yes No
Yes No
Consider nonoperative
treatment, with THA as salvage
Stable hip on if painful arthritis develops Consider institutional factors:
fluoroscopic stress • Surgeon experienced?
view under anesthesia? • Institution capable of
managing injury?

Yes No
Yes No

Nonoperative
management ORIF Transfer patient

Displaced both-column acetabular fracture

Secondary congruence present?

Yes No

Consider patient factors:

• Age >50?
Consider institutional factors:
• Serious comorbidities?
• Surgeon experienced?
• Increased surgical risk?
• Institution capable of managing injury?
• Preexisting hip arthritis?
• Very low-demand patient?
• Demented patient?
• Patient refuses transfusion?

Yes No
Yes No

ORIF Transfer patient

Nonoperative management

Figure 4 Top, Algorithm for treatment of displaced acetabular fractures (except both-column fractures). Bottom, Algorithm for treat-
ment of displaced both-column acetabular fractures. ORIF = open reduction and internal fixation; THA = total hip arthroplasty.

24 Journal of the American Academy of Orthopaedic Surgeons

 Paul Tornetta III, MD

A B C

Figure 5 A, AP radiograph of a 19-year-old woman with a posterior hip dislocation, a

transverse acetabular fracture, and a symphyseal dislocation. After reduction of the
dislocation, Judet views (B and C) and a CT scan confirmed that the patient had intact
45-degree roof arcs, no posterior wall fracture, an intact subchondral ring, and a con-
gruent relationship of the head to the roof on all three views. Although the patient met
the criteria for nonoperative management, the hip was stressed in the operating room
and found to be unstable. D, The femoral head lost congruence with the roof and
became congruent with the ischiopubic segment in abduction. ORIF of the acetabulum
and the symphysis was performed to maintain hip stability.

and the hip is stable, nonoperative
management permits early mobi-
lization without an increased risk of
early arthritis while avoiding the
risks of surgery.
This same principle may be ap-
plied to one component of an ace-
tabular fracture. If one fragment of
a complex fracture (usually in a
low-column or small posterior-wall
fracture) meets the criteria for non-
operative management, then open
reduction and internal fixation
(ORIF) of the rest of the acetabu-
lum may be all that is required.
This is especially likely if a second
approach would be needed, such
as for a T-shaped fracture in which
only one column can be accurately
reduced through a nonextensile
approach (Fig. 7). Nonoperative
management of such fractures
avoids the morbidity associated
with operative management due to
use of a second approach or an ex-
tensile approach. The CT arc is
most often useful in determining
which component of the fracture
affects the roof. However, after fix-
ation of a portion of a complex ace-
tabular fracture, the same criteria
for nonoperative management pre-
viously described must be met re-
garding the remaining displaced
portion.
Notably, Olson and Matta8 ex-
cluded both-column fractures in
their analysis of nonoperative frac-
ture management. This pattern de-
serves special mention, as the
results of nonoperative manage-
ment for displaced both-column
fractures are better than those for
other displaced fractures affecting
the roof. In both-column fractures,
the entire articular surface is sepa-
rated from the intact ilium. The
columns rotate away from each
other, allowing the head to medial-
ize, but they may maintain a con-
gruent relationship with the head.
This is referred to as “secondary
congruence.”
Letournel reported very good or
excellent results in 11 (85%) of 13
patients with both-column fractures
treated nonoperatively an average
of 4.3 years after injury if secondary
congruence was present. 5 How-
ever, the long-term follow-up of
these injuries is not known. One
recent biomechanical study demon-
strated statistically significant in-
creases in the contact pressures in
the roof of the acetabulum in the
presence of perfect secondary con-
gruence.35
Patient Factors
Patient factors, such as age, bone
quality, comorbidities, preinjury
function, type of employment, and
personal expectations, all have a
bearing on treatment. For young
patients, there is no good alterna-

Vol 9, No 1, January/February 2001 25

Displaced Acetabular Fractures

tive to ORIF of displaced fractures

and no long-term salvage solution
if clinically significant arthritis
develops. However, in older pa-
tients, salvage is possible with a
87° 60°
hip arthroplasty; thus, nonopera-
tive management may be consid-
ered a more viable option for older
patients.
Clinical results after surgery are
better in younger patients than in
A B
older patients. Older patients are
more likely to have poor bone stock
and suffer a loss of reduction if
treated operatively.5-21 Other factors
that may predispose to complica-
70° tions, such as diabetes and obesity,
must be evaluated. Preexisting
symptomatic arthritis is a relative
contraindication to internal fixation,
as the long-term result will likely be
poor and hip arthroplasty may even-
C D
tually be necessary.
Figure 6 An 18-year-old motorcyclist sustained a right femur fracture, a symphysis dis- The patient’s activity level may
location with bilateral ramus fractures, an anterior left sacroiliac joint injury, and a dis- also influence the decision. A house-
placed T-shaped left acetabular fracture. The roof arc measurements are drawn for clarity. hold ambulator does not have the
The anterior column is not significantly displaced (B), but the posterior column is dis-
placed 1.5 cm (C). The roof arc measurements are more than 45 degrees on the AP (A) and same requirements as a vigorous
Judet (B and C) views. The 10-mm subchondral ring was intact and the head was congru- community ambulator and may not
ent with the roof in all views. Because the hip was stable on the fluoroscopic stress views, choose the same management. The
the acetabular fracture was treated nonoperatively. The symphysis and rami were
reduced and fixed. Although the sacroiliac joint would not normally require fixation, it patient in Figure 8 is a 72-year-old
was fixed because the iliac wing fragment remained mobile after nonoperative manage- obese woman who is a household
ment of the acetabular fracture. D, Four years after surgery, the hip was rated excellent ambulator with insulin-dependent
clinically and showed no signs of arthritis.
diabetes mellitus. She suffered a
both-column fracture in a fall.
Given her lifestyle, physical de-
mands, and fracture pattern, she
chose nonoperative management
and had a very good result at 4
years. Figure 9 depicts a similar
fracture pattern in an active, well-
developed 70-year-old man with-
out identifiable comorbidities. He
chose operative management and
had an excellent result at 5 years.
Thus, management must be tai-
A B C lored to the patient as well as to the
fracture pattern.
Figure 7 A, AP view of a 42-year-old woman who sustained a T-type fracture in a motor
vehicle accident. The femoral head is subluxated medially and follows the posterior col-
umn. B, CT section obtained 15 mm below subchondral bone reveals the anterior-column Institutional Factors
fracture (arrow) entering the joint (but outside the weight-bearing surface of the acetabu- Just as each patient is different,
lum). C, After the posterior-column fracture was reduced anatomically and fixed, all three so, too, is each surgeon and institu-
views showed that the head was congruent with the roof and stable (AP view is shown).
Thus, the anterior component of the fracture met the criteria for nonoperative management tion. Specialized equipment is used
and was not reduced or fixed. by surgeons who frequently treat
acetabular fractures. This includes

26 Journal of the American Academy of Orthopaedic Surgeons

 Paul Tornetta III, MD

special traction tables, reduction

clamps, oscillating drills, and nerve
monitoring apparatus. The pres-
ence of qualified assistants is also
an important factor. Special anes-
thetic techniques, such as hyper-
volemic hypotension and the use of
a cell saver, may decrease the need
for transfusion. Many institutions
are not equipped to properly sup-
port acetabular surgery. Thus, the
individual surgeon must assess, in
A B addition to his or her own experi-
ence in dealing with these injuries,
Figure 8 A, A 72-year-old diabetic woman who was a household ambulator sustained a the institutional support available
both-column fracture after a fall. The relationship of the head to the displaced roof in all
three views indicated reasonable secondary congruence. The patient opted for nonopera- when making the decision to operate
tive management, which included immediate mobilization with a walker and wheelchair. or to transfer the patient to a center
B, Four years after her injury, she had no hip pain, and there was radiographic evidence of that specializes in the care of these
preservation of the joint space.
patients.

Summary

Acetabular fractures are complex

injuries and should be viewed as an
operative problem unless the crite-
ria for nonoperative management
are met. If the nonoperative criteria
are not met, the ultimate decision as
to whether to operate depends on
many factors, including the pa-
tient’s expectations. The individual
surgeon must evaluate his or her
own experience and the institu-
tional support available in deciding
A B
whether to operate on or transfer a
Figure 9 A 70-year-old man who had been an active community ambulator and enjoyed patient who would benefit from
walking daily sustained an acetabular fracture after a fall. A, Judet views demonstrate a operative management. Regardless
both-column fracture with imperfect secondary congruence on the iliac oblique view. After of the treatment chosen, manage-
discussion of the risks and benefits of operative and nonoperative management, the patient
chose ORIF. The immediately postoperative AP and Judet views demonstrated anatomic ment should include early mobili-
reduction of the acetabulum. B, After 5 years, the patient had minimal pain with weather zation to avoid the complications of
changes and no radiographic signs of arthritis and still enjoyed walking several miles daily. recumbency.

References
1. Baumgaertner MR, Wegner D, Booke
J: SSEP monitoring during pelvic and
acetabular fracture surgery. J Orthop
Trauma 1994;8:127-133.
2. Helfet DL, Anand N, Malkani AL, et
al: Intraoperative monitoring of motor
pathways during operative fixation of
acute acetabular fractures. J Orthop
Trauma 1997;11:2-6.
3. Middlebrooks ES, Sims SH, Kellam
JF, Bosse MJ: Incidence of sciatic
nerve injury in operatively treated
acetabular fractures without soma-
tosensory evoked potential monitor-
ing. J Orthop Trauma 1997;11:327-329.
4. Hak DJ, Olson SA, Matta JM: Diag-
nosis and management of closed inter-
nal degloving injuries associated with
pelvic and acetabular fractures: The
Morel-Lavallee lesion. J Trauma
1997;42:1046-1051.
5. Letournel E, Judet R (eds); Elson RA
(trans-ed): Fractures of the Acetabulum,
2nd ed. Berlin: Springer-Verlag, 1993.
6. Rowe CR, Lowell JD: Prognosis of
fractures of the acetabulum. J Bone
Joint Surg Am 1961;43:30-59.

Vol 9, No 1, January/February 2001 27

Displaced Acetabular Fractures
7. Matta JM, Anderson LM, Epstein HC,
Hendricks P: Fractures of the acetabu-
lum: A retrospective analysis. Clin
Orthop 1986;205:230-240.
8. Olson SA, Matta JM: The computer-
ized tomography subchondral arc: A
new method of assessing acetabular
articular continuity after fracture—A
preliminary report. J Orthop Trauma
1993;7:402-413.
9. Olson SA, Bay BK, Pollak AN, Sharkey
NA, Lee T: The effect of variable size
posterior wall acetabular fractures on
contact characteristics of the hip joint.
J Orthop Trauma 1996;10:395-402.
10. Brumback RJ, Holt ES, McBride MS,
Poka A, Bathon GH, Burgess AR:
Acetabular depression fracture accom-
panying posterior fracture dislocation
of the hip. J Orthop Trauma 1990;4:42-48.
11. Letournel E: Acetabular fractures:
Classification and management. Clin
Orthop 1980;151:81-106.
12. Calkins MS, Zych G, Latta L, Borja FJ,
Mnaymneh W: Computed tomogra-
phy evaluation of stability in posterior
fracture dislocation of the hip. Clin
Orthop 1988;227:152-163.
13. Keith JE Jr, Brashear HR Jr, Guilford
WB: Stability of posterior fracture-
dislocations of the hip: Quantitative as-
sessment using computed tomography.
J Bone Joint Surg Am 1988;70:711-714.
14. Vailas JC, Hurwitz S, Wiesel SW:
Posterior acetabular fracture-disloca-
tions: Fragment size, joint capsule, and
stability. J Trauma 1989;29:1494-1496.
15. Tornetta P III: Nonoperative manage-
ment of acetabular fractures: The use
of dynamic stress views. J Bone Joint
Surg Br 1999;81:67-70.
16. Tornetta P III, Mostafavi HR: Hip dis-
location: Current treatment regimens.
J Am Acad Orthop Surg 1997;5:27-36.
17. Fassler PR, Swiontkowski MF, Kilroy
28
AW, Routt ML Jr: Injury of the sciatic
nerve associated with acetabular fracture.
J Bone Joint Surg Am 1993;75:1157-1166.
18. Chrisman OD, Ladenbauer-Bellis IM,
Panjabi M, Goeltz S: The relationship
of mechanical trauma and the early
biomechanical reactions of osteo-
arthritic cartilage. Clin Orthop 1981;
161:275-284.
19. Donohue JM, Buss D, Oegema TR Jr,
Thompson RC Jr: The effects of indi-
rect blunt trauma on adult canine
articular cartilage. J Bone Joint Surg
Am 1983;65:948-957.
20. Johnson EE, Matta JM, Mast JW,
Letournel E: Delayed reconstruction of
acetabular fractures 21-120 days follow-
ing injury. Clin Orthop 1994;305:20-30.
21. Matta JM: Fractures of the acetabu-
lum: Accuracy of reduction and clini-
cal results in patients managed opera-
tively within three weeks after the
injury. J Bone Joint Surg Am 1996;78:
1632-1645.
22. Mayo KA: Open reduction and inter-
nal fixation of fractures of the acetabu-
lum: Results in 163 fractures. Clin
Orthop 1994;305:31-37.
23. Mayo KA, Letournel E, Matta JM,
Mast JW, Johnson EE, Martimbeau CL:
Surgical revision of malreduced ace-
tabular fractures. Clin Orthop 1994;
305:47-52.
24. Ruesch PD, Holdener H, Ciaramitaro
M, Mast JW: A prospective study of
surgically treated acetabular fractures.
Clin Orthop 1994;305:38-46.
25. Wright R, Barrett K, Christie MJ,
Johnson KD: Acetabular fractures:
Long term follow-up of open reduc-
tion and internal fixation. J Orthop
Trauma 1994;8:397-403.
26. Matta JM, Merritt PO: Displaced
acetabular fractures. Clin Orthop
1988;230:83-97.
Journal of the American Academy of Orthopaedic Surgeons
27. Cole JD, Bolhofner BR: Acetabular
fracture fixation via a modified Stoppa
limited intrapelvic approach: Descrip-
tion of operative technique and pre-
liminary treatment results. Clin Orthop
1994;305:112-123.
28. Kaempffe FA, Bone LB, Border JR:
Open reduction and internal fixation
of acetabular fractures: Heterotopic
ossification and other complications of
treatment. J Orthop Trauma 1991;5:
439-445.
29. Brueton RN: A review of 40 acetabu-
lar fractures: The importance of early
surgery. Injury 1993;4:171-174.
30. Bosse MJ, Poka A, Reinert CM, Ell-
wanger F, Slawson R, McDevitt ER:
Heterotopic ossification as a complica-
tion of acetabular fracture: Prophylaxis
with low-dose irradiation. J Bone Joint
Surg Am 1988;70:1231-1237.
31. Ghalambor N, Matta JM, Bernstein L:
Heterotopic ossification following
operative treatment of acetabular frac-
ture: An analysis of risk factors. Clin
Orthop 1994;305:96-105.
32. Moed BR, Smith ST: Three-view radio-
graphic assessment of heterotopic ossi-
fication after acetabular fracture sur-
gery. J Orthop Trauma 1996;10:93-98.
33. Moed BR, Letournel E: Low-dose irra-
diation and indomethacin prevent het-
erotopic ossification after acetabular
fracture surgery. J Bone Joint Surg Br
1994;76:895-900.
34. Alonso JE, Davila R, Bradley E:
Extended iliofemoral versus triradiate
approaches in management of associ-
ated acetabular fractures. Clin Orthop
1994;305:81-87.
35. Tornetta P III, Levine R, Renard R, et
al: The biomechanical consequences of
both column fractures with perfect sec-
ondary congruence. J Orthop Trauma
(in press).
 Strength Training for Children and Adolescents

Jeffrey A. Guy, MD, and Lyle J. Micheli, MD

Abstract

Strength, or resistance, training for young athletes has become one of the most strength training because of insuffi-
popular and rapidly evolving modes of enhancing athletic performance. Early cient circulating levels of andro-
studies questioned both the safety and the effectiveness of strength training for gens.6 However, this has been dis-
young athletes, but current evidence indicates that both children and adoles- proved over the past decade, as
cents can increase muscular strength as a consequence of strength training. research has documented that young
This increase in strength is largely related to the intensity and volume of load- athletes do in fact gain strength
ing and appears to be the result of increased neuromuscular activation and coor- with a properly planned and super-
dination, rather than muscle hypertrophy. Training-induced strength gains are vised training regimen.4,7-13
largely reversible when the training is discontinued. There is no current evi- The second misconception is that
dence to support the misconceptions that children need androgens for strength athletes participating in strength
gain or lose flexibility with training. Given proper supervision and appropriate training lose both the flexibility and
program design, young athletes participating in resistance training can increase the range of motion necessary for
muscular strength and do not appear to be at any greater risk of injury than optimal performance in their chosen
young athletes who have not undergone such training. sport. This has also been refuted by
J Am Acad Orthop Surg 2001;9:29-36 recent studies, with some research-
ers reporting increased flexibility
when flexibility training was incor-
porated into a training regimen.10
Because of the increasing demands ticipate in some form of strength The third misconception is that
for performance and the decreasing training to enhance performance strength training is dangerous and
ages of participation and peak per- and endurance and to reduce the exposes the young athlete to unnec-
formance, young athletes are con- risk of injury. While the effective- essary risk of injury. This particu-
tinually being asked to perform at ness, risks, and methods of training lar question remains a cause for
higher levels and to improve at a for the adult population have been concern for parents and general
quicker pace than ever before. As extensively studied, 1,2 the role of physicians. The persistence of this
the demands increase, the athletic strength training for children and concern is largely due to the inap-
community has been asked to sup- adolescents remains a topic of con- propriate comparison of injury
ply the means to increase athletic troversy and often heated debate.3-5 rates with different modes of train-
performance, and the medical com- A number of important questions
munity has been asked to validate have been asked. Can strength
the safety of these methods. training increase the muscular
Dr. Guy is Fellow in Sportsmedicine, Boston
Strength training has become one strength in young athletes? Is
Children’s Hospital, Boston, Mass. Dr.
of the most popular and rapidly strength training safe? Can strength Micheli is Director, Division of Sports
evolving modes of enhancing ath- training result in increased athletic Medicine, Boston Children’s Hospital; and
letic performance. Although initial- performance? Associate Clinical Professor of Orthopaedic
ly limited to those sports thought to The initial controversy surround- Surgery, Harvard Medical School, Boston.
require strength for optimal perfor- ing strength training for the young
Reprint requests: Dr. Micheli, Boston
mance, such as football and rugby, athlete evolved from unfounded
Children’s Hospital, 319 Longwood Avenue,
some form of strength training has statements and three misconcep- Boston, MA 02115.
now been adopted in virtually every tions regarding the risks and poten-
sports activity. tial benefits to the athlete. The first Copyright 2001 by the American Academy of
It is commonplace for adult ath- misconception is that the prepubes- Orthopaedic Surgeons.
letes, both male and female, to par- cent athlete cannot benefit from

