A Field Guide To Joint Disease in Archaelogy - J. Rogers and T. Waldron OCR Reduit

A Field Guide
to Joint Disease
in Archaeology
A Field Guide
to Joint Disease
in Archaeology
JULIET ROGERS
University of Bristol, UK
TONY WALDRON
Institute of Archaeology, London, UK
J IN Wl Y & SONS
c l il t IH .. :II 'r N!'W Yorl ll ri : h:11H Toront o Si ngaporP
Copyright 1995 by John Wiley & Sons Ltd,
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Libran; of Congress Cataloging-in-Publication Data
Rog rs, Juliet.
A field guide to joint disease in archaeology I Juliet Rogers, Tony Waldron.
p. cm.
In hides bibliographical references and index.
I BN 0-471-95506-X
1. Joints - Diseases. 2. Paleopathology. I. Waldron, T. (Tony)
II. Title.
[DNLM: 1. Joint Diseases - pathology. 2. Paleopathology. WE 300
R727f 1994]
R134.8.R64 1994
616.7'207-dc 20
DNLM/DLC
for Library of Congress
British Library Cataloguing in Publication Data
A catalogue record for this book is available from the British Library
ISBN 0-471-95506-X
Typeset in 11/13pt Palatino from authors' disks by
Mayhew Typesetting, Rhayader, Powys
Printed and bound in Great Britain by
Biddies Ltd, Guildford and King' s Lynn
94-45111
CIP
Contents
Preface
List of Abbreviations
1. The Definition of Joint Disease
2. The Palaeopathological Classification of Disease
3. Osteophytes
4. Osteoarthritis
5. Diffuse Idiopathic Skeletal Hyperostosis
6. Rheumatoid Arthritis
7. Ankylosing Spondylitis
8. Other Seronegative Spondlyoarthropathies
9. Gout
10. Infections Causing Joint Disease
11 . Implications for Archaeologists
App ndix
C; n r n 1 Bibliography
llttrll er R nd ing
vii
ix
1
8
20
32
47
55
64
69
78
87
97
108
111
112
11 5
Preface
I' tl ttopathology is both exciting and intensely frustrating. The
1 t i I ment stems from the fact that of all those interested in the
li e of our remote ancestors, palaeopathologists and archaeol-
"1', 11-1 come nearest to them by handling what remains of their
1 d 1 1-1 i al presence. They can come literally face-to-face with
I hn 1.' who lived centuries ago and it really is a privilege and a
1 tl c111H tr to try to find out as much as one possibly can about
II H Il l. lt is wanting to do just this, however, which provokes
11 11 f' rtt stration because the amount of information which can be
' lt'lll t d from human bones is not great, and certainly not as
I' 11 ' If , many archaeologists would like it to be, or many
utlhl'opologists assert it to be.
l11 tddili n to general details such as age, sex and height about
lite individuals they have recovered, archaeologists would like
111 I now what diseases the individuals suffered from, what they
ol e l of, what their occupation was, what their state of nutrition
1
1
1nd . much as possible about their way of life, and the
l11 dth of 1+1 population of which they were once a part. It is
ol ' 11 1 d to hav to say that, in actual fact, very little such
tile" 111 I! ion iH going t b- forthcoming, and we have the dis-
llrH I "IIH'<' ion th. t. gr nt many bon reports are a profound
dt tppninlnwnl In lh ir r il i r tR.
111 cl 11 lite l w I I l l!' t' 111, 111 1 Hopnlhologi l-l l l-l OWl.' it to then -
' I e
1
rnd In I ilo .t w1 who t htl udf ll w worl , to do wh.1t
viii Preface
they can do well. They do this best by not exaggerating the
claims for their discipline, and by ensuring that the information
they do provide is soundly based and conforms to generally
accepted clinical notions of disease. Although one does not
necessarily have to have a medical education to undertake
palaeopathological work it can certainly be an advantage, if
only because one is thereby imbued with a sense of the unpre-
dictability of disease, the uncertainty of diagnosis, and some
concepts of pathological processes.
One of the important ways in which the palaeopathologist can
provide information about the health of past populations is by
describing the frequency of diseases over time, and suggesting
ways in which environmental and other influences may have
affected such changes as are seen. To do this, however, requires
that the diagnostic criteria which are used are reliable and
consistent, and it is to suggest some ways in which these
objectives can be met that this book was written. We hav
concentrated on the joint diseases because these are by far th
most commonly found in human skeletal remains, and becau
they have been our field of special study for a number of year .
We had non-medical bone specialists particularly in mind and
hope that the book will encourage them to be circumspect in
their conclusions.
Over the years we have had much help and encouragem nl
from our colleagues, clinical and archaeological, and we would
like to thank them all. In particular, however, we would lik to
thank Professor Paul Dieppe and Dr lain Watt, who have b en
willing and valuable colleagues and collaborators over tht
years and who have guided our feet into the paths of rheumn
to logical righteousness on many an occasion. We would a I t'
like to take the opportunity to thank the medical illu trat r 11
Bristol for their enormous help with the photograph and otlwr
illustrations.
Juli 't Rogtr
Tony Wnldwn
13ris/'ol nnd I .o11tloll, I
1
)%
List of Abbreviations
, ankylosing spondylitis
Ill ' ill diffuse idiopathic skeletal hyperostosis
I 111 ' I i tal interphalangeal (joint)
11 '1' m tatarsophalangeal (joint)
r; ost oarthritis
1 11 l ost ochondritis dissecans
I ' I I proximal interphalangeal (joint)
I 'I
1'1
l P
1 soriatic arthropathy
rh umatoid arthritis
rheumatoid factor
1
The Definition of Joint
Disease
joints are the organs which form the junction between different
I 1ones and in skeletal material are most frequently the site of
pn thological change. As well as the two bone ends, joints have
n l'lubstantial soft tissue component which can also be involved
11 joint disease; however, evidence for this can only be inferred
I mm the bone.
'I 'here are three types of joint:
( I) fibrous, such as the sutural junction between the bones of
the skull;
(: ) artilaginous, of which the symphysis pubis is one of the
f w examples; and
('I) synovial, which forms the majority of those in the skeleton,
in luding the hip, knee and apophyseal joints of the spine.
' l'ht Hlructure of synovial joints differs fundamentally from the
ni l wr lypes to allow free motion between the bone ends. The
I H 1111 , r joined by a fibrous capsule. The ends of the bones,
lht ll'li ulntions, are covered with cartilage which is lubricated
lty llw Hy novinl fluid within the joint cavity, the synovial fluid
lu ng tcrd d b ~ h Hynovi al rn rnbran whi h )in th joint
' IV ly (Ht Jligttt' t 1.1). ' l'ht H novinl fluid iH. lso involv I in the
tilili' I Oil (]{' lht tl'l it tdill' (' lrlill)',i' ,
2 A Field Guide to joint Disease in Archaeology
BONE
CAPSULE
SYNOVIUM ---
JOINT SPACE ---
HYALINE ARTICULAR -----J
CARTILAGE
Figure 1.1
SKIN AND
SUBCUTANEOUS TISSUE
BURSA
ENTHESIS
TENDON
LIGAMENTOUS
THICKENING
OF THE MUSCLE
Diagram of a typical synovial joint
Any, or all these structures, as well as the ligaments inserting
into the joint capsule and the juxta-articular areas can become
diseased. The type of disease present in a joint depends upon
which of these tissues is mainly affected and which disease
process is involved-such as inflammation or infection. These
factors will determine which particular signs may be present on
the bony elements of the joints. Many different types of joint
disease have been recognised and described, not all involving
the bones; the causes of some are unknown.
There have been many different classifications of joint disease
through the ages, depending on the contemporary concepts of
disease and on the investigative techniques which were th n
available. Until relatively recently all classification of di al5
has depended on the clinical skill of the phy i ian nnd wl n t
could be l arn d fTom obs rving, H t ning to or x. mlnl r g lhv
The Definition of joint Disease 3
p tient and his or her body fluids, and finally, on the results of
post-mortem examination.
The earliest classification of joint disease was into acute and
, hronic arthritis depending on the observed differences in the
progress of the disease under consideration. A few of the early
clinical descriptions are very precise and enable us still to
r cognise the disease being described; gout is one such
1xample. The term gout, however, was used to refer to other
conditions not now recognised as gout.
lr 1 the seventeenth and eighteenth centuries the advent of the
rnicroscope introduced a further dimension into the under-
1 I mding of joint disease. For instance, urate crystals were then
'llntified from the tophi (swellings) found in patients with
11out. The introduction of X-rays in 1895 quickly allowed the
P pansion of the classification of joint disease using the results
obtained from their radiographic examination. By looking for
ll ll' first time directly at the bony changes involved in live
1 "1 Licnts it was seen that there were two main categories of joint
pn thology and that these coincided with two types of joint
1l h; ase. The first was termed atrophic; it affected younger
1 "ople and many joints were involved and there was a
lnd ncy to inflammation of the soft tissues of the joint with
of the joint margins and loss of bone density. The
1 cond type recognised radiographically was termed hyper-
lt'OJ hie joint disease because of the hypertrophy or overgrowth
, ,( marginal and articular bone manifested by osteophytosis and
, llr sis. Pathological examination revealed a focal loss of
1 uUiage and this second set of changes tended to occur in older
p1opl and to affect fewer joints than the atrophic variety of
tl'lhri ti s.
11 Wnl' sub equent to these first X-ray classifications that Garrod
11 1904 all d the atrophic, erosive form rheumatoid arthritis
(I' A) n nd the hypertrophic form, osteoarthritis (OA). Some
nllwr j' roups f ro iv arthropathy, formerly included within
llw Jl' ' l rum of RA l av sin b n r lassifi d as parat
l ' tll titll in 1'1 Pir owr rigl t, th rnoRt irnportnnt 111tt di vi sion
lu 111; lh 11 o l i lt' cnll <d tt'<HH'g 1tlv< HJ ond lo l l' lhtopnLI it
Wh tl! W l ' l 'l ' dt f l ll ' d I) fi ll' 1
1
)(,()1 ,
It is thus clear that the manner in which diseases are classified
depends partly on the set of examinations that can be made
and how these are interpreted, and partly on the current
concept of the disease process. However, there is always a
tendency for observations to be made to fit the original concept
of the disease. This has an important bearing on the way in
which we attempt to classify joint disease in skeletal material
because the majority of information on which clinicians may
base their diagnostic criteria is absent. Thus, there is no living
patient from whom to take a history or to examine, and no soft
tissue for pathological or biochemical examination. The palaeo-
pathologist's investigations are limited to the bony changes
only, and in some joint diseases these may be minimal. The
only routine investigation available is some form of radiology
although it is possible that biochemical and immunological
analyses will become available in the near future.
Bone reacts in a restricted number of ways so that the final
pathological appearances of a joint in the skeleton may be the
end result of any one of a number of diseases. However, the
propensity for these bony changes to be distributed both within
the joints and around the skeleton in a distinct and sometimes
specific manner helps in many cases to clarify which particular
joint disease has caused the skeletal changes.
The criteria which are for palaeopathological diagnosis are
distinct from but related to strictly clinical criteria (Figure 1.2a
and b). They are based on a visual assessment of the mor-
phology of the bones with special note being made of the
distribution and type of bone change within the joints and the
distribution of the affected joints around the skeleton. There are
characteristic patterns typical of certain diseases which can
allow a reasonable chance of classification in typical cases. It is
important to remember that typical changes will not be found
in all cases, however (Figures 1.3 & 1.4). In clinical practice a
disease evolves and a diagnosis may not be possible until it has
progressed to a relatively advanced stage and clinicians hav
many opportunities to review the changes in their pati nts. fn
any one skeleton it is impossible to tell how Ion th dis a:,;'
has been present or when during th di as th ind ividua l
di d. Mor ov r, th bony hang s di. I, y 'd on tlw kl' II'IOn
(a)
(I>)
The Definition of joint Disease
CLINICAL
RADIOLOGICAL
CLINICAL
PALAEO-
PATHOLOGICAL
5
I Hllr 1. ' (.1) Vnnn dl.1gr.ui1 of l'ti latl onship b tw n v;Jriou lini <I di agnosti
1 illl tin (11) I ol.lllilll'il p hntwn<'ll p.li.H'Opnthologlcal and r llnl <d ell. p,nn. tl
n Ill rl.,
OA uncommon.:: ......
OA

OA-... .'.'.
Psoriatic_...,...
RA ........ .
Psoriatic ........... .
........ RA I atlanto-axi al l
OA C/4/5
DISH
...... ...... RA & OA
............ RA
.. ........... OA/Gout
Figure 1.3 Pattern of characteristic skeletal involvement in various
arthropathies
may be from an early or a late stage of the disease.
In the following chapters, the main categories of joint disease
that can be expected in the skeleton are discussed and we
describe how they can be usefully diagnosed or classified in
earlier skeletal populations.
NORMAL
RA
marginal
ADVANCED
PSORIATIC
ARTHROPATHY
cup & pencil
deformity
The Definition of joint Disease
OA
sclerosis of
I eburnation I
osteophyte
GOUT
bone noc>K .... fl
pararticular
erosion
ANKYLOSIS
occasional feature
of Psoriatic/Reiters
or AS of
peripheral joints
NEVER In RA
l lgure 1.4 Characteristic peripheral joint changes in various arthropathies
7
2
The Palaeopathological
Classification of Disease
In normal living bone there is a dynamic equilibrium between
the cells that make bone (the osteoblasts) and those which
resorb it (the osteoclasts), and this serves to maintain the
integrity of the skeleton. This equilibrium is disturbed in bone
affected by disease, but since bone has only a limited capacity
to react to disease processes, one may greatly oversimplify the
outcome by saying that diseased bone is characterised by there
being too much or too little present. The diseases which affect
bone, however, rarely do so in isolation. For example, the joint
diseases may not have their origin in the bone, but in the other
tissues of the joints, the articular cartilage or the synovial
membrane (see Figure 2.1), and it may be difficult to under-
stand the changes seen in the skeleton unless some thought is
also given to what is going on in the surrounding soft tissues.
Another general point which needs to be clearly understood is
that diseases may affect the skeleton in a selective manner.
Thus in some joint diseases the distal interphalangeal joints
(DIP) will be found to be involved, whereas in others it will be
the proximal interphalangeal (PIP) joints; one arthropathy will
present with multiple symmetrical changes, another with a
lesion affecting only a single joint. Because of this, the more
complete the skeleton, the better the chance of b ing r hably
able to classify the disea es whi h ar pr s nt. Th nvcrs of
Figure 2.1
The Palaeopathological Classification of Disease 9
AREA OF CHANGE
JOINT MARGIN
ARTICULAR SURFACE
PERIARTICULAR
JUXTA-ARTICULAR
Diagram of a typical synovial joint showing areas in which
pathological changes may be observed
this is obviously also true; and our advice, especially to the
beginner is, if there is not much bone, do not say much about
it.
FIRST STEPS IN CLASSIFICATION
The first step in classifying joint diseases must be to make an
inventory of all the bones which are present in the well washed
skeleton and note which joints are present. The \!Se of fixatives,
which might impart a shine to the joints should be noted; and
occasionally archaeologists or finds assistants will write the
skeleton number on the joint surface; this is a practice strongly
to be discouraged. If, as sometimes happens, the age and sex of
the skeleton are to be determined by another worker you
should agree criteria in advance if only to ensure that joint
hanges are not used as an ageing criterion, since if they are,
1 otentially useful epidemiological information will be lost.
It is essential to use forms devised specially for recording
1 urposes and not rely on free-form notes otherwise details will
in vitably b mi s ed off. An example of the recording forms
whi I w ro11fi1 ' ' Y us ar hown in the app ndix. The joint
lnvtnlor l lll' t 't 't nr wl t' n th pal t rn of joint
1 0 A Field Guide to joint Disease in Archaeology
involvement and for providing the denominator data for
subsequent epidemiological analyses (see below).
Having recorded these details, the skeleton is carefully
examined for abnormalities. The position of joint lesions
should be recorded on a skeletal diagram from both the
anterior and posterior view; in the spine, the level of each
lesion should be recorded and, in the case of the facet joints, the
side or sides affected. It may be useful to make a more detailed
record of some of the individual joints; for example, we
routinely use separate charts for the hands and feet and for the
shoulder, hips and knee, but there is no reason why others
should not be used if required. When collecting data for
research purposes, rather than for routine bone reporting, con-
siderably more information is likely to be required and when
deciding on the level of data to record, bear in mind the
possibility of further studies; also bear in mind that it may not
be feasible to go back to re-examine individual skeletons again,
especially if they are to be reburied, and that yours may be the
definitive set of observations made on a particular group of
skeletons. Obviously a balance has to be struck between what is
practicable to record, given the constraints of time and money,
and what one might wish to preserve for posterity.
