You are on page 1of 8

Periodontology 2000, Vol.

30, 2002, 123130 Copyright C Blackwell Munksgaard 2002


Printed in Denmark. All rights reserved
PERIODONTOLOGY 2000
ISSN 0906-6713
The periodontalendodontic
controversy
GrnnIn W. HnnniNc1oN, Dnvin R. S1riNrn & WiIIinr F. ArroNs, Jn
Over the past century the dental literature has con-
sistently reected a controversy related to the effect
of periodontal disease on the dental pulp and more
recently the effect of pulpal necrosis on the initiation
and progression of marginal bone loss. Two basic
questions have been raised and continue to be mat-
ters of dispute. Is periodontal disease a cause of pulp
necrosis? Can a pulpless tooth be the cause of peri-
odontal disease? The answers to these basic ques-
tions are of utmost clinical importance. The appro-
priateness of treatment planning hangs in the bal-
ance. For example, should root canal treatment be
carried out prophylactically for a tooth associated
with moderate or advanced periodontal disease?
Should a pulpless tooth be retained or should it be
removed and replaced with an osseointegrated im-
plant?
Many of our clinical impressions related to the
dental pulp, and indeed many of our misinterpret-
ations, stem from early histological observations.
Adequate xation of pulp tissue has always been,
and continues to be, a challenge, and artefacts re-
sulting from inadequate xation continue to be de-
scribed as evidence of pathosis. Stanley & Weaver
(39) listed the following progression of tissue break-
down resulting from inadequate xation: vacuoliz-
ation in the odontoblastic layer and subsequently in
the general body of the pulp, displacement of
odontoblasts into the dentinal tubules as vacuoliz-
ation progresses, reticular atrophy, and the appear-
ance of advanced brosis in the body of the pulp.
Fibrosis and reticular atrophy are historical histo-
logical descriptions of pulp pathosis attributed to
many causes, including periodontal disease. A clas-
sic example of how inadequate pulp xation effects
an attempt to interpret the response of the dental
pulp to periodontal disease is the often quoted
paper by Mazur & Massler (26). Although it is obvi-
ous from the histological description in this paper
that many of the pulps suffered from inadequate
123
xation, the paper continues to be one of the more
commonly quoted in the periodontalendodontic
literature (9, 31, 34, 43). Most of the papers written
prior to 1975, as well as some written since, need to
be reviewed carefully to determine if their descrip-
tions of perceived pulp pathosis are in fact simply
histological artefacts.
The potential for the dental pulp to survive the
various challenges presented during the lifetime of a
patient is also by and large related to presumptions
made in interpretation of histological data. The his-
tology of a specic dental pulp, however, represents
only one frame of a picture in time for that particular
pulp. What has occurred before and what will subse-
quently occur must be a matter of conjecture and
interpretation. For example, Swerdlow & Stanley (40)
report the presence of intrapulpal abscesses at an
early time-point in one of their many pulp studies,
yet at later time-points in the same study there were
no intrapulpal abscesses and healing of pulp lesions
was evident. Does this mean that intrapulpal ab-
scesses can resolve and the pulp heal itself? Or is it
simply the luck of the draw in a histological study,
in that the pulps which had early intrapulpal ab-
scesses would subsequently become completely ne-
crotic if observed over a longer period of time, and
the pulps from the later time-points would have
shown less evidence of pathosis if observed at the
earlier time? While one cannot discount this latter
possibility, Stanleys interpretation was that oc-
casionally there will occur beneath cavity prepara-
tions certain abscess-like conditions which will re-
solve. (38) Hence, each pulp studied is from one mo-
ment in time, and observations are subject to
interpretation and projection beyond that moment.
Such projections may or may not conform to fact.
Was Stanley correct, or incorrect? We may never
know, and such interpretations become references
to authority.