Vol 9, No 1, January/February 2001 29

Strength Training for Children and Adolescents
ing, such as weight training, resis-
tance training, and power lifting.
Injury rates with these modes of
training can vary greatly, and ex-
trapolation from one to another can
be misleading.
The literature in recent years has
helped dispel some misconceptions
about strength training for children
and adolescents. Unfortunately,
however, information from the med-
ical community on these topics may
appear to be inconsistent, depending
on the experience of the practitioner
and his or her knowledge of recent
studies on strength training. Not
surprisingly, parents, coaches, and
trainers remain confused and uncer-
tain about strength training and
often refrain from its use.
Definitions
The term “strength training” is
defined as the use of progressive
resistive methods to increase one’s
ability to exert or resist force.4 The
term “resistance training” may also
be used in the same context and is
often considered synonymous.
This type of training is both con-
trolled and progressive, often utiliz-
ing various modalities, such as free
weights, individual body weight,
hydraulics, and elastic bands, to
name a few. To be successful, a par-
ticular training regimen must be
individualized and must involve a
timely progression in intensity,
thereby stimulating strength gains
that are greater than those associ-
ated with normal growth and de-
velopment.
One particular area of confusion
is in the use of the terms “strength
training” and “resistance training”
in relation to the terms “weight lift-
ing” and “power lifting.” The latter
terms should be used only to de-
scribe techniques of training at high
intensities with the goal being to lift
maximal amounts of weights, often
in competition.
30
When reviewing the literature,
the age group involved in discus-
sion can be particularly confusing.
For the purposes of this review, the
definitions by Faigenbaum and
Bradley4 will be utilized. The terms
“prepubescent” and “child” refer to
girls and boys prior to the develop-
ment of secondary sex characteris-
tics, roughly defined as up to the
age of 11 years for girls and up to
age 13 for boys. The terms “pubes-
cent” and “adolescent” are applied
to girls aged 12 to 18 and boys aged
14 to 18. The term “young athlete”
is a more comprehensive term and
will be used when discussion in-
cludes both the prepubescent and
the pubescent athlete.
Effectiveness of Strength
Training for Young
Athletes
The topic of strength training by
adult athletes has been the subject
of extensive research.14 However,
the role of strength training for the
young athlete remains controversial
despite recent studies at a number
of centers.
During the 1970s, there were few
studies available. As a result, many
clinicians discouraged strength
training for children. It was felt
that prepubescent children were
incapable of developing much
strength and that physical weak-
ness after puberty is merely the
result of insufficient physical exer-
tion.15 This stance was reflected in
a 1983 position paper of the Ameri-
can Academy of Pediatrics in which
it was stated that “prepubertal boys
do not significantly improve strength
or increase muscle mass in a weight
training program because of insuffi-
cient circulating androgens.”6
Furthermore, several early stud-
ies failed to demonstrate increased
strength in children engaged in
strength-training programs.16,17 In
1978, Vrijens16 reported no strength
Journal of the American Academy of Orthopaedic Surgeons
gains in a study of 10- to 17-year-
old boys undergoing training ses-
sions three times a week for a total
of 8 weeks’ duration. Of interest,
the training program involved low
resistance and employed only one
set of exercises per session. In a
similar study, Docherty et al 17
found that 12-year-old boys did not
benefit from strength training fol-
lowing their competitive season.
The frequency of training was three
times weekly for a total of 4 to 6
weeks. However, both the low
intensity of two sets per session and
the short duration of the study may
have compromised the results of
the study.
These studies have been cited in
the literature as proof that strength
training is ineffective for young ath-
letes; however, careful evaluation
suggests that these results may
have been flawed by methodologic
shortcomings. The nature of con-
trol groups is important because as
children continue to grow, a prepu-
bescent athlete may in fact develop
an increase in strength from normal
growth alone, thus confounding
any benefit from a training pro-
gram. In addition, the training pro-
gram itself may not provide the
intensity, frequency, or length of
training necessary to allow the
prepubescent athlete to develop
enough muscular strength to over-
come differences observed with
normal growth alone.
The past 15 years has seen a pro-
gressive and increased interest in
the topic of strength training, and a
number of controlled studies have
examined the benefits and risks of
youth strength training. One of the
earliest clinical studies supporting
strength training for prepubescent
children was by Sewall and Mich-
eli.10 Eighteen prepubescent boys
and girls participated in pneumatic
resistance training for three 30-
minute sessions per week for a total
of 9 weeks. The children involved
in training had a statistically signif-

icant (P<0.05) mean increase in
strength of 42%, compared with a
9% increase for control subjects.
The study also showed that, even
over a 9-week period, prepubescent
children have a baseline increase in
strength due to normal growth and
maturation.
Similar findings were demon-
strated by Weltman et al, 18 who
examined the effects of hydraulic
strength training on prepubertal
boys. Twenty-six boys participated
in a strength training program three
times a week for 14 weeks, and dif-
ferences in isokinetic strength for
flexion and extension at the knee
and elbow joints were evaluated.
Compared with an untrained con-
trol group, subjects involved in
training had an increase in strength
of up to 36% for concentric work
and an increase in torque of up to
45% for all eight motions tested
(P<0.05). The findings in this study
suggest that short-term, supervised
concentric strength training with
use of hydraulic resistance is both
effective and safe for prepubertal
boys, with no injuries sustained
while training.
As further evidence in support of
strength training for prepubescent
children accumulated, researchers
began to manipulate training regi-
men variables (e.g., frequency, in-
tensity of exercise, and duration of
training) in search of an optimal pro-
gram. Because overuse injuries are
not uncommon in the pediatric pop-
ulation,19,20 Faigenbaum et al7 investi-
gated the effects of a shortened fre-
quency of training (twice a week)
while maintaining a high level of in-
tensity. In an 8-week study, prepu-
bescent subjects underwent a twice-
weekly training schedule based on an
individual’s 10-repetition-maximum
(10-RM) strength (i.e., the maximum
weight that could be lifted ten times
with good form). The prepubescent
children were found to have a mean
increase of 74% in 10-RM strength
values compared with nontrained
Vol 9, No 1, January/February 2001
Jeffrey A. Guy, MD, and Lyle J. Micheli, MD
control subjects. Faigenbaum et al8
found similar results in prepubescent
subjects in a 1996 study: a mean
increase of 53% in leg extension and a
41% mean increase in chest-press val-
ues after 8 weeks of strength training.
Thus, at a given intensity, twice-
weekly training programs appear to
increase strength in children to a
level equivalent to that found with
schedules requiring participation
three times per week.
Taking into consideration the
number of variables involved in
determining the effectiveness of
resistance training, Falk and Tenen-
baum5 conducted a meta-analysis
of nine studies demonstrating in-
creased strength. All children in the
studies were under the age of 13
years. In the combined studies, the
resistance training group had a
71.6% increase in strength over the
control group. There was no ad-
vantage at any particular age, and
there were no differences between
the sexes.
Thus, current evidence indicates
that resistance training can result in
marked strength gains in the pre-
pubescent child. While the ultimate
duration and intensity continue to be
debated, children develop strength
gains with workouts as infrequent
as twice weekly. At this time, there
do not appear to be any sex- or age-
related differences.
Physiologic Mechanisms
for Strength Development
Although the literature supports
the contention that children may
demonstrate strength gains with a
proper training regimen, it is more
difficult to define how and why this
occurs and what the underlying
mechanisms are. Numerous fac-
tors, including muscle hypertrophy,
increase in muscle cross-sectional
area, motor-unit coordination, cen-
tral nervous system activation, and
psychological drive, may all con-
tribute to increases in strength.
These factors have been extensively
studied in adults, but few studies
have evaluated the underlying
mechanism of strength gains in
children.
In an attempt to determine the
contribution of muscle hypertrophy
to increased strength, several re-
searchers have included morpho-
logic variables in their evaluation of
strength changes.7,9,18,21-23 Weltman
et al18 found little or no change in
anthropometric and body composi-
tion measures in prepubescent boys
over a 14-week training period. No
statistically significant differences
were found in body circumference
or skin-fold measurements. Body
density as measured by hydrostatic
weighing was also unchanged.
Ramsay et al9 found no statistically
significant changes in anthropomet-
ric indicators in prepubescent boys
over a 20-week resistance training
period. No changes were seen in
the cross-sectional area of either the
midportion of the upper arm or the
midthigh as measured with com-
puted tomography.
Because prepubescent children
lack circulating androgens, it is not
surprising that strength gains seen
in resistance training are not associ-
ated with the muscle hypertrophy
seen in the adult population (at least
not in short-term studies). Neural
adaptations have been implicated
by some as primarily responsible
for strength gains.9,22 Ozmun et al22
addressed this issue in a study of
the effects of thrice-weekly biceps
curls on prepubescent children over
the course of 8 weeks. Significant
isotonic and isokinetic strength in-
creases were found in the trained
group (22.6% and 27.8%, respective-
ly), with no changes in either skin-
fold or arm-circumference measure-
ments. While these findings confirm
that strength gains are not the result
of muscle hypertrophy, the increased
electromyographic measurements
(17% greater amplitude in the trained
31
Strength Training for Children and Adolescents

group) suggest that the early gains
in strength seen in prepubescent
children are due in part to increased
muscle activation.
Only one other study has ad-
dressed the neural adaptations in
strength training in children.
Blimkie et al,12 looking at isotonic
strength changes in prepubescent
children, found a significant (P<
0.05) increase in strength over a 10-
week training period. Although
there were no differences in muscle
cross-sectional area, an increasing
trend in motor unit activation was
noted, as determined by interpolar
twitch. It has also been suggested
that intrinsic muscle adaptations,
increased motor activation, im-
proved motor skill performance,
and coordination of the involved
muscle groups may all play a role
in the muscle strength seen with
resistance training.9
Although at this time it may be
difficult to separate out the contri-
butions and relative importance of
each variable, it appears that neu-
romuscular activation, motor coor-
dination, and intrinsic muscular
adaptations all contribute to the
increased strength seen in prepu-
bescent athletes undergoing resis-
tance training. Similar mechanisms
are found in adolescents and
young adults,14 but strength gains
a decrease in athletic performance.8
There are few studies of detraining
in adults and even fewer in the pre-
pubescent population. Furthermore,
attempts to evaluate the persistence
of resistance-induced strength gains
in prepubescent subjects after with-
drawal of a training stimulus may
be confounded by the concomitant
growth-related strength increases.24
In a study of detraining in pre-
pubescent children, Sewall and
Micheli10 suggested that the loss of
strength due to withdrawal from
training was greater than, and not
offset by, the anticipated growth-
related increases in strength over
the same time period. In 1989,
Blimkie et al12 proposed a model of
the effects of growth, resistance
training, maintenance training,
and detraining on strength devel-
opment in children. In a study
using that model, 13 the strength
gains seen in the training group
regressed over time in both the
maintenance and detraining groups
to levels close to, but still above,
those of the untrained control sub-
jects (Fig. 1).
75
In a study by Faigenbaum et al8
evaluating the effects of strength
training and detraining on children,
the results were consistent with those
of Blimkie.13 Despite a 53% increase
in training-induced leg-extension
strength over 8 weeks, a subsequent
8 weeks of detraining led to rapid
and significant (P<0.05) decreases in
both leg extension (−28%) (Fig. 2) and
chest press performance (−19.3%). In
the same period, the performance of
the untrained control subjects in-
creased slightly. The magnitude of
loss for the trained group was ap-
proximately 3% per week. A com-
parison of groups at completion of
detraining found no statistically sig-
nificant difference in leg extension.
Although the available data are
limited, it appears that strength
gains secondary to resistance train-
ing during prepubescence are tran-
sient and regress toward untrained
control levels. The degree of regres-
sion appears to depend on the mag-
nitude of strength gains, level of
inactivity, and duration of detrain-
ing. Unfortunately, the amount of
training required to maintain or at
T
MT

seen in prepubescent children ap-

Leg strength, N • m

pear to be largely independent of 65

muscle size. Not surprisingly, the DT

training-induced gains in strength
C
seen in postpubertal boys are
accompanied by increased cross- 55
sectional area of muscle.16

Persistence of Training- 45
Induced Gains Pretraining Posttraining Detraining

Figure 1 Graphic illustration of Blimkie’s model demonstrating the effects of resistance

The removal of stimulus, or “de-
training,” is defined as the tempo-
rary or permanent reduction or with-
drawal of a training stimulus, which
may result in the loss of physiologic
and anatomic adaptations, as well as
training (T), maintenance training (MT), and detraining (DT) on strength development
during normal growth (C) during childhood. The values for both the maintenance and
detraining groups regressed with time to levels close to, but above, those of the untrained
control subjects. (Adapted with permission from Blimkie CJR: Resistance training during
pre- and early puberty: Efficacy, trainability, mechanisms, and persistence. Can J Sport Sci
17;4:264-279.)

32 Journal of the American Academy of Orthopaedic Surgeons

 Jeffrey A. Guy, MD, and Lyle J. Micheli, MD

these injuries happen at home or

35
school and are not the result of su-
pervised activity. In several stud-
ies of adolescents, the incidence of
*
30
injury ranged between 7% and
40%.26,27 Almost 75% of the inju-
(6 repetition maximum), kg

ries were strains, with the most

Leg-Extension Strength

common site being the lower spine.

25 * There are also numerous case re-
ports or small series of serious
weight-lifting and power-lifting
injuries, such as cardiac rupture
20
due to impact by a dropped bar-
bell,28 spondylolysis and spondy-
lolisthesis, 29 and growth-plate
injuries in the wrist. 30 Most of
15
these injuries were attributed to
improper lifting techniques, exces-
sive loading, or inadequate teaching
10 or supervision. Not surprisingly,
Pretraining Posttraining Mid-detraining Post-detraining recommendations about the partici-
pation of young athletes in these
Figure 2 The effects of strength training and detraining on children demonstrated in the
study by Faigenbaum et al8 were consistent with Blimkie’s model.13 The trained group activities vary from supervised par-
(solid circles) had a 53% increase in training-induced leg-extension strength over 8 weeks, ticipation only25 to proscription of
but a subsequent 8 weeks of detraining led to a rapid and significant decrease (−28%) in weight lifting, power lifting, and
leg-extension performance, while the performance of the untrained control subjects (open
circles) increased slightly (asterisk indicates statistically significant [P<0.05] difference body building, as well as the use of
between control value and previous value for trained group). A comparison of groups at maximal amounts of weight in
the completion of the 16-week detraining period revealed no significant difference from training programs, for both chil-
the control value for leg extension. (Adapted with permission from Faigenbaum AD,
Westcott WL, Micheli LJ, et al: The effects of strength training and detraining on children. dren and adolescents.31
J Strength Cond Res 1996;10:109-114.) Strength training for young ath-
letes has received widespread sup-
port. 3,4,10,11,18,24,32,33 Rians et al, 33
looking at subclinical musculo-
least slow down this regression has based sports programs. 3 To ad- skeletal injury (as evaluated on
yet to be determined. While these dress the question of whether bone scan) or muscle damage (as
findings may bring into question strength training by the prepubes- estimated on the basis of serum
the need for maintenance programs cent child is associated with an un- creatine phosphokinase determina-
for children, more information is acceptable risk of injury, we must tion), found no evidence of injury
required before specific recommen- first revisit the relevant definitions. in prepubescent boys after 14 weeks
dations can be made. The terms “strength training” and of resistance training. Similar find-
“resistance training” are used to ings by Blimkie et al21 found only
refer to progressive resistance to mildly elevated creatine phospho-
Risks of Resistance enhance performance or ability by kinase values and concluded that
Training for Young using submaximal amounts of short-term (duration of 20 weeks)
Athletes weight. The terms “weight lifting” resistance training by prepubertal
and “power lifting” usually refer to boys did not pose any particular
The past 20 years have seen a the use of maximal amounts of risk in terms of subclinical or clini-
marked increase in the participation weight at high intensities during cal musculoskeletal injury.
of children in competitive sports, competition. Perhaps a better assessment of
and the popularity continues to It has been estimated that more the risk of injury associated with
grow. Approximately 30 million than 17,000 weight-lifting or power- resistance training would come
children (50% of boys and 25% of lifting injuries in adolescents re- from prospective studies of closely
girls) are involved in either competi- quiring emergency room visits oc- monitored and supervised training
tive organized sports or community- cur annually.25 However, most of programs with appropriately pre-

Vol 9, No 1, January/February 2001 33

Strength Training for Children and Adolescents
scribed training loads. There have
been no reported cases of serious
injuries in these studies.9,10,18 There-
fore, it appears that the risks and
concerns associated with youth
strength training are no greater than
those associated with other sports
and recreational activities common
to this age group.4 However, this is
based on the understanding that a
given strength training program is
competently supervised and the
young athlete is properly instructed
and underscores the need for pre-
participant history, blood pressure
measurements, flexibility screening,
and a preparticipation physical
examination. As with adult ath-
letes, while no studies have demon-
strated enhanced performance with
strength training, experience strong-
ly supports its use.
Anabolic Steroid Use
For years, athletes have taken exog-
enous substances to manipulate
their athletic performance. It is not
surprising that modern athletes
often turn to ergonomic aids like
anabolic androgenic steroids to
enhance muscle growth, increase
strength, and improve physical
performance. It has been esti-
mated that over 1 million persons
in the United States are currently
using anabolic steroids, with a
total expenditure of more than
$100 million a year. 34 Although
there is a potential for enhancing
performance, anabolic androgenic
steroids can have severe physio-
logic and emotional side effects,
such as a heightened risk for coro-
nary disease, cholestatic jaundice,
abnormal liver function, hepatic
tumors, stunted growth, gyneco-
mastia, and many psychotic disor-
ders. In addition, there is the risk
of transmission of diseases such as
acquired immunodeficiency syn-
drome and viral hepatitis through
needle sharing.
34
Early use of anabolic steroids in
the United States was primarily by
individuals involved in weight
training. However, gains in size
and strength prompted their use by
other athletes. Today, anabolic
steroids are consumed by both
male and female power athletes,
endurance athletes, and nonath-
letes. Given the increasing pres-
sure for athletes to perform better
and earlier, it is no surprise that the
use of anabolic steroids has breached
the boundary of age.
The use of steroids in the adoles-
cent population brings with it an
additional level of concern com-
pared to its use by older athletes.
Estimates of steroid use in the ado-
lescent population have placed the
prevalence at approximately 5% to
7% for boys and 1% to 3% for
girls.35-37 In a recent study of pre-
adolescent middle-school students
ranging in age from 9 to 13 years,
approximately 2.7% of the students
admitted using steroids. 38 The
majority of the students felt that
steroids would make their muscles
bigger and stronger. While usage is
not exclusive to any segment of the
population, the literature suggests
that the highest level is among ado-
lescents from more affluent neigh-
borhoods, presumably because of
easier access to this relatively ex-
pensive drug.39 Most of the steroids
used by young athletes appear to
have been obtained illegally, in-
creasing the risk of purchasing mis-
labeled or impure agents.
The physical side effects in ado-
lescent boys can range from acne
and gynecomastia to more serious
conditions, such as priapism, sodium
retention edema, and liver dysfunc-
tion after prolonged use. In girls,
clitoromegaly, hirsutism, and amen-
orrhea are common, as well as per-
manent deepening of the voice after
prolonged use. Use by children of
both sexes may also result in dimin-
ished adult height, as premature
closure of the physis is possible.
Journal of the American Academy of Orthopaedic Surgeons
Perhaps the most serious side
effects of steroid use occur in the
behavioral sphere; in the transition
to adulthood, adolescents may be
particularly vulnerable to the conse-
quences of heightened aggression.40
As the relatively high consump-
tion of steroids by young athletes
continues, the need for early educa-
tional intervention concerning their
effects is becoming more apparent.
One such intervention is the ATLAS
(Adolescents Training and Learn-
ing to Avoid Steroids) program.34
The goal of that program is to edu-
cate adolescent athletes, enhance
healthy behaviors, and minimize
the factors that encourage steroid
use. Although such programs ap-
pear to be quite successful, they are
limited in both number and avail-
ability. Therefore, one cannot over-
emphasize the role of health pro-
fessionals, educators, and parents
in providing a healthy and informed
atmosphere for young athletes.
Initiation of Training
The proper initiation of strength
training for children and adoles-
cents is critical. Those supervising
young athletes—coaches, trainers,
and parents—should address several
issues before initiating a program of
training. First is whether the ath-
lete is prepared psychologically and
physically to participate in the pro-
gram. This includes making sure
that the athlete has had a prepartici-
pation physical at school or at a
physician’s office. In addition,
supervising adults should strive to
minimize pressure and stress placed
on the athlete to perform.
The second issue is whether the
athlete understands what strength
training is and what the goals of the
program are. This point cannot be
overemphasized, as misinformed
athletes are at increased risk for
injury. The athlete should under-
stand the fundamental differences