When preparing diagrams of lesions it is helpful to show
different features in separate colours: red for proliferation, blue
for erosions, green for eburnation and so on, as in this way the
patterns of change throughout the skeleton are much more
easily detected. Some work has been started in the United
States to computerise skeletal diagrams, and when this has
finally been achieved it should be possible to use computer-
aided classification; but this is still some way off. Nevertheless,
with any but the smallest site the data relating to joint numbers
and some form of coding for the pathology present will have to
be entered into a database the precise nature of which will
almost certainly be a matter of personal preference.
In addition to the systematic recording of the sites and distri-
bution of lesions, a clear and detailed description should also
be made, especially as not all lesions will fall into a p i fi
category. Photographs hould b tak n and illu m. tk
wherever possible; this is especially important if the skeletons
are to be reburied or cremated.
EROSION AND PROLIFERATION
We have said that bone has only a limited capacity to express
pathological change; it may gain substance through the
proliferation of new bone and it may lose it in the form of
erosions which are manifestations of osteoclastic activity or
sometimes the result of direct pressure from adjacent soft
tissues or abscess cavities.
During the examination of the skeleton, each lesion which is
found should be assessed to decide whether it is erosive or
proliferative, or, as not infrequently happens, a combination of
both. It will also be necessary to record the presence of other
abnormalities affecting the joints of which the most important
in the present context is eburnation.
Proliferation
Detecting the presence of new bone around a joint margin or
on the surface of a joint is relatively straightforward although it
may be difficult sometimes to determine whether minimal
change is within the spectrum of . normality or not, remem-
bering that there is no abrupt change from normal to abnormal,
and only experience will help on this point. Some workers like
to grade the changes which they see on a simple three- or four-
point scale and this may be useful. However, if you decide to
do so, remember that your gradings will probably not bear
much relationship to those of another worker in the field unless
rt'f r nee can be made to type specimens; and there is also
lik ly to b a ood d al of inconsistency in grading from day to
dny (Ace . IAo h. pl:l'r 3 on ost phyt . f r furth r d tails on
w ring nw t hod ).
Erosions
As used here, the term erosion applies only to pathological
lesions in or around joints. The term is often more widely
applied to post-mortem damage around joints or on the bone
surface. We would prefer that the term 'erosion' is restricted to
the lesions accompanying joint disease and that other terms
such as abrasion be used for post-mortem damage.
Erosions can present much more of a problem diagnostically
than proliferation, and they must be carefully distinguished
from post-mortem damage and from the other holes which may
be found around the joint. These other holes may include
vascular foramina, cysts and canals produced by roots or
fungal hyphae. There is no simple way to discriminate true
erosions from other holes around joints but there are some
pointers. For example, in a true erosion the cortical bone is lost
and the underlying trabeculae may be exposed and under the
scanning electron microscope, signs of osteoclastic activity may
be seen (Figure 2.2). Any hole in which the cortex is completely
intact (such as the entry site for a nutrient artery) is not an
erosion, although you must remember that there will be an
attempt at repair and some remodelling may be present in a
true erosion. Differentiating post-mortem damage from a true
erosion usually presents a greater difficulty, but post-mortem
damage is seldom symmetrical and may extend well beyond
the confines of the joint. Damage sustained during or after
excavation may have fresh edges but even this is not an
infallible distinction, however, as some erosive arthropathies
are accompanied by osteoporosis, which makes the bone more
fragile and more easily damaged during handling. In some
erosions there is an undercut edge which is not usually present
in an artefactual lesion.
The lesions in some of the joint diseases start at the joint
margin, in others in the centre of the joint and in others outside
the joint capsule; if it is possible to make this distinction it can
help with the classification, but in many cases the disease will
be too advanced or the bone too damaged to p rmit su h an
observation.
Figure 2.2 Electron micrograph showing in vitro osteoclastic activity. (Courtesy
of Dr Adrianne Flannigan)
Eburnation
Eburnation is an important feature in joint disease since it is
pathognomonic of OA. It manifests itself in dry bones by highly
polished areas on the joint surface and is caused by an area of
bare bone moving over other structures. Eburnation is almost
always found on the reciprocal surfaces of a joint, although this
is not necessarily the case. Eburnation is never found in a joint
which has been immobile. There is generally no excuse to miss
'burnation, although small areas on, say, a distal phalanx may
not be seen unless the bones are examined in a good light as
I hey always should be.
Osteoporosis
< )Hit'op<H"OHi. iH lh' loHA of bote Hubstc n resulling in orti al
thhmi11p, or 1 d1cn Hil' in llw lltllllhtr of lrnl trtllnt. 11 iH
secondary sign of some joint diseases and can be suspected if
a bone feels unduly light but can only be confirmed by
radiography.
Compound joints
Some joints, such as the elbow and the knee, consist of more
than one anatomical compartment-in both the elbow and the
knee there are three-and these are known as compound joints.
Changes found in such joints should be recorded for each
compartment, and for epidemiological purposes it is legitimate
to consider each compartment separately (see Chapter 4). Some
complicated systems for scoring these joints have been
described in which each compartment is considered to be a
fraction of a joint and a score is assigned to the joint depending
on how many 'fractions' are involved. This kind of scoring
system has no clinical correlates and should be completely
avoided unless a special research topic is being pursued. For
epidemiological purposes, the rule should be that a compound
joint is treated as a single joint, although its compartments may
be treated separately in any subsequent analyses.
SUPPLEMENTARY EXAMINATIONS
There are relatively few supplementary examinations that are of
value to the bone specialist and the only one which is used
frequently is radiography. Radiography is most likely to be
helpful with the classification of the erosive arthropathies and
we would go so far as to say that under normal circumstances
there is no virtue in X-raying joints with OA since little further
information is likely to emerge which would cause you to
change your classification, assuming that the proper procedures
have been followed in the first place. The advice of an experi-
enced skeletal radiologist is absolutely essential in drawing
conclusions from the films which are taken.
The Palaeopathological Classification of Disease 1 r.
CLASSIFYING INTO MOST PROBABLE CAUSE
Having recorded all the lesions and noted their character and
distribution, the next step is to classify these changes into their
most probable cause; for the joint diseases which are most
likely to be found in skeletal material this procedure is
described in the following chapters.
It is often intensely frustrating trying to classify joint lesions
since, with the exception of eburnation in OA, there are no
pathognomonic signs and so often critically important parts of
the skeleton are missing. You will probably find that in a
substantial number of cases you are able to do no more than
note that you are dealing with an erosive arthropathy of some
kind and will have to admit that further classification has
defeated you. You may take some comfort, however, from
knowing that your clinical counterparts may not be doing a
great deal better even with their ability to interrogate their
patients and their access to a large array of investigations.
Moreover, clinicians have an opportunity to see disease in
'volution, and see it as a changing, dynamic process. Palaeo-
pathologists, by contrast, have only one view of disease in their
1-mbjects and that at a most unfortunate time for them, the time
of their death. There is no telling where in the progress of the
lisease the subjects were and the appearances may or may not
'Onform to modem textbook appearances; it is just a matter of
chance.
DETERMINING THE FREQUENCY OF DISEASE
Reporting on disease in the skeleton can take one of two forms:
the case report or the population model. Case reports, where
I h number of subjects is small- perhaps even a single case--
I r often used when dealing with rare or unusual diseases but
I h y provide no useful information about the frequency of
'llRcas in pa t populations. If this is the aim, then population
d tn hnv to b u A d and "om stimate of th frequ ncy of tb
' C' ondN con ' idNnllon hn to b mod ; thi s is o hi v<>d y
1 tll'!tllling lr jH't y tlt t)l ' t ' ,
I() A Fi Id Guide to joint Disease in Archaeology
The prevalence of a disease is expressed simply as the ratio of
the number of those with the disease to the total population;
that is
where P = prevalence,
p = .!!__
N
n = the number of cases with the disease, and
N = the total population.
You may see the frequency of a disease in skeletal populations
referred to as an 'incidence' or an 'incidence rate'; epidemio-
logically this is incorrect for reasons which are gone into more
fully elsewhere; suffice it to say, incidence should never be used
when referring to the frequency of a disease in a skeleton
population.
As it is a simple ratio, the prevalence of a disease is strictly
speaking not a rate, but the term 'prevalence rate' is often used
as the normal expression. Whether the correct or incorrect term
is used, however, prevalence is almost never given as a
percentage but depending on the size of the base population
(the denominator), as so many cases per 10
3
-10
6
; the size of
skeletal populations would generally preclude referring to a
base population greater than a thousand.
CALCULATION OF PREVALENCE
In contemporary populations the calculation of prevalence is an
extremely straightforward exercise-in so far as anything is
simple in epidemiology; just count the number of cases, the
number in the base population and divide the first by the
second. When trying to carry out this elementary aritlunetic on
skeletal populations, one very soon comes across a diffi ulty
which relates to the number to put in th d nomi:nat r; in other
words, what is th population?
The Palaeopathological Classification of Disease 1 7
onsider for a moment a simple example. You have a group of
175 skeletons and you find that nine have OA of the hip. The
apparent prevalence of this condition is 9/175 = 51.4/10
3
; this
i referred to as the crude prevalence. Suppose, however, that 26
of the skeletons are so badly damaged that they have no hip
joints, then it is clear that they should not appear in the
denominator and the prevalence now can be calculated as
9/{175-26) = 60.4/10
3
. However, there is yet a further compli-
ation to consider befpre one can let the matter finally rest. We
now have 149 skeletons with hip joints, but what if 13 of these
have only one normal joint present? We know nothing about the
Htatus of the missing joint-it might have been either diseased
or normal, but as we do not know, we are obliged to exclude
lhese 13 from the denominator and so the final calculation
becomes 9/{149-13) = 6.2/10
3
. (It should be noted that this
1 rocedure can be somewhat simplified by considering the left
nnd right joints separately, but this would be an unusual
pidemiological practice.)
What should be remembered from this exercise is that the total
number of skeletons in a group may not be the appropriate
denominator when calculating the prevalence of joint disease;
nlmost never in the case of OA, which is far and away the most
'Ommon disease seen in the skeleton, and this is why it is so
vital to have an accurate inventory of the number of joints
1 resent.
AGE- AND SEX-SPECIFIC PREVALENCE
Prevalence can be calculated for the different sexes and for
different age classes, in which case one refers to sex-specific and
nge-specific prevalence, respectively. It would generally not be
worthwhile to do this with the less common joint diseases but it
rtainly is when dealing with OA and if, for example you were
lo find th t th pr val ne of OA did not increase considerably
wi lh ngl 11 mi)"ht ho s tor vi w th ag s all o at d to your
(' (i'IOII H,
COMPARING PREVALENCE IN DIFFERENT
SKELETAL GROUPS
One reason to study skeletons is to compare the frequency of
disease in different groups and investigate whether variations
in frequency may be related to environmental, social or other
factors. Comparisons such as this will be made using the
prevalence of the disease but, if the crude prevalence is used,
like may not always be compared with like, and the reason for
this lies in the fact that the age structure of different popu-
lations may be dissimilar. This point can be illustrated simply
by considering a disease where the prevalence is highly age-
related; OA or diffuse idiopathic skeletal hyperostosis (DISH;
see Chapter 5) would be good examples.
Imagine we have two skeletal populations (A and B) each of
350 individuals. In A there are 19 cases of a disease in which
we are interested, whereas in B there are 46. The apparent
prevalences of the disease in A and Bare 19/350 and 46/ 350 =
54.3 and 131.4/ 10
3
respectively; these are known as the crude
prevalences. It appears that the disease is almost 2lh times more
common in B than in A. When we look at the age-specific
prevalences, however, there is an anomaly as the age-specific
prevalences are identical in both populations; see Table 2.1. The
reason for the apparent excess in B is that there are more older
individuals in this population, in whom the disease is much
more frequent, than in A, where young individuals with a low
prevalence predominate. By comparing the age-specific
prevalences it is clear that the frequency of the disease is
exactly similar in the two populations.
Table 2.1 Age-specific prevalence of disease in two popul ations
A
Age-group n N P/10
3
25-34 4 200 20
35-44 5 100 50
45+ 10 50 200
Total 19 350 54.3
n = number of inviduals with the disease
N = tota.l number in age-group
P = pr valcn c
B
n N P/10
3
1 50 20
5 100 50
40 200 200
46 350 1 1.4
It is perfectly respectable to compare age-specific prevalence
between populations using appropriate techniques, including
that of comparing odds or risk ratios. One can also use the so-
called method of direct standardisation. Any of these methods
can produce a summary statistic which can be compared
between populations. You should be aware of how these
procedures are carried out but this is not within the remit of the
present book and we must refer you elsewhere.
3
Osteophytes
Osteophytes are growths of new bone which arise round the
margins of a joint and which may vary considerably in size and
shape. They are extremely common in any skeletal population
and their prevalence increases markedly with age, and almost any
skeleton over the age of 50 or so will be found to have osteo-
phytes around at least one joint if examined carefully enough.
DISTRIBUTION
Osteophytes may be found around any joint but they appear
around some more commonly than others. For example, they
occur round the knee and hip joints more often than around the
ankle, around the DIP joints more frequently than the PIP joints.
They are especially common around the margins of the vertebral
bodies but are found more often in the cervical and lumbar
vertebra regions than in the thoracic. Osteophytes are also
commonly seen around the margins of the facet joints of the
spine and, especially in older individuals, on the odontoid peg.
MORPHOLOGY
Osteophytes around joint generally tak th ir origin nt the
point at whi h th . ynovia'l m mbrnr is onlinuot tH wi th llw
Osteophytes 21
articular cartilage, that is, at the joint margins. On occasion the
osteophyte forms a complete ring around the joint, demarcating
it exactly from the surrounding normal bone and a normal joint
tourface. The degree of bone formation can vary enormously
from a minute rim to an massive outgrowth which may some-
times form a phlange several millimetres deep around the joint.
Large osteophytes are likely to be seen especially around the
margins of a concave joint such as the acetabulum or the
glenoid; very rarely we have seen the head of a femur so
nclosed by osteophytes arising from the acetabulum that the
two could not be separated.
In the spine, osteophytes on the vertebral bodies are somewhat
different from those in other sites (Figure 3.1) in that they take
their origin from the point of attachment of the fibres of the
, nnulus fibrosa. Osteophytes here tend to develop horizontally,
I ut may turn vertically if they become sufficiently large (Figure

,' ince there is such variation in the degree of osteophytosis
nround joints, some workers have devised rating scales to
r cord its presence. These usually have three or four points,
nnd individual joints are rated either as 0, when no osteophyte
is present, or from 1 to 3 (or 4) when it is, depending on the
ize and extent of the new bone formation. These scales may
1 rovide useful information for individual observers but they
11 re not particularly helpful for interstudy comparisons as it is
t mlikely that there will be a high level of concordance between
1 he ratings of different observers since they reflect qualitative
rather than quantitative differences. The discrepancies are noted
1 articularly with specimens which are considered to be
'borderline' between the categories and many observers experi-
tnce a problem with knowing exactly when to rate minimal
change as being of significance, that is, worthy of inclusion into
I h lowest category. Rating scales are sometimes used to
rn. asure the 'severity' of the degree of osteophytosis present,
but this concept has very little meaning since it implies that the
OHt phytes may have impaired the individual to lesser or
gr '( t r d gr s during life and there is no evidence that this is
rdually th as . It is b tter not to use rating scales in this way
111d 114 r ot much to omm-nd th ir use at all,
22
A Field Guide to joint Disease in Archaeology
NORMAL
DISH
or
Forrestiers
Disease
huge
paravertebral

bone extensions \:'::::::::::::::::::::::::::::::::::::::::::::::::
ANKYLOSING
SPONDYLITIS
squaring of
corners of
vertebrae r ~ = ' " " " " ' = = ~
OSTEOPHYTOSIS
Figure 3.1 Characteristic changes in the vertebral bodies in some spinal
diseases
except where some particular research interest is being
pursued.
OSTEOPHYTES AT OTHER SITES
Osteophytes occur at sites other than around joint margins and
although their significance is outside the scope of the present
book, it is, nevertheless, worth giving them a passing mention.
They may occur on joint surfaces, appearing as flat, irr !lady
hap d plaqu of bon u ually in a"' o iation with mnrginnl
Osteophytes 23
Figure 3.2 Spinal osteophytosis
osteophyte. They may or may not be associated with OA. They
are not often referred to clinically as they do not usually show
up on an X-ray.
Growths of new bone may also be found elsewhere on the
skeleton and are often associated with injury as it is assumed
t- hat they represent the calcification or ossification of hae-
matomas. For example, fractured ribs may be found joined by
thin bands of bone that can be interpreted to be the results of
ossification of a bleed which occurred at the time of the
fracture. These growths of new bone are sometimes referred to
lS osteophytes, but ought more correctly to be called exostoses.