Most histological interpretations of the past dec-
Harrington et al.
ades have suggested that the dental pulp resides in
a rather precarious environment. Even some current
texts list a litany of ills (43) which may befall a pulp
from exposure to periodontal disease and sub-
sequent periodontal treatment. Such projections,
however, fail to recognize more recent physiological
data which demonstrate that the pulp has a quite
sophisticated vasculature for such a relatively primi-
tive tissue. Vast networks of capillary beds have been
demonstrated as well as sophisticated control sys-
tems including precapillary sphincters and arterio-
venous shunts. An active lymphatic system has also
been demonstrated. As the effectiveness of a tissues
vasculature is key to its adequate function, such
physiological observations suggest that the dental
pulp has mechanisms which provide a signicant
capacity for survival.
The effects of periodontal disease
and procedures on the dental pulp
Periodontal disease
Over the years there has been a consistent stream of
speculation as to the effect of periodontal disease on
the dental pulp. Recent publications have suggested
that periodontal disease is a direct cause of pulpal
atrophy and necrosis (35), periodontal disease is
more deleterious to the pulp than both caries and
restorations combined (35), and periodontal dis-
ease and periodontal treatments should be regarded
as potential causes of pulpitis and pulpal necrosis
(43). Such interpretations have little basis in current
scientic fact, but do demonstrate the persistence of
an often repeated point of view in our literature. A
review of recent studies related to the periodontal
endodontic controversy therefore seems in order.
The pathways for communication and therefore
for the extension of disease from a periodontal
pocket to the pulp are through patent dentinal tu-
bules, lateral canals, and the apical foramen or for-
amina. Demonstration of the presence of such path-
ways is commonly identied as evidence that speci-
c periodontal disease must have some effect on the
health of the dental pulp. The following histological
and clinical studies suggest, however, that such re-
lationships rarely, if ever, result in pulp necrosis.
Kirkham (23) examined 100 periodontally involved
teeth and found that only 2% had lateral canals
located in a periodontal pocket. Tagger & Smukler
(41) removed roots from molar teeth so extensively
involved with periodontal disease that root ampu-
124
tation was required, and found that none of the
pulps of the resected roots showed inammatory
changes. Haskell et al. (16) also removed roots from
maxillary molars with total or nearly total peri-
odontal involvement and found no inammatory
cells or very few inammatory calls present in the
pulps of the periodontally involved resected roots.
Czarnecki & Schilder (11) performed a histological
study of intact, caries-free teeth and compared the
pulps of teeth which were periodontally within nor-
mal limits with teeth which had periodontal disease.
The pulps in the intact, caries-free, periodontitis
group were all histologically within normal limits re-
gardless of the severity of the periodontal disease.
In the same study they found that only teeth with
extensive decay or extensive restorations showed
evidence of pulp pathosis. A case report by Torabine-
jad & Kiger (42) of a patient with extensive peri-
odontal disease supports the position that advanced
periodontal disease has little or no effect on the
pulps of humans.
Ross & Thompson (36) evaluated the progress of
100 patients with maxillary molar furcation involve-
ment over a period of 524 years. Sixty-two of the pa-
tients were followed for over 10years. Of the 387
maxillary molars, 79% had at least 50% or less bone
support around one root prior to periodontal treat-
ment. Only 4% (14 of 380 vital teeth) required root ca-
nal treatment subsequent to periodontal therapy, and
it was the opinion of the authors that in all cases the
need for root canal treatment resulted from caries or
pulp degeneration under restorations. None were as-
cribed to the effects of the advanced periodontal dis-
ease on the pulp. Two per cent of the teeth in this
study had root canal treatment prior to periodontal
therapy for reasons unknown to the authors.
Bergenholtz & Nyman (4) evaluated 52 patients
with advanced periodontal disease over a 4- to 13-
year period. Of 417 nonabutment teeth, 60% had
crestal bone level in the apical two-thirds of the root.
Three per cent (14 of 417 teeth) required root canal
treatment during the recall period. The reasons cited
by the authors were progression of periodontal dis-
ease to involve the root apices in four teeth, decay
into the pulp in ve, one with internal resorption,
two with crown fractures, and two for unknown rea-
sons. For abutment teeth, 15% (38 of 255) needed
root canal treatment during the 413-year recall
period. Progression of periodontal disease to involve
the root apices was cited as the reason for root canal
treatment in two teeth, decay into the pulp in 10,
and unknown reasons for 24 teeth or 9% of the abut-
ment teeth.