between strength training and
weight lifting and the goals of each.
Athletes should understand that
while increasing one’s performance
is a reasonable and attainable goal,
increasing muscle size prior to the
onset of puberty is not. Safety while
training should also be emphasized.
The third issue is which strength
training program the athlete should
follow. While the specifics of indi-
vidual training programs are be-
yond the scope of this article, the
program chosen should be tailored
to the athlete in question on the
basis of age, size, experience, and
sport.41 Access to certain facilities
and specific types of supervision
are important considerations, as not
everyone has a gym membership or
the finances to hire a personal trainer.
Parents interested in being involved
in the training process can also con-
sult the wealth of information in the
literature on strength training for
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3. Faigenbaum AD, Kraemer WJ, Cahill
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adolescents.41-43 The objective is to
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dren need androgens for strength
gain, lose flexibility with training, or
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the proper supervision and appropri-
ate instruction and program design,
children involved in resistance train-
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injury and is not recommended.
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ment in the pre- and post-pubescent
age. Med Sport 1978;11:152-158.
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Quinney HA: The effects of variable
speed resistance training on strength
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The effects of hydraulic resistance
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19. Outerbridge AR, Micheli LJ: Overuse
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20. Micheli LJ: Sports injuries in children
and adolescents: Questions and con-
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727-745.
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Thonar E, Smith K, Garner S: Soft-
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23. Sailors M, Berg K: Comparison of
responses to weight training in pubes-
cent boys and men. J Sports Med Phys
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24. Blimkie CJR: Resistance training dur-
ing preadolescence: Issues and contro-
versies. Sports Med 1993;15:389-407.
25. Mazur LJ, Yetman RJ, Risser WL:
Weight-training injuries: Common
injuries and preventative methods.
Sports Med 1993;16:57-63.
26. Risser WL, Risser JMH, Preston D:
Weight-training injuries in adolescents.
Am J Dis Child 1990;144:1015-1017.
27. Brown EW, Kimball RG: Medical his-
tory associated with adolescent pow-
erlifting. Pediatrics 1983;72:636-644.
28. George DH, Stakiw K, Wright CJ:
Fatal accident with weight-lifting
equipment: Implications for safety
standards. CMAJ 1989;140:925-926.
29. Kotani PT: Studies of spondylosis
found among weight lifters. Br J
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30. Ryan JR, Salciccioli GG: Fractures of
the distal radial epiphysis in adoles-
cent weight lifters. Am J Sports Med
1976;4:26-27.
31. American Academy of Pediatrics
Committee on Sports Medicine:
Strength training, weight and power
lifting, and body building by children
and adolescents. Pediatrics 1990;86:
801-803.
32. Duda M: Prepubescent strength train-
ing gains support. Phys Sportsmed
1986;14:157-161.
33. Rians CB, Weltman A, Cahill BR,
Janney CA, Tippett SR, Katch FI:
Strength training for prepubescent
males: Is it safe? Am J Sports Med
1987;15:483-489.
34. Goldberg L, Elliot DL, Clarke GN, et
al: The Adolescents Training and
Learning to Avoid Steroids (ATLAS)
prevention program: Background and
results of a model intervention. Arch
Pediatr Adolesc Med 1996;150:713-721.
35. Windsor RE, Dumitru D: Anabolic
steroid use by athletes: How serious
are the health hazards? Postgrad Med
1988;84:37-38, 41-43, 47-49.
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anabolic steroids. N Engl J Med 1993;
328:922-926.
37. Buckley WE, Yesalis CE III, Friedl KE,
Anderson WA, Streit AL, Wright JE:
Estimated prevalence of anabolic
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seniors. JAMA 1988;260:3441-3445.
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Gardner DE, Micheli LJ: Anabolic
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39. Windsor R, Dumitru D: Prevalence of
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40. Rogol AD, Yesalis CE III: Anabolic-
androgenic steroids and the adolescent.
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Strength and Power for Young Athletes.
Champaign, Ill: Human Kinetics, 2000.
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 Cartilage Substitutes:
Overview of Basic Science and Treatment Options

Douglas W. Jackson, MD, Mark J. Scheer, MD, and Timothy M. Simon, PhD

Abstract

Articular cartilage defects that are symptomatic and refractory to nonoperative tis is expected to affect almost 60 mil-
treatment represent a clinical management challenge. Although there have been lion persons in the United States and
important advances in stimulating intrinsic repair mechanisms, cartilage to limit the activity of 11.6 million.2
regeneration, and other substitution techniques, to date none has unlocked the
understanding necessary to duplicate normal articular cartilage. The objectives
of treatment of cartilage lesions are to obtain pain relief, reduce effusions and Incidence of Cartilage
inflammation, restore function, reduce disability, and postpone or alleviate the Lesions
need for prosthetic replacement. As the field of articular cartilage repair contin-
ues to evolve rapidly, the most appropriate treatment option for an individual The total incidence of symptomatic
patient should be based on the pathologic characteristics of the lesion and the and asymptomatic localized trau-
patient’s symptoms and expectations. The orthopaedic surgeon needs to be matic articular cartilage and osteo-
familiar with both the existing and the newly emerging cartilage treatment chondral lesions is unknown. Clin-
techniques in order to best educate patients and meet their expectations for ically, the deleterious effect of an
long-term benefits. isolated traumatic impact to articu-
J Am Acad Orthop Surg 2001;9:37-52 lar cartilage may take time to mani-
fest, and the ability of standard
radiography and magnetic reso-
nance imaging to depict partial-
Articular cartilage is a unique tis- cartilagelike substitutes so as to pro-
sue, and any substitute used to vide pain relief, reduce effusions
replace it is subjected to marked and inflammation, restore function,
demands and stresses. Although a reduce disability, and postpone or Dr. Jackson is Medical Director, Southern
number of articular cartilage sub- alleviate the need for prosthetic re- California Center for Sports Medicine,
Memorial Orthopaedic Surgical Group, Long
stitutes have been developed for placement.
Beach, Calif. Dr. Scheer is Sports Medicine
treatment of chondral and osteo- Not all degenerative articular Fellow, Southern California Center for Sports
chondral defects, to date none has cartilage changes are symptomatic. Medicine, Memorial Orthopaedic Surgical
successfully replaced normal artic- However, osteoarthritis is one of Group. Dr. Simon is Director of Research,
ular cartilage. Patients who have the most common disorders of the Southern California Center for Sports
Medicine, Memorial Orthopaedic Surgical
isolated traumatic chondral and musculoskeletal system, and the
Group.
osteochondral defects in an area symptoms caused by it are among
without surrounding degenerative the most common reasons for One or more of the authors or the department
articular cartilage have the most patients to seek medical attention. with which they are affiliated have received
favorable results. While the natural Osteoarthritis is the leading cause something of value from a commercial or other
history of isolated chondral defects of disability and impairment in party related directly or indirectly to the sub-
ject of this article.
is unknown, 1 it is assumed that middle-aged and older individuals,2
these chondral and osteochondral entailing significant economic,
Reprint requests: Dr. Jackson, 2760 Atlantic
defects may progressively enlarge social, and psychological costs. Avenue, Long Beach, CA 90806.
with time and play a role in the Each year, osteoarthritis accounts
development of more generalized for as many as 39 million physician Copyright 2001 by the American Academy of
osteoarthritic changes. The surgical visits and more than 500,000 hospi- Orthopaedic Surgeons.
goal is to replace these defects with talizations. By the year 2020, arthri-

Vol 9, No 1, January/February 2001 37

Cartilage Substitutes
thickness and smaller localized
full-thickness lesions is limited.
Even with arthroscopic examina-
tion, the traumatized area of articu-
lar cartilage may initially appear
intact without obvious pathologic
changes and then later degenerate.
It has been proposed that 5% to 10%
of all patients who present with
acute hemarthrosis of the knee after
a work- or sports-related traumatic
event in fact have a full-thickness
chondral injury.3 In a retrospective
review of 31,516 knee arthroscopies,
chondral lesions were reported in
19,827 (63%) of the patients. On
average, there were 2.7 articular car-
tilage lesions per knee, with unipo-
lar grade IV injuries to the medial
femoral condyle found in 1,729 (5%)
of patients younger than 40 years of
age.4 The actual incidence of asymp-
tomatic articular cartilage lesions in
the contralateral knee of these pa-
tients and in asymptomatic individ-
uals of the same age in the general
population can only be inferred.
Basic Science
Developing a substitute for articular
cartilage requires an understanding
of its complex, highly ordered struc-
ture (Fig. 1). Cartilage is a viscoelas-
tic material that exhibits a time-
dependent behavior when subjected
to a constant load. It provides the
diarthrodial joint with a low-friction
surface, allowing a smooth, gliding
movement, and functions to trans-
mit loads across the joint and to dis-
sipate peak stress on the underlying
subchondral bone.
A large percentage of extracellu-
lar matrix is composed of collagen,
proteoglycans, and water, with
only a sparse population of cells.
In the matrix of mature articular
cartilage, type II collagen fibers
constitute 50% of the dry weight,
and type V, VI, IX, X, and XI colla-
gens are present in small amounts.
The type II collagen exists in a
38
triple-helix configuration (Fig. 2) affinity to the negatively charged
that provides the tensile strength proteoglycans, it helps resist very
and mechanical integrity of carti- high compressive loads as it is being
lage and acts as a framework to displaced. This resistance to loading
immobilize and restrain the proteo- depends on pressurization of water,
glycans in the extracellular matrix. and it is the pore size of the matrix,
Proteoglycans constitute 12% of dictated by the concentration of pro-
the total weight of articular carti- teoglycans, which determines the
lage and are the major macromole- permeability of the tissue and its
cules occupying the interstices with- frictional resistance to flow. Water
in the collagen fibrils. The glycos- also contributes to joint lubrication
aminoglycans contain carboxyl and the transport of nutrients.
groups and/or sulfate groups (ker- Chondrocytes occupy approxi-
atan sulfate and chondroitin sul- mately 2% of the total volume of
fate). The negative charge of the gly- normal adult articular cartilage and
cosaminoglycans is largely re- are the only cell type therein. Their
sponsible for the high affinity for metabolism is affected by factors in
water displayed by the tissue, help- their chemical and mechanical envi-
ing it to resist compressive loading. ronment, such as soluble mediators
Moreover, the adjacent negatively (e.g., growth factors and interleu-
charged branches of aggrecans repel kins), matrix composition, mechani-
each other, which allows them to cal loads, hydrostatic pressures,
occupy the largest possible domain. and electrical fields. Due to the rela-
This, in turn, traps the proteoglycan tively low-oxygen-concentration en-
within the collagen meshwork and vironment in which chondrocytes
contributes to stiffness and strength exist, their metabolism is mainly an-
(Fig. 3). aerobic. Because chondrocytes syn-
Water makes up 65% to 80% of thesize all the extracellular matrix
the total weight of articular cartilage, macromolecules (collagen fibrils,
depending on the load status and noncollagenous proteins, and proteo-
the presence or absence of degenera- glycans) and degradative enzymes in
tive changes.3 Through its strong normal articular cartilage, they are
Cellular Collagen Fiber
Articular cartilage
Arrangement Arrangement
surface
Superficial
Lamina
zone (10%-20%)
splendens
Intermediate
zone
(40%-60%)
Deep zone
(30%) Tidemark
Mineralized
Calcified zone Subchondral cartilage
bone
Cancellous
bone
Figure 1 Major zones of cellular organization (left) and collagen fiber arrangement (right)
in articular cartilage. Chondrocytes are elongated in the superficial tangential zone with
their long axis aligned parallel to the surface. The chondrocytes gradually become rounded
and are often arranged in columns; in deeper zones, they are completely surrounded by the
extracellular matrix. (Adapted with permission from Mow VC, Proctor CS, Kelly MA:
Biomechanics of articular cartilage, in Nordin M, Frankel VH [eds]: Basic Biomechanics of the
Musculoskeletal System, 2nd ed. Philadelphia: Lea & Febiger, 1989, p 32.)
Journal of the American Academy of Orthopaedic Surgeons
 Douglas W. Jackson, MD, et al

sion in response to stimuli decreases

Alpha with age.5-7

200-400 nm
chain Link
protein
Triple
helix Hyaluronate Cartilage Injuries and
Repair
Collagen
molecule
The long-term effects of a localized
Collagen fibril cartilage injury are dependent on
with quarter-
Hole Overlap stagger array chondrocyte and matrix survival.
1,200 nm The extent of injury, the depth of
A B
the injury, and the location of the
Hyaluronate
injury affect the eventual outcome
(Fig. 5). Mechanical damage that
results in injury only to the matrix
components, not to the chondro-
cytes, has the potential that the sur-
viving chondrocytes can synthesize
Collagen fibril new matrix and restore normal
properties. However, if the mechan-
Attached ical destruction involves all com-
aggrecan ponents of the articular cartilage,
C monomer
including the chondrocytes, spon-
Figure 2 Formation of collagen fibrils. A, The triple helix is composed of three alpha taneous repair to the damaged tis-
chains forming a procollagen molecule (intracellular). Once outside the cell, the N- and C- sue is limited and does not dupli-
terminal ends of the alpha chains are cleaved off, which allows fibril formation in a quarter- cate normal articular cartilage.
stagger manner. B, Aggrecan molecules attach to the hyaluronate backbone to form the
proteoglycan aggregate. C, Matrix organization within articular cartilage. The meshwork Each of these scenarios produces a
of collagen fibrils entraps the proteoglycans. The underhydrated proteoglycans create a different biologic and structural
swelling pressure that keeps the network inflated. (Parts A and C reproduced with per- response. Trauma to articular car-
mission from Mow VC, Zhu W, Ratcliffe A: Structure and function of articular cartilage
and meniscus, in Mow VC, Hayes WC [eds]: Basic Orthopaedic Biomechanics. New York: tilage beyond a critical level causes
Raven Press, 1991, pp 143-198. Part B reproduced with permission from Simon SR [ed]: reduction in the viscoelasticity and
Orthopaedic Basic Science. Rosemont, Ill: American Academy of Orthopaedic Surgeons, stiffness of the cartilage. As a re-
1994, p 10.)
sult, more force is transmitted to
the subchondral bone, with conse-
quent thickening and eventual stiff-
important in directing cartilage re- in the adult animal, mitotic activity ening of the subchondral plate.
modeling and regeneration. ceases with the development of a The increased stiffness of the sub-
Embryologically, articular carti- well-defined calcified zone (the chondral bone allows more impact
lage forms from mesenchymal cells tidemark) and, in some species, stresses to be transmitted to the
that cluster together and synthesize with closure of the epiphyseal cartilage, creating a vicious circle of
a matrix. These cells become orga- plate. The lack of pluripotent cells cartilage degeneration and sub-
nized and can be recognized histo- within mature cartilage, with their chondral stiffening.
logically as cartilage cells after the ability to migrate, proliferate, and The thinnest zone of articular
accumulation of a sufficient amount participate in a repair response, cartilage is the superficial zone, the
of matrix separates the cells and they hinders the healing potential of so-called skin of articular cartilage,
acquire the characteristic spherical articular cartilage. In addition, which acts as a barrier against the
shape. This immature cartilage is mature chondrocytes have only a movement of molecules between
considerably more cellular than limited ability to increase synthesis the synovial fluid and the cartilage.
mature tissue, with a higher num- of the components of the surround- This zone typically consists of two
ber of cells per unit volume (Fig. 4). ing matrix to repair tissue defects. layers. MacConaill 8 described a
Besides being more cellular, this There is a programmed cellular bright layer at the articular surface
early cartilage tissue demonstrates senescence, such that the capacity visualized on phase-contrast study
abundant normal mitotic figures. to synthesize some types of proteo- of articular cartilage and named it
Compared with articular cartilage glycans and increase cellular divi- the “lamina splendens.” This portion

Vol 9, No 1, January/February 2001 39

Cartilage Substitutes

of the superficial zone covers the

Aggrecan molecule joint surface and corresponds to
the adherent clear film that can be
Secondary globular
mechanically stripped from the
domain (G2)
underlying deeper portion of the
HA-binding KS-rich CS-rich C-terminal
domain (G1) region region domain (G3)
superficial layer. It consists of fine
fibrils with little polysaccharide
Hyaluronate and no cells.5 Deep to this are the
ellipsoid chondrocytes, which are
aligned parallel to the articular sur-
Protein core face. This deeper area has a high
KS chains CS chains concentration of collagen and a low
A Link protein
concentration of proteoglycans. The
fibrils give this zone greater tensile
strength than the deeper zones of
articular cartilage.9-11
Removal of the superficial zone
increases the permeability of the tis-
Fetal
aggrecan/proteoglycan sue and probably increases loading
structure Aggrecan/proteoglycan of the macromolecular framework
structure with age during compression. It has been
Postnatal shown that disruption or remodel-
B maturation ing of the dense collagenous matrix
of the superficial zone is one of the
first detectable structural changes in
experimentally induced degenera-
tion of articular cartilage. 12 This
suggests that alterations in this zone
may contribute to the development
Decreased pressure
of osteoarthrosis by changing the
mechanical behavior of the tissue.
Furthermore, disruption of this
zone could release cartilage mole-
cules into the synovial fluid, which
Increased pressure
may stimulate an immune or in-
flammatory response. The lamina
splendens and the underlying dense
C
collagen fibril layer are an example
of the site-specific organization of
Figure 3 Component areas of the aggrecan molecule. A, The protein core has three glob-
ular domains (G1, G2, and G3) and specific areas containing the keratan sulfate (KS) and articular cartilage, which is difficult
chondroitin sulfate (CS) glycosaminoglycan chains. Binding of the protein core to the to duplicate with a substitute tissue
hyaluronate (HA) molecule is specific; it occurs through the N-terminal globular domain or synthetic.
and is stabilized by link protein. Numerous monomers of the aggrecan molecule can bind
to the hyaluronate, forming a proteoglycan aggregate. These enormous structures are Articular cartilage is isolated
immobilized within the network of collagen. (Reproduced with permission from Simon SR from the marrow cells by the dense
[ed]: Orthopaedic Basic Science. Rosemont, Ill: American Academy of Orthopaedic Surgeons, subchondral bone and does not
1994, p 9.) B, The change in structure of proteoglycans from fetal epiphyseal cartilage and
mature articular cartilage. Fetal cartilage proteoglycan monomers are uniformly larger in have access to its vascularity. This
size and length than the monomers in mature articular cartilage. (Reproduced with permis- lack of blood supply contributes to
sion from Rosenberg LC, Buckwalter JA: Cartilage proteoglycans, in Kuettner KE, the inability to repair itself. The
Schleyerbach R, Hascall VC [eds]: Articular Cartilage Biochemistry. New York: Raven Press,
1986, pp 41.) C, Pressure from loading of cartilage results in compression of the proteogly- usual response to injury that occurs
can molecules, which provides increased resistance to loading compared with the normally in other tissues throughout the body
extended molecule. (Reproduced with permission from Buckwalter J, Hunziker E, is dependent on hemorrhage, fibrin
Rosenberg L, Coutts R, Adams M, Eyre D: Articular cartilage: Composition and structure,
in Woo SL, Buckwalter JA [eds]: Injury and Repair of the Musculoskeletal Soft Tissues. Park clot formation, and the mobilization
Ridge, Ill: American Academy of Orthopaedic Surgeons, 1988, p 412.) of cells and important mediators
and growth factors. Trauma that