Occasionally large, curiously shaped exostoses may be found
1 rising from the shafts of long bones-the femur seems often to
I) involved-and these are considered to be ossification into
bleeds that have taken place into the body of a muscle which
was damaged by some unusually strenuous exertion. This
mndition is frequently referred to as myositis ossificans but
tHtght p rhaps to be qualified as myositis ossificans traumatica
lo diff r nti t it clearly from the rare, hereditary condition,
111 oHi li H (or fibrodyspla ia) o sifi ans progr s iva. Th
24
Table 3.1 Types of bony outgrowth in the spine
Type of outgrowth Morphology Associated with
Ossification of annulus
fibrosa (syndesmophyte)
Osteophyte
Anterior ossification
Vertical outgrowth
extending from the
edge of adjacent
vertebral bodies
Horizontal outgrowth
from edge of vertebral
body
Flowing growth along
anterior border of the
spine into the anterior
longitudinal ligament
Paravertebral ossification Outgrowth of bone
separated from the
edge of the vertebral
body and the
intervertebral disc
Ankylosing spondylitis
Degenerative disc
disease
DISH
Psoriatic arthropathy
Reiter's syndrome
exostoses are sometimes considered to be indicators of occu-
pational stress or injury.
In the spine, bony outgrowths may be seen as a result of
ossification of the annulus fibrosa of the intervertebral disc, as a
longitudinal, flowing ossification into the anterior longitudinal
ligament, intervertebral disc and the paravertebral connective
tissue, and as ossification of the paravertebral tissues alone.
These are all generally referred to as osteophytes and although
some authorities might object to this usage, it is so ingrained in
the literature that it would be perverse to try to change it. The
characteristics of these different types of spinal bony
outgrowths and some of their causes are shown in Table 3.1.
Enthesophytes
Osteophytes may also be seen at the site of tendon
the area known as the enthesis; the preferred term for them IS
enthesophytes (Figure 3.3). They may re ult from r p at d
trauma to t ndon ons qu nt 11pon r p t d u R ul. r < N I ion
Osteophytes 25
Figure 3.3 Enthesophyte on olecranon process of the ulna at the point of
insertion of the triceps muscle
but they are also found as a concomitant of other diseases and,
again, their interpretation as indicators of occupation or activity
needs carefully to be qualified; this is discussed further in
Chapter 11.
SIGNIFICANCE OF OSTEOPHYTES
There is no difficulty in recognising the presence of osteophytes
in the skeleton and there are no diagnostic problems in that
respect. The question is to what extent do they represent
disease in the skeleton? In the absence of any other abnormali-
ties in the skeleton, then marginal osteophytes are probably not
pathological. Indeed, they appear to be a normal accompani-
ment of ageing; the prevalence of osteophytosis increases
markedly with age and in some joints-the spine and the hip,
for example-they appear to be independent of other signs of
OA. Because their frequency increases with age there is a
ltmptation to use the presence of osteophytes as a means of
ng ing; this is at best an imprecise method and we would not
Hlvo at its u e. If one is trying to study the age-specific
Table 3.2 Some conditions associated with
osteophytosis or new bone formation
Ageing
Osteoarthritis
Intervertebral disc disease
DISH
Trauma
Ankylosing spondylitis
Reiter's syndrome
Acromegaly
Fluorosis
Ochronosis
Neuroarthropathy
prevalence of osteophytes then their presence is absolutely
contra-indicated as an ageing technique.
OA is by far the most common condition in which osteophytes
are seen and they are one of the minor criteria for classifying
this disorder (see Chapter 4) but they may be seen in many
other conditions, some of which are shown in Table 3.2. The
conditions are listed in probable order in which they might be
expected to be found in the skeleton and none but the first five
is at all common.
Although they are common in OA, osteophytes must not form
the basis of the palaeopathological diagnosis if there are no
other signs such as eburnation, new bone on the joint surface,
pitting on the joint surface or change in joint contour. Although
the presence of osteophytes around a joint is used radio-
logically to diagnose OA, there is no justification for doing so in
palaeopathology and those who use this as the sole criterion for
classifying OA in the skeleton are in error.
DEGENERATIVE DISC DISEASE AND
SCHMORL'S NODES
These conditions are so common in the skeleton and so oft n
associated with osteophytes that this ms an appropri. t
pla to consid r th m.
Osteophytes 27
Degenerative disc disease
Degenerative, or intervertebral disc disease is diagnosed by
coarse pitting, sometimes associated with new bone growth, on
the superior or inferior surfaces of the vertebral bodies (Figure
3.4). It is most commonly found in the mid- and lower cervical,
upper thoracic and lower lumbar regions of the spine and may
be on one or both surfaces of an individual vertebra. Marginal
osteophytosis is an almost invariable accompaniment and these
changes are presumed to reflect degeneration in the inter-
vertebral disc. In some cases osteophyte may be observed
encroaching on to the intervertebral foramen, through which
the nerve roots leave the spinal cord, and in some instances the
foramen is so narrowed that it seems likely that the nerve root
must have been compressed during life. This is the course of
events which gives rise to cervical spondylitis which is a
condition commonly met with in clinical rheumatology or
neurology.
Schmorl's nodes
These are recognised in the skeleton as indentations in the
superior or anterior surfaces of the vertebra, and are most
common in the lower thoracic and lumbar regions. They
represent the herniation of material from the intervertebral disc
through the end plate and they are pressure defects. They are
often irregular in shape and have a lining of intact cortical bone
and may be found in any position on the vertebra depending
in which direction the disc has herniated. With posterior
herniation the lesions may be found in communication with
the spinal canal, and if anteriorly there may be some associated
kyphosis and osteophytosis, in which case the condition is
referred to as Scheuermann' s disease.
Osteophytosis and Schmorl' s nodes are both common con-
ditions and so both are frequently found together. However,
Lh re is no evidence that, with the exception noted above, they
1 r ausally r lated.
OSTEOCHONDRITIS DISSECANS AND
METATARSAL PITTING
(
These conditions are seen commonly in association with
osteophyte formation and will be considered here as they do
not fit neatly into any other category.
Osteochondritis dissecans (OD)
OD is referred to quite often in the palaeopathological
literature, but it is probably considerably overdiagnosed. The
lesion is the result of fragmentation and probable disruption of
articular cartilage probably consequent upon trauma. The result
is a defect in subchondral bone which is generally in line with
the long axis of the joint surface; the lesion is variable in size,
shape and depth and may be surrounded by a rim of
(
osteophyte (Figures 3.4, 3.5 & 3.6). OD has a peak age of onset
between the ages of 15 and 20, is more common in males than
in females and is much more often unilateral than bilateral. It
occurs only on
Figure 3.4 Characteri stic changes of degenerati ve disc disease showing plll'lng
and rough ning f th nd plat s and som ostcorhyto. ls
Osteophytes 29
Figure 3.5 Osteochondritis dissecans on the medial femoral condyle
Figure 3.6 Radiograph of specimen shown in Figure 3.5
other sites at which the condition occurs at all frequently are
the humeral compartment of the humeroradial joint and on the
dome of the talus.
D must be differentiated from small pits or other lesions
whi h ar ornrnonly seen on the concave surfaces of joints and
10 A I i Id Guide to joint Disease in Archaeology
Figure 3.7 Pitting on inferior surface of third metatarsal and lateral cuneiform.
Scale in cm
which have a different aetiology. Such pseudo lesions are
frequently seen on the proximal joint surface of the first
( phalanx of the foot, for example, and David Burkitt referred to
\ them as osteochondritis non-dissecans. It is all too easy to
record any defect on the joint surface as true OD and care
should be taken not to perpetuate this error.
Metatarsal pitting
This is a curious condition in which fine pitting is seen on the
\ reciprocal joint surfaces of the third metatarsal 1 1:91
\ Cl,J.neiform (Figure 3.7). The ones may l:ie
\ sligfit y enlarged and the pitting confined there, alternatively it
may cover the entire surface. The condition is generally
bilateral and may be accompanied by marginal osteophyte. Its
prevalence is variable; in some North American Indian
populations it may be 10% or more but in this country it i
( much less common. The cause and ignifi an of it er cnlin'ly
\ unknown.
Osteophytes 31
haracteristics of osteophytes
growths of new bone around joint margins and at other
sites
vary in size .
increase in prevalence with age
commonly seen in osteoarthritis .
found in diffuse idiopathic skeletal hyperostosis.
cannot be used to diagnose osteoarthritis as an Isolated
finding . .
should not be used as an agemg technique
4
Osteoarthritis
OA is the commonest joint disease in both modem and ancient
populations but was not well described until Heberden did so
in the eighteenth century. It is characterised by a focal loss of
articular cartilage and subsequent bony reaction of the
subchondral and marginal bone.
OA affects only synovial joints and the prevalence of the
disease increases markedly with age; in modem populations it
tends to be more common in females than in males. In theory,
any synovial joint can be affected by OA but, in practice, it
(
occurs in some much more commonly than in others. The major
sites are thej:lli!s (especially the joints around the trapezium),
the facet joints of the the acromioclavicular joint, the
first metatarsophalangeal (MTP) joint, the hip and the knee.
Clinically, many patterns of OA have been described and it is
now felt that there are a number of more or less distinct forms.
(
, For example, bilateral OA of the hip is thought to be a distinct
entity and it tends to affect younger males. By contrast,
generalised OA, in which the DIP joints of the hands, the
thumb base and the knees are involved, is more often found in
, middle-aged women. Examination of skeletal material makes it
obvious that there is a wide variation of joint involvement and
much work has been done on localising this differential joint
involvement in skeletal populations and equating the diff r-
ences found to various activities and oc upatio:ns. B au th y
hav the opportunity to xamin v ry joint in l'lw bod ,
Osteoarthriti 'I I
palaeopathologists see OA in sites which the nd
radiologist seldom, if ever, have to th:II notice. For
xample, OA affecting the odontoid peg IS
in skeletal populations but scarcely recogrused as a _clinical
ntity; other unusual sites at which OA
the inter-metacarpal and inter-metatarsal JOmts.
< bility to examine the articular system in detail than IS
ossible in a live population, palaeopathologiSts are able to
ontribute substantially to our understanding of this disease.
The association of OA with the concept of wear and tear, or as
degenerative disease, and hence the result of over-use
through activity or occupation is a long one and probably arose
in the first place from observations on the focal nature of the
loss of cartilage which occurs in the disease. However, our
present understanding of the pathogenesis of OA a
much less straightforward association. The changes seen m the
artilage are not necessarily but represent real or
1ttempted repair, rather than OA IS the
1
roduct of a normal repair IS the
natural reaction of a synovial JOmt to JOmt failure. The
nlteration of the mechanics of the joint, either through injury or
, tivity is only one element in the process; the age,_ systemic
md genetic predisposition of the are Important
factors in the development of the disease (see Figure 4.1). The
mechanical element probably acts to determine which joints are
involved in an otherwise predisposed individual.
EROSIVE OA
In a very few cases, erosions are noted in the
joints in individuals with true OA. Erosive OA: IS
fmm the other erosive arthropathies as the lesiOns are articular
m ther than marginal; on X-ray they produce a 'gull-wing'
'I pcarance (Figure 4.2). Althou?h once a separate
1
1 iHca e, erosive OA is now considered to be JUSt a severe stage
of n rmal int r h. lnng al A. To the best of our
only on , s I o f 11 ppcar d in the palaeopatholog1cal
I It ' 1' 1 t1 ur<.
Systemic factors ~
Genetic
predisposition
Predisposition
toOA
Local
biomechanical
factors
Site & severity
ofOA
Figure 4.1 Model of factors influencing the pathogenesis of osteoarthritis. (After
Klippel & Dieppe)
OA IN ANIMALS
OA is common in animals and is probably the disease found
most frequently in animal bones from archaeological sites.
There is no difference in the pathology between species,
although the rate of progress may be extremely rapid,
especially in large animals. Some forms of OA in animals have
particular names in the veterinary literature and archaeological
bone specialists should perhaps be aware of them.
Ringbone
This refers to OA of the interphalangeal joints of ungulates,
especially horses. It principally affects the joints of the forelimb.
Th 'ringbone' is osteophyte which may ompletely n ir lt' th
joint.
Osteoarthritis . 5
Figure 4.2 Radiograph of palaeopathological specimen showing typ_ical
changes of erosive osteoarthritis with 'gull wing' of left second d1stal
interphalangeal joint
Spavin
This is OA of the tarsus of the horse and sometimes the ox. The
disease usually begins first in the joint between the second and
third tarsal bones but may spread to involve all the joints.
PATHOLOGY
The initial pathological change in OA is fibrillation of the
artilage, which may lead to complete degradation. Where this
h< ppens, the bony articular surfaces become bare and rub
together forming a dense shiny surface which is referred to as
1burnation (from the Latin eburnea, meaning ivory); this tends
to ccur at the point of maximum mechanical loading of the
joint. New bone is formed around the margin of the joint and it
tfl, y 1 o b form d on the joint surface. This new bone
n1 r \ nts an att mpt f th joint to tabilise itself and although
t i r of 'IT I to HI-I Ol-! 1('01 hytt, it Rh ul b cliff r ntiated from
tlu oHl!oph lt which i ottnd nroun th joints a a
](> A Field Guide to joint Disease in Archaeology
concomitant of ageing. In some forms of OA (so-called atrophi
forms) the production of new bone may be minimal, but by
contrast, it may be extremely florid in the hypertrophic form ,
especially if OA develops in association with a bone formin
condition such as diffuse idiopathic skeletal hyperostosis (se
Chapter 5).
Until recently some forms of hypertrophic OA have been
considered as separate entities caused by the shedding of
calcium pyrophosphate crystals into the joint; it was referred to
as calcium pyrophosphate disease. This condition was also
sometimes known as pseudo-gout in the clinical literature by
analogy with true gout in which uric acid crystals precipitat
the pathological process (see Chapter 9). However, most
authorities include pyrophosphate arthropathy within th
general spectrum of OA and believe that the presence of
crystals within the joint is a post hoc rather than a propter hoc
phenomenon.
If eburnation has occurred this is a sign that the articular
cartilage has completely disappeared from the areas of bone
contact and this is the pathognomonic sign that the joint ha
been affected by OA. Sometimes the ebumated area is grooved
or scored to a greater or lesser extent, the grooves usually
running in the direction of movement of the joint (Figures 4.3 &
4.4). Some eburnated surfaces are also pitted, but pitting and
porosity often occur in the absence of eburnation. Occasionally
pitted areas on the joint surface are observed to overli .
subchondral cysts on X-ray, but this is less often observed than
other radiographic changes.
OA COMPLICATING OTHER DISEASES
Manifestation of osteoarthritic changes, in particular ebmna-
tion, are frequently observed where a joint has been damag
by other diseases or by trauma. For example, eburnation may
be noted in an erosive arthropathy such as RA, wh nth joint
has been disrupted so that the me hanics ar di tort . ;\
may also complicate an infectious ro ss or foll ow t r 111nn.
Po t-traumatic OA mt y aris w h n I lw In H of bonl' h11 1 I u 'I' ll
1
11
ure 4.3 Osteoarthritis of the facet joint <?f a cervical
nhurnation and grooving. Marginal osteophytos1s and some p1ttmg on the JOint
surface are also evident
1 ,roken and healed in poor alignment; it is almost
when a fracture line extends into a joint and is also common m
11
1
, knee following damage to the and
11
1 ,nisei. OA may also occur when a jomt
1
nd not reduced, in which case a new articulation will be
formed (Figure 4.5).
RADIOLOGY OF OA
'l' h cardinal sign of OA on an X-ray is of the
joint space which is taken to represent loss of articular
(Pigure 4.6). This sign is no help at all .to the
hut other less important signs can confirm the diagnosiS arnved
11 from visual inspection of the bones. The presence of
1
burnation is recognised radiologically by the _Presence of
cl erosi that is dense white subchondral bone (Figure 4.7a &
h) . In a ' s, ub h ndral cysts may be seen _which may
1
on
1111
unk. t<-' with 1 ltli ng 0 1 th surface. Changes m the bony
A n Id Guide to joint Disease in Archaeology
Figure 4.4 Macerated post-mortem specimen with osteoarthritis of the
patellofemoral joint showing extensive grooving and bony contour change with
marginal osteophytosis
contour of the joint may also be seen radiologically and these
may occur in the absence of any change on the articular surface.
The most extreme changes in bony contour tend to occur in the
femoral head which may become flattened and widened to
resemble a mushroom (Figure 4.8).
As with all palaeopathological material there is a considerabl
disparity between the visual and the X-ray app aran s.