Periodontalendodontic controversy
Jaoui et al. (21) studied patients with advanced
periodontal disease for 514years after completion
of active periodontal treatment. Of the 571 teeth that
did not have root canal treatment at the time of
completion of periodontal treatment, only one tooth
(0.175%) required root canal treatment over the 5- to
14-year recall period.
As one surveys the preceding human research
studies and considers the often discussed pathways
of communication between the pulp and the oral
cavity which may be exposed as a result of progress-
ive periodontal disease, the weight of evidence sup-
ports the position presented by Langeland et al. (25)
some years ago but largely ignored in more philo-
sophical discussions of purported periodontalen-
dodontic relationships. They presented some evi-
dence at the time that periodontal disease must ex-
tend all the way to the apex of a tooth before an
accumulation of plaque in the area of the apical for-
amen or foramina can cause signicant pulp in-
volvement. The aforementioned histological and
clinical outcome studies appear to support this posi-
tion and suggest that pulpal insults through patent
dentinal tubules or the occasional exposed lateral
canal have relatively insignicant effects on the abil-
ity of the dental pulp to survive.
From very practical clinical observations, it is sel-
dom that we nd a virgin tooth (no decay, no res-
torations) with evidence of periapical pathosis for
which we cannot determine a cause for the pulp be-
coming necrotic. More commonly we can identify a
traumatic incident with anterior teeth, developmen-
tal defects such as palatal grooves in anterior teeth
or Leongs tubercles in bicuspids, incomplete co-
ronal fractures in bicuspids and molars, or a history
of a disease process such as herpes zoster as the
cause for pulp necrosis. As clinicians we seldom nd
a pulpless virgin tooth to which we cannot attribute
a reasonable cause for the necrosis of the pulp. It is
seldom then that we nd a pulpless virgin tooth for
which we nd no clinically acceptable reasonable
cause for pulp necrosis. Therefore we rarely have to
search for a cause for a tooth becoming pulpless and
resort to the possibility that necrosis of the pulp was
caused by advanced periodontal disease or the se-
quelae of periodontal treatment. If it is correct that
the majority of adults age 35 years or more suffer
from gum disease at some point in their life, and that
periodontal disease is considered to be a signicant
cause of pulp necrosis, the magnitude of the num-
bers make it seem only reasonable that by now some
astute clinician would have identied a signicant
group of virgin teeth with necrotic pulps for which
125
advanced periodontal disease would have been
identied not only as the likely cause of pulp ne-
crosis but as the only possible cause. It does not ap-
pear that this is the case in the many clinical studies
which have been carried out by either periodontists
or endodontists.
Periodontal procedures
The aforementioned clinical research studies by
Ross & Thompson (36), Bergenholtz & Nyman (4)
and Jaoui et al. (21) evaluated patients who pre-
sented with advanced periodontal disease, received
what was considered to be appropriate periodontal
treatment, and received follow-up maintenance care
for periods ranging from 4 to 24years. There were
1,623 teeth in the combined studies which were
treated for advanced periodontal disease and were
assumed to have vital pulps at the completion of
treatment and the beginning of the recall period.
Four per cent (67 of 1623 teeth) required root canal
treatment subsequent to periodontal disease, peri-
odontal treatment, and follow-up periodontal care.
The cause of pulp necrosis could be identied by the
clinicians in most cases. Recurrent decay resulting in
pulp exposure was the primary cause. Extension of
periodontal disease to involve the root apices is also
cited as a reason for root canal treatment, but it is
not known if the pulps of these teeth were in fact
necrotic or whether root canal treatment was ac-
complished to facilitate additional periodontal treat-
ment. But few of the teeth requiring root canal treat-
ment were listed as having unknown cause. In the
Bergenholtz & Nyman 1984 study (4) all nonabut-
ment teeth, as well as abutment teeth, were involved
in xed prosthetic reconstructions, so it can at least
be speculated that the cause for at least some of the
unknowns could be extensive restorations. While
Bergenholtz & Nyman found that 15% of pulps of
vital teeth prepared for abutments in xed bridge-
work became necrotic, a study by Karlsson (22)
found this gure to be 11%.