40 Journal of the American Academy of Orthopaedic Surgeons

 Douglas W. Jackson, MD, et al

chondrocytes capable of restoring

F the biomechanical and structural
P
integrity of the articular surface.
Primitive mesenchymal cells retain
the ability to differentiate into spe-
cific cell types depending on regula-
tory conditions (Fig. 8). These cells
T are found in the bone marrow,
peripheral blood, perichondrium,
periosteum, skin, muscle, and growth
A plate. They can become osteoblasts,
fibroblasts, or chondroblasts de-
pending on local and systemic stim-
P uli. This population of cells naturally
becomes reduced in number with
age but can be grown in large num-
bers in cell culture. These cells can
then be implanted in chondral and
T osteochondral defects, where they
appear to have an enhanced poten-
B C tial for repair and regeneration. On-
going research aims to induce the dif-
Figure 4 A, Histologic appearance of a human fetal knee joint (F = femur; P = patella; T =
tibia)(hematoxylin-eosin, original magnification ×10). B, Higher-magnification view of ferentiation of these newly attracted
area demarcated in A demonstrates an abundance of cells in lacunae in area where articu- or transplanted cells into mature
lar cartilage will form (hematoxylin-eosin, original magnification ×50). C, Histologic chondrocytes, which will promote
appearance of adult human articular cartilage (femoral condyle) (ruthenium hexamine
trichloride, original magnification ×120). (Part C reproduced with permission from the formation of hyaline cartilage.
Hunziker EB: Articular cartilage structure in humans and experimental animals, in Growth factors are polypeptides
Kuettner KE, Schleyerbach R, Peyron JG, Hascall VC [eds]: Articular Cartilage and that act in a paracrine manner and
Osteoarthritis. New York: Raven Press, 1992, pp 185.)
have a wide variety of regulatory
effects on cells mediated by binding
to cell surface receptors. Various
significantly disrupts the chondro- tion, cell migration from the bone factors have been identified, such as
cytes and extracellular matrix but marrow, and associated vascular fibroblastic growth factors, platelet-
does not penetrate the subchondral ingrowth. Larger osteochondral derived growth factors, insulinlike
bone has little or no capacity to defects are often filled with fibro- growth factors, transforming growth
heal.13 cartilage, which is principally type I factors (TGFs), and bone morphoge-
The only spontaneous repair collagen.17 Some rounded forms of netic proteins (BMPs). These factors
reaction that occurs in superficial chondrocytelike cells can develop have an influence on cell functions,
articular cartilage lesions is the and even synthesize type II colla- including migration, proliferation,
transient proliferation of chondro- gen in certain portions of the defect. and matrix synthesis and differentia-
cytes near the edges of the defect.6 The repair tissue is usually inter- tion, depending on their concentra-
Similar cell clusters have been re- mixed with fibrous tissue, fibrocar- tion, the presence of cofactors, the
ported in the early stages of osteo- tilage, and hyalinized tissue. This type of target cell present, and the
arthritis and have been referred to reparative tissue differs from nor- number of cell receptors available.
as cell-clones.14,15 Their size remains mal articular cartilage in that it is Bone morphogenetic proteins are
within constrained limits, and they less organized, more vascular, and characterized as members of the
do not proliferate significantly into biochemically different in water TGF superfamily (except BMP-1)
the void of the lesion or produce ade- content, proteoglycan content, and because they have seven highly con-
quate extracellular matrix (Fig. 6).16 collagen type. Mechanically, the re- served carboxyl-terminal cysteines.
In full-thickness and osteochon- parative tissue is less durable and is More than a dozen members of the
dral lesions, when the subchondral structurally different (Fig. 7). BMP family have been identified, all
plate is penetrated or removed, a For actual regeneration of articu- of which have different actions on
reparative response is generated, lar cartilage to be accomplished, the specific types of bone-forming and
which involves fibrin clot forma- cells present must become mature cartilage-forming cells.18 Types 2

Vol 9, No 1, January/February 2001 41

Cartilage Substitutes

Normal articular cartilage Articular cartilage defect Articular cartilage defect to Defect penetrates
does not penetrate subchondral bone but does bone marrow
subchondral bone not penetrate into marrow
A B C D

Figure 5 The various types and depths of articular cartilage defects or lesions that can be created in animal models to evaluate repair
processes in articular cartilage. A, Normal articular cartilage is typically organized histologically into zones. B, A partial-thickness (superfi-
cial or shallow) defect penetrating to the middle zone is isolated from the blood supply and marrow space. Such a defect typically does not
elicit or demonstrate a repair response. C, A lesion that penetrates to the subchondral bone but does not penetrate into the marrow space, if
truly isolated from the marrow, will not repair. However, even a very small communication of the lesion with the marrow blood supply
will elicit a repair response. Full-thickness lesions usually are in this category. D, A defect that penetrates through all zones of the articular
cartilage and penetrates into the marrow space typically demonstrates a repair response that results in fibrocartilaginous tissue.

through 7, which have been found Sellers et al 36 investigated the chondral bone and improved histo-
in extracts of demineralized bone, effect of rhBMP-2 on the healing of logic appearance of the overlying
have the capacity to induce the for- full-thickness osteochondral defects articular cartilage. At 24 weeks, the
mation of cartilage and bone at het- in rabbits. The results showed greatly thickness of the healing cartilage
erotopic sites.18,19 Several studies accelerated formation of new sub- was 70% of that of the normal adja-
have established a regulatory role
for BMPs in the initiation of the dif-
ferentiation of cartilage-forming and
bone-forming cells from pluripotent
mesenchymal stem cells.20-24
In particular, recombinant human
BMP-2 (rhBMP-2) appears to be
closely involved with the growth
and differentiation of mesenchymal
cells to chondroblasts and osteo-
blasts in developing limb buds.25,26
There is also increasing evidence
that these proteins have many influ-
ences on the differentiation and pro-
liferation of cells in embryogenesis,
depending on the presence of target
cells and the prevailing environmen-
tal conditions.25,27,28 In vitro studies
in adults have shown that rhBMP-2
induces expression of cartilage and Figure 6 Chondrocyte cloning after articular cartilage transplantation in a goat model.
bone markers29,30 and can enhance Cloning of chondrocytes is usually observed at the margins of articular cartilage lesions or
in cartilage demonstrating an attempted reparative response. They are believed to form in
the production of articular cartilage response to alterations in the articular cartilage matrix that signal the chondrocytes to pro-
matrix without inducing the forma- liferate or combine. The extracellular matrix they produce usually has properties different
tion of bone. 31-33 In vivo studies from those of normal articular cartilage (safranin O and fast green, original magnification ×63).
(Adapted with permission from Jackson DW, Halbrecht J, Proctor C, VanSickle D, Simon
have also shown that rhBMP-2 can TM: Assessment of donor cell and matrix survival in fresh articular cartilage allografts in a
induce the formation of cartilage and goat model. J Orthop Res 1996;14:255-264.)
bone at ectopic and skeletal sites.34,35

42 Journal of the American Academy of Orthopaedic Surgeons

 Douglas W. Jackson, MD, et al

clinically applicable. Regeneration

of the exact matrix composition and
structure and restoration of the
complicated interactions between
chondrocytes and their matrix are
the essential features necessary to
FC AC
biologically engineer articular carti-
lage substitutes.

Nonoperative Treatment
Options

The vast majority of articular carti-

lage defects and degenerative artic-
ular cartilage changes do not cause
symptoms or any significant disabil-
Figure 7 Development of fibrocartilage (FC) repair tissue in a marrow-penetrating artic-
ular cartilage lesion in the trochlear sulcus in a sheep model. The interface (solid arrow)
ity. However, some patients with
between the original articular cartilage (AC) and the fibrocartilage appears integrated. A chondral and osteochondral lesions
new subchondral bone plate has developed, but the tidemark has not developed to the may present with complaints of
original level (open arrow) at the 6-month postoperative interval (toluidine blue, original
magnification ×10).
pain, swelling, giving way, and
mechanical symptoms of locking,
catching, or crepitus. The pain and
swelling are believed to be related to
cent cartilage, and a new tidemark tribution of the bioactive molecules the presence of cartilage-breakdown
usually had formed between the throughout the matrices all affect products and the release of enzymes
new cartilage and the underlying the result. Any substitute will need and cytokines. This combination
subchondral bone. Immunostaining to be stable under the loads and cleaves articular cartilage and may
for type II collagen showed its dif- forces that articular cartilage is sub- produce painful synovitis and even-
fuse presence throughout the repair jected to with the daily activities of tual further discomfort associated
cartilage in treated defects.36 living. with capsular distention due to sy-
Lietman et al37 investigated the Stimulation of repair of superfi- novial effusion. Another source of
influence of rhBMP-7 on the synthe- cial chondral lesions is more diffi- symptoms is the stimulation of peri-
sis, release, and maintenance of pro- cult because articular cartilage con- arterial nerve fibers located in the
teoglycans in explants of porcine tains dermatan sulfate and other subchondral bone. As sclerosis of
articular cartilage held in chemically proteoglycans that confer antiadhe- the subchondral bone occurs, there
defined serum-free media. The au- sive properties on the surface of the may be secondary vascular changes
thors found a 70% to 120% increase cartilage. These hinder the ability of in the bone that result in increased
in synthesis after 7 to 10 days in cul- repair cells or tissue to bind to the venous blood flow and congestion
ture and decreased release of pro- lesion surface.38-40 By first treating and further stimulation of the nerve
teoglycans from the explants of ar- the surface of the defect with the fibers.
ticular cartilage. Overall, there was enzyme chondroitinase ABC (which The immediate goal for the symp-
a net increase in the proteoglycan digests the antiadhesive proteogly- tomatic patient seeking treatment of
content in extracts treated with cans) and then adding fibrin clot localized articular cartilage lesions
BMP-7.37 and mitogenic growth factors (par- is to decrease the secondary symp-
The successful manipulation of ticularly TGF-β1, or basic fibroblastic toms of pain and disability. Most
the microenvironment to enhance growth factor), increased coverage of symptoms related to articular carti-
or promote the synthesis of a re- a defect by mesenchymal cells from lage lesions can be managed effec-
placement with characteristics sim- the synovium can be achieved. 17 tively with either conventional or
ilar to those of hyaline cartilage This healing response generates a alternative management modalities.
will require both extensive preclini- loose fibrous connective tissue, These include patient education
cal and clinical trials to establish its rather than cartilage. To date, this about the underlying process, as
efficacy. The dose, method of de- methodology has not created an well as lifestyle and activity modifi-
livery, timing of delivery, and dis- articular cartilage substitute that is cations. Weight reduction and spe-

Vol 9, No 1, January/February 2001 43

Cartilage Substitutes
Proliferation
Commitment
Chondrocyte
Osteoblast
Lineage progression
Chondrocyte
Osteocyte
Differentiation
and maturation
Cartilage
Bone
Figure 8 Potential lineage of mesenchymal stem cells. Once the cell is committed to a
specific developmental pathway, it begins a differentiation process in which it no longer
proliferates, but instead synthesizes unique components (e.g., extracellular matrix, cell sur-
face receptors, bone, muscle) characteristic of the newly developing tissue these cells are
targeted to make.
cific muscle-strengthening and non-
aggravating fitness programs can
also be helpful. The patient is usu-
ally receptive to treatments that
minimize joint discomfort if the
need for surgery is delayed or elimi-
nated. Nonpharmacologic treat-
ment of osteoarthritis includes
application of heat and cold, selec-
tive use of bracing, physical thera-
py, and nonirritating aerobic condi-
tioning. Pharmacologic therapies
are more specific in their effects.
These include mild analgesics; anti-
inflammatory drugs, such as cyclo-
oxygenase-2 (COX-2) inhibitors;
local corticosteroid injections; and
chondroprotective agents, such as
oral glucosamine and chondroitin
sulfate and injectable hyaluronic
acid for viscosupplementation.
Patients with osteoarthritis are
looking for safer disease-altering
treatments and are even exploring
alternative therapies. Nonsteroidal
44
Mesenchymal stem cell
Tenoblast Stromal
fibroblast
Myoblast fusion Preadipocyte
Tenocyte Stromal cells
Myocyte Adipocyte
Tendon Stroma
Muscle Adipose
anti-inflammatory drugs (NSAIDs)
are the medications most commonly
prescribed for osteoarthritis. How-
ever, although more than 16 million
individuals are now taking NSAIDs,
there is no evidence that these drugs
alter the natural history of cartilage
degeneration. Furthermore, both
patients and physicians are con-
cerned about the possible long-term
effects of NSAIDs. At least 16,500
deaths a year have been caused by
gastrointestinal bleeding associated
with NSAID usage.41 The new COX-
2 inhibitors are reported to have a
lower rate of associated gastroin-
testinal bleeding side effects.
Viscosupplementation therapy
for articular cartilage defects and de-
generation by means of hyaluronic
acid injections has been available in
Europe for over a decade, in Canada
since 1992, and in the United States
since 1997. The use of viscosupple-
mentation is based on the observa-
Journal of the American Academy of Orthopaedic Surgeons
tion that there is a decrease in vis-
cosity and elasticity of the synovial
fluid in osteoarthritis and that the
native hyaluronic acid in osteoar-
thritic knees has a lower molecular
weight than that found in normal
healthy knees. Replenishing the
hyaluronic acid component of nor-
mal synovial fluid may play a role
in supplementing the elastic and
viscous properties of synovial
fluid,42,43 which may help relieve
the signs and symptoms related to
osteoarthritis and improve function.
In vitro studies of human synovio-
cytes from osteoarthritic joints have
revealed that exogenous hyaluronic
acid stimulates de novo synthesis
of hyaluronic acid,44 inhibits release
of arachidonic acid, and inhibits
interleukin-1α–induced prostaglan-
din E2 synthesis by human synovio-
cytes.45 Recent clinical trials have
evaluated the efficacy and safety of
intra-articular hyaluronic acid injec-
tions.46-50
Overall, viscosupplementation
often does not replace the need for
some alteration of specific aggra-
vating activities by means of mus-
cle strengthening and weight re-
duction. However, it may decrease
the medical costs and morbidity as-
sociated with NSAIDs by allowing
patients to use less medication.51,52
It represents an adjunct to current
treatments for osteoarthritis and an
alternative treatment when other
forms of medical treatment are con-
traindicated or have failed.
There is a need for further studies
to clarify the specific indications for
the various nonoperative treatment
modalities and to evaluate their
effectiveness with randomized, con-
trolled clinical trials. When eval-
uating both nonoperative and opera-
tive treatments, the placebo effect of
treatments of osteoarthritis and car-
tilage lesions must be taken into con-
sideration. Furthermore, symptoms
secondary to articular cartilage
lesions and osteoarthritis may have
peaks and valleys independent of

treatment, and relief may not neces-
sarily be due to the particular treat-
ment rendered. For patients for
whom nonpharmacologic or phar-
macologic modalities have been
unsuccessful, and for those who are
unable or unwilling to take the med-
ications, the utilization of surgical
interventions can be considered.
Operative Treatment
Options
There are a number of surgical op-
tions for the treatment of chondral
and osteochondral defects that are
refractory to nonoperative manage-
ment. Each of these options has
variable reported success rates de-
pending on patient age and activity
level and the location, size, shape,
and depth of the defect. The tech-
niques currently being most widely
utilized clinically for cartilage defects
and degeneration are not articular
cartilage substitution procedures,
but rather lavage, arthroscopic de-
bridement, and repair stimulation.
The direct transplantation of cells or
tissue into a defect and the replace-
ment of the defect with biologic or
synthetic substitutes accounts for
only a small percentage of surgical
interventions at this time.
“Healing” related to articular car-
tilage is a rather nonspecific term.
Healing has been defined as restor-
ing the structural integrity and func-
tion of a damaged tissue. A biologic
reparative process implies replacing
the damaged or lost cells or matrix
with new cells or matrix, but not
necessarily restoring the tissue to its
original structure. It is the term
“regeneration” that implies that the
damaged tissue has been replaced
by tissue—specifically, new cells
and matrix identical to the original
tissue.13 “Substitution” implies re-
placement of the damaged cartilage
with biologic or synthetic polymers
that possess mechanical properties
similar to those of articular cartilage
Vol 9, No 1, January/February 2001
Douglas W. Jackson, MD, et al
but does not necessarily require the duction of hemorrhage or clot forma-
exact duplication of normal articu- tion. Consequently, there is no migra-
lar cartilage. tion or proliferation of repair cells
to the defect, and thus there is limited
Lavage and Debridement or no potential for further healing.
Lavage and arthroscopic debride-
ment are techniques that do not in- Repair Stimulation
duce repair but instead are directed The goal of repair stimulation (by
toward temporary relief of the means of drilling, abrasion arthro-
symptoms and disability associated plasty, or microfracture) is to induce
with articular cartilage lesions. Ar- the migration of high concentrations
throscopic lavage has been reported of potential repair cells into the
to have beneficial effects on mild to chondral or osteochondral defects.
severe osteoarthritis of the knee.53-56 Various techniques for enhance-
The benefit of arthroscopic lavage ment of the migration of marrow
is believed to be due to the removal cells and hemorrhage have been
of degenerative articular cartilage developed (Fig. 9). The usual result
debris, proteolytic enzymes, and of these penetrating techniques is
inflammatory mediators. In addi- the partial filling of the articular
tion to the benefits of lavage, ar- defect with fibrocartilage that con-
throscopic debridement is believed tains principally type I collagen.
to be helpful by virtue of removal Unlike the desired hyaline cartilage
of partially detached flaps or de- (which is principally type II colla-
generative articular cartilage and con- gen produced by the chondrocytes),
touring of the articular surface.57-59 this fibrocartilage has diminished
Because neither technique pene- resilience and stiffness, poor wear
trates the tidemark or subchondral characteristics, and a predilection
bone, there is no significant pro- for deterioration over time.
A B C
Figure 9 Various methodologies currently used to elicit repair tissue in articular carti-
lage defects. A, Current methods involve penetrating the underlying bone endplate by
drilling, as proposed in the Pridie procedure. Variations include abrasion (B) and
microfracture (C). All these techniques penetrate the subchondral bone to open communi-
cation with a zone of vascularization to initiate fibrin clot formation and to obtain the
potential benefit of vascular ingrowth or migration of more primitive mesenchymal cells
from the bone marrow. These communications open the defect to the migration of many
types of cells, including fibroblasts and inflammatory cells. These cells may compete with
a limited number of the primitive mesenchymal cells to occupy the fibrin matrix, con-
tributing to a variety of repair scenarios. These methods penetrate the subchondral bone
plate and tidemark, but the intent is not to disrupt the integrity of the subchondral bone.
Large disruption or removal of the subchondral bone endplate may result in detrimental
mechanical, structural, and biologic changes.
45
Cartilage Substitutes

Varying amounts of fibrous tis-
sue, fibrocartilaginous tissue, and
articular cartilage–like tissue have
been reported to fill these defects
after the use of penetrating tech-
niques.5 Microfracture studies in an
equine model have suggested that
type II collagen may predominate in
the repair tissue from the fibrin clot,
which may increase in amount over
a period of 4 to 12 months.60 Correc-
tion of any malalignment defor-
mities and institution of an early-
motion rehabilitation program have
been reported to be beneficial in im-
proving the quality of replacement
tissue. Overall, this heterogeneous
tissue has inferior mechanical char-
acteristics, which leads to deteriora-
tion of clinical results with time.
The outcomes have been particularly
poor in cases of malalignment. These
findings have stimulated the explo-
ration of other treatment modalities
that yield tissue that more closely
simulates native cartilage.
implanted into the defect. Other ap-
proaches to cartilage regeneration
involve the use of different types of
autologous cells that are less differ-
entiated precursor cells with chon-
drogenic potential. These stem cells
can be derived from skin, muscle,
perichondrium, periosteum, synovi-
um, bone marrow, epiphyseal plate,
and peripheral blood sources. Un-
der the influence of environmental
conditions and growth factors, these
cells can be induced to differentiate
into mature chondrocytelike cells
that may produce a hyalinelike car-
tilage.
Several methods of regeneration
have been applied to articular carti-
lage defects. Both Grande et al62 in
1989 and Brittberg et al 63 in 1996
demonstrated in rabbit models that
by adding cultured chondrocytes
under a transplanted periosteum
graft (cambium layer facing the
defect), an enhanced repair could be
achieved, rather than generation of
periosteal tissue alone. With these
techniques, chondrocytes were re-
leased enzymatically and subjected
to proliferative expansion in vitro.
The resulting increased populations
of cells were transplanted into carti-
lage defects and covered by a peri-
osteal flap. The cells that filled the
defects appear to produce a hyaline
cartilage–like tissue. A periosteal
flap with the cambium layer down
was used to seal the transplanted
cells in place and act as a mechani-
cal barrier, which was considered to
have a beneficial humoral or para-
crine effect on the synthesis of re-
parative tissue (Fig. 10). Migration
of chondrogenic cells directly from
the periosteal cambium layer may
also contribute undifferentiated
cells to the repair process.
The autologous chondrocyte
implantation technique preserves
the subchondral bone plate, with a