Changes in the dry bone are much mor bvious in th fl si
(so to speak) than on X-ray. n Htu :ly whi h wt- nrrhd Ottl
Figure 4.5
Osteoarthritis
Dislocated glenohumeral joint showing original articulation and
formation of new joint
t lgurc 4.6 R di graph fr m m d rn p.ati ent with characteri stic changes. of
1
,. ,,
1
o: uthri tl s. Not ' joint sp.t ct n:mowlng 111 lat ral ompartment, margmal
ostl'ophyto Is and sriNosis (in r a d ban d nstty)
40
(a)
(b)
Figure 4.7 Archaeological specimen with osteoarthritis of the humeral head
with (a) eburnation, pitting on the joint surface, change in bony contour and
marginal osteophyte; (b) subchondral sclerosis with marginal osteophyte
showed a great disparity between the frequency of OA when
the same set of joints were assessed by a palaeopathologist
(Juliet Rogers) and a radiologist. Depending on which criteria
were used, the frequency of OA ranged from 2% to greater than
60% (see Table 4.1).
OA AT THE SHOULDER JOINT
OA of the glenohumeral joint is rare, but there are a number of
patterns of what are still generally referred to as degenerative
disease around the shoulder joint which are common, may lead
to the development of eburnation and may be due to changes
in the rotator cuff, which helps to stabilise the shoulder joint.
So-called rotator cuff disease is common and incr ases
markedly with age and it is possible to reco is a nttmlwr
of patholo ical patt rn .
Osteoarthri tis
"'
Figure 4.8 Mushroom-shaped femoral head
Table 4.1 Comparison of morphological and radiological appearance of
24 knee joints
Morphological appearance Radiological
appearance
Normal Osteophyte only Osteoarthritis
1
Osteoarthritis
2
8 11 5 2
33.3% 41% 21% 8%
The appearances were judged by a and a radiologist. Both
Investi gators agreed that eight of the 24 JOmts were normal. .
1
Based on the finding of eburnation, or of pitting, osteophyte and change m the bony
contour.
2
Based on standard radiological criteria.
(a) Rotator cuff enthesopathy in which new bone is found on
the greater and lesser tuberosities of the humerus, on th
anatomical neck of the humerus where the glenoid labium
inserts, around the rim of the glenoid and on the coracoid
process of the acromion. The insertion of the supraspinatus
tendon is said to be most typically affected.
(b) Humero-acromial impingement following disruption of the
rotator cuff and upward displacement of the head of the
humerus. There is eburnation on the head and greater
tuberosity of the humerus and the inferior surface of the
acromion and generally new bone around the rotator cuff
insertions. Rarely a subacromial spur may be seen arising
from the insertion of the coraco-acromial ligaments. This
arises in response to subacromial bursitis.
(c) Osteophytosis around the bicipital groove. The position of
the new bone formation reflects different pathological
events. Osteophytes on the medial wall of the groove
indicate tension in the transverse humeral ligament; on the
floor of the groove they are probably the result of chronic
bicipital tendinitis. Along the length of the groove or on
both sides, osteophytes represent ossification of the
bicipital sleeve. If a tunnel of osteophyte is present over
the groove, this reflects ossification in the transverse
humeral ligament. Good bone preservation and careful
examination are necessary to make these distinctions.
OA OF THE KNEE JOINT
As mentioned in Chapter 2, the knee joint is anatomically a
compound joint with three compartments, the patellofemoral
joint (see Figure 4.4), and the medial and lateral tibiofemoral
joints (Figure 4.9). Recently, clinical research has drawn atten-
tion to the fact that OA in the three compartments behaves
differently, with distinct incidence and prevalence rates in th
population and with distinct risk factors for each. In a recent
study we have found a similar pattern in skeletal material with
patellofemoral OA being three times as common a tibi f m ra I
OA. Because of the clinical acceptanc that th diff r nt , n. H
are likely to hav diff r nt aus s or ri nk f tonl, , n I diffn, nl
Osteoarthritis 4
1
11
urc 4.9 Archaeological specimen showing oste?arthritic change on. medial
llil.
1
1 joint surface. Roughening, pitting, and som_e 1n bony
contour are all evident. There was no eburnation on th1s spec1men
lll'<'valences in males and females, it is legitimate to record and
11
wlyse the compartments of the knee separately in skeletal
l11dies.
PALAEOPATHOLOGICAL CLASSIFICATION
' l'h ' clinical diagnosis of OA depends upon the presence of pain
1
n I certain clinical signs; the radiological diagnosis
ltpon demonstrating joint space narrowing. None of IS
lwlpful for a palaeopathological and. so different
n it ria have to be adopted while bearmg m mmd fl_lat
1111tst correlate as closely to the clinical and
dingnoses as possible; this is particularly important. in the
of r, di lo ical diagnosis since it is on this that our information
un mod rn pr valence data derives.
'l 'lw P 1. o . thologi AI diagn i of OA should be simple and
t l1' 1lghlforwnrd; il dl' l ndH fin; t . nd for mo t on demon-
ll' lling ll w pn1 t' lll'l ' of 1hurn !l ion (Plp urts 'I. - 4.13). Whcr
Figure 4.10 Post-mortem specimen showing area with total loss of articular
cartilage on the patellofemoral joint and subsequent eburnation
eburnation is absent, then we suggest that it should be
diagnosed only when at least two of the following are present:
marginal osteophyte and/ or new bone on the joint surface;
pitting on the joint surface; or
alteration in the bony contour of the joint.
In practice, little will be lost by restricting the diagnosis to
include only those joints which show eburnation, although in
some special circumstances, such as with a mushroom-shaped
femoral head, the changes in joint contour and pitting on the
joint surface are so obviously abnormal as to leave no doubt
about the diagnosis.
OA must never be diagnosed if marginal osteophytosis is the
only abnormality, and whatever criteria are used these should
be clearly stated in a paper or bone report.
When calculating the prevalence of OA in sk letal opulntionH,
the precautions noted in hapt r 2 hould b borrw i11 nind.
Osteoarthritis IJ !,
Figure 4.11 Osteoarthritis of the thumb base (first joint)
:bowi ng eburnation on the plantar aspect and osteophyte
formation. (Note archaeological numbering on. the JOint surface. Please
discourage wherever poss1ble)
haracteristics of osteoarthritis
disease of articular cartilage
probably represents the end product of normal re-
modelling of a failed joint
prevalence increases with age
more common in females and males
eburnation is pathognomonic
marginal osteophyte is usual
may be n w bon or pitting on joint surface
joint r tour m, y b alt r d
A I i Id Guide to Joint Disease in Archaeology
Figure 4.12 Osteoarthritis of the odontoid peg with eburnation and p'tf
the joint surface
1
mg on
Figure 4.13 Skeleton ~ n .situ ~ r i o r to lifting showing osteoarthritis of th
JOint With marginal osteophytosis left hip
5
Diffuse Idiopathic Skeletal
Hyperostosis
rn 1950 Forestier and Rotes-Querol described a disease of the
spine in old people with a form of fusion different from anky-
losing spondylitis (AS) and which they called senile ankylosing
hyperostosis of the spine. The disease was relatively painless
and was thought to be a variant of OA, under which heading it
is still sometimes included. The spines of affected individuals
have typical and striking X-ray changes with fusion on the
anterolateral aspect of adjacent thoracic vertebral bodies, almost
invariably on the right-hand side. After the original description
of the condition in the spine it came to be referred to
ponymously as Forestier' s disease.
Resnick subsequently reported that many of those with
Forestier's disease also had ossification of ligament insertions
(or entheses) at peripheral sites in addition to the typical
changes in the spine. Resnick referred to this set of signs as
diffuse idiopathic skeletal hyperostosis (DISH) and considered
that it was an enthesopathy in which there was ossification of
the entheses and fusion of at least four adjacent thoracic
vertebrae. Fusion was often present in more than four thoracic
v rt brae and could also occur in the cervical and lumbar
r ion , although in these regions it was not limited to the
ripht-hnnd sid . The facet joints of the spine are not usually
involv d . nd 1'11 dis s a s r maintained unl ome other
pin tl di t>n t iH ol. o 1 rl' l'lll..
Jn the 1970s Julkunnen carried out a survey of several
thousand people in Finland and confirmed the prevalence of
DISH to be between 6 and 12% as others had shown before
him. He found that males were affected more often than
females and that 85% of those with the condition were over 50
years of age. He also confirmed that symptoms were minimal
and, where present, usually confined to some stiffness and
aches and pains. In 25% of cases of DISH Julkunnen found an
association with adult-onset diabetes and there was an
association also with obesity.
In the palaeopathologicalliterature, especially before the 1950s
when DISH was first described clinically, skeletons with the
condition were frequently misclassified as having AS. This is
especially the case in some of the earlier reports of Egyptian
material. Re-reading some of the detailed descriptions of the
distribution and form of the spinal fusion, however, it is clear
that the majority of these cases are actually DISH. DISH has
been found in skeletal material from all archaeological periods
from Neanderthal to the most recent.
The prevalence of DISH in most skeletal populations is, in
general, similar to that in modem populations but there are
some striking variations within burial grounds. At Wells
Cathedral all the cases of DISH were found buried in side
chapels with a prevalence of 20-30%, confirming a trend noted
earlier at Merton Priory that there was a notably high preva-
lence of DISH in monastic and often high status burial grounds,
such as those where benefactors of ecclesiastical institutions
might be buried. Although this is a trend which has been noted
elsewhere in skeletal assemblages, care must be taken not to
assign a particular status to an individual skeleton on the basis
of the presence of DISH, nor inferences drawn about its
association with other conditions such as diabetes or obesity;
this can be attempted only at a population level.
PATHOLOGY
DISH is characterised by ossification of th ant ri or longi-
tudinal spinal li gament and by o sifi < li n ir to l' I rn 1 in d
Diffuse Idiopathic Skeletal Hyperostosis
4
rigure 5.1 Spine showing typical of diffuse id!opathic
hyp rostosis with flowing candle-wax-lrke new bone on the nght-hand s1de of
the thoracic vertebrae
t>nth.eses. The development of new bone in the skeleton may
nn h prolific proportions and has been likened to candle
llowin down the spine and may reach up to 20 mm m
thi kn (Figures 5.1 & 5.2). In the thoracic spine the restriction
of h ng to the right side is said to be due to the presence of
t I w pul H ting d s nding aorta on the left. There .have
,.,.
1
orL of I ft-Aid d 'fSH in pati nts whose descendmg aorta IS )
m
1
tlw rl ghl Hidt bul to our kr c wl dg th r hav b n no su h
In n flkchl on to d lit .
',() A Field Guide to joint Disease in Archaeology
Figure 5.2 Radiograph of specimen shown in Figure 5.1 . Note the normal disc
spaces and normal facet joints
Other spinal ligaments may also become ossified; it is common
to find the ligamentum flavum, the supraspinous ligaments and
the ligaments around the sacrum ossified. When the sacral
ligaments are ossified they may bridge across the joint line,
completely or not, bilaterally or unilaterally, and in this way
fuse the joint (Figure 5.3). This type of fusion may be dis-
tinguished from that which is found in the seronegative
arthropathies (Chapters 7 and 8) since in the latter, the fusion is
the result of intra-articular pathology.
Outside the spine, any enthesis may become ossified but the
common sites are around the elbow, particularly the triceps
insertion, the insertion of the quadriceps femoris into the
patella, the insertion patellar ligament into the tibia and the
insertion of the Achilles tendon into the calcaneum (Figure 5.4).
It is important to remember, however, that entheses may
become ossified for other reasons, including mechanical
trauma, such as occurs in tennis elbow.
In patients with DISH there is often evid ne of al ifi lion
into soft tissues including and bl od Vl'RIwl nnd in
Figure 5.3
Fusion of sacro-iliac joint by ossification of sacral ligaments in a
case of DISH
keletons which have been well excavated with good bone
recovery it is not uncommon to find ossified tracheal rings.
laryngeal cartilages; the costal cartilages are. also often
These features are also found in skeletons w1thout DISH and m
themselves are not diagnostic.
PALAEOPATHOLOGICAL DIAGNOSIS
DISH is one of the easiest conditions to diagnose in skeletal
material. The fused block of thoracic vertebrae with exuberant
new bone flowing down the right side of the vertebral bodies
should be immediately obvious. To conform to the clinical
de cription of DISH, at least four vertebrae be
fu ed, but it is not at all uncommon m skeletal matenal to
find skeletons which obviously have DISH in which less than
four are fused although the ossification of the anterior longi-
tudinal Jigament involves many contiguous vertebrae. The
pol-llC'rior v rt brc I joinlA . nd th disc are preserved
111
d ll w( ft tlll l'l 'l e H\ nHii l b onfumd on X-ray.
A Field Guide to j oint Disease in Archaeology
Figure 5.4 Enthesophytes on the patella and Achilles tendon insertion of the
calcaneum characteristic of diffuse idiopathic skeletal hyperostosis or bone
forming
Enthesophytes will be apparent at extraspinal sites, some of
which may be extremely florid. Fusion of the sacro-iliac joints
at the ) anterosuperior margins is common but X-rays will
demonstrate that the joint surfaces are normal and the joint
space is preserved.
Where DISH is coexistent with OA the degree of osteophyt
around the affected joints may be considerable (Figure 5.5) and
we have seen a single case of DISH in which the detach d
lamina of a lumbar vertebra with spondylolysis had b om
reunited to the vertebra with new bon whi h h, d form I
around the sit s of th (Ta tur .
Diffuse Idiopathic Skeletal Hyperostosis
!d
Figure 5.5 Florid marginal osteophytosis in a case of diffuse skeletal
hyperostosis without osteoarthritis. Also note enthesophytes on t1b1al tubercles
Bone formers
'fhere is a subset of the skeletal which
of the entheses, fusion of the sacro-iliac JOmts, ossification of
< rtilage and large marginal osteophytes is and these
w have termed bone formers. Some of these md1v1duals may
go on to develop DISH, which in itself may be of the
11
p tt:um of bone forming (Figure 5.6). Hypertrophic OA
t! Ho fit into this category. If bone formers develop another JOIDt
< 1 h-1 'nH u h RA, its morphology may well be altered or
1110dlfil' I by tl ir bon formin t nd n y.
Figure 5.6 Excess bone formation after rib fracture in a case with diffuse
idiopathic skeletal hyperostosis
Characteristics of DISH
disease of ligaments and entheses
ossification of anterior longitudinal spinal ligament
produces candle wax appearance
spinal fusion with preservation of facet joints and disc
spaces
ossification of entheses at extraspinal sites
prevalence increases with age
more common in males than females
associated with diabetes and obesity
6
Rheumatoid Arthritis
RA is one of the diseases which is generally considered to be
of recent origin. It was first described clinically in a thesis in
L800 by Landre-Beauvais who believed that it was a variant of
gout and referred to it as goutte asthaenique primitive: There
have been very few cases recorded in the palaeopathological
literature, although some are now beginning to come to light
rmd we have described two recently. Claims such as those of
Wood Jones that RA was the most common disease to afflict
the skeletons which he examined from Nubia are explained by
the fact that he was actually referring to what we now call OA,
and not RA.
fn modem populations, RA is a common condition, affecting
about 1% of the total population. Women are more likely to be
affected than men in a ratio of about 3:1, and perhaps as many
as 5% of the female population over the age of 65 has the
disease. The disease is universal in occurrence, although some
populations, such as those of black Africa are relatively spared.
fn the countries of western Europe, the disease is declining in
incidence but it is becoming more common in the developing
ountries. In some developing countries, such as Pakistan and
Malaysia, the expression of RA is different from that in the
W st. For example, the feet are relatively spared compared with
West rn ea es. It is quite likely the expression and distribution
of RA in past population w r different from those in con-
lt'nq Ol'fli'Y rorul. lion nd l'hi s is an important con ideration
1
)(, A Fi Id Guide to joint Disease in Archaeology
for palaeopathologists. The same stricture almost certainly
applies for other diseases also.
The disease has its onset most commonly in the fourth and fifth
decades but no age-group seems to be exempt and classic
adult-type disease may be found in children and it may also
make its first appearance in the elderly. There is a tendency for
the disease to run in families but this probably reflects a shared
environment rather than hereditary factors.
r The cause of the disease is not known with any certainty
although the modem tendency is to consider it to be multi-
factorial in origin which is to say that any number of different
possibilities have been considered. As with AS there is some
evidence of a link between tissue antigens and a predisposition
towards the disease. In the case of RA there is an association
between the possession of some of the subtypes of the HLA-
DR4 antigen and the occurrence of the disease.
PATHOLOGY
RA is a disease of the synovial membrane that becomes
infiltrated with inflammatory cells, which cause it to become
thickened and vascular. Continued inflammation produces a
chronic state in which the diseased synovium is referred to as a
pannus. This grows out from the joint margin to cover and then
destroy the articular cartilage with the formation of erosions
which are first seen at the margins of the joint. As the disease
progresses, the joints become deformed and may dislocate;
however, it is rare for joints other than the wrist or the tarsus to
fuse in RA. Patients in the end stage of RA may be extremely
disabled with crippling deformities of the hands and such
individuals are still not uncommonly seen. It is hard to imagine
that such extreme manifestations of the disease would have
escaped the attention of writers or artists in the past had they
been as common as they are now.