From these studies and from many other recall
studies in the periodontics literature, it appears that
periodontal treatment, as well as periodontal dis-
ease, has a negligible effect on the dental pulp.
In summary, unless periodontal disease extends all
the way to the tooth apex, the weight of evidence in
the literature suggests that the dental pulp is capable
of surviving signicant insults and that the effect of
periodontal disease as well as periodontal treatment
on the dental pulp is negligible. It also appears that
the clinical signicance of the relationship between
Harrington et al.
periodontal disease and the dental pulp has been
greatly exaggerated in historical and much of the
current periodontalendodontic literature.
The effects of endodontically
involved teeth on periodontal
health and healing
Historically the effect of periodontal disease on the
dental pulp has been a source of discussion for the
better part of the past century. Only in recent years
has the reverse been discussed, the potential effect
that a tooth with a necrotic pulp or a tooth that has
had root canal treatment may pose as a risk factor
in the initiation of periodontal disease, the pro-
gression of periodontal disease, and the resolution
of periodontal pockets. Position papers have recently
appeared making a case for such relationships (9, 24,
34). The projected negative effects of pulpless teeth
appear to be based on studies related to the simi-
larity of the microbial ora in root canals and deep
periodontal pockets, negative effects on periodontal
healing in replantation studies, and a series of retro-
spective statistical studies by Jansson, Ehnevid, Lind-
skog and Blmlof (12, 13, 1719). The latter series
suggests that a pulpless tooth with a periapical
lesion promotes the initiation of periodontal pocket
formation, promotes the progression of periodontal
disease, and interferes with healing of a periodontal
lesion after periodontal treatment. The presumed
pathway is primarily through patent dentinal tu-
bules. The clinical consequences suggested by this
series of studies are signicantly deeper probing
depths, more bone loss, impaired periodontal heal-
ing following nonsurgical periodontal treatment, and
enhanced progression of periodontal disease.
The ve Jansson and Ehnevid papers are multiple
regression analyses of different parameters of the
same cohort of patients. The selected patients had
been treated for advanced periodontal disease and
had at least one single-rooted tooth with a periapical
lesion or a root canal lling. While stated to be statis-
tically signicant, the differences in periodontal
pocket depth between teeth with no periapical
lesions and teeth with periapical lesions is somewhat
hard to interpret in these papers. Jansson et al. (17)
does break out a smaller group to evaluate intraindi-
vidual comparisons and reports a mean pocket
depth difference of 0.27mm to 0.66mm in ve tooth
groups and 0.98mm in a sixth group. In a second
paper (18) Jansson et al. state, Mean probing depths
126
for each tooth were approximately 0.2mm deeper in
teeth with the same degree of radiographic attach-
ment in the presence of angular destructions when
periapical pathology was present compared to teeth
without periapical pathology. The recorded mean
differences in probing depths therefore appear to be
less than one millimeter.
In an evaluation of clinical radiographs, Jansson
et al. (18) state that teeth with periapical lesions had
lost signicantly more proximal marginal bone, ap-
proximately 2mm. Relative bone loss is difcult to
evaluate from the data presented. As the radiographs
evaluated in this study were those taken during the
course of routine periodontal treatment, differences
in projection geometry between the test and control
radiographs would be of concern. It is interesting to
note that for over 50% of the teeth identied as
having periapical radiolucencies, the size of the
lesions was too small to be measured (less than 0.1
mm
2
). It is also of interest to note that of the teeth
that had root canal treatment, 70% were evaluated
to be inadequate.
In their 1995 paper, Jansson et al. (19) extrapolate
their data to estimate that the rate of marginal proxi-
mal radiographic bone loss for teeth with active peri-
apical lesions in periodontitis-prone patients is 0.19
mm/year vs. 0.06mm/year for teeth with no peri-
apical lesion or where there is evidence of reduction
in lesion size. While these numbers are relatively
small, they have been magnied in the literature by
being referred to as a three-fold amplication (19)
and three times the rate of proximal bone loss (24).