Cell and Tissue Transplantation

Generating a biologic substitute
tissue that resembles native articu- Periosteum
Fibrous layer
lar cartilage requires living cells that
Cambium layer
are capable of synthesizing and
Cortical
maintaining their surrounding carti- bone
laginous matrix. These living cells, Cambium layer
or tissue containing living cells, may faces down Incorrect
be directly transplanted into an ar-
ticular cartilage defect. Once the Correct
cells have been implanted in the de-
fect, they need to remain viable and
Cambium layer
to replicate and synthesize a dur- faces down
able matrix to be effective. Experi-
mental and preliminary clinical
Articular
work with tissue regeneration tech-
cartilage
niques has shown that both autolo-
gous committed chondrocytes and Periosteal cambium-
undifferentiated mesenchymal cells Release of factors by cambium cell harvest site
placed in articular cartilage defects cells (paracrine effect?)
survive and are capable of produc-
Figure 10 Autologous chondrocyte implantation technique. Articular cartilage is pro-
ing a new cartilagelike matrix.61 cured, and its chondrocytes are enzymatically released and expanded in cell culture.
One method of trying to generate When a sufficient number of cells are obtained, a second operation is performed for
cartilage is autologous chondrocyte implantation of the cultured cells. A periosteal flap with matching geometry is harvested
and sutured in place with the cambium cell layer facing the defect (down). The edges of
implantation, in which mature artic- the flap are sealed with fibrin glue. Inset, Care must be taken when harvesting periosteum
ular chondrocytes are harvested, to ensure that the cambium cells remain attached to the periosteal fibrous layer.
expanded in cell culture, and then

46 Journal of the American Academy of Orthopaedic Surgeons


reported high success rate.64 In a
retrospective study, Peterson et al65
evaluated the clinical, arthroscopic,
and histologic results in 101 pa-
tients who underwent autologous
cultured chondrocyte transplanta-
tion. At a follow-up interval of 2 to
9 years, 92% of the patients with
isolated femoral condyle lesions,
65% with chondral lesions on the
patella, 67% with multiple lesions,
89% with osteochondritis dissecans
lesions, and 75% with femoral con-
dyle defects treated simultaneously
with anterior cruciate ligament re-
construction had good or excellent
results. Follow-up arthroscopic ex-
aminations of 53 patients showed
good fill with repair tissue, good
adherence to underlying bone, and
hardness close to that of the adja-
cent tissue. Histologic analysis of
37 biopsy specimens showed an
association between hyalinelike tis-
sue and improved clinical outcomes
and, conversely, between fibrous
repair tissue and poor outcomes. In
addition, the authors concluded
that instability of the knee or abnor-
mal weight distribution may ad-
versely affect the results.
The current indication for im-
plantation of autologous cultured
chondrocytes is for repair of symp-
tomatic, cartilaginous defects of the
femoral condyle (medial, lateral, or
trochlear) in patients who had an
inadequate response to prior ar-
throscopic or other surgical repair.
It should be used only in conjunc-
tion with debridement, placement
of a periosteal flap, and rehabilita-
tion. It is not indicated for the treat-
ment of cartilage damage associated
with osteoarthritis, and any accom-
panying instability or abnormal
weight distribution within the joint
should be corrected prior to implan-
tation.
Osteochondral Plugs
Large untreated (empty) lesions
created in weight-bearing surfaces
of the medial femoral condyles in a
Vol 9, No 1, January/February 2001
Douglas W. Jackson, MD, et al
goat model have demonstrated pro- effect of defect size in the distal fe-
gressive changes in both the bone mur of horses and demonstrated
and the articular cartilage compart- that a large (9-mm-diameter) lesion
ment over time, with an associated did not heal, but that a smaller (3-
abortive spontaneous repair process mm-diameter) lesion was fully re-
and deleterious effects in a zone paired by 3 months. In addition to
surrounding the defect (Fig. 11). the size of the defect, other factors
Without reestablishment of a bone that may affect a reparative process
base that includes a subchondral include the location of the defect in
plate, it is highly unlikely that a car- a weight-bearing area and early
tilaginous reparative process will loading in weight-bearing areas
progress to a functional, nondegen- during the initial healing process.
erative end point in larger defects. For full-thickness articular carti-
If the defect is beyond a critical lage defects and osteochondral de-
size, it appears to be difficult to fects, another repair option includes
achieve complete repair spontane- the transplantation of autologous
ously. Convery et al66 assessed the living chondrocytes with their im-
A B C
D E F
Figure 11 Appearance of a 6-mm articular cartilage lesion in the medial femoral condyle
in a goat model at various time intervals after creation of the lesion. Gross appearance at
time zero (immediately after lesion creation) (A) and 1 year postoperatively (D). Articular
cartilage adjacent to the defect was also affected, undergoing changes in a region called the
“zone of influence,” which is characterized by flattening and cartilage thinning and matrix
alterations that remained abnormal throughout the study period. Coronal-section micro-
radiographic appearance of the lesion at time zero (B) and computed tomographic scan
obtained at 1 year (E) demonstrate changes in lesion geometry. Histologic sections of the
lesion at 48 hours after its creation (C) and at 6 months show that the wall of the lesion has
enlarged, and the surface articular cartilage appears to be collapsing into the defect, form-
ing a cystlike structure (F). The articular cartilage at the margins migrated over the edges
of the defect, and cloned cells remained at the margins of the lesions. Furthermore, while
bone has the potential to spontaneously regenerate itself, these bone defects did not regen-
erate or repair completely. It appears that following destruction of the subchondral plate,
the reparative bone response was altered in association with the size of a defect (hema-
toxylin-eosin, original magnification ×10). (Adapted with permission from Jackson DW,
Lalor PA, Aberman HM, Simon TM: Spontaneous repair of full-thickness defects of articu-
lar cartilage in a goat model: A preliminary study. J Bone Joint Surg Am 2001;83:53-64.)
47
Cartilage Substitutes
mediate normal matrix intact. This
substitution replacement involves
the transplantation of single or multi-
ple osteochondral grafts, commonly
referred to as mosaicplasty or the
Osteochondral Autograft Transplant
System. This technique can be per-
formed as an arthroscopic or limited
open procedure. It involves excising
all injured or unstable tissue from
the articular defect and creating cy-
lindrical holes in the base of the de-
fect and underlying bone. These
holes are filled with cylindrical plugs
of healthy cartilage and bone in a
mosaic fashion (Fig. 12). The osteo-
chondral plugs are harvested from a
weight-bearing area of lesser impor-
tance in the same joint. The goal is
to fill the defect as completely as
possible (usually 60% to 80% of the
surface area). Histologic evidence
demonstrates that the hyaline carti-
lage on the cylindrical graft has the
Implanted osteochondral plugs
Potential
harvest
sites
Figure 12 Osteochondral plug transplan-
tation technique. The lesion site is pre-
pared by debriding any loose articular car-
tilage, and the number and size of the
plugs to be used for repair are determined.
The holes to receive the plugs are drilled in
the floor of the lesion. With use of special-
ized harvesting instrumentation, the osteo-
chondral plugs are procured from suitable
sites so as to approximate the surface
geometry of the lesion site. The plugs are
then implanted to the appropriate depth
into the holes placed in the lesion base.
48
ability to survive in its new setting
and maintain its structural integrity.
In a study on 227 patients, Han-
gody et al67 reported that mosaic-
plasty had superior results com-
pared with abrasion arthroplasty,
microfracture, and Pridie drilling
in articular lesions ranging in size
from 1 to 9 cm2. The authors con-
cluded that the results of proce-
dures penetrating the bone endplate
deteriorate over time, with improve-
ments ranging from 48% to 62%,
while mosaicplasty results stabilize
at 86% to 90% at 5 years.
Overall, the transplantation of
osteochondral autografts has been
shown to be an effective technique
for replacing confined areas of dam-
aged articular cartilage. The tech-
nique of fixation and the value of
continuous passive motion, with al-
tered weight bearing, are reported
to be important in obtaining optimal
results. Factors that can compro-
mise the results include donor-site
morbidity, the effects of joint incon-
gruity on the opposing surface of
the donor site, damage to the chon-
drocytes at the articular margins of
the donor and recipient sites dur-
ing preparation and implantation,
and collapse or settling of the graft
over time. In addition, articular mis-
matches of the surface curvature
after implantation may compromise
results and affect the opposing sur-
face of the recipient site. Accurate
restoration of the normal contour
of the articular surface may depend
on the size of the defect and the con-
tour of the donor autograft plug, as
well as appropriate depth place-
ment of the graft.
Osteochondral Allografts
Transplantation of large allo-
grafts of bone and overlying articu-
lar cartilage is another treatment
option after trauma to articular car-
tilage and underlying bone that
involves a greater area than is suit-
able for autologous cylindrical
plugs, as well as for a noncontained
Journal of the American Academy of Orthopaedic Surgeons
defect. Allografts have been used
successfully after severe acute joint
trauma and in the treatment of neo-
plasms involving the joint or adja-
cent bone. The advantages of osteo-
chondral allografts are the potential
to restore the anatomic contour of
the joint, lack of morbidity related
to graft harvesting, and the ability
to reconstruct large defects. Better
clinical results from these grafts are
related to the higher percentage of
chondrocytes remaining viable to
maintain the extracellular matrix,
healing of the junction site to the
host bone, and revascularization of
the graft without excessive col-
lapse.68 In one study,69 the viability
of chondrocytes after osteochondral
allograft transplantation ranged
from 69% to 99% in three grafts
studied at 12, 24, and 41 months.
Stored frozen irradiated osteochon-
dral allografts were also tested as
controls; no viable cells were dem-
onstrated. Even when failure oc-
curred, 66% of the failed grafts had
viable chondrocytes.69 However,
not all studies have shown this de-
gree of chondrocyte survival.
The success of fresh osteochon-
dral grafts has been reported to be
75% at 5 years, 64% at 10 years, and
63% at 14 years.68,70 Frozen allo-
grafts appear to produce results
that compare favorably with those
obtained with fresh grafts when
used to replace localized defects of
the distal femoral articular surface.
The failure rate was higher for
bipolar grafts than when either the
tibia or the femur alone was re-
placed (success rate of 25% vs 70%
at 10 years).68,70 It is also less suc-
cessful for patients older than 60
years of age. Unloading osteoto-
mies have been used to enhance
the success of these allografts. The
best results are in single, well-
demarcated, full-thickness osteo-
chondral defects that are 2 to 5 cm
in diameter in an otherwise normal
knee.68,70 Concerns related to preser-
vation techniques, disease transmis-

sion, tissue viability, tissue availabil-
ity, and immune responses to the cells
or matrix (graft-host interactions)
limit the use of this technique.
Biologic and Synthetic Matrices
Recent interest and research
have been directed toward finding
different types of both biologic and
synthetic polymers to fill osteo-
chondral defects. They may be
used to cover and cushion underly-
ing exposed bone, reestablish a con-
gruent articulating surface, reduce
crepitation and contact of bone-on-
bone surfaces, act as a pain-free sur-
face, stabilize progression of the
zone of influence on adjacent tissue,
and provide physical and mechani-
cal properties of articular cartilage.
Biologic scaffolds may act as carri-
ers for transplanted cells and/or
may be vehicles for delivery of sig-
naling substances (bioactive factors)
that stimulate cells to grow into
them (inductive) and on them (con-
ductive). They have the potential to
minimize the number of cells lost in
the synovial fluid and allow easier
delivery of the cells into a defect.
Polymers can be produced in
different forms and shapes and can
be modified for porosity and the
number of cells they contain. They
may be composites and may vary
in structural characteristics (e.g.,
hard vs soft, permanent vs bioab-
sorbable). Potentially, the synthetic
matrices can bridge the void of the
osteochondral defect to overcome
the deleterious effects seen with
larger lesions and can facilitate the
restoration of an articulating sur-
face. Important points in develop-
ing matrices to replace articular
cartilage are mechanical stability,
bonding to the host tissue, biocom-
patibility, internal cohesiveness,
and the three-dimensional organi-
zation within the matrix. Implants
may be formed from a variety of
biologic and nonbiologic materials,
including treated cartilage and
bone matrices, collagens with or
Vol 9, No 1, January/February 2001
without hyaluronan, fibrin, carbon
fiber, hydroxyapatite, porous poly-
lactic acid, polytetrafluoroethylene,
polyester, and other synthetic poly-
mers.
An example of one of these syn-
thetic polymers for localized re-
placement of articular cartilage
lesions is flowable in situ curable
polyurethane, which is being de-
veloped by Advanced Bio-Surfaces,
Inc (Minnetonka, Minn). 71 This
elastomer is biocompatible and has
mechanical characteristics that
mimic those of articular cartilage.
It allows customized restoration of
some articular cartilage defects
with the use of minimally invasive
techniques. This biomaterial is a
two-part reactive system; the reac-
tive components are liquid at room
temperature but form a solid elasto-
meric implant within minutes after
mixing and delivery. The cured
polymer is cross-linked, segmented
polyurethane that exhibits high
tensile strength and excellent tear
and fatigue resistance under physio-
logic conditions. The elastic deforma-
tion of the material allows impact
absorption and load distribution
across the implant. Some plastic
deformation also occurs, allowing
improved congruency with the ar-
ticulating surface. Postoperative
immobilization is necessary.
Although the durability of such
substances after human implanta-
tion has not been established, it is
hoped that synthetic polymers used
for focal articular cartilage lesions
may postpone or delay the need for
a total joint replacement in adult
patients. Utilization of these sub-
stances has the potential to delay or
avoid major surgery, reduce the
need for postoperative rehabilita-
tion, and allow rapid return to full
functional status. The use of local
cartilage restoration procedures
should not preclude a patient with
osteoarthritis from undergoing a
total knee replacement in the future.
Until the ideal substitute is devel-
Douglas W. Jackson, MD, et al
oped, achieving pain relief, restor-
ing function, and delaying the need
for joint replacement are short-term
goals directing research around the
world.
Rehabilitation After Cartilage
Substitution
The effects of weight bearing
and movement on any new articu-
lar surfaces will vary depending on
the type of procedure. Rehabilita-
tion must include appropriate lev-
els for maintaining the surround-
ing articular cartilage and muscle
strength. Reducing joint loading
can lead to atrophy or degeneration
of normal articular cartilage. In-
creasing joint loading through ex-
cessive use or increased magnitude
can be deleterious to articular carti-
lage. Joint loading influences chon-
drocyte function beneficially or
detrimentally over a very broad
range and is an important part of
any repair, replacement, or regen-
erative process. The tolerance for
temporal loading of new surfaces
will vary depending on the repair
process and the substitute used.
Breinan et al72 demonstrated in
animal studies that there are three
phases of tissue repair with cell-
based therapies: the proliferative
phase, which occurs at 0 to 3 months;
the transitional phase, which in-
volves macromolecular matrix pro-
duction at 3 to 6 months; and finally
the ongoing remodeling phase. In
an environment conducive to stimu-
lation and maturation, mechanical
overloading must be avoided through
protected weight bearing and func-
tional use of the limb without im-
pact loading, as well as correction of
any malalignment or ligamentous
instabilities before or during admin-
istration of cell-based therapies.
Failure to recognize overloading
before mechanical integration of the
repair tissue is complete may result
in degradation and failure of the
tissue. Simultaneous correction of
any factors that produced or con-
49
Cartilage Substitutes
tributed to the initial lesion, such as
malalignment or ligamentous insta-
bility, is critical to the success of the
procedure.
Summary
Surgical considerations when utiliz-
ing cartilage substitutes should
include the cause and chronicity of
the defect, the general medical and
systemic history of the patient, the
depth of the defect, the size of the
lesion, the degree of containment,
the location and number of defects,
ligament integrity, meniscal integrity,
alignment, and previous treatments
rendered. It is important to remem-
ber that not all chondral or osteo-
chondral lesions found at magnetic
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Clin Sports Med 1991;10:569-593.
71. Jackson DW, Felt JC, Song Y, Van
Sickle DC, Simon TM: Restoration of
large femoral trochlear sulcus articular
cartilage lesions using a flowable poly-
mer: An experimental study in sheep.
Trans Orthop Res Soc 2000;25:670.
72. Breinan H, Minas T, Barone L, et al:
Histological evaluation of the course
of healing of canine articular cartilage
defects treated with cultured chondro-
cytes. Tissue Eng 1997;4:101-114.
 Wrist Arthrodesis: Review of Current Techniques

Peter J. L. Jebson, MD, and Brian D. Adams, MD

Abstract

Wrist arthrodesis is a well-established procedure that predictably relieves pain inserting the Steinmann pin into
and provides a stable wrist for power grip. Although a variety of techniques for the radius via the second or third
achieving a solid fusion have been described, the combination of rigid stabiliza- web space of the hand. In 1982,
tion with a dorsal plate and autogenous cancellous bone grafting results in a Feldon and co-workers9 described
high fusion rate and obviates the need for prolonged postoperative cast immobi- the use of two smaller Steinmann
lization. Successful results with dorsal plating with or without local bone graft pins inserted through the second
have recently been reported for patients with posttraumatic conditions. Rod or and third web spaces and between
pin fixation is an established procedure for patients with inflammatory arthritis the metacarpal shafts into the
or a connective tissue disorder; however, plate fixation for these conditions is medullary canal of the radius. This
becoming a more acceptable alternative. Complications are relatively common technique improved stability and
and range from minor transient problems to major problems, such as wound obviated the need for supplemen-
dehiscence, infection, extensor tendon adhesions, and plate tenderness, which tary staple or wire fixation. Viegas
may require implant removal. Preoperatively, patients should be assessed for et al10 recommended placing a sin-
the presence of carpal tunnel syndrome, distal radioulnar joint arthritis, or gle large Steinmann pin adjacent to
ulnocarpal impaction syndrome, which may become or remain symptomatic the base of the second metacarpal,
after arthrodesis. Wrist arthrodesis results in a high degree of patient satisfac- through the carpus, and into the
tion with respect to pain relief and correction of deformity. Patients are able to medullary canal of the radius. They
accomplish most daily tasks and activities by learning to adapt to, and compen- suggested that this insertion posi-
sate for, the loss of wrist motion. tion places the wrist in extension
J Am Acad Orthop Surg 2001;9:53-60 and ulnar deviation, thus improving
grip strength.
Proponents of intramedullary
rod or pin techniques have sug-
Since the original report by Ely in high rates of pseudarthrosis and gested a number of advantages.
1910, arthrodesis of the wrist has graft failure led to the use of inter- These include decreased operative
become a well-established recon- nal fixation devices to augment the time, simplicity, ability to perform
structive procedure for a number of arthrodesis.
upper extremity disorders. A vari- In 1965, Clayton6 described a tech-
ety of methods for achieving wrist nique for achieving wrist arthrod-
fusion have been described.1-5 The esis in patients with rheumatoid Dr. Jebson is Assistant Professor, Hand and
earliest techniques relied on cancel- arthritis. The technique involves Microvascular Surgery, Section of Orthopaedic
Surgery, University of Michigan Medical
lous or corticocancellous bone-graft the insertion of a single 3Ú 32-inch-
Center, Ann Arbor. Dr. Adams is Professor,
stabilization alone and varied with diameter Steinmann pin down the Division of Hand and Microsurgery, De-
respect to donor site; type, size, and third metacarpal shaft into the partment of Orthopaedic Surgery, University
shape of the graft; and method of medullary canal of the radius. The of Iowa Hospitals and Clinics, Iowa City.
graft insertion. Postoperative cast pin maintains alignment and stabil-
immobilization was required to ity after the placement of a dorsal Reprint requests: Dr. Jebson, Section of
Orthopaedic Surgery, University of Michigan
maintain wrist position until a solid corticocancellous bone graft. In
Medical Center, 1500 East Medical Center
fusion was achieved. Concerns re- 1971, Mannerfelt and Malmsten 7 Drive, TC2912, Ann Arbor, MI 48109-0328.
garding the inconvenience and modified the procedure by using a
morbidity of prolonged immobi- Rush rod reinforced with a staple. Copyright 2001 by the American Academy of
lization, the morbidity of extensive In 1973, Millender and Nalebuff8 Orthopaedic Surgeons.
bone grafting, and the unacceptably further modified the technique by