(
The onset of RA characteristically involves the small joint of
th hands and feet, especially the PIP, the m ta lang at
1 an th m tatarsophalang al (MTP); th Tl jointA n tnu h
7
I ss frequently involved (Figures 6.1-6.3). distribution is
11 uall symmetrical and the sacro-iliac joint IS almost never
and when it is, the lesions seldom severe. Other
. oints become affected as the progresses, most
I mmonly the wrist, knee, cervical spme, shoulder, subtalar
joint, elbow and hip (Figures 6.4-6.6).
I t is usual for bones around an affected to
ost o aenic and eburnation may supervene an ec e
. . t th wake of the destruction of the articular cartilage.
1otl'l m
(
'I' . lly ut thr <.- lh rt rs f pati nts with RA are found
tnt , 1 ) I ol ul s
to h wt .ml ibodil (tt l4 tt dl of tlw lgM a. 8 to g m .
I
I
1\ I i Id Guide to joint Disease in Archaeology
Figure 6.2 Carpals, one metacarpal and one proximal phalanx from the same
case as shown in Figure 6.1 showing non-proliferative erosions
in their blood and these antibodies are referred to as
rheumatoid factor (RF). It was the discovery that patients with
what were thought to be atypical forms of RA did not have RF
in their blood which gave rise to the concept of the sero-
negative arthropathies. (The differences between RA and these
disorders are discussed in Chapters 7 and 8.)
The diagnosis of RA in the skeleton depend upon finding th<
presence of ymm trical, non-prolif re tivC' roslor H nffccling llw
Figure 6.3 X-ray of Saxon skeleton with erosions at the metacarpophalangeal
joint typical of rheumatoid arthritis
small joints of the hands and feet. One difficulty which is very
likely to be encountered is that, since the bones in an affected
ase will almost certainly be osteopaenic, there is a great risk of
them suffering post-mortem damage and important elements of
the skeleton will be lost. We must emphasise that in our view it
would be well nigh impossible to sustain a diagnosis of RA in a
sk leton in which the hands and the feet were missing; the
I iagnosis must never to be made on the basis of lesions which
n r found in a ingle, large joint, although this will un-
doubt dly t net to unci<'r stimate its prevalence in the past. For
,, nm1 1<, W<' h lV ' t '<' ll th mgi'A whi h look typi al of RA in
Figure 6.4 Elbow joint from the case shown in Figure 6.1 with non-
proliferative erosions
Figure 6.5 Radiograph of the proximal ulna shown in Fi rur 6.4. N 1.
scl eroti c margin of erosions indi ting r m d lling
Rheumatoid Arthrit'is (, 1
Figure 6.6 Erosions on the facet joints of a thoracic vertebra from the case
shown in Figure 6.1
isolated large joints but in the absence of the hands and feet we
have been reluctant to make a definite classification.
The lesions must be true erosions. There are many occasions on
which skeletons are found with what might be called
rosions'; these are particularly common in the wrist, ankle and
around the shoulder and these must not be confused with the
lrue erosions found in RA although we believe that this is
sometimes done (Figures 6.7 & 6.8). Radiology is helpful in
istinguishing true erosions from pseudo-erosions and good
films will show the loss of cortex and the trabeculae ending in
mid-air. The advice of an experienced skeletal radiologist may
prove invaluable where there is any doubt as to the nature of
I ions around a joint.
'l'h rosions in RA begin at the joint margins and encroach
furth r ov r th joint urface as the disease progresses. If there
nr(' 11 0 I . ions on th joint margins, you should think of some
c 111. (' for tlwm c I her lh 111 RA.
A h Id Guide to joint Disease in Archaeology
Figure 6.7 Head of humerus with remodelled erosion at the joint margin.
There are numerous 'pseudo-erosions' in the floor of this lesion
Many of the large joints can be symmetrically affected as we
have mentioned above, but the sacro-iliac joint is usually
spared and the cause of erosive lesions in a skeleton with
disease of the sacro-iliac joints is not likely to be RA
There are no signs in the skeleton which are pathognomonic of
RA, but it is possible that RF survives in the bone as many
other bone proteins are now known to do. If this were to be the
case-and this possibility is presently being investigat d- then
finding RF in a skeleton which was thought to hav RA would
be strong supporting evidence; the abs n of RP, I .ow v r,
could not b tak n to prov th diH a. c wnH 110/ RI\ .
Figure 6.8 Scaphoid showing presence of a large marginal
and several smaller ones. In neither this case, nor the one shown m figure 6.7,
were there any X-ray changes or any othe.r changes to support a
diagnosis of rheumatoid arthntis
Characterisitics of rheumatoid arthritis
disease of the synovium
( non-proliferative symmetrical erosions beginning at the
\ margins of the joint
proximal interphalangeal, and
metatarsophalangeal joints charactenstically
may also affect wrist, knee, shoulder, subtalar JOmt,
cervical spine, elbow and hip
sacro-iliac joints not usually affected
bony ankylosis not common except occasionally at
carpus
osteopaenia common
may be eburnation on affected joints
annat be diagnosed confidently if hands and feet are
miRAing
7
Ankylosing Spondylitis
AS is a disease which appears to be of considerable antiquity
0\ and it is probably the most likely of the seronegstixe arthro-
pathies to be reported in the palaeopathological literature.
While some of these are undoubtedly genuine cases, many
more are probably misdiagnoses and the nature of these is
presently under review. In the older medical literature, and
occasionally elsewhere, it may be referred to as Marie-
Striimpell, or von Bechterew's disease; however, there is
nothing to commend the continuation of such usage.
AS is a disease characterised in the living by an inflammat cy
Cl'--- and by involvement of the entheses. In modem
populations it is more common, and more severe, in males than
in females; the disease declares itself with significant symptoms
in approximately 0.5% of men and 0.05% of women and the
peak onset is in the late teens or early 20s. Milder forms of the
disease with radiological evidence of sacro-iliitis may be seen in
up to 3% of males and 2% of females. There seems to be an
important genetic component in the aetiology of this condition
and there is a strong association between the occurrence of th
disease and a tissue antigen referred to as HLA-B27. Approxi-
mately 95% of patients with AS have this antig n compar d
with less than 10% of the general population. It is id to o ur
in some animals, including do , attl and pi gH.
ILIOLUMBAR
LIGAMENT
l.UMBOSACRAL
LIGAMENT
VENTRAL
!l ACRO - ILIAC
l iGAMENT
Ankylosing Spondylitis
THE SACRO-ILIAC JOINT
Figure 7.1 Diagram of the sacro-iliac joints
PATHOLOGY
INTEROSSEOUS
SACRO - ILIAC
LIGAMENT
SYNOVIAL
SACRO-ILIAC
JOINT
The disease usually begins in the sacro-iliac the
lumbar spine. The sacro-iliac joint is a JOmt; the
lower two-thirds is synovial and the upper third ligamentous
but both compartments are affected in AS 7.1). Both
sacro-iliac joints are invariably affected and er?swns . be
t The Pa
tholooical changes are symmetncal within the
presen . o- . . . f th t
joints but are more obvious on . the . side o e ,
perhaps because the articular cartilage IS thinner ?I_l the
than on the sacrum. As the disease progresses the JOIDt space IS
narrowed and fusion occurs across it.
In the spine the disease begins as an at the
t . of the outer fibres of the annulus fibrosa mto the
mser 1on . his Th
vertebral body and erosions may be seen m t positw.n. e
I
. ts then become ossified and the vertebral bodies are
1 amen t th
Haid to become ' squared' (Figure 7.2). Inflammation m o . . e
nth r spinal ligaments follows all.become ossified
1 'c ding to a completely ossified, n g1d spme which may. then. be
r .f 'rr d to as a 'bamboo spine' because of the
, . Th li am nt around th costovertebral JOmts may
l m an . f d t tl
11 .
0
be omc i
1
v l v d s tl nt thr ribs b om IX on o 1
pi rw.
A Field Guide to Joint Disease in Archaeology
Figure 7.2 Radiograph of patient with ankylosing spondylitis to show
typ1cal bamboo spine'
One of_ the im.J?ortant features of the spinal pathology in AS is
that spmal fuswn begins in the lower lumbar region and as it
none of the vertebra is spared so that there
are skip leswns as there may be in Reiter's disease or
psonabc arthropathy (P A), for example (see Chapter 8).
The feature in a sk 1 ton with A is tl n t tlw
sacro-Iliac JOmt wj]l b fl.1, d and the t th r wi ll b(
1
vnl'l lhlt
Ankylosing Spondylil'i
Figure 7.3 Fused spine from an archaeological case of ankylosing spondyl itis.
Note complete fusion of vertebrae with no skip lesions. Several ribs have been
fused to the vertebrae, although subsequently damaged; the sacro-i liac joints
are fused
degree of fusion throughout the spine (Figure 7.3). The fusion
will always affect the lowest parts of the vertebral column and
if it advances upwards it will usually do so without missing
out any elements. As the fusion increases upwards there is
often a degree of kyphosis. In advanced cases the ribs may be
f us d to the vertebra and the entire vertebral column and
thora ic cage may be lifted up as a single entity.
' J'Iw , . ro-i l i. j ints may fus in DISH and the ribs may also
on 1 ion 11ly lw fu.- td to tl t' v(rt('brr , but spinal fu ion du to
1111 A I idd Guide to joint Disease in Archaeology
I I ' 11 is generally easily distinguished from AS because in
DISH the osteophytes are much more massive and irregular,
and in the thoracic spine at least are almost entirely confined to
the right-hand side.
In the cases which we have observed there may be very little
change outside the spinal column, although conversely there
may be prominent entheses at almost any muscle insertion; it is
unusual to find other joints affected but, of course this cannot
be ruled out.
Radiography may be helpful in demonstrating the typical
bamboo spine (Figure 7.2) and there may be some virtue in
trying to obtain radiographs of the sacro-iliac joints to demon-
strate the presence of erosions, although those inexperienced at
X-raying dry bones may find some difficulty in lining the joints
up in the correct position.
It is possible that in the future HLA antigens may be
extractable from bone and the presence of HLA-B27 would be
confirmatory evidence of AS but its absence could not preclude
the diagnosis. We are some way off being able to do this,
however, and even if the technique becomes available, it would
probably not be widely available. The extension of palaeo-
immunology to the study of the rheumatic diseases in
antiquity, however, is something which should be welcomed
and may provide useful information in the future.
Characteristics of ankylosing spondylitis
disease of synovium and entheses
sacro-iliac joints affected symmetrically
sacro-iliac joints often fused in the skeleton
X-ray of sacro-iliac joints may show erosions
erosions may occur in large joints
spinal fusion begins in lower lumbar region and pro-
gresses steadily upwards
no 'skip' lesions
kyphosis is often a feature
ribs may be fused to vertebrae
8
Other Seronegative
Spondlyoarthropathies
The seronegative spondyloarthropathies are a group of erosive,
inflammatory polyarthropathies, which also affec: entheses.
Thus the inflammatory process involves the ligamentous
insertions (the entheses) as well as the internal of the
joints. They were originally to vanants of
it was when it was found that patients with these
did not have RF in their blood they were categonsed
eparately. They all have overlapping clinical features . .
which, so far as the skeleton is concerned, include
pondylitis and peripheral arthritis. There . are maJOr
seronegative spondyloarthropathies: AS (considered m Chapter
7), PA and Reiter's disease.
Pathologically and radiologically, PA and Reiter's disease
everal features in common although they can be readily
distinguished clinically. In the absence of clinical informa.tion It
may be difficult to differentiate one from other the
sk 1 ton, although in typical cases there are differences
morph logy of the lesions and in their distribution, both within
th, fl in an riph rally, which may enable a palaeo-
pathologi . I linpno i to b mn
PATHOLOGY
As in RA, the target area for pathological change is the synovial
membrane and the same series of inflammatory changes as is
observed in RA occurs in the seronegative arthropathies also.
The synovium becomes infiltrated with inflammatory cells,
proliferates and becomes thickened. As the disease process
progresses the articular cartilage is destroyed and there is a
much greater tendency for the joints to fuse; this is particularly
the case with P A and AS. Marginal and central erosions may be
observed and there is a good deal of new bone formation,
unlike the situation in RA. There may be joint destruction,
especially in P A when changes reminiscent of those seen in RA
may be found.
The other major characteristic of the seronegative arthropathies
is the involvement of tendons and ligaments which may be
ossified and may also be the site of proliferative erosive lesions
(Figure 8.1). The ossification of the spinal ligaments accounts
for the spinal fusion which is almost always seen. Periosteal
new bone may also develop, particularly in Reiter's disease,
and may gives rise to 'whiskering' on X-ray.
X-rays of affected skeletons may show the presence of erosions,
proliferation and ankylosis, and in addition there may be
evidence of resorption of the tufts of the distal phalanges in P A.
Osteoporosis is much less common than in RA. The changes in
the sacro-iliac joints are asymmetrical and may be unilateral.
PSORIATIC ARTHROPATHY
The first association between the skin disease psoriasis and
arthritis was made by Alibert in the 1850s. The condition was
first thought to be part of the spectrum of RA or a variant of it,
and was only separated from it in 1964. Psoriasis affects about
1% of the population but only about 5-8% of patients with th
condition go on to develop the arthropathy; mal and f mal s
ar aff cted qually.
Figure 8.1
Other Seronegative Spondlyoarthropathi s 7 1
Erosive lesion on the olecranon process in a case of psoriatic
arthropathy
The arthropathy is usually asymmetrically distributed with a
preferential involvement of the DIP, PIP and MTP joints. The
changes in P A are often not very marked but there is a severe,
mutilating form in which the interphalangeal joints are
destroyed leading to bony ankylosis and telescoping of the
digits (Figure 8.2). The proximal end of the distal phalanx is
often widened while the distal end of the middle phalanx
undergoes osteolysis and becomes pointed to produce what is
known radiologically as a 'cup and pencil' deformity. This
condition is often referred to as arthritis mutilans. The appear-
ance of this form of P A can mimic the deformities found in
j pro y and many cases of leprosy described in the past may
, tually hav b n PA, especially considering the skin changes.
'onv rs0ly, som s of pala opatholo ical cases of PA may
H' lll nll lw ltpro .
I
I
I
I
\ _
Figure 8.2 Psoriatic arthropathy showing fusion and shortening of the proximal
and middle phalanges. Note also the erosion at the proximal end of the
proximal phalanx
In the sacro-iliac joints the changes are similar to those seen in
AS but they are usually unilateral or asymmetrical in
distribution (see Table 8.1). In the spine there may be some
fusion of adjacent vertebrae with the cervical spine being
affected more frequently than the thoracic or lumbar. The
ankylosis in the spine often takes the form of paravertebral
ossification, that is, large chunky outgrowths of bone situated
unilaterally. In the cervical spine the facet joints may also be
involved and there may be marked bone excrescences alon th
margins of the vertebral bodies.
Other Seronegative Spondlyoarthropathi s 7J
Figure 8.3 X-ray of the foot from case as 8.2 showing fusion of the tarsus and
the tarsometatarsal joints. There are erosions at the first distal interphalangeal
joint with expansion of the proximal end of the first distal phalanx
Radiographs will confirm the presence of marginal and central
erosions, of bony ankylosis and proliferation of new bone
(Figure 8.3).
REITER'S DISEASE, OR REACTIVE ARTHRITIS
Tn 1916, Hans Reiter first described the association of signs and
. ymptoms whi h has ub qu ntly taken his name. In addition
t) nn a rthriti., o th r P< ti ntR had onjun tiviti and urethritis
md l'lw !' nfl1n OC<' tlrr'!'d 1fl cr n dinrrho nl illn BR, Btl h RA
A held Guide to joint Disease in Archaeology
dy ntery. The possibility that arthritis might be a complication
of urethritis or might follow a gut infection, however, had been
noted much earlier, in the sixteenth and seventeenth centuries.
This type of arthritis, which occurs after some triggering
infection usually affecting the gyt or acquired during sexual
intercourse, is a reaction to the infectious organism and differs
from septic arthritis in which there is a direct and immediate
infection of the joint tissues.
Reiter's original case was a male and it is still the case that
males are more commonly affected than females; the prime age
of onset is between 15 and 35 years.
The pathological lesions on the bone look very similar to those
of P A, as do the radiological changes, but their distribution
may be different. The erosions in Reiter's disease are marginal
as in P A and there is adjacent proliferation of new bone; they
are also asymmetrical but they tend primarily to affect the
lower extremity. The preferred sites are the small joints of the
foot, the calcaneum, the ankle and the knee (Figure 8.4). The
sacro-iliac joint is affected and there may be paravertebral
ossification. The cervical vertebrae are affected less often than
in PA, and throughout the spine there may be so-called 'skip'
areas where normal vertebrae are found interspersed between
the affected ones.