Ehnevid et al. (12,13) deal with evaluation of treat-
ment results. The mean pretreatment pocket depth
was 3.9mm and depths post-treatment ranged from
2.9mm at 46months to 3.3mm at 2836months.
Multiple regression analysis was again used. Non-
surgical treatment of periodontal pockets in teeth
with horizontal marginal defects was identied as re-
sulting in signicantly less mean pocket depth re-
duction in teeth with periapical lesions compared to
teeth with no periapical lesions. It is quite interesting
to note that there was no correlation between peri-
apical pathosis and mean pocket depth reduction for
nonsurgical treatment of vertical marginal defects,
nor was there any correlation between periapical pa-
thosis and mean pocket depth reduction after surgi-
cal management of either horizontal or vertical de-
fects.
In a later 1998 study, Jansson & Ehnevid (20)
evaluated the periodontal status of mandibular mo-
lars. They reported that the mean periodontal prob-
ing depth of a nonroot-lled molar with a periapical
Periodontalendodontic controversy
lesion was 0.7mm deeper than corresponding teeth
with no periapical lesions, and that the mean prob-
ing depth difference at proximal sites was 0.2mm. It
is quite curious to note that they found that molars
with root canal llings, but no evidence of periapical
pathosis, were not signicantly correlated to peri-
odontal probing depth nor to degree of furcation in-
volvement. How could it possibly be that pulpless
teeth with periapical lesions have signicantly
deeper periodontal pockets and furcation involve-
ments, whereas teeth which have had root canal
treatment but at the time of evaluation have no peri-
apical pathosis do not have deeper pockets nor
deeper furcation involvements? From their data sug-
gesting that pulpless teeth which have had micro-
organisms in their pulp chambers and root canals
have increased pretreatment pocket depths, how can
no evidence of increased pocked depths be found
post-treatment? How can the difference possibly be
accounted for? Does it mean that all of the teeth
evaluated in this study that had root canal treatment
and no periapical pathosis, or at least a majority of
them, had no history of having microorganisms in
their pulp chambers and root canals prior to root
canal treatment? It is possible, but unlikely. Or does
it mean that there is no difference because the peri-
odontal pathosis healed after root canal treatment?
Again, quite unlikely.
While it is difcult to evaluate adequately the
series of papers by the groups of Jansson & Ehnevid,
the data presented appear equivocal at best, appear
to present triing distinctions, and appear to have
little clinical signicance. If there is a clinical mess-
age, it would seem to be that root canal treatment
should be completed before periodontal therapy and
that root canal treatment should be accomplished at
a very high technical level.
One credible human study in the literature sup-
ports the position that endodontically obturated
teeth may interfere with the effectiveness of attach-
ment regeneration procedures. Sanders et al. (37) re-
ported in 1983 that after the use of freeze-dried bone
allografts 65% of the teeth that did not have root ca-
nal treatment showed complete or greater than 50%
bone-ll in periodontal osseous defects, while only
33% of the teeth which had root canal treatment
prior to the periodontal surgical procedure had com-
plete or greater than 50% bone-ll. While the sample
size of teeth in the root canal group was relatively
small (eighteen), the results appear to be worth
further evaluation. In the discussion, it is of interest
to note that the authors state that the adequacy of
a number of obturations was suspect. With all of the
127
variables considered in this study, it would appear
that it would require control of the signicant vari-
ables in a matched-pair study design to resolve the
issue.
In 1979 Nyman & Lindhe (33) evaluated a group
of patients who had lost 50% or more periodontal
bone support. After periodontal and restorative
treatment they were followed for a period of 58
years. In comparing bone height measurements of
patients who had both an endodontically treated
abutment and a vital abutment tooth, they found
that the bone height was maintained equally well
around the root-lled teeth as around the vital teeth.
Miyashita et al. (32) recently used a paired sample
in which the test tooth had been endodontically
treated or not treated but had a periapical radio-
lucency, but not the control tooth. The selected pa-
tients had minor or no signs of periodontal disease.