Vol 9, No 1, January/February 2001 53

Wrist Arthrodesis
concomitant procedures at the
metacarpophalangeal joints in
patients with inflammatory arthri-
tis, short recuperation period, low-
ered cost compared with other
implants, and flexibility in posi-
tioning the wrist in the desired
amount of flexion or extension.
In 1972, Meuli 11 performed a
wrist arthrodesis with a dorsal plate
applied from the second metacarpal
to the radius. Manetta and Tavani12
recommended axial compression of
the radiocarpal joint and fixation of
the plate on the third metacarpal.
Wright and McMurtry13 reviewed
their experience with arthrodesis
with a 3.5-mm dynamic compres-
sion plate. Using a dorsal plate for
wrist arthrodesis was advocated as
a method of achieving immediate
rigid fixation that obviated the need
for postoperative cast immobiliza-
tion and avoided the complications
of hardware failure and pseudar-
throsis (Fig. 1). Although there
were high rates of fusion and sub-
Figure 1 Wrist arthrodesis performed
with the single-intramedullary-rod tech-
nique. The patient had a painful pseud-
arthrosis involving the scaphotrapezio-
trapezoid articulation. The rod is broken,
most likely the result of failure to include
the third carpometacarpal joint in the
fusion.
54
jective satisfaction with respect to
pain relief, several patients in their
series required plate removal be-
cause of tenderness and/or extensor
tendon irritation. In addition, precise
contouring of the plate into slight
wrist extension and ulnar deviation
was time-consuming and difficult
to achieve. A recent development
is the precontoured, low-contact,
dynamic-compression titanium
plate (Fig. 2), which was specially
designed for wrist arthrodesis.
Despite immediate rigid stabi-
lization with a dorsal plate and
advances in implant design, supple-
mentation of the fusion site with
autogenous cancellous bone graft
from the iliac crest continues to be
common practice. Significant donor-
site morbidity, including persistent
pain, hematoma formation, infec-
tion, and nerve injury, has led to the
use of alternative techniques, such
as obtaining bone graft from the
distal radius or fusion without bone
graft.14,15 Use of the iliac crest is
reserved for those patients with
poor bone quality or large defects.
Supplemental autogenous bone
grafting is usually not necessary for
patients with inflammatory arthritis.
Indications
The most common indication for
wrist arthrodesis is symptomatic
posttraumatic or degenerative arthro-
sis of the radiocarpal and midcarpal
joints that is severe and unrespon-
sive to conservative nonoperative
treatment and will not be improved
by a motion-saving procedure.
Additional indications include con-
ditions that cause destruction, insta-
bility, or contracture of the wrist
joint, such as the inflammatory
arthritides, infection, nerve palsy,
and paralytic, spastic, and connec-
tive tissue disorders, as well as bone
loss due to trauma or following
tumor resection. Wrist arthrodesis
is also indicated for the treatment of
Journal of the American Academy of Orthopaedic Surgeons
complex carpal instability problems
and salvage of a failed implant ar-
throplasty, proximal row carpectomy,
or limited intercarpal arthrodesis.
Performing bilateral wrist ar-
throdeses in the patient with in-
flammatory arthritis is controver-
sial. Patients with bilateral wrist
arthrodeses are believed to have
less dexterity and greater functional
compromise than those with an
arthrodesis of one extremity and
arthroplasty of the other. However,
there is disagreement with respect
to which extremity should be fused.
Arthrodesis of the nondominant
extremity and arthroplasty of the
dominant extremity has been advo-
cated. There is no consensus re-
garding optimal positioning when
arthrodesis is performed in both
extremities. Several authors recom-
mend the neutral position for the
dominant extremity and 5 to 10 de-
grees of flexion for the nondomi-
nant side.16,17 Brumfield and Cham-
poux18 recommend 10 degrees of
extension for both extremities.
Clayton and Ferlic19 recommend a
neutral position for both wrists.
Contraindications
Contraindications to wrist arthrod-
esis include a lack of adequate soft-
tissue coverage and the presence of
active wrist infection. Arthrodesis is
also contraindicated when motion-
preserving procedures are possible
means of preserving function.
Because of the technical require-
ments, wrist arthrodesis should
also be avoided for the skeletally
immature patient with open epiphy-
seal plates.
Surgical Technique Using
the Wrist Fusion Plate and
Local Bone Graft
This procedure can be performed
with the use of either brachial plexus
 Peter J. L. Jebson, MD, and Brian D. Adams, MD

A B

Figure 2 A, The three plate options: the standard-bend (top), short-bend (middle), and straight plates (bottom). The precontoured titani-
um plates are manufactured by Synthes USA (Paoli, Pa). B, Note the low profile, tapered end, and built-in fusion angle of 10 degrees of
dorsiflexion in the standard-bend and short-bend plates.

block or general anesthesia. If iliac-
crest bone graft is required, general
anesthesia is usually necessary, al-
though on occasion local anesthesia
and a brief period of sedation may
be used for that portion of the pro-
cedure. Under tourniquet control, a
straight incision is made from
the distal third of the index finger–
middle finger interosseous space
across Lister’s tubercle and over the
radial shaft to the proximal border
of the abductor pollicis longus mus-
cle. Full-thickness skin flaps are ele-
vated, with care taken to protect the
cutaneous nerves and dorsal veins.
The third dorsal compartment of the
extensor retinaculum is opened, and
the extensor pollicis longus muscle
and tendon are retracted radially.
The second and fourth dorsal com-
partments are elevated subperiosteal-
ly in the radial and ulnar directions,
respectively. The dorsal aspect of
the third metacarpal is exposed by
sharply incising and elevating the
periosteum, with care taken to avoid
damaging the adjacent interosseous
muscles.
The incision is deepened proxi-
mally to expose the third carpo-
metacarpal, capitolunate, and ra-
diocarpal articulations. Distraction
is applied to the hand, and the ar-
ticular surfaces of the third car-
pometacarpal, capitolunate, radio-
scaphoid, and radiolunate joints
are denuded to cancellous bone
(Fig. 3, A). Articular cartilage may
be removed with a curette and/or
a rongeur. Alternatively, a burr
may be used, particularly for scle-
rotic bone. The triquetrohamate,
capitohamate, and scaphotrapezio-
trapezoid surfaces are similarly
prepared for fusion if symptomatic
arthritic involvement is identified
on preoperative radiographs or
clinical examination. Lister’s tuber-
cle is removed, and the dorsal sur-
faces of the scaphoid, lunate, and
capitate are decorticated to provide
a flat surface for plate application
(Fig. 3, B).
Cancellous bone graft is harvested
from within the distal metaphyseal
region of the radius through a corti-
cal window created 2 cm proximal
to the distal radial articular surface
and radial to the intended plate
position. One centimeter of sub-
chondral and metaphyseal bone
should be preserved during harvest-
ing of the graft. Bone graft is inserted
into the prepared joint spaces that
will lie beneath the plate.
The appropriate plate type is then
selected. If the AO wrist arthrod-
esis system is used, there are three
choices of plates. A standard-bend
plate is used in larger individuals.
A short-bend plate is used in small-
stature patients and in those with a
failed proximal-row carpectomy. A
straight plate is used in patients
with unusual wrist anatomy or a
severely deformed joint or when a
large intercalary bone graft is nec-
essary.
Proper plate position and align-
ment should be confirmed before
screw insertion. The plate is fixed
to the third metacarpal shaft with
three 2.7-mm bicortical screws.
Alternatively, the plate may be
fixed to the second metacarpal to
position the wrist in slight ulnar
deviation, thus enhancing power
grip. The holes must be drilled
exactly from dorsal to volar in the
sagittal plane; otherwise, rotational
malalignment of the middle finger
will occur when the plate is se-
cured to the radius. The holes
should also be drilled in the mid-
line of the metacarpal to optimize
screw fixation and to prevent meta-
carpal fracture. The plate should
be properly seated and secured as

Vol 9, No 1, January/February 2001 55

Wrist Arthrodesis

Before decortication

After plate application

Always fused Figure 3 A, Joint surfaces to be included in the fusion.

The inclusion of optional joints into the arthrodesis is based
Optional on the presence of deformity or arthritis on preoperative
examination or radiographs. B, Lister’s tubercle is os-
teotomized. The dorsal aspects of the third carpometacarpal
joint, scaphoid, capitate, and lunate are decorticated.
A

far proximally as possible on the
metacarpal shaft to avoid irritation
of the overlying extensor tendons
by the distal edge of the plate. An
additional 2.7-mm bicortical screw
is placed into the capitate. The
plate is fixed to the radius with
four fully threaded 3.5-mm screws
placed in bicortical fashion. The
fusion mass is compressed by
drilling the radial-shaft screw holes
eccentrically away from the wrist
joint.
Appropriate plate position and
screw lengths are confirmed with
intraoperative radiographic imag-
ing. Wound closure is performed
over a suction drain. The distal por-
tion of the plate is covered with the
dorsal hand fascia and periosteum
if possible. The capsule may also
be covered over the plate; alterna-
tively, a distally based slip from
one of the wrist extensor tendons
may be used. The extensor pollicis
longus is transposed above the
extensor retinaculum as the third
dorsal compartment is closed. The
tourniquet is deflated, and hemosta-
sis is obtained. Skin closure is per-
formed with nonabsorbable suture
placed in interrupted horizontal-
mattress fashion to facilitate ever-
sion of the wound edges. A soft,
bulky dressing is applied.
Postoperatively, the patient is
encouraged to elevate the extremity
and perform active and passive dig-
ital range-of-motion exercises. Su-
tures are removed at 10 to 14 days,
and a volar forearm-based splint is
applied. Only light activities are
permitted. Strengthening exercises
are begun 6 weeks after surgery.
Splinting is discontinued at 6 to 8
weeks, and full unrestricted use of
the extremity is usually permitted
by 10 to 12 weeks postoperatively
when healing is complete and radio-
graphs confirm successful fusion.
Figure 4 illustrates a case of wrist
arthrodesis performed with the cus-
tom plate in a patient with post-
traumatic arthritis.
Surgical Technique Using
an Intramedullary Rod
Exposure of the distal radius and car-
pus is performed through a dorsal
longitudinal incision, as described
for the dorsal-plate technique. In
the patient with inflammatory ar-
thritis, it is particularly important to
handle all skin flaps gently, to pre-
serve dorsal veins, and to maintain
thick skin flaps. The skin flaps and
subcutaneous tissue are elevated
from the extensor retinaculum,
which is incised longitudinally over
the sixth compartment. The remain-
ing compartments are released in an
ulnar-to-radial direction, preserving
the broad, radially based retinacular
flap for transposition of all or a por-
tion of the retinaculum beneath the
extensor tendons.
A longitudinal wrist capsulotomy
is made, followed by exposure of
the radiocarpal and intercarpal
joints. A complete radiocarpal and
intercarpal synovectomy is per-
formed. Articular cartilage from
the radiocarpal, intercarpal, and
midcarpal joints is removed. Con-
comitant procedures involving the
extensor tendons and the distal
radioulnar joint (DRUJ) are per-
formed as indicated. If the distal
ulna is excised, the resected bone
may be morcellized and used as
bone graft. In patients with post-

56 Journal of the American Academy of Orthopaedic Surgeons


traumatic or degenerative arthritis,
the fusion site is supplemented
with cancellous bone harvested
from the distal radius or iliac crest.
There are several acceptable
methods of pin or rod placement.
The single-Steinmann-pin technique
of Millender and Nalebuff8 and the
dual-rod technique of Feldon9 dem-
onstrate the principles of this ap-
proach.
Millender-Nalebuff Technique
With this technique, the wrist is
palmar-flexed, and the intramedul-
lary canal of the distal radius is
carefully entered with a pointed
awl or large curette. A Steinmann
pin is advanced into the radius
manually or with a power drill.
The size of the pin is sequentially
increased until the largest possible
pin that can be accommodated by
the radial shaft is identified. This
pin is drilled in a proximal-to-distal
direction through the carpus until
A B
Figure 4 AP (A) and lateral (B) radiographs of the wrist demonstrate the scapholunate advanced collapse (SLAC) pattern of arthritis,
with narrowing of the radioscaphoid joint and midcarpal arthritis. Posteroanterior (C) and lateral (D) radiographs 10 weeks after wrist
arthrodesis performed with a titanium custom wrist fusion plate and local bone graft.
Vol 9, No 1, January/February 2001
Peter J. L. Jebson, MD, and Brian D. Adams, MD
it exits through the second or third
intermetacarpal space dorsally.
The pin is then withdrawn distally,
the hand is reduced on the wrist,
and the pin is advanced proximally
into the previously prepared med-
ullary canal of the radius. The pin
is countersunk beneath the skin
into the intermetacarpal space with
a bone tamp.
Because the pin is not bent, the
wrist is subsequently fused in a
neutral flexion-extension position.
Alternatively, if concomitant meta-
carpophalangeal joint implant ar-
throplasties are to be performed, the
Steinmann pin can be placed down
the third metacarpal shaft after
resection of the metacarpal head.
The pin should be sufficiently coun-
tersunk to avoid interfering with
subsequent implant placement.
Feldon Dual-Rod Technique
Instead of a single large Stein-
mann pin, two smaller (3Ú32- to 7Ú64-
C D
inch-diameter) pins are inserted
dorsally across the carpus into the
second and third intermetacarpal
spaces. The pins may be bent be-
fore or after insertion to obtain the
desired degree of wrist extension
and ulnar deviation. The pins are
cut short and impacted beneath the
skin.
In both methods, the capsule is
reapproximated, and the radially
based extensor retinacular flap is
transposed beneath the extensor
tendons. If there is a tendency to-
ward bowstringing, one half of the
retinaculum can be placed over the
tendons. The tourniquet is released,
and hemostasis is obtained. The
skin is closed, and a sterile dressing
is applied, followed by a short plas-
ter arm cast or splint immobili-
zation.
Postoperative management is
similar to that used after arthrode-
sis with a dorsal plate with one
exception. Following suture re-
57
Wrist Arthrodesis
moval, the wrist is immobilized in a
short arm cast for 6 weeks. The de-
cision to discontinue immobiliza-
tion is based on radiographic con-
firmation of successful arthrodesis.
Capitate-Radius
Arthrodesis
An alternative technique for achiev-
ing radiocarpal arthrodesis in pa-
tients with a severe flexion defor-
mity of the wrist due to congenital
or acquired spastic deformities of
the upper extremity has been re-
ported by Louis et al.20 The tech-
nique involves excision of the prox-
imal 80% of the scaphoid, the entire
lunate and triquetrum, and a por-
tion of the hamate. A trough is cre-
ated in the subchondral region of
the distal radius to facilitate seating
of the denuded proximal pole of the
capitate. The hand is positioned in
neutral or slight palmar flexion and
ulnar deviation, and the fusion site
is augmented with Kirschner wires,
transfixing staples, or a dorsal plate
as needed. Concomitant sectioning,
lengthening, or transfer of wrist
and digital flexor tendons may be
needed to allow satisfactory posi-
tioning of the hand. Postopera-
tively, plaster cast immobilization
is maintained until there is clinical
and radiographic evidence of union.
The advantages of the capitate-
radius arthrodesis include the in-
trinsic stability created by excision
of the proximal carpal row and in-
sertion of the capitate into the ra-
dius and the elimination of autog-
enous bone grafting. In addition,
the shortening accommodates the
contracted volar wrist and digital
flexor tendons. The cosmetic ap-
pearance of the severely flexed ex-
tremity is significantly improved
after capitate-radius arthrodesis.
However, functional improvement
is dependent on the preoperative
diagnosis, functional abilities, and
the severity of spasticity.
58
Comparative Results
In one retrospective series of 89
consecutive patients who had un-
dergone wrist arthrodesis for a
posttraumatic disorder, patients
treated with dorsal-plate fixation
were compared with those treated
with various other techniques.14 In
the former group, fusion was more
successful (98% versus 82%) and oc-
curred earlier (average, 10.3 weeks
versus 12.2 weeks postoperatively).
When performed in patients with
posttraumatic or degenerative con-
ditions, dorsal-plate fixation and
autogenous bone grafting results in
highly reliable fusion rates, ranging
from 93% to 100%.13,21,22 Preliminary
data demonstrate similar success
with the use of the specially de-
signed low-profile precontoured
plate and local bone graft.22
Most of the patients reported in
the literature who have had wrist
arthrodesis with dorsal-plate fixa-
tion had diagnoses of degenerative,
posttraumatic, or neurologic condi-
tions. There are very few studies
involving patients with inflamma-
tory arthritis. In the largest series
of rheumatoid patients with a wrist
arthrodesis performed with a dorsal
plate, successful union occurred in
all 23 patients.23 The arthrodesis was
performed with a self-compressing
six-hole plate applied on the sec-
ond metacarpal. In the series of
Zachary and Stern,24 all 5 patients
with inflammatory arthritis had a
successful wrist arthrodesis with
the dorsal-plate technique. How-
ever, all three failures in the series
of Wright and McMurtry13 occurred
in patients with rheumatoid arthri-
tis. Similarly, Bracey et al25 reported
a nonunion rate of 17% after wrist
arthrodesis performed with a dor-
sal T-plate in patients with rheu-
matoid arthritis. In one patient, the
arthrodesis was performed after
failure of a cemented wrist prosthe-
sis. The other failure occurred after
a postoperative infection. Because
Journal of the American Academy of Orthopaedic Surgeons
of plate prominence, the higher
rates of nonunion, delicate skin, and
osteoporotic bone, and the greater
risk of infection, the intramedullary-
rod technique remains an accept-
able and popular alternative for
patients with inflammatory ar-
thritis.
Satisfactory results have also
been reported when wrist arthrod-
esis is obtained with intramedullary
fixation. 6-8,26 However, these re-
ports predominantly involved pa-
tients with rheumatoid arthritis. In
Clayton’s original report,6 all 5 pa-
tients with rheumatoid arthritis had
a successful fusion. Mannerfelt and
Malmsten7 reported successful wrist
fusion using a Rush pin and staple
in all but 1 of their 43 rheumatoid
patients. The same technique was
used in 1 patient with a congenital
deformity and 5 patients with a
posttraumatic or neurologic disor-
der; however, their outcome was
not reported.
In the series of Millender and
Nalebuff,8 all but 2 of the 60 rheu-
matoid patients (70 arthrodeses)
had a successful fusion with a
Steinmann pin supplemented with
a staple or single Kirschner wire.
Postoperatively, up to 5 months of
immobilization in a long or short
arm cast was necessary. Clendenin
and Green 27 reported successful
union in all but 1 of their 12 pa-
tients in whom arthrodesis was
performed with the technique of
Millender and Nalebuff. Vahvanen
and Tallroth 26 reported a 100%
fusion rate in 38 patients with
rheumatoid arthritis (45 wrists) in
whom arthrodesis was performed
with a single Rush pin. In the only
series of nonrheumatoid patients
in whom arthrodesis was per-
formed with a modification of the
Millender-Nalebuff intramedullary
technique, all 10 patients (7 with
posttraumatic arthritis, 2 with
Kienböck disease, and 1 with pso-
riatic arthritis) achieved solid
fusion.10