In addition to new bone around the erosions, there may be
proliferation of the entheses on the plantar surface of the
calcaneum, on the ischial tuberosities, the femoral trochanters
and the sacro-iliac joints. Periosteal new bone may also be seen
in some cases along the shafts of the metacarpals, metatarsals,
phalanges and on the tibiae (Figure 8.5).
In practice it is very difficult to differentiate P A from R iter'
disease and this may also be the case clinically, but th r ar
some pointers which will h lp in thi task ( T. t If' 8.1 ).
Other Seronegative Spondlyoarthropathies
Figure 8.4 Metatarsals from a case of seronegative spondyloarthropathy with
proliferative erosions on the head of the first metatarsal and fusion of the
tarsometatarsal joint with some hypervascularity; probable case of Reiter's
syndrome
The first stage in palaeopathological classification depends
upon finding the presence of an asymmetrical erosive arthro-
pathy with proliferation of new bone around the margins. The
distribution of the lesions will be a guide towards the
classification; in P A the small joints of both the hands and the
feet are affected, whereas in Reiter's disease, the feet are much
more often the preferred site. In both conditions bony ankylosis
may occur but it is more common in P A; arthritis mutilans does
not occur in Reiter's syndrome.
In both conditions there may be sacro-iliitis with fusion of the
acro-Hiac joints, and there may be paravertebral ossification. In
PI\ th c rvi cal pine is more commonly affected than the other
rcgionH, ~ nd in R it r's dis AS th r may be skip lesions. In
R<' ii N'Ii di Nl ' t' llw tnll w t'. on Jh plantar surfa of th
Figure 8.5 Radiograph from a modern case of Reiter's syndrome showing
periostitis on the shaft of the fourth metatarsal with thickening of the distal part
of the shaft
calcaneum may be involved and there may be periostitis on the
shafts of the long bones of the hands and the feet and on the
tibiae.
Where a definite classification cannot be achieved, and this may
well be the case with damaged or incomplete skeletons, it i
best merely to classify the changes as those of an rosive
arthropathy of the seronegative or r activ typ an not
attempt any furth r di tinction.
Other Seronegative Spondlyoarthropathi s
Table 8.1 Some features of psoriatic arthropathy and Reiter's di sease
77
Lesions peripheral and axial
Generally asymmetrical
Upper extremity affected more
often than lower
Marginal and central erosions
with proliferation of new bone
Tuftal resorption
Arthritis mutilans with pencil
and cup lesions
Sacro-iliac joint involved
Changes may affect entire spine,
especially cervical
Reiter's disease
Lesions peripheral and axial
Generally asymmetrical
Lower extremity affected more
often than upper
Marginal and central erosions with
proliferation of new bone
Sacro-iliac joint involved
Lower spine tends to be
affected, skip lesions present
Enthesopathy around calcaneum
Periosteal new bone on shafts of
long bones of hands and feet and
on tibiae
Characteristics of seronegative arthropathies other than anky-
losing spondylitis
lesions asymmetrically distributed
erosions marginal and central with proliferation of new
bone
sacro-iliac joint involved
paravertebral ossification with spinal fusion
may be skip lesions in spine
ossification of entheses
periosteal new bone on shafts of long bones of hands
and feet
11
9
Gout
Gout can be recognised from descriptions written by early
clinicians, including the authors of the Hippocratic corpus,
although the term gout, from the Latin gutta, meaning a drop,
was applied indiscriminately to many joint afflictions.
Gout is caused by an inflammatory response to the deposit of
crystals of uric acid with the joint tissues. The deposition of
crystals is secondary to high uric acid levels in the blood
(hyperuricaemia) which may be due to genetic or environ-
mental factors. Hyperuricaemia may be present in a patient for
many years before an attack of gout occurs and indeed, in
some of these people, gout never manifests itself. The classic
site for the disease is the first MTP joint but other sites may
also be affected, those most commonly involved being the
hand, wrist, elbow, knee and ankle. In the clinical literature it
is said that the shoulder, sternoclavicular joint and sacro-iliac
joint are less commonly affected and the hip and spine rarely,
but this may not be the case in palaeopathology. In between
75 and 90% of all patients with gout the MTP will eventually
be affected.
Attacks of gouty arthritis can occur in two forms, acute or
chronic. The first attack of acute gout usually occurs in middle-
aged men or post-menopausal women. Urate crystal ar
deposited in the tissues causing exquisite pain, w lling and
r dn s and th on t roay b v ry Au d n; th di s< H<' m. y
Gout 7<)
attack a single joint or more than one. The attacks are If-
limiting but nowadays are treated to speed recovery. Betw en
attacks the patient is unaffected, but as time passes attacks may
occur more frequently and each can last longer and affect more
joints.
In about 50% of cases chronic gout eventually supervenes. It is
characterised by the formation of tophi; these are firm, nodular
swellings which may be yellowish in colour or exude white
chalky material. The tophi are deposits of urate crystals which
can be found in articular cartilage, subchondral bone, the
synovial membrane, joint capsule and tendons, ligaments and
bursae. Thus all the structures within and around the joint may
be affected.
Until a few years ago very few cases of gout had been reported
in the palaeopathological literature despite the undoubted
reports of its occurrence in the early medical literature. One
case was reported in an Egyptian mummy in which urate
crystals were identified in a tophus and Calvin Wells reported a
case in a male skeleton excavated from the Romano-British
cemetery at Cirencester. This skeleton showed the typical X-ray
changes and juxta-articular, punched-out erosions with under-
cut edges around the feet (Figures 9.1 & 9.2). Since then many
further examples have been recognised.
PATHOLOGY
It is the presence of tophi which cause the typical bony changes
from which gout can be recognised in skeletal material. The
bony erosions which give rise to the typical appearance can be
situated in three locations around a joint. They can be marginal,
sometimes extending towards the centre of the joint, they can
be away from the margins or para-articular and eccentrically
placed, or they can be somewhat remote from the joint, or
juxta-articular when they are also typically eccentric in location.
.ouly ro ions are generally round or oval in shape and are
ofl<'l'l in lh long axis of th bon . They appear punched out
HO A Field Guide to joint Disease in Archaeology
Figure 9.1 Romano-British skeleton from Cirencester with extensive erosive
lesions of both ankle joints
with overhanging edges (Figures 9.1-9.3). The distribution of
the lesions is asymmetrical and on X-ray the margins frequently
have a sclerotic margin and the overhanginge edges are
sometimes referred to as Martell hooks; this latter appearance is
typical of gout. Occasionally there is proliferation of new bone
around the margins of an erosion and rarely bony fusion
occurs. Osteoarthritic changes are also noted frequently both on
X-ray and in -the skeleton.
Gout should be suspected on finding asymmetric, punch d-out
lesions around or within a joint. The fe t ar m r fr u ntly
aff t d than th r part of th k l ton, but gout r Y ~ r nL o t
G ul' Ill
Figure 9.2 X-ray of one of the ankle joints shown in Figure 9.1 with undercut
and sclerotic margins typical of gout
found in the hands, wrists, elbows and knees. This is a
condition in which radiography is particularly helpful in
making a diagnosis. The X-ray will usually show that the
lesions have sclerotic, overhanging margins and that there is no
significant osteoporosis associated with them. In some rare
a es there may still be deposits of uric acid within the lesion
an if th. ir presence can be confirmed, this will leave the
dingr o iA in n doubt (Figur 9.4).
H2 A Field Guide to joint Disease in Archaeology
Figure 9.3 Phalanges, metatarsals and navicular from a skeleton from Barton
on Humber with extensive marginal erosions. Note Martell hook on the left-
hand side of the proximal joint surface of the first metatarsal
OTHER EROSIVE CONDITIONS
A small number of other joint diseases may also include
erosions among their pathological changes. 1bree will be
mentioned here.
The commonest of these conditions is hallux valgus of the first
MTP joint (Figure 9.5). The erosions may be single or multiple
and usually have smooth margins and are morphologically
difficult to tell apart from the erosions due to gout or the
seronegative spondylarthropathies. However, an X-ray read by
an experienced skeletal radiologist should usually be able to
distinguish between these various conditions.
Other erosions encountered in the hands, feet or-
occasionally-in the knee, may be caused by synovial mass
lesions (Figures 9.6 & 9.7). Synovial chondromatosis or pig-
mented villonodular synovitis may produce thickened
nodularities in the synovium which in turn may cause juxta-
articular single or multiple erosions. There may b som
difficulty in differ ntiating th ro ion from oth rs and
X-r< ys will b rcquir to h lp I. rify 1'1 dingn08iH.
Gout
Figure 9.4 Urate crystals from a modern case of gout
Characteristics of gout
lesions caused by deposits of uric acid (tophi)
lesions may involve all the structures within and around
the joint
first metatarsophalangeal joint involved in about 75% of
cases
common sites include feet, ankle, hands, wrist and knee
lesions distributed asymmetrically and have punched-
out app arance with overhanging edges
continued overleaf
Figure 9.5 Erosions on head of first metatarsal in a case of hallux valgus
continued ------------------------,
may be proliferation of new bone around margins of
lesion
X-ray usually shows sclerotic margin around lesions and
confirms overhanging edges-Martell hook
osteoporosis uncommon
Gout 8
Figure 9.6 Knee joint with large juxta-articular erosions. There were no
erosions elsewhere in the skeleton. This is a possible case of synovial
chondromatosis or pigmented villonodular syndrome
Figure 9.7 Single large erosion on the posterior surface of the distal femur. The
rest of the skeleton showed changes characteristic of treponema! disease and
this lesion is likely to have been the result of a gumma
10
Infections Causing Joint
Disease
Many infectious organisms, bacterial, viral and fungal, may
involve the joints but the most common, and those which we
need to consider in detail here, are the organisms that cause
osteomyelitis and tuberculosis.
OSTEOMYELITIS
Osteomyelitis is an infection of the bone and bone marrow
most usually with bacteria and the most common infectious
organism is Staphylococcus aureus, a bacterium most frequently
encountered when it causes boils. The organism may gain entry
to the bone by one of three routes:
(1) haematogenous spread (through the blood stream), the
organism having got into the blood from a septic focus
somewhere in the body;
(2) direct spread from infected soft tissues; and
(3) by the direct implantation of an infected object such as
might occur with a penetrating wound.
T l a mntog nous F!pr od is th mo t usual m an by which
oAtcom <liliH i (' t 1hliHiwd in bon -. st -omy l l t i ~ : ~ i, mor
IlB A Field Guide to joint Disease in Archaeology
ommon in children than in adults and the preferred site of
jnfection is at the growing end of long bones where the blood
supply is richest. The organisms multiply in the bone marrow,
which is an excellent culture medium, and an intense
inflammatory reaction sets in with the formation of pus;
regarding this, the infection is often referred to as pyogenic.
The pus drains from the bone through channels which are
called cloacae and during the course of the infection, portions
of bone may become cut off from their blood supply and die,
forming sequestra, which may only be visible on X-ray. The
infection provokes the formation of a great deal of periosteal
new bone formation and a collar of new bone may be formed
around the shaft of the bone, when it is known as an
involucrum. In long-standing infections the shaft of the bone
may appear ~ n ; in some cases the infected bone may
become weak and fracture. The combination of cloacae,
sequestra and periosteal new bone is very characteristic of
pyogenic osteomyelitis (Figure 10.1).
The age of onset of the infection may to some extent determine
the appearance of the changes seen in osteomyelitis (see Table
10.1). Thus with an adult onset, the presence of sequestra and
an involucrum are uncommon but pathological fractures are
common; this is the converse of what is generally the norm in
childhood cases. Joint involvement, by contrast, is common in
adult-onset cases (and in infancy) but less common in
childhood cases.
PYOGENIC ARTHRITIS
A pyogenic organism can spread to a joint through any of the
three routes described above, but in general only a single joint
is affected. The process is highly destructive; the erosive lesions
tend to appear first at the margins of the joint but eventually
virtually all the joint surface may be destroyed. The disease
stimulates the production of much new bone and the end stage
of the disease is usually bony ankylosis of the joint (Figur
10.2).
Infections Causing joint Disease 89
Figure 10.1 Tibiae in .a case of osteomyelitis. Both bones are swollen in their
distal ends and, in addition, there is a cloaca on the right tibia, on the medial
surface at the junction of the lower third and upper two-thirds of the bone. Scale
in cm
TUBERCULOSIS
Tuberculosis is caused by a mycobacterium and there are two
principal species which affect humans, Mycobacterium bovis and
M. humanis. The first organism is contracted from cattle by the
ingestion of contaminated milk or dairy products. It spreads
from the gut to the lymph nodes throughout the body and may
come to be lodged in other tissues, including bone. The human
organism probably evolved from the bovine type and it is
pr ad through the air and so the site of entry is the lungs.
Wh n inhnl d, fh organism provok s what is known a a
prirnnr nHponHt', which 11 unll rcsul tR inn AmL 111 Rion in th
1
10 A I i Id Guide to joint Disease in Archaeology
L1hll I 0.1 Features of osteomyelitis at different ages
loacae
Sequestra
Involucrum
Joint involvement
Pathological fractures
Infant Child
(<1 year) (1-16 years)
Uncommon
Common
Common
Common
Uncommon
Variable
Common
Common
Uncommon
Uncommon
Adult
(>16 years)
Common
Uncommon
Uncommon
Common
Common
Figure 10.2 Proximal tibia showing destruction of joint surface with
proliferation of new bone typical of pyogenic arthropathy
apex of the lung and swelling of lymph nodes within the chest.
In many of those exposed the disease spreads no further but in
some, after a variable time, the disease flares up and spreads
through the lung and to distant parts of the body.
Both organisms can affect bone and the idea which is still
current that skeletal infection is more common in the bovine
than the human type is not true. The preferred site for infection
is the spine, and usually the lower thoracic or lumbar region.
The anterior parts of the vertebrae are affected in pr f r n t
the posterior and th r ult is an r iv 1 sion whi h provoke,
Figure 10.3 Spine showing destruction of bodies of some thoracic vertebrae
with collapse and resultant kyphosis. These are the typical appearances in Pott's
disease of the spine
little, if any, proliferation of new bone. In time the vertebrae
become substantially weakened as they are destroyed and they
may collapse resulting in an angular kyphosis, which may be
seen referred to as Pott's disease of the spine (Figure 10.3).
Virtually any other bone may be affected by tuberculosis,
but they will all show the characteristic erosions without
proliferation. In children the metacarpals and phalanges are
often affected, the condition being referred to then as tuber-
u1ou dactyliti . In addition to swelling of the bones and lytic
1 ' AionA (Pigur 1 0.4), th r' mny b som p ri titi on th
hnft H, tnd thh 1111 11 li11w, lw quil l' (' ul ('l' nt.
\ I
Figure 10.4 Radiograph from a modern child with tuberculosis affecting the
shoulder joint. A large erosive lesion on the lateral aspect of the humeral head is
easily seen
Tuberculous arthritis
Tuberculosis tends to affect the large joints such as the hip and
knee, but others may also be involved, including the elbow,
wrist, sacro-iliac joints and the glenohumeral joint; it is rare for
more than one joint to be involved in the process. The erosions
in the joint tend to start at the margin, particularly in weight-
bearing joints such as the knee, hip and ankle. There is little
proliferation of new bone but the bones around the infected
joint become porotic early in the disease. The end stage of a
tuberculosis joint is usually fibrous ankylosis; bony ankylosis is
unusual, which is in contrast with pyogenic arthritis where
bony ankylosis is the norm. (Some of the features of tuber-
culous and pyogenic arthritis are shown in Table 10.2.)
Tuberculous discitis
Radiologically, early lesions may be e n in th ant dor sub-
chondral portion of a v rt ra just b n ath tl int rvc rt ' I rnl
Table 10.2 Comparis9n of some features of tuberculous and pyogenic arthriti s
Erosions
Proliferative new bone
Bony ankylosis
Osteoporosis
Tuberculous arthritis Pyogenic arthritis
Yes
Little if any except in
tuberculous dactylitis
Rare
Common
Yes
Much
Common
Rare
disc. Extension of this lesion may cause it to perforate through
the end plate and infect the disc and subsequently spread into
the adjacent vertebra. This process cannot be observed directly
in the skeleton but radiography of the vertebra may sometimes
reveal a lytic lesion in the body, which may correspond to this
early lesion. It may also be possible to observe defects in the
end plate where such a lesion has erupted through (Figure
10.5). These are not to be confused with Schmorl's nodes, which
are distinctive and will not be associated with any lytic lesions
in the vertebral body.
Spread from this type of lesion may result in infection
spreading to the anterior longitudinal ligament with erosions of
the anterior face of the vertebral body and lesions of this type
are sometimes seen in the skeleton.
BRUCELLOSIS
Brucellosis is an infection caused by one of the species of
Brucella, which are transmitted from animals including the cow
(B. abortis), the goat (B. mellitensis) or the pig (B. suis). It is
transmitted through contaminated milk or dairy products or
from direct contact with infected secretions and it is likely to
have been common during periods when societies were living
in close contact with their animals. It produces a monoarticular
arthritis affecting the hip, knee and sacro-iliac joint most often,
and it also affects the lumbar spine (Figure 10.5). The lesions
may b difficult to diff r ntiate from tuberculosis, although
th r t nd. to b mor n w bon formation in bruc llo i than
h tulwrc111o i 111d o r - ~ l . t ot orotliH i I<'RR ommon th, n in
Figure 10.5 Lumbar vertebrae showing erosive lesions on the end plate_s ~ ~ t h
considerable proliferation of new bone. Probable case of tuberculous d1sc1tls
tuberculosis. There are no pathognomonic signs, however, and
it is possible that some cases of vertebral lesions may, in the
past, have been wrongly diagnosed as tuberculosis. With
advances in the technique of polymerase chain reaction applied
to bacterial DNA, it may be possible to differentiate the two
diseases in the skeleton.
LEPROSY
Arthritic lesions due to the causative organism of leprosy (M.
leprosa) are rare, but it is common for secondary infection to
occur in patients with leprosy due to the loss of sensation,
which results from the lesions in the nerves. In the foot this
may lead to secondary osteomyelitis with involvement of any
of the joints of the foot. The loss of sensation may also lead to
recurrent trauma to the joints of the lower limb with
subsequent malalignment and destruction; these are the so-
called Charcot joints and they may occur also in syphilis wh n
in the tertiary stage of the disea e th n rvous syst m is
involv d.
FUNGAL DISEASES
Fungal diseases affecting bone and joints are rare in Europe but
they are much more common in North and South America, and
those who examine skeletons from sites in those countries
should be aware of them. The two fungi which account for
most skeletal disease are Blastomyces dermatitidis and Cocci-
dioides immitis causing blastomycosis and coccidioidomycosis,
respectively. In blastomycosis the vertebrae, ribs, tibia, tarsus
and carpus may be involved with areas of moth-eaten bony
destruction. Vertebral collapse may be seen which may be
difficult to distinguish from tuberculosis. The joints are usually
affected by the spread of the disease from adjacent sites but
occasionally a monoarthritis is observed most frequently
involving the knee or ankle joints. In coccidioidomycosis
multiple symmetrical lesions are found in the spine, ribs and
pelvis and sometimes in other bones; spinal collapse is
uncommon. As with blastomycosis, joint involvement usually
results from direct spread but a monoarthritis may also be
found, and again the ankle and knee are the commonest sites.
There may be great difficulty in distinguishing fungal diseases
from other infectious diseases, and in the case of coccidioido-
mycosis sclerotic changes in the vertebral bodies may simulate
prostatic carcinoma. In the future, fungal DNA studies may
help in the diagnosis of these conditions.
Both osteomyelitis and tuberculosis are ancient diseases and
there are examples from virtually all archaeological periods. In
pyogenic arthritis there may well be signs of osteomyelitis in
the long bones or there may be evidence of trauma around the
joint. Where there is not, then the diagnosis depends upon the
presence of proliferative new bone on the surface of the joint
and, in some cases, ankylosis. There may be cloacae through
whi h th pu drained from the joint during life. Radiography
w i 11 show slru ti n and di or anisation of the joint.
Tlw di. r.n(H it o lttlunulo i i rcl. liv<' ly (',, y in the f11ll bl wn
spinal case with erosion of the vertebral bodies (massive in
some cases) and little or no proliferation of new bone. Pott's
spines are extremely characteristic and cannot easily be
mistaken. The more difficult case is where joints outside the
spine are involved. Here again, however, the combination of
erosion without proliferation, and joint fusion are good
indicators of the likely diagnosis. Recently, it has become
possible to demonstrate the presence of bacterial DNA in bones
from cases of putative tuberculosis. A positive result in such a
test is confirmatory evidence for the diagnosis, assuming that
the possibility of contamination can be ruled out. On the other
hand, a negative result does not rule out the diagnosis since the
DNA that might have been present in life could have been lost
by any of the processes which disrupt the body and its
component parts after death.
Characteristics of pyogenic and tuberculous arthritis
Pyogenic arthritis
usually monoarticular
erosive lesions
much proliferation of new bone
bony ankylosis
may be the sequel to injury
Tuberculous arthritis
lower thoracic and lumbar spine most commonly
affected
fingers affected in children
erosive lesions
little proliferation of new bone
spinal collapse with Pott's disease
fibrous ankylosis
11
Implications for
Archaeologists
Skeletal studies, including palaeopathology, are generally
undertaken with the main aim of informing the archaeologist
about the physical attributes of the population being examined.
Palaeopathological studies have, over the years, provided much
information about some of the diseases and abnormalities
which were experienced by early populations. Much infor-
mation has been gained about the natural history and evolution
of disease which is of interest to both biologists and clinicians.
Skeletal assemblages can serve as a unique resource for some
aspects of medical research, which may also be of great value
to palaeopathologists and thus to archaeologists.
Recently, there has been a move towards expanding skeletal
studies into a more biocultural approach which aims to
diminish the emphasis on palaeopathology and its so-called
clinical approach and to focus more on the general health of the
populations under consideration. Even in this reduced role,
however, palaeopathology will provide an essential framework
for the study of health in a population as correct diagnosis is
the basis of population or epidemiological studies.
Palaeopathology is the study of all diseases which may be
found in an ient human remains; but we have chosen to
on nlrat on th . ln Rifi ation of joh1.t diseases because these
1 r{ Hw OtH'H l'lw t t ll'h<wH know n bout lh moRt and th y ar also
by far the most commonly found in the skeleton. In this final
chapter we would like to make some general comments which
are pertinent both to the bone specialist and to the archae-
ologist. These comments come under three main headings:
diagnosis, interpretation and epidemiology.
DIAGNOSIS
When starting to examine human bones and seeking a
diagnosis for the joint changes which may be seen, there is an
almost instinctive tendency to turn to a clinical textbook for
help and guidance. If that fails then the second step may be to
consult a textbook of radiology. There is a great likelihood,
however, that neither will be very helpful for reasons which we
have mentioned in earlier chapters, but which we now wish to
reinforce.
Diagnosis in clinical practice is a means to an end-the end
being treatment of a patient's symptoms-and not an end in
itself. In palaeopathology, on the other hand, the diagnosis is
the end, as there is nothing more that palaeopathologists can do
other than say what conditions their subjects were afflicted
with at the time of their death. And in arriving at a diagnosis,
the clinician and the radiologist use methods which differ in
kind very much from those which are available to the
palaeopathologist. We can illustrate these differences most
clearly by reference to OA.
For the clinician, the diagnosis of OA relies very heavily on the
patient's complaint of pain in a joint perhaps supplemented by
clinical signs such as swelling around the joint or crepitus on
movement. But, put simplistically, a middle-aged patient who
has pain in his hip has OA until proved otherwise. For the
radiologist, on the other hand, the cardinal signs of OA are
joint space narrowing, indicating degradation of the articular
cartilage, and the presence of marginal osteophyte. In the large
population studies of the prevalence of OA which Lawrence
and his colleagues carried out in England in th 1 r.::o and
1960 , and oth r authors have 11nd rtc ken ci H(wh t'<
1
th
Implications for Archaeologists 99
presence of OA has been determined on the basis of these
radiological signs.
Palaeopathologists need no reminding that none of these
clinical or radiological diagnostic criteria is available to assist
them in their task-except for the presence of marginal
osteophyte, but radiology is never needed to confirm what can
be seen much better by the naked eye. To arrive at their
diagnosis, then, palaeopathologists must rely on criteria which,
although they must have a grounding in the clinical science of
rheumatology, nevertheless are specific to their discipline. In
the case of OA, there is one obvious sign on the joint surface
which infallibly indicates the presence of the disease, and that is
eburnation. Eburnation occurs only in a joint in which the
articular cartilage has disappeared, leaving areas of bare bone
to rub against each other. There is no dispute that eburnation
allows OA to be diagnosed with absolute certainty, but where
it is not present then we have suggested other criteria (see
Chapter 4) which may be used instead. We have thus proposed
what the epidemiologists would call an operational definition
of OA for palaeopathologists to use. If it were to gain universal
acceptance, then this would ensure that the diagnosis of this
most common disease in the skeleton enjoyed some com-
monality which it does not have at present, judging from a
reading of the literature.
The reader will have noted that nowhere in this discussion do
we mention the contribution which pathologists make to the
diagnosis of joint disease in the skeleton. Since we describe the
process of determining disease in bones as palaeopathology, it
might seem strange that modem pathology has so little to offer.
The explanation has to do with the nature of contemporary
pathology which is based on cellular or subcellular rather than
gross appearances, and in this respect palaeopathologists have
more in common with the pathologists who worked before the
advent of the microscope.
Th re is a need for some agreement on operational definitions
of th j int di as other than OA, although this is a much
more diffic11 lt tnHk, I ut it Hhould not be shirked merely on that
t<'<'Ottnl. 11 i ' lnqmrl nnt th 11 o nw <or H('nAUH iH r a hcd flR to
which signs in the skeleton really are the result of diseases such
as RA, otherwise the disagreement and argument which are
found in the scientific press at present will continue to the
detriment of palaeopathology as a whole. We have gone some
way towards arriving at some definitions and we hope that we
may be able to present them elsewhere in the future. Clearly,
without some consensus of what constitutes, say, AS or DISH,
in the skeleton, there will be great opportunity for error and
this will distort any estimates of prevalence; this applies
particularly with the less common joint diseases, where mis-
diagnosis in a small number of cases may lead to large errors in
the apparent relative frequencies between populations.
The importance of agreed diagnoses cannot be over-emphasised
and discussions of the aetiology of disease, of its relative
frequency and its cultural implications will be rendered
meaningless unless different authors refer to the same entities
in their work.
Although we have dealt with the most common and most
reliably recognised joint diseases which are likely to be seen in
the skeleton, it must be remembered that the classic appear-
ances described here will not always be seen, especially where
two or more diseases occur together; this may be confusing for
the' beginner. It must also be borne in mind that an explanation
will not be found for every single lesion. There are very many
conditio:ris other than those mentioned here that may affect the
joints; these include, for example, trauma, congenital dislocation
of the hip, juvenile arthritis, acromegaly, rickets, osteoporosis,
thyroid disease, hypertrophic osteoarthropathy, Paget's disease;
the list, if not endless, could be extended for several more lines.
Failure to diagnose a case is often more to do with the protean
nature of joint disease than with the competence of the
examiner; this may be a comforting thought to those struggling
in vain to fit a name to a lesion.
INTERPRETATION
Those who examine the bones of their anc stors f 1 an
understandable urge to xplain what th y fin ; th re iH
Implications for Archaeologists 1 01
feeling that each lesion must have its cause and that once this is
known, this will throw light on the way of life of the individual
concerned. The interpretation of the observations which they
make is, of course, an important aspect of any palaeo-
pathologist's work but often-all too often-the conclusions
which are made outstrip the evidence and we would like to
urge caution in one or two areas in relation to joint disease.
The severity of lesions
Many authors writing in respect of OA in particular, refer to
the severity of the lesions, referring generally to the degree of
marginal osteophyte. The thinking is that the larger the lesion,
or the more extensive, then the more severe the disease.
Alternatively, a more severe lesion may be considered to be a
later stage in the disease than one which is milder.
Neither of these notions has any basis in clinical practice nor )
are they epidemiologically sound as we hope to show.
Taking the clinical point first. We assume that when authors
consider a lesion to be severe then they assume that it had
more impact on the individual during life than one which they
deem to be less severe. This is a completely unfounded notion.
As we have said, patients report to their doctors complaining of
pain in a joint or some other symptom, and the degree of pain
bears very little relationship to either the X-ray findings or to
the morphological appearances which may be observed in a
postoperative or autopsy specimen. For example, a patient who
complains of severe pain in the knee may have a normal X-ray
(Figure 11.1) and postoperative specimens following knee
replacement may show little other than a small amount of
eburnation or marginal osteophyte on one or other of the tibial
plateaux (usually the medial in practice). Similarly, we have
seen femoral heads that have been removed during hip
replacement and show no change at all in their macerated state,
which we would have considered normal had we encountered
th 1n fr m , n or hn ol ogi al sit .
'C HI VI' I' H' I
1
fl ol'i d \'1)111)\l' 111 y lW cf jA OVCl'<'d in fl joint wh n i t
I
r
l ~
Figure 11.1 Radiograph of knee joints from a patient with clinical
osteoarthritis. Note that the radiographic appearances are normal, although
the patient was in considerable pain
is in the field of an X-ray being taken for some other purpose.
These may include joint space narrowing, sclerosis and
marginal osteophyte, and yet the patient has no symptoms
referrable to that joint (see Figure 11.2).
Clinical experience, therefore, shows that the correlation
between the appearances of a joint, either radiologically or
morphologically, and an individual's symptoms is poor and
attempts to judge the magnitude of symptoms-the severity of
disease-from the appearances of a joint are wasteful and can
serve no useful purpose.
The attempt is often made to place lesions seen in a skeletal
sample in a progression based on their severity- generally
some aspect of their morphology, such as their size, so that
some inference can be drawn about the natural history of the
disease. We feel that this, too, may lead to error. We can
illustrate this point by reference to a simple model. In Figure
11.3 we have shown the progression of a lesion- let us suppo
that it is marginal osteophyte around the kn joint in A- in
three individual , p, q and r. Th s v rily of th ir lcHion (in lhi
Implications for Archaeologists 103
Figure 11.2 Radiograph of the hips in a modern patient. Although the patient
had no pain, there is radiographic evidence of osteoarthritis, especially on the
left-hand side
case, the extent to which the osteophyte develops) increases in
each of the three at different rates, which is perfectly consistent
with clinical observation. Let us further suppose, however, that
each dies at a different time in the development of their disease;
p dies at time a, r at time b and q at time c. The palaeo-
pathologist now examines their skeletons and notes the severity
of the lesions which are a', b
111
and c". Using the standard
approach under these circumstances, he/ she will grade them in
order of severity as:
b"'--+ a'-+ c"
whereas reference to the figure will show that the temporal
relationship is incorrect and that the severity of none can be
used to predict the severity of the others, which is what one
would hope to be the case if one were trying to determine the
nalural hi tory f th di ease.
In pni:W!)J nlhology wt> hnvt no ml'nns of knowing , t wh. t
tl ltgt' in 111 11d v d11 tl 't diHII t lh tl individt l I ditN, nor of
11
c
0
'iii
(])
-0
~
;::
(])
>
(])
(J)
b'
a' . bu
- -QJ
c'
p
cu
q
Figure 11.3 Progression of hypothetical lesion in three cases, p, q and r.
Assume that p dies at time a, rat time b and q at time c, then the presumed
order of severity will be given as b"', a', c", although, in fact, this temporal
relationship is incorrect
knowing the rate of progress of that disease. That is to say, we
do not know-in the case in point-whether an individual
skeleton is like p, q or r in respect of the speed of development
of the lesion, or if he/she died at a, b or c. The problem is well
recognised in epidemiology and it is that one cannot make
inferences about a dynamic process from a series of stati
observations; to be able to do so r quir s that individuals an
b follow d up ov r tim . How v r, in r I. o nth lopy, we . re
Implications for Archaeologists 1 OS
able only to make cross-sectional observations. And that is a
problem which no amount of tinkering with the data can
overcome.
Occupation and activity
The final inference we would like to discuss briefly relates to
occupation. It is a widely held belief that the distribution of OA
in a skeleton can be used to predict the occupation or activity of
the individual. We recognise that this is a perfectly laudable
attempt on the part of palaeopathologists and anthropologists
to extract the maximum amount of information from the rather
meagre amount of data at their disposal, but it is mistaken. If
we refer back to Figure 4.1 we can see that there are several
factors which determine the development of OA; these include
age, sex, race, genetic disposition and activity. Now in no case
could one start with a skeleton which shows the presence of
OA and say with any confidence which of the aetiological
factors was responsible for the development of its disease.
Moreover, even if we could be sure that activity were the prime
mover, how would it be possible to say what activity was the
cause?
Let us pursue this a little further with a consideration of OA of
the hip. We know from recent epidemiological work that
farmers are much more likely to develop this condition than the
general population; their risk is approximately nine times that
of the general population. If we encountered OA of the hip in a
male skeleton it is reasonable to consider whether he might
have been a farmer. However, although farmers are more at
risk of getting OA of the hip, they are by no means the only
people in whom it appears and if there were five male
skeletons with OA of the hip (see Figure 11.4), only one of
whom really was a farmer during life, there is no way at all by
which we could say which he was. In Figure 11.4 we have
shown the farmer as the shaded figure of the five, but we have
no m ans at our disposal by which we can determine which he
is; H'w nowA in th diagram ar all unidir tional, and . o it i.