Functional Outcome
Wrist arthrodesis results in high
subjective patient satisfaction with
respect to pain relief and correction
of deformity.8,13,28 Grip strength,
digital range of motion, and fore-
arm rotation do not significantly
change from preoperative values.22
Improvements in pinch and grip
strengths have been reported fol-
lowing wrist arthrodesis in patients
with osteoarthritis, but not in those
with rheumatoid arthritis.13
In a recent study assessing the
functional capabilities of patients
after unilateral wrist arthrodesis
performed for a variety of post-
traumatic conditions, most tasks
and daily activities could still be
performed, but required adapta-
tion and modification by the pa-
tient. 28 The most difficult tasks
were perineal care, manipulating
the hand in tight spaces, and activi-
ties that required forceful prona-
tion and supination with a simulta-
neous strong grip. Manual laborers
have difficulty crawling, pushing,
carrying, and using tools, particu-
larly a hammer, because of the loss
of wrist extension. Interestingly,
maximum improvement in function
did not occur for an average of 14.5
months after arthrodesis.28 Most
patients returned to their original
occupation with some job modifica-
tion, such as lifting restrictions. In
the retrospective study of Hastings
et al, 21 those patients in whom
arthrodesis had been performed
with a dorsal plate returned to
work earlier than those in whom
arthrodesis had been performed
with various other methods.14
Complications
Complications after wrist arthrode-
sis occur regardless of the technique
used.27 However, review of the lit-
erature suggests that plate fixation
is associated with a lower incidence.
Vol 9, No 1, January/February 2001
Peter J. L. Jebson, MD, and Brian D. Adams, MD
Hastings et al21 reviewed the data
on 89 patients with 90 wrist arthrod-
eses performed for various post-
traumatic disorders. In 56 patients
(57 wrists), arthrodesis was per-
formed with plate fixation. In 33
patients (33 wrists), the arthrodesis
was performed with a variety of
other methods. In 28 of these 33,
arthrodesis was performed with an
onlay corticocancellous bone graft
temporarily transfixed with Stein-
mann pins or Kirschner wires. Four
patients had an onlay graft alone;
the remaining arthrodeses involved
intramedullary fixation without
bone grafting. A 3.5-mm dynamic
compression or reconstruction plate
was used for plate fixation. Autog-
enous iliac-crest bone graft was
used in all but 1 of the 57 arthrodeses.
Nonunion occurred in 2% of the
arthrodeses performed with a plate,
compared with 18% of the arthrod-
eses performed with other meth-
ods. Additional complications oc-
curred in 51% of patients with plate
fixation, compared with 79% of the
patients in whom arthrodesis had
been performed with alternative
methods. Complications associated
with plate fixation included exten-
sor tendon adhesions or tenosyn-
ovitis, intrinsic muscle contracture,
tenderness over the plate, poor
wound healing, painful nonunion
of the third carpometacarpal joint,
and carpal tunnel syndrome. Fifty-
nine percent of these complications
required operative treatment.
Complications associated with the
alternative arthrodesis techniques
included tendon adhesions, carpal
tunnel syndrome, DRUJ pain, pin-
track infection, and pin migration
or breakage. Twenty-one percent
of these complications required
operative treatment.
Complications related specifically
to dorsal-plate fixation and iliac-
crest bone grafting were analyzed
by Zachary and Stern.24 Although
the union rate was 100%, there
were a total of 82 complications in
50 of the 73 wrist arthrodeses.
Approximately 80% of these com-
plications resolved spontaneously
or with nonoperative treatment.
Nineteen patients required surgery,
which most commonly involved
plate removal because of promi-
nence, loosening, or the development
of a symptomatic bursa. Resection
of the distal ulna was necessary in
3 patients and was recommended
for 5 additional patients with symp-
tomatic DRUJ arthritis or ulnar im-
paction syndrome.
Failure to identify or anticipate
DRUJ problems in the wrist arthrod-
esis patient is a well-recognized
source of postoperative dissatisfac-
tion.17,24,27,29 Concomitant DRUJ dis-
orders and the potential for “iatro-
genic” ulnar impaction syndrome or
compression of the median nerve in
the carpal tunnel after wrist arthrod-
esis should be addressed preopera-
tively or intraoperatively, as these
conditions may be aggravated, po-
tentially compromising an otherwise
successful arthrodesis. The manage-
ment of extensor tendon irritation by
the plate can be particularly chal-
lenging. Nonoperative treatment
modalities include icing, nonsteroi-
dal anti-inflammatory medication,
and the judicious use of corticoste-
roid injections. Plate removal is re-
served for patients with persistent,
chronic symptoms. Removal is typi-
cally performed after successful ar-
throdesis. Some patients continue to
have persistent symptoms despite
plate removal.
Although wrist arthrodesis with
intramedullary fixation is relatively
simple and safe, complications
directly attributable to the various
intramedullary devices do occur.
Rod or pin migration with irritation
of the surrounding tendons and
skin necessitates bending of the pin,
which makes subsequent implant re-
moval difficult. Breakage of the rod
or pin can be associated with pseud-
arthrosis. Fortunately, the incidence
of these complications is low.6-8,26
59
Wrist Arthrodesis
Summary
Wrist arthrodesis results in pre-
dictable pain relief and a high de-
gree of patient satisfaction. Some
adaptation and modification of
functional activities is required, and
certain tasks, such as perineal care,
are difficult. The traditional tech-
nique of intramedullary rod or pin
fixation is most applicable for pa-
tients with inflammatory arthritis or
a connective tissue disorder.
Plate fixation is indicated for pa-
tients with posttraumatic or degen-
erative arthrosis. The advantages
of this type of fixation include im-
mediate rigidity, thus permitting
References
1. Carroll RE, Dick HM: Arthrodesis of
the wrist for rheumatoid arthritis. J
Bone Joint Surg Am 1971;53:1365-1369.
2. Haddad RJ Jr, Riordan DC: Arthrod-
esis of the wrist: A surgical technique.
J Bone Joint Surg Am 1967;49:950-954.
3. Wood MB: Wrist arthrodesis using
dorsal radial bone graft. J Hand Surg
[Am] 1987;12:208-212.
4. Benkeddache Y, Gottesman H, Four-
rier P: Multiple stapling for wrist
arthrodesis in the nonrheumatoid pa-
tient. J Hand Surg [Am] 1984;9:256-260.
5. Louis DS, Hankin FM: Arthrodesis of
the wrist: Past and present. J Hand
Surg [Am] 1986;11:787-789.
6. Clayton ML: Surgical treatment at the
wrist in rheumatoid arthritis: A review
of thirty-seven patients. J Bone Joint
Surg Am 1965;47:741-750.
7. Mannerfelt L, Malmsten M: Arthrod-
esis of the wrist in rheumatoid arthri-
tis: A technique without external fixa-
tion. Scand J Plast Reconstr Surg 1971;5:
124-130.
8. Millender LH, Nalebuff EA: Arthrod-
esis of the rheumatoid wrist: An evalu-
ation of sixty patients and a descrip-
tion of a different surgical technique. J
Bone Joint Surg Am 1973;55:1026-1034.
9. Millender LH, Nalebuff EA, Feldon
PG: Rheumatoid arthritis, in Green
DP (ed): Operative Hand Surgery. New
York: Churchill Livingstone, 1982, vol
2, pp 1161-1262.
10. Viegas SF, Rimoldi R, Patterson R:
Modified technique of intramedullary
60
early postoperative rehabilitation
with little or no immobilization.
Wrist arthrodesis with dorsal-plate
fixation and autogenous bone graft-
ing is associated with higher fusion
rates and a lower incidence of com-
plications than the alternative tech-
niques. Plate prominence may re-
sult in tenderness or extensor tendon
irritation, necessitating removal.
Recent developments in plate
design and the use of local bone
graft in selected patients may de-
crease morbidity and complications.
However, there are as yet no data to
suggest that use of the custom wrist
fusion plate reduces the incidence of
plate-associated complications or
fixation for wrist arthrodesis. J Hand
Surg [Am] 1989;14:618-623.
11. Meuli HC: Reconstructive surgery of
the wrist joint. Hand 1972;4:88-90.
12. Manetta P, Tavani L: Arthrodesis of
the wrist with a compression plate.
Ital J Orthop Traumatol 1975;1:219-224.
13. Wright CS, McMurtry RY: AO ar-
throdesis in the hand. J Hand Surg
[Am] 1983;8:932-935.
14. Laurie SWS, Kaban LB, Mulliken JB,
Murray JE: Donor-site morbidity after
harvesting rib and iliac bone. Plast
Reconstr Surg 1984;73:933-938.
15. Younger EM, Chapman MW: Morbid-
ity at bone graft donor sites. J Orthop
Trauma 1989;3:192-195.
16. Straub LR, Ranawat CS: The wrist in
rheumatoid arthritis: Surgical treat-
ment and results. J Bone Joint Surg Am
1969;51:1-20.
17. Rayan GM, Brentlinger A, Purnell D,
Garcia-Moral CA: Functional assess-
ment of bilateral wrist arthrodeses. J
Hand Surg [Am] 1987;12:1020-1024.
18. Brumfield RH, Champoux JA: A bio-
mechanical study of normal functional
wrist motion. Clin Orthop 1984;187:23-25.
19. Clayton ML, Ferlic DC: Arthrodesis of
the arthritic wrist. Clin Orthop 1984;
187:89-93.
20. Louis DS, Hankin FM, Bowers WH:
Capitate-radius arthrodesis: An alter-
native method of radiocarpal ar-
throdesis. J Hand Surg [Am] 1984;9:
365-369.
21. Hastings H II, Weiss APC, Quenzer D,
Journal of the American Academy of Orthopaedic Surgeons
the need for plate removal. The cus-
tom plate is easier to use and was
developed to theoretically reduce
the incidence of complications.
However, other factors, such as im-
plant cost, patient size, bone quality,
and clinical diagnosis, should be
considered when selecting the ap-
propriate implant type or method
for wrist arthrodesis. Careful pre-
operative clinical and radiographic
evaluations are essential to detect
the presence of other conditions,
such as intercarpal arthritis, carpal
tunnel syndrome, DRUJ arthritis, or
ulnocarpal impaction, that may
need to be treated at the time of
wrist arthrodesis.
Wiedeman GP, Hanington KR, Strick-
land JW: Arthrodesis of the wrist for
post-traumatic disorders. J Bone Joint
Surg Am 1996;78:897-902.
22. Weiss APC, Hastings H II: Wrist
arthrodesis for traumatic conditions: A
study of plate and local bone graft
application. J Hand Surg [Am] 1995;
20:50-56.
23. Larsson SE: Compression arthrodesis
of the wrist: A consecutive series of 23
cases. Clin Orthop 1974;99:146-153.
24. Zachary SV, Stern PJ: Complications
following AO/ASIF wrist arthrodesis.
J Hand Surg [Am] 1995;20:339-344.
25. Bracey DJ, McMurtry RY, Walton D:
Arthrodesis in the rheumatoid hand
using the AO technique. Orthop Rev
1980;9:65-69.
26. Vahvanen V, Tallroth K: Arthrodesis
of the wrist by internal fixation in
rheumatoid arthritis: A follow-up
study of forty-five consecutive cases. J
Hand Surg [Am] 1984;9:531-536.
27. Clendenin MB, Green DP: Arthrodesis
of the wrist: Complications and their
management. J Hand Surg [Am] 1981;
6:253-257.
28. Weiss APC, Wiedeman G Jr, Quenzer
D, Hanington KR, Hastings H II,
Strickland JW: Upper extremity func-
tion after wrist arthrodesis. J Hand
Surg [Am] 1995;20:813-817.
29. Trumble TE, Easterling KJ, Smith RJ:
Ulnocarpal abutment after wrist ar-
throdesis. J Hand Surg [Am] 1988;
13:11-15.
 Use of Ergogenic Aids by Athletes

Marc D. Silver, MD

Abstract

“Ergogenic aid” is defined as any means of enhancing energy utilization, roid supplements; and (5) nutritional
including energy production, control, and efficiency. Athletes frequently use aids, such as creatine supplementa-
ergogenic aids to improve their performance and increase their chances of win- tion.6,7 The latter three categories
ning in competition. It is estimated that between 1 and 3 million male and are of the most interest. Some of the
female athletes in the United States alone have used anabolic steroids. In re- more commonly used substances
sponse to the problem of drug use, many athletic organizations have established are highlighted in Table 1.
policies prohibiting the use of certain pharmacologic, physiologic, and nutritional Ergogenic aids can be specifically
aids by athletes and have implemented drug testing programs to monitor com- tailored to enhance performance in
pliance. Therefore, it is important for physicians to be knowledgeable about the a particular sport. For example,
available ergogenic aids so they can appropriately treat and counsel the athletic some athletes involved primarily in
patient. strength-dependent activities, such
J Am Acad Orthop Surg 2001;9:61-70 as weight lifting, use anabolic ste-
roids to increase muscle mass. Some
endurance athletes, such as mara-
thon runners, use blood doping
Sports have become phenomenally actions, even when that involves (also known as “blood boosting”
popular worldwide. Successful ath- taking substances with major side and “blood packing”) to increase
letes frequently become instant effects that can cause permanent their oxygen-carrying capacity.
celebrities, with lucrative commercial physical harm and even death.2-4
opportunities. Unfortunately, some For example, it is estimated that as
of those athletes use illegal sub- many as 3 million athletes in the Historical Perspective
stances to give themselves a compet- United States have used anabolic
itive edge. A 1997 poll in Sports steroids for non–medically pre- The first Olympic games took place
Illustrated1 asked current and aspir- scribed applications.5 Therefore, it in Greece in 776 BC. From sources
ing US Olympic athletes two ques- is important for the physician, espe- documenting specific training and
tions. The first was whether they cially one who deals with athletes, dietary regimens for athletes in
would take a banned performance- to be knowledgeable about the vari- ancient times,3,8 we know that some
enhancing drug if they were guaran- ous ergogenic aids available. of them ate hallucinogenic mush-
teed to both win their athletic event rooms and sesame seeds to enhance
and not get suspended for drug use.
The second question was whether Types of Ergogenic Aids
they would take the same substance
Dr. Silver is Assistant Clinical Professor of
if it would enhance their ability to An “ergogenic aid” is defined as Orthopaedics and Rehabilitation, Yale
win every competition for the next 5 any means of enhancing energy University School of Medicine, New Haven,
years but then result in death. Re- production and utilization.6 Ergo- Conn.
markably, 98% responded “yes” to genic aids have been classified into
the first question, and more than five categories: (1) mechanical aids, Reprint requests: Dr. Silver, Department of
Orthopaedics and Rehabilitation, Yale
50% responded “yes” to the second such as lightweight racing shoes;
University School of Medicine, One Long
question. (2) psychological aids, such as hyp- Wharf Drive, New Haven, CT 06511.
Because successful athletes are nosis; (3) physiologic aids, such as
looked on as role models in our so- “blood doping” (administration of Copyright 2001 by the American Academy of
ciety, many people in the general packed red blood cells); (4) pharma- Orthopaedic Surgeons.
population try to emulate their cologic aids, such as androgenic ste-

Vol 9, No 1, January/February 2001 61

Ergogenic Aids in Athletics
Table 1
Common Ergogenic Aids
Substance/Method
Pharmacologic substances
Anabolic steroids (e.g., metandieone,
mesterolone, nandrolone
Growth hormone
Recombinant human erythropoietin
Beta-blockers (e.g., metoprolol)
Stimulants (e.g., caffeine)
Nutritional aids
Creatine
Vitamin A
Vitamin C
Vitamin E
Carnitine
Androstenedione
Blood doping
performance.9 Although the mod-
ern Olympic games commenced in
1896, scientific and medical interest
in the diet and training of Olympic
athletes did not begin until 1922.8
In 1889, Charles Edward Brown-
Séquard, a French physiologist,
claimed to have reversed his own
aging process by self-injecting tes-
62
Proposed Mechanism of Action
Induce protein synthesis in muscle,
stimulate release of growth
hormone, reverse effects of cortisol
Accelerates incorporation of amino
acids into proteins, stimulates
utilization of lipids from
adipose tissue
Stimulates erythropoiesis (thought
to increase oxygen uptake)
Has antitremor and antianxiety effects
Stimulates sympathetic nervous system,
stimulates intracellular utilization
of free fatty acids as energy source
Enhances intracellular production
of ATP (needed for muscle
contraction)
Acts as an antioxidant
Acts as an antioxidant
Acts as an antioxidant
Thought to spare muscle glycogen
breakdown and decrease
lactic acid production
Induces protein synthesis in muscle,
stimulates release of growth hormone,
reverses effects of cortisol
Increases oxygen-carrying capacity
of blood
ticular extracts.10 Testosterone, the
primary male hormone, was first
synthesized in 1935, and in the
1940s, athletes began taking ana-
bolic steroids to increase their mus-
cle mass.10 Throughout the 1950s
and 1960s, amphetamines and ana-
bolic steroids were used extensively
in sports.7 Concerned about that
Journal of the American Academy of Orthopaedic Surgeons
Athletes’ Expectation
Increase muscle mass, strength,
lean body mass
Increases muscle mass, strength,
lean body mass
Increases endurance and time to
exhaustion
Improve shooting scores
Increase endurance
Increases strength and power
performance
Decreases cellular damage
Decreases cellular damage
Decreases cellular damage
Increases endurance
Increases muscle mass, strength,
lean body mass
Increases endurance
trend, the International Olympic
Committee (IOC) banned their use
by Olympic athletes in the early
1960s. Formal drug testing began
with the 1968 Olympics.7 In 1988,
Canadian Olympic sprinter Ben
Johnson was stripped of his gold
medal after testing revealed he had
used an oral anabolic steroid; this
 Marc D. Silver, MD

Adverse Effects US Organizational Policies

Effects on multiple organ systems (e.g., hypertension, elevated lipoproteins Banned by NCAA, NFL, and USOC
and liver enzymes, increased risk of tendon and muscle injury, testicular
or uterine atrophy, depression, psychosis, immunosuppression)
Acromegaly-like effects (e.g., heart disease, heart failure, glucose Banned by NCAA and USOC
intolerance, hyperlipidemia, impotence, menstrual
irregularities, myopathy, osteoporosis)

Thromboembolic events, ischemic events, hyperkalemia Banned by NCAA and USOC

Bronchospasm, diminished performance capacity, atrioventricular Banned for certain sports (e.g., shooting)
block, cardiac insufficiency, hypoglycemia, hallucinations, by NCAA and USOC
insomnia, depression, nightmares
Anxiety, jitters, inability to focus, gastrointestinal discomfort, insomnia, Maximum urinary concentration allowed
irritability, cardiac arrhythmia, hallucinations by USOC, 12 µg/mL; maximum urinary
concentration allowed by NCAA,
15 µg/mL

Muscle cramping, dehydration, gastrointestinal distress, nausea, No organizational policy

seizures, possible effects on kidney function

Drowsiness, headache, vomiting, papilledema, hair, skin, and nail changes No organizational policy
Diarrhea, renal stones No organizational policy
Muscle weakness, fatigue, headache, nausea No organizational policy
Diarrhea No organizational policy

Decreased high-density lipoprotein levels, increased estrogen levels Banned by NCAA, USOC, and NFL

Allergic reaction, bacterial contamination, disease transmission, immune Banned by NCAA and USOC
sensitization, polycythemia, ischemic events, thromboembolic events

was the first time a gold medalist
in track and field was disqualified
from the Olympics for using illegal
drugs. 11 Criminal investigations
are proceeding against former Ger-
man Democratic Republic sports
officials for systematically using
banned substances in their athletes’
training programs.12
Incidence of Use of
Ergogenic Aids
Most studies of pharmacologic aids
used by athletes have dealt with
steroid use. The prevalence of self-
reported use of anabolic steroids by
adolescent athletes is as high as
11% for boys and 2.5% for girls.13
Buckley et al14 found that 4.4% of
all male high school seniors had ini-
tiated steroid use at 16 years of age
or younger. In studies of adults,
the prevalence of self-reported ste-
roid use has been as high as 15%.15
In projected-use studies, in which
subjects were asked about the prac-
tices of other athletes, the preva-

Vol 9, No 1, January/February 2001 63

Ergogenic Aids in Athletics
lence was even higher.15 In all age
groups, the prevalence was always
higher for males.15 The greatest use
of androgens is not by competitive
athletes, but rather by recreational
bodybuilders who take them for
cosmetic purposes15 and continue
their use indefinitely in order to
maintain their effects.16 The National
Football League (NFL) first tested
for anabolic steroids in 1988 and
announced that 6% of professional
football players had taken them.11
There have been rumors that
various national teams, especially
European bicycling teams, use
blood doping during competition,
but the extent of this practice is
largely unknown. Blood doping has
been replaced primarily by admin-
istration of recombinant human
erythropoietin (r-EPO), which is
the recombinant form of a normal
hormone that regulates erythro-
poiesis in the bone marrow. The
lay sports literature reports wide-
spread use of erythropoietin to ele-
vate the red blood cell concentra-
tion in endurance athletes; however,
there are no scientific data to quan-
tify the extent of its use among
competitive athletes.17
Nutritional supplements, such
as creatine and vitamins, are con-
sidered legal ergogenic aids.7 Al-
though researchers disagree about
their effectiveness, athletes con-
sume certain nutrients, often in
large doses, in the hope of enhanc-
ing their performance. A recent
survey of 13,914 collegiate athletes
revealed extensive use of nutritional
supplements, such as creatine (13%),
amino acid supplements (8%), and
dehydroepiandrosterone (DHEA),
which is a precursor to testosterone
and estrogen (1%).18 In a 1998 poll
of 56 professional sports teams, cre-
atine supplements were reportedly
used by fewer than 25% of players
on 36 teams, by 25% to 50% of
players on 15 teams, and by more
than 50% on 5 teams.19 Use of crea-
tine appears to be higher in profes-
64
sional football than in other team
sports.20
Drug Testing
To address the problem of poten-
tially life-threatening use of drugs
by athletes and use contrary to the
ethics and ideals of fair competi-
tion, in 1963 the Council of Europe
established the definition of dop-
ing, as follows:
The administration or use of sub-
stances in any form alien to the body
or of physiological substances in
abnormal amounts and with abnor-
mal methods by healthy persons with
the exclusive aim of attaining an arti-
ficial and unfair increase in perfor-
mance in competition. Furthermore,
various psychological measures to
increase performance in sports must
be regarded as doping. Where treat-
ment with a medicine must be under-
gone, which as a result of its nature
or dosage is capable of raising physi-
ological capability beyond normal
level, such treatment must be consid-
ered doping and shall rule out eligi-
bility for competition.21
In 1967, the IOC established a
medical commission, which was
charged with enforcing the prohibi-
tion of illegal drug use (Table 2). In
response to the Congressional hear-
ings in 1973 on improper drug use
in sports, major athletic organiza-
tions in the United States, including
the National Collegiate Athletic
Association (NCAA), the NFL, USA
Track and Field, and the United
States Olympic Committee (USOC),
implemented drug programs.
The first drugs to be used for per-
formance enhancement were stimu-
lants, such as amphetamines. The
initial testing for stimulants (using
gas chromatography) occurred at
the 1972 Olympic Games in Mu-
nich.21 Widespread testing (using
gas chromatography–mass spec-
trometry) for anabolic steroids in
the urine began at the 1983 Pan-
American Games.21 Peptide hor-
Journal of the American Academy of Orthopaedic Surgeons
mones, such as growth hormone,
are detectable in the urine by means
of immunoassay, but they are diffi-
cult to test for and to confirm as a
positive result. Many of these com-
pounds have a short half-life in the
blood and a low concentration in the
urine. With the greater availability
made possible by the production of
recombinant proteins, this class of
compounds threatens to become the
most abused.21 Urine testing may
reveal the presence of substances
that are not performance-enhancing
drugs themselves but that are used
to mask the presence of banned sub-
stances. Diuretics can be used to re-
duce the urinary concentration of
prohibited drugs. Probenecid and
bromantan can also interfere with
the detection of anabolic steroids.21
Anabolic Steroids
Anabolic-androgenic steroids are
synthetic derivatives of testosterone.
In clinical practice, they are used to
treat men with hypogonadism or
impotence and to reverse the wast-
ing effects of conditions such as
burns and chronic debilitating ill-
nesses.10 Under appropriate condi-
tions, administration of anabolic
steroids can result in increases in
muscle size and strength.13,16 The
benefits of anabolic-androgenic ste-
roids are more notable in strength-
dependent sports, such as weight
lifting and football, than in aerobic
sports.16 Bodybuilders use anabolic
steroids primarily to gain lean mass
and lose body fat.9
Mechanism of Action
Anabolic steroids induce protein
synthesis in muscle cells, stimulate
the release of endogenous growth
hormone, and can reverse the ef-
fects of cortisol, a catabolic hor-
mone.16 Their psychological effect
may allow a more intense and sus-
tained workout. 13 The extent to
which anabolic steroids can increase
 Marc D. Silver, MD

as diuretics, antiestrogens, human

Table 2 chorionic gonadotropin, and antiacne
Substances and Methods Prohibited or Restricted by the USOC*
medications, concurrently with ana-
bolic steroids to counteract some of
Prohibited substances the more common adverse effects.
Stimulants (e.g., amphetamines, caffeine [>12 µg/mL on urinary testing])
Narcotics (e.g., morphine, meperidine)
Adverse Effects
Anabolic agents (e.g., dehydroepiandrosterone, androstenedione)
Diuretics (e.g., furosemide, acetazolamide) Much of the information about
Peptide hormones, mimetics, and analogues (e.g., erythropoietin, growth the adverse effects of anabolic
hormone) steroid administration is anecdotal
Over-the-counter medications containing prohibited stimulants or extrapolated from its effects in
Desoxyephedrine (e.g., Vicks Inhaler) therapeutic use.5,13 Organs and sys-
Pseudoephedrine (e.g., Actifed, Co-Tylenol) tems affected include the liver,
Phenylpropanolamine (e.g., Alka-Seltzer Plus, Contac, Dexatrim) reproductive system, musculoskele-
Ephedrine (e.g., Bronkaid, Collyrium With Ephedrine) tal system, skin, cardiovascular sys-
Ma-huang (e.g., “Mexican tea,” “Bishop’s tea,” ephedra) tem, and genitourinary system.
Propylhexedrin (e.g., Benzedrex inhaler)
Anabolic steroids also have psycho-
Prohibited methods logical and immunologic effects13
Blood doping (Table 3). There is evidence that
Pharmacologic, chemical, and physical manipulation
anabolic steroids can induce tendon
Use of substances and methods that alter the integrity and validity of urine
rupture, osteonecrosis of the hip,
samples in drug testing (e.g., probenecid and bromantan)
psychosis, and suicidal behav-
Substances subject to certain restrictions
ior.16,24,25 The masculinizing effects
Alcohol
in women, such as male-pattern
Cannabinoids
Local anesthetics baldness and deepening of the
Corticosteroids voice, may be irreversible, as may
Beta-blockers growth retardation in children. 13
Specific β2-agonists Synthetic steroid derivatives with
Caffeine (<12 mg/mL on urinary testing) primarily anabolic or virilizing
activity have been manufactured.
* Source: Drug Status Guide: Athlete Reference. Colorado Springs, Colo: US Olympic
The degree of virilization depends
Committee, May 1999. on the dosage, duration of treat-
ment, and particular steroid used.26
Although the incidence of seri-
ous side effects of anabolic steroid
strength and lean body mass and are less hepatotoxic than the oral administration has been relatively
the factors that influence their preparations; however, they are low,22 fatal effects have been docu-
effects are not yet completely under- detectable via drug testing for a mented. Athletes have died of he-
stood or documented.9 There is a longer period of time.9,16 patocarcinoma, myocardial infarc-
lack of consensus as to the effect of Athletes frequently use a combi- tion, and stroke as a consequence
anabolic steroids on humans be- nation of anabolic steroid prepara- of prolonged steroid use. There
cause of differences in technique tions, a practice called “stack- has also been one reported case of a
and methodology in the various ing.”9,13,16 Individuals often take bodybuilder who contracted ac-
studies that have been performed. anabolic steroids in 6- to 12-week quired immunodeficiency syn-
cycles and may “pyramid” their ad- drome as a result of sharing nee-
Athletic Dosing ministration by increasing the dose dles for steroid injections.16
Some effects of exogenous ana- through the cycle.9,13 Even though
bolic steroid administration are re- there is as yet no scientific proof of
versible. For instance, once the ath- effectiveness, athletes often use Growth Hormone
lete discontinues use of the anabolic cycling and pyramiding in the hope
steroid, the increased size and of maximizing the beneficial effects Growth hormone is the most abun-
strength disappear. Anabolic ste- of anabolic steroids while mini- dant substance produced by the
roids can be administered orally or mizing their harmful effects.13 Ath- pituitary gland, and it acts on most
parenterally. The injectable forms letes may also use other drugs, such organs and tissues in the body. 16

Vol 9, No 1, January/February 2001 65

Ergogenic Aids in Athletics
Table 3
Adverse Effects of Anabolic Steroids16,22,23
Cardiovascular
Hypertension
Thrombosis
Increased total cholesterol
Increased low-density lipoprotein
Decreased high-density lipoprotein
Endocrine
Decreased glucose tolerance and
thyroid function
Masculinization in women
Musculoskeletal
Premature physeal arrest
Increased risk of tendon or
muscle injury
Bilateral hip osteonecrosis
Male reproductive system
Abnormal spermatogenesis
Testicular atrophy
Gynecomastia
Impotence
Priapism
Prostatic carcinoma
Prostatic hypertrophy
Female reproductive system
Menstrual abnormalities
Uterine atrophy
Breast atrophy
Teratogenicity
Overproduction leads to gigantism
or acromegaly; underproduction
causes dwarfism. Some athletes use
growth hormone because it increases
muscle mass and is more difficult to
detect than anabolic steroids.25
Mechanism of Action
Growth hormone has an anabolic
effect on the body, accelerating in-
corporation of amino acids into
proteins. In addition, growth hor-
mone stimulates utilization of lipids
from adipose tissue as an energy
source, thereby sparing muscle
glycogen.16 Although strength and
performance may improve with the
use of growth hormones, no one
has yet investigated the ergogenic
effects of growth hormone adminis-
tration on athletes.16
66
increased endurance with specific
amounts of caffeine ingestion. 27
Caffeine taken in doses of 3 to 9 mg
per kilogram of body weight ap-
Liver pears to enhance performance of
Elevated liver enzymes
both prolonged endurance exercise
Hepatocellular damage
and more intense short-duration
Hepatocarcinoma
Hepatoadenoma exercise (lasting up to 5 minutes).
Most of these results are based on
Urinary system
laboratory tests on athletes; more
Wilms’ tumor
studies during actual sports com-
Immunologic
petition are needed.28
Decreased immunoglobulins
Hepatitis B and C infection (from
shared needles) Mechanism of Action
HIV infection (from shared Although the mechanism of its
needles) effects is not entirely known, caf-
Integument feine may stimulate the sympathetic
Acne nervous system. Another theory is
Hirsutism that caffeine enhances intracellular
Male-pattern baldness utilization of free fatty acids as an
Edema energy source, thereby sparing mus-
Coarsening of skin cle glycogen stores.6,27
Psychological
Mood swings Adverse Effects
Irritability Some of the potential side effects
Aggressiveness of caffeine ingestion include anxi-
Increased libido ety, jitters, inability to focus, gas-
Psychosis trointestinal discomfort, insomnia,
Depression
and irritability. At higher doses,
Addiction
cardiac arrhythmia and hallucina-
Suicide
tions may occur.28 The IOC currently
allows only low levels of caffeine
ingestion by athletes. By limiting
Adverse Effects coffee consumption to a maximum
The adverse effects of exogenous of three cups throughout the day,
administration of growth hormone most athletes remain safely under
in athletes can be extrapolated from the limit of a urinary concentration
the findings in patients with endog- of 12 µg/mL.29
enous oversecretion of this hor-
mone. These include gigantism in
children and acromegaly in adults. Recombinant Human
Acromegaly can lead to heart dis- Erythropoietin
ease or cardiac failure, glucose
intolerance, hyperlipidemia, impo- As mentioned previously, the earlier
tence, menstrual irregularities, my- practice of blood doping by admin-
opathy, osteoporosis, and death.16,25 istration of packed red blood cells
has been largely replaced by the
use of r-EPO. The objective is to en-
Caffeine hance performance.
Caffeine has a stimulant effect on Mechanism of Action
the body and is used by athletes to Recombinant human erythropoi-
improve endurance performance. etin, like the naturally occurring
Several studies have demonstrated substance, regulates erythropoiesis
Journal of the American Academy of Orthopaedic Surgeons

in the bone marrow. The rate at
which the hematocrit increases
depends on the dose of r-EPO. 30
Ekblom and Berglund 31 demon-
strated increased maximum oxygen
consumption and increased time
to exhaustion in male athletes after
6 weeks of r-EPO administration.
Adverse Effects
Risks from r-EPO administration
include hyperviscosity of the blood,
which leads to ischemic and throm-
boembolic events, hypertension, flu-
like symptoms, and hyperkalemia.32
The use of r-EPO has been banned
by the IOC since 1990. Unfortunately,
it is extremely difficult to detect
with current testing standards.
Beta-Blockers
Beta-blockers are used by athletes
in certain sports (e.g., riflery and
archery) for their antianxiety and
antitremor effects.23 Beta-blockers
are clinically used primarily for the
treatment of hypertension, angina
pectoris, and cardiac arrhythmias.23
Mechanism of Action
There are two types of beta-
receptors in the body: β1-receptors
primarily mediate cardiac stimula-
tion and intestinal motility, and
β2-receptors primarily mediate bron-
chodilation and relaxation of vas-
cular and uterine smooth muscle.33
Beta-blockers were added to the
IOC list of prohibited substances in
1986, when it was discovered that
their use by marksmen improved
their pistol shooting scores.34 In the
study by Kruse et al, 34 athletes
given metoprolol, a β 1 -receptor
blocker, showed improvement in
their shooting performance com-
pared with those who received
placebo. This effect was considered
to be primarily due to the ability of
the drug to decrease hand tremors.
Increases in heart rate and systolic
blood pressure were eliminated,
Vol 9, No 1, January/February 2001
which might also explain improved
performance.
Adverse Effects
Beta-blockers have an ergolytic
effect on endurance athletes and
affect thermoregulation during ex-
ercise.35 Beta-blockers can induce
bronchospasm and cause atrioven-
tricular block, cardiac insufficiency,
hypoglycemia, hallucinations, in-
somnia, depression, and night-
mares.33
Creatine
The use of creatine by athletes in-
creased after Harris et al showed in
1992 that administration of high
doses of creatine resulted in a 20%
increase in skeletal muscle creatine
concentration.36 Creatine has become
popular among football players and
athletes in power sports who are
seeking to increase strength.18
Mechanism of Action
Creatine is an amino acid deriva-
tive found in skeletal muscle, cardiac
muscle, and brain, retinal, testicular,
and other tissues.7,36 Creatine is syn-
thesized primarily by the liver, kid-
neys, and pancreas, and is excreted
by the kidneys.21 Total creatine in
skeletal muscle is the sum of free cre-
atine and phosphocreatine (PCr),
both of which are important in the
production of adenosine triphos-
phate (ATP) during anaerobic activ-
ity. Oral creatine supplementation is
considered ergogenic because of its
potential to enhance ATP production
during exercise.18 Theoretically, this
can be accomplished by increasing
PCr availability, accelerating PCr
resynthesis, and improving the pH-
buffering capacity of muscle.18 The
buffering action may allow im-
proved tolerance of anaerobic metab-
olism, thereby lengthening its poten-
tial ergogenic effect.18
Research on the ergogenic effect
of creatine supplements has pro-
Marc D. Silver, MD
vided mixed results. 18 Several
studies carried out on untrained
subjects under laboratory condi-
tions have shown that oral creatine
supplementation can improve
sprint and power performances
during repeated short-duration
bouts of high-intensity exercise.37,38
However, studies performed on
highly trained or elite athletes en-
gaging in a high-intensity sprint
activity showed no performance
improvement. 37 The majority of
available data concerning creatine
supplementation and endurance
exercise suggest that it does not im-
prove performance.18,37
Athletic Dosing
The athlete typically starts with a
loading dose of creatine ranging
from 15 to 30 g per day for the first
week. Afterward, a maintenance
dose of 2 to 5 g/day is taken for as
long as 3 months. A month’s sup-
ply typically costs $30 to $50.19 The
athlete then discontinues creatine
supplementation for 1 month to
allow the creatine level to return to
baseline before resuming the cycle
again. 20 Risks are thought to be
minimized with this regimen. There
are no added benefits of increasing
creatine intake above this level.
Skeletal muscle has a specific maxi-
mum creatine storage capacity; sup-
plemental creatine that exceeds this
maximum is excreted by the kid-
neys.39
Adverse Effects
Short-term creatine supplemen-
tation for as long as 8 weeks has not
been associated with major health
risks.38 However, creatine supple-
mentation can cause weight gain
due to an increase in cellular water
in muscle and possibly increased
protein synthesis within muscle.18
Some of the observed side effects
of long-term use include muscle
cramping, dehydration, gastroin-
testinal distress, nausea, and sei-
zures.20 There is also concern about
67
Ergogenic Aids in Athletics
the effects of creatine supplementa-
tion on kidney function.20,36 There-
fore, creatine supplementation should
not be used by persons with under-
lying kidney disease or potential for
renal dysfunction.36 More studies
are needed to fully understand the
long-term effects of chronic creatine
supplementation.
Vitamins
Vitamins are generally classified
as water-soluble or fat-soluble.
Water-soluble vitamins (e.g., vita-
mins B and C) are metabolized and
excreted in the urine. Fat-soluble
vitamins (e.g., vitamins A, D, E,
and K) are stored in the liver and
metabolized more slowly. The fat-
soluble vitamins, therefore, are
potentially more toxic when con-
sumed in large amounts. In general,
most athletes who eat well-balanced
meals and have no dietary restric-
tions do not benefit from vitamin
supplementation.6,18
Mechanism of Action
Some of the more common vita-
min supplements taken by athletes
include vitamin E (α-tocopherol),
vitamin C (ascorbic acid), and vita-
min A precursor (beta carotene).
The belief is that these vitamins are
antioxidants and therefore are able
to act as free-radical scavengers,
especially with the increase in free-
radical production during exercise.
Studies of the effects of antioxidant
supplementation have had varied
results.18 Current research does not
support their use to benefit perfor-
mance.40
Adverse Effects
Some of the adverse side effects
of overconsumption of vitamin A
include drowsiness, headache, vom-
iting, papilledema, hair loss, scaly
skin, brittle nails, hepatospleno-
megaly, anorexia, and irritability.
Excessive intake of vitamin E can
68
cause muscle weakness, fatigue,
headache, and nausea. Excessive
intake of vitamin C can lead to diar-
rhea and renal stone formation.41
Carnitine
Carnitine is a quaternary amine
that exists in several forms in the
body. L-Carnitine is the physiolog-
ically active form. Carnitine sup-
plementation is believed to reduce
muscle glycogen breakdown and
lead to a decrease in lactic acid pro-
duction during exercise, thereby
primarily benefiting the endurance
athlete.6,18 Studies of carnitine and
athletic performance have been
inconclusive. 18,27 Large doses of
carnitine can cause diarrhea, which
is obviously a considerable distrac-
tion from top athletic performance.
Androstenedione
Androstenedione, an androgen
produced in small quantities by the
adrenal glands and gonads, re-
ceived a lot of attention in 1998,
when professional baseball player
Mark McGwire admitted consum-
ing this nutritional supplement
during his record-setting season.
Mechanism of Action
Androstenedione has little in-
trinsic activity but is a direct pre-
cursor of testosterone, a potent
androgen. Androstenedione is also
produced by some plants, from
which can be derived a natural
alternative to anabolic steroids. It
is sold as a nonprescription nutri-
tional supplement. Users and man-
ufacturers of androstenedione sup-
plements claim that they encourage
the buildup of muscle mass and
promote rapid recovery from
injury.42 Whether this claim is true
is unknown, as there is almost no
published information available on
the effects of taking androstene-
Journal of the American Academy of Orthopaedic Surgeons
dione.43 A recent study by King et
al44 showed no increase in muscle
mass or increased testosterone lev-
els in men given daily doses of 300
mg of androstenedione compared
with control subjects given placebo.
Adverse Effects
King et al44 found decreased lev-
els of high-density lipoprotein and
elevated levels of estrogens in sub-
jects who received androstene-
dione. Low levels of high-density
lipoprotein can contribute to car-
diovascular disease risk. Increased
concentrations of estrogens may
increase the risk of cardiovascular
disease, breast cancer, pancreatic
cancer, and gynecomastia. Several
athletic organizations, including
the NCAA, NFL, USOC, and IOC,
have banned the use of androstene-
dione. Major-league baseball and
some other athletic organizations
still permit its use.
Blood Doping
There have been several highly
publicized scandals involving
blood doping in endurance ath-
letes. 45,46 The practice has been
prohibited by the IOC. (The con-
ceptually related practice of train-
ing at high altitudes in order to ele-
vate hemoglobin concentration is
considered to be a legitimate way
to enhance performance.)
Mechanism of Action
Red blood cell infusions are clas-
sified as ergogenic because they
increase the oxygen-carrying ca-
pacity of the blood and thereby in-
crease the performance of the
working muscles.45 The effective-
ness of blood doping indicates that
it does improve athletic perfor-
mance.3,7,30,45,46 It has been hypoth-
esized that blood doping benefits
the endurance athlete, who depends
primarily on the aerobic cycle for
energy, rather than the sprinter,

who depends primarily on the ana-
erobic cycle for energy.45
Adverse Effects
Risks as a result of blood trans-
fusions include allergic reactions,
bacterial contamination, disease
transmission, and immune sensiti-
zation.46 Autologous transfusion
minimizes the obvious risks, but
there is still the potential of harm,
especially if the storage and trans-
fusion are performed in suboptimal
conditions. 30 In addition, over-
transfusion can lead to polycythe-
mia, which can cause decreased
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