In 1 t1 "'"I, llholog ; nil our nrrOWH 1 oint fr'Oi11 ouR' to (ffN:t,
Figure 11.4 Diagram showing five males who develop osteoarthritis of the hip.
One (shaded) is a farmer, but there is no means whereby palaeopathological
examination of the bone will determine which hip came from the farmer and so
any inferences made regarding occupation from the joint will be erroneous
we cannot reverse them and go from effect to cause, which is so
often the direction in which the bone specialist seems so
desperate to go.
The only possibility of safely inferring the occupation of an
individual skeleton from the pattern of OA would b if that
pattern were unique to one occupation, and, of o n, , w
know that this is not th case. Th sam.c nrgurncnt nppl it
Implications for Archaeologists 1 07
when occupation or activity is inferred from any other skeletal
attribute; unless it is unique to that occupation, it has no
predictive value.
On a population basis, however, it is permissible to make some
inferences. For example, if in two populations the prevalence of
OA of the hip was markedly dissimilar, and if one knew that
the pattern of activity was different in the two groups-if one
was rural and one urban, for example, then it would be
reasonable to infer that the differences in activity were related
to the variation in the expression of OA. Even then it would be
a probability and not a certainty.
EPIDEMIOLOGY
Some epidemiological points have been dealt with earlier and
we do not wish to stress many more here. However, because it
seems so often misunderstood, we must emphasise that the
frequency of joint disease (or any other) in past populations can
only be expressed in terms of its prevalence. A palaeo-
pathological examination is, epidemiologically speaking, a
cross-sectional study and thus can only be used to measure
prevalence and it is always incorrect to talk about the incidence
of a disease in palaeopathology.
In order to determine the prevalence, however, it is necessary
to take care about the denominator data, for it is only rather
rarely that the total number of skeletons in an assemblage will
be the denominator used to determine prevalence. As described
in Chapter 2, prevalence is a simple ratio of those with the
disease to the total population at risk, but when dealing with
joints the denominator, putting things simply, is the number of
joints present, not the number of individuals. It is for this
reason that we have stressed, in Chapter 2, the necessity to
keep a record of the total number of each type of joint.
11 0 A Fi eld Guide to joint Disease in Archaeology
(b) Spinal sites
Present OA OP Fusion IVD SN LF
Cl
C2
C3
C4
CS
C6
C7
T1
T2
T3
T4
T5
T6
T7
T8
T9
TlO
Tll
T12
L1
L2
L3
L4
L5
Sl
OA = osteoarthritis; OP = osteophyte; SN = Schmorl's nodes; IVD = intravertebral di
disease; LF = calcified ligamentum flavum.
General Bibliography
J. Baker & D. Brothwell, Animal Diseases in Archaeology, London,
Academic Press, 1980.
D.R. Brothwell, Digging up Bones, 3rd edition, London, Oxford
University Press, 1981.
J.H. Klippel & P.A. Dieppe, Rheumatology, London, Mosby, 1994.
D.J. McCarty & W.J. Koopman, Arthritis and Allied Conditions,
Philadelphia, Lea & Febiger, 1993.
D.J. Ortn.er & W.G.J. Putschar, Identification of Pathological Conditions in
Human Skeletal Remains, Washington, Srnithsonian Institution, 1981.
D. Resnick & G. Niwayama, Diagnosis of Bone and Joint Diseases, 2nd
edition, Philadelphia, W.B. Saunders, 1988.
P.A. Revell, Pathology of Bone, Berlin, Springer-Verlag, 1986.
C. Wells, Bones, Bodies and Diseases, London, Thames & Hudson, 1964.
Further Reading
CHAPTER 2
J. Rogers, T. Waldron, P. Dieppe & I. Watt, Arthropathies in
palaeopathology: the basis of classification according to most
probable cause, Journal of Archaeological Science, 1989, 16, 611-625.
T. Waldron, Counting the Dead. The epidemiology of skeletal populations,
Chichester, John Wiley & Sons, 1994.
CHAPTER 3
S. Ahlback, Osteoarthrosis of the knee. A radiographic investigation,
Acta Radiologica, Supplementum 277, 1968.
CHAPTER 4
P. Dieppe, Osteoarthritis. A review, Journal of the Royal College of
Physicians, 1990, 24, 262-267.
J. Rogers & P.A. Dieppe, Ridges and grooves on the bony surfaces of
osteoarthritic joints, Osteoarthritis and Cartilage, 1993, 1, 167- 170.
J. Rogers & P.A. Dieppe, Is tibiofemoral osteoarthritis in the knee joint
a new disease? Annals of Rheumatic Diseases, 1944, 53, 612- 613.
J. Rogers, T. Waldron & I. Watt, Erosive osteoarthritis in n m di vnl
skeleton, International Journa.l of Osteoar ha olo8y, 19 1, 1, 1 ')1 1 3.
Further Reading 11 3
J. Rogers, I. Watt & P. Dieppe, Arthritis in Saxon and medieval
skeletons, British Medical Journal, 1981, 283, 1688-1670.
J. Rogers, I. Watt, & P. Dieppe, Comparison of visual and
radiographic detection of bony changes at the knee joint, British
Medical Journal, 1990, 300, 367-368.
L.C. Vaughan, Osteoarthritis in cattle, Veterinary Record, 1960, 72,
534-538.
H.A. Waldron, Prevalence and distribution of osteoarthritis in a
population from Georgian and early Victorian London, Annals of the
Rheumatic Diseases, 1991, 50, 301-307.
T. Waldron, The distribution of osteoarthritis of the hands in a
skeletal population, International Journal of Osteoarchaeology, 1993, 2,
213-218.
T. Waldron & J. Rogers, Inter-observer variation in coding osteo-
arthritis in human skeletal remains, International Journal of
Osteoarchaeology, 1991, 1, 49-56.
CHAPTER 5
J. Forestier & J. Rotes-Querol, Senile ankylosing hyperostosis of the
spine, Annals of the Rheumatic Diseases, 1950, 9, 321-330.
H. Julkunen, O.P. Heinonen & K. Hyperostosis of the spine
in an adult population, Annals of the Rheumatic Diseases, 1971, 30,
605-612.
T. Waldron, DISH at Merton Priory: evidence for a 'new' occupational
disease? British Medical Journal, 1985, 291, 1762-1763.
T. Waldron & J. Rogers, An epidemiologic study of sacroiliac fusion
in some human skeletal remains, American Journal of Physical
Anthropology, 1990, 83, 123- 127.
CHAPTER 6
P. Hacking, T. Alien & J. Rogers, Rheumatoid arthritis in a medieval
skeleton, International Journal of Osteoarchaeology, 1994, 4, 251-255.
B.H. Rothschild, K.R. Turner & M.A. DeLuca, Symmetrical erosive
peripheral polyarthritis in the late archaic period of Alabama,
ien e, 198 , 241, 1498-1501.
T. J. Rog rs & I. Watt, Rheumatoid arthritis in an En li h
nd v tl lthlo, l llli'rnal ional Joumal of steoar haeolo&y, 1 4, IJ.,
1!1
1
1 111'/
114 Further Reading
CHAPTER 7
J. Rogers, I. Watt & P. Dieppe, The palaeopathology of spinal
osteophytosis, vertebral ankylosis, ankylosing spondylitis and
vertebral hyperostosis, Annals of the Rheumatic Diseases, 1985, 44,
118- 120.
CHAPTER 8
P.A. Dieppe & J. Rogers, The Antiquity of the Erosive Arthropathies,
Conference Proceedings No. 5, Arthritis & Rheumatism Research
Council, 1988.
CHAPTER 9
C. Wells, The human burials. In: Romano-British Cemeteries at
Cirencester, edited by A. McWhirr, L. Viner & C. Wells, Cirencester,
Cirencester Excavation Committee, 1982, pp. 135-196.
CHAPTER 10
J. Rogers & T. Waldron, Infections in palaeopathology: the basis of
classification according to most probable cause, Journal of
Archaeological Science, 1989, 16, 611- 625.
D. Morse, D.R. Brothwell & P.J. Ucko, Tuberculosis in ancient Egypt,
American Review of Respiratory Diseases, 1964, 90, 524- 541.
A. Stirland & T. Waldron, The earliest cases of tuberculosis in Britain,
Journal of Archaeological Science, 1990, 17, 221- 230.
CHAPTER 11
H. Bush & M. Zvelebil, Health in Past Societies, Oxford, BAR, 1991.
Index
Alibert, J.L., 70
Ankylosing spondylitis, 5, 64-9,
100
characteristics of, 68
diagnosis of, 66- 8
esthesopathy in, 64, 68
HLA-antigens in, 64, 68
in animals, 64
kyphosis in, 67
pathology, 65-6
prevalence of, 64
radiography in, 65- 6, 68
bamboo spine, 65, 68
sacro-iliitis in, 64, 65- 6
skip lesions in, 66
vertebrae in, 65- 6
Annulus fibrosa, 24
Arthritis, see joint diseases
Arthritis mutilans, 71, 75
Articular cartilage, 1, 8
!31rH;torny si , 95
)ltl lll ' fol'llwr , , 4
lltllt 'l' lht 1 1):1 /)
l llld 11 11 Ill
Calcium pyrophosphate, 36
Coccidioidomycosis, 95
Degenerative disc disease,
26-7
osteophytes and, 27
Diagnosis in palaeopathology,
98- 100
Diffuse idiopathic skeletal
hyperostosis, see DISH
DISH, 36, 47- 54, 67-8, lOO
at Merton Priory, 48
at Wells Cathedral, 48
bone formers and, 53
diagnosis of, 51- 3
entheses in, 49-50
marginal osteophytes and,
53
pathology, 48- 51
prevalence of, 48
radiology of, 50
sacro-iliac fusion in, 52
DIP, 8
in psoriatic arthropathy, 71
in rh umatoid c rthrili H, ,
o. ll 'OJ h to, L of, 0
116 Index
Distal interphalangeal joints, see
DIP
DNA, 96
Eburnation, 13, 35-6, 43, 99
in osteoarthritis, 13
in rheumatoid arthritis, 57
pathognomonic of
osteoarthritis, 43
Enthesopathy, 42
in ankylosing spondylitis, 64,
68
in DISH, 48-9
rotator cuff disease and, 42
Enthesophytes, 24-5
in DISH, 52
Erosions, 11, 12
in gout, 79
in Reiter's disease, 74
in rheumatoid arthritis, 58-62
in sero-negative
spondylarthropathies, 70
marginal, 12
Exostoses, 23
Forestier, J., 47
Gout, 3, 78-82
characteristics of, 83-4
diagnosis of, 80-1
erosions in, 79
of MTP, 78
radiology of, 80-1
Martell hook, 80
tophi, 79
uric acid in, 78, 81, 83
Gumma, 86
Hallux valgus, 82
HLA-antigens, 56, 64, 68
Impingement syndrome, 42
Joint capsule, 1
Joint(s)
cartilaginous, 1
compound, 14, 42-3
counting and recording, 8-11
diseases, 2
acute, 3
atrophic, 3
classification of, 4, 8-15
chronic, 3
diagnostic criteria for, 4
hypertrophic, 3
fibrous, 1
infections of, 87-96
pathology
classification of, 15
recording forms for, 10
patterns of skeletal
involvement in, 6-7
structure of, 1
synovial, 1
Julkunen, H., 48
Juxta-articular area, 2
Knee joint, 42
compartments of, 42
osteoarthritis of, 41, 42-2
Landre-Beauvais, A.J., 55
Lawrence, J.S., 98
Leprosy, 71, 94
Martell hook, 80
Metatarsal pitting, 30
Metatarso-phalangeal joint, see
MTP
MTP
hallux valgus of, 80
in gout, 78
Mushroom head, of femur, 38, 41
Myositis ossificans, 23
Odds ratio, 19
Odontoid peg, 20, 46
Ossification, 24
into anterior longitudinal
ligament, 24
paravertebral, 25
Osteoarthritis, 3, 26, 32-47, 98
atrophic, 36
at the shoulder joint, 40, 42
at unusual sites, 33
calcium pyrophosphate crystals
and,36
changes in joint contour and,
38
classification of, 43-5
criteria for, 43-5
common sites of, 32
complicating other diseases,
36-7
eburnation in, 35, 43-4
erosive, 33-4
gull-wing appearance in, 33
grooving of joint surfaces in,
36- 8
hyp rtrophic, 35, 45, 53
in onirnals, 34- 5
joint di fl lc Lion , nd, 37
occttp lll ott ttttl , ((),) 7
of o d t H t l t ~ d fi' ')',, ' ~ ' '
ell lftt h l' r l0
1
c '/
Index
of the knee joint, 42-3
osteophytes and, 15
pathology of, 35-6
prevalence of, 44, 98
117
radiology of, 37-40, 43, 101-2
joint-space narrowing, 43
sclerosis, 37
sub-chondral cysts, 37
rheumatoid arthritis and, 36
severity of, 101-5
trauma and, 36
Osteoblasts, 8
Osteochondritis dissecans,
28-30
location of, 28-9
Osteoclasts, 8, 12, 13
Osteomyelitis, 87-9, 90
cloacae in, 88
diagnosis of, 95
features of, 93
involucrum in, 88
new bone formation in, 88
Osteophytes, 20-31, 66
bicipital groove and, 42
causes of, 26
degenerative disc disease and,
27
distribution of, 20
marginal, 21, 30, 44
classification of osteoarthritis
and,44
in DISH, 53, 68
morphology of, 20-2
of DIP, 20
of odontoid peg, 20
of PIP, 20
osteoarthritis and, 25
rating scales for, 21 -2
s v rity of, 21
Hignifi 011 f, 2r: - 6
lruttnlll nnd, 23
Vtl'lclll' d, ' ()
I Ill Index
Ost oporosis, 13-14, 93, 100
in sero-negative
Pigmented villonodular synovitis,
82, 85
PIP, 8
osteophytosis of, 20
Pott' s disease, 91, 96
Prevalence, 15, 107
age-specific, 17
calculation of, 16-17
comparison between groups,
18
crude, 18
definition of, 16
of DISH, 48
of osteoarthritis, 4
of rheumatoid arthritis, 55
sex-specific, 17
Proliferation, 11
in sero-negative
rating scales for, 11
Proximal interphalangeal joints,
see PIP
Pseudo-erosions, 30, 61, 63
Psoriatic arthropathy, 66, 69,
70- 3
arthritis mutilans, 71, 75
diagnosis of, 74- 7
distribution of, 71- 2
erosions in, 73
prevalence of, 70
proliferation in, 73
radiology in, 71, 73
cup and pencil deformity,
71
sacro-iliitis in, 72
spinal fusion in, 72
Pyogenic arthritis, 88
Radiography
in ankylosing spondylitis, 65-6
in DISH, 50
in osteoarthritis, 14, 37-40
Rating scales
for osteophytes, 21-2
for proliferation, 11
Reiter, H., 73
Reiter's disease, 66, 69, 73- 7
diagnosis of, 74- 7
enthesis in, 75
erosions in, 7 4
radiology of, 76
sacro-iliitis in, 74
skip lesions in, 74-5
Resnick, D., 47
Rheumatoid arthritis, 3, 36, 53,
55- 63, 69-70, 100
diagnosis of, 58- 63
distribution of affected joints,
56- 7
eburnation in, 57
erosions in, 58- 62
HLA-antigens and, 56
osteoarthritis in, 36
osteopaenia in, 57
pathology of, 56- 8
prevalence of, 55
radiology in, 61
rheumatoid factor (RF) in,
57-8, 62
sacro-iliac joints and, 57
synovial m mbranc in, 5 1
Rheumatoid factor, 57, 62, 69
Ring-bone, 34
Risk ratio, 19
Rotes-Querol, J., 47
Sacro-iliac joints, 52-3, 65-6
in ankylosing spondylitis, 64
Scheuermann' s disease, 27
Schmorl's nodes, 27, 93
Sclerosis, 37
Skeleton, recording forms for, 10
Skip lesions, 65- 6, 74-5
Spavin, 35
Spondylarthropathy, 3
sero-negative, 3, 69- 77
pathology of, 70
Spondylolysis, 52
Sub-chondral cysts, 37
Synovial chondromatosis, 82, 85
Index 11 9
Synovial membrane, 1, 8
in sero-negative
Tuberculosis, 89-93
bacterial DNA in, 96
in the fingers, 91
in the spine, 90
of the joints, 92
Tuberculous arthritis, 92
dactylitis, 91
diagnosis of, 95-6
discitis, 92-3
features of, 93
Uric acid, 36, 78, 81, 83
Wells, C., 79
Wood Jones, F., 55
ISBN 0-471-95506-X
9 78047 95506
0 WILEY &SONS
:::- : : : : : - ~ e ew York Brisbane Toronto Singapore

A Field Guide To Joint Disease in Archaelogy - J. Rogers and T. Waldron OCR Reduit

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