The distance from the cementoenamel junction to
the marginal bone level was measured using intra-
oral radiographs. A somewhat larger loss (mean
value 0.1mm) of alveolar bone support was found in
test teeth vs. the controls, but the difference was not
statistically signicant and the study failed to show
a correlation between a reduced marginal bone sup-
port and endodontic status. It is of interest to note
that 61% of the root canal llings were judged inad-
equate in the cervical third of the canal.
In contrast to the preceding clinical studies,
McGuire & Nunn (2730) attempted to relate disease
etiology and progression of periodontal disease with
a pretreatment-assigned prognosis, and found that
some commonly accepted clinical parameters did
not accurately predict a tooths survival. Their stat-
istical model (27) had predicted that endodontic in-
volvement would be associated with the probability
that the prognosis for such a tooth would worsen
over time. In their clinical study (29), however, the
actual outcome was that none of the 131 teeth lost
from a total of 2,509 teeth had endodontic involve-
ment. Endodontic involvement at the time of peri-
odontal treatment planning therefore was deter-
mined not to be a signicant clinical factor associ-
ated with tooth loss.
As extraction is the alternative to maintaining a
pulpless tooth, long-term prognosis studies are sig-
nicant when considering treatment planning. The
previously discussed clinical research studies by
Ross & Thompson (36), Bergenholtz & Nyman (4),
and Jaoui et al. (21), as well as that by McGuire &
Nunn (29), point to the long-term retention of teeth
with advanced periodontal disease if managed ap-
propriately and for periodontally involved teeth
Harrington et al.
which have had root canal treatment. In the Jaoui
et al. study (21), for example, tooth loss was 2% of
the 911 periodontally involved teeth and the overall
failure rate of the 340 endodontically treated teeth
was 1.2%.
Recent studies (3, 5, 7) have demonstrated that the
prognosis is quite good even for molars so exten-
sively involved with periodontal disease as to require
root amputation. It has also been suggested that sur-
vival rates of teeth with root resections is not sub-
stantially different than that for osseointegrated im-
plants (6). In fact, a current periodontics textbook (8)
suggests that substituting a furcation-involved tooth
with an osseointegrated implant should be con-
sidered with extreme caution and only if the implant
will improve the prognosis of the overall treatment
plan.
In summary, while it has been suggested that a
pulpless tooth may represent an etiological risk fac-
tor related to periodontal disease, the comparative
risk must be considered negligible based on clinical
outcomes.
Diagnosis
Pulp testing procedures and periodontal probing are
critical to accurate diagnosis. The authors believe
that the contour of a defect in the attachment can be
identied by careful probing around the periphery of
the tooth and that the contour is important in deter-
mining the appropriate treatment for resolving the
lesion (14, 15). For example, it is usually easy to
identify a sinus tract through the periodontal liga-
ment space from a periapical lesion or lateral lesion.
By careful probing, a break in the integrity of the
sulcus is found and can be probed some distance
down the root surface. The break is about 1mm wide
and probing a millimeter to either side is within nor-
mal limits. It is usually referred to as a narrow sinus
tract-type of probing. This type of probing will be
associated with a tooth with a necrotic pulp or a
tooth which has had root canal treatment a very high
percentage of the time. In such cases it simply indi-
cates a draining sinus tract associated with a peri-
apical or lateral lesion. It is no different from a drain-
ing sinus tract in the alveolar mucosa or attached
gingiva. It simply exits through the gingival sulcus.
Although it involves the attachment and there is a
defect that can be probed, it is strictly an endodontic
problem and will resolve after adequate root canal
treatment. No periodontal treatment is necessary,
128
and in fact, periodontal treatment of any type is
contraindicated.
But what if the same type of probing is associated
with a tooth that responds within normal limits to
cold and the electric pulp tester? This presents a di-
lemma. Should the positive pulp tests be ignored
and root canal treatment be performed in an
attempt to resolve the probeable lesion? There are,
in fact, a number of clinical situations which can be
identied where a narrow sinus tract-type of probing
is associated with a tooth with a vital pulp:
O A sinus tract through the periodontal ligament of
a vital tooth which comes from an adjacent pulp-
less tooth or a pulpless tooth several teeth away.
Such a sinus tract could also be related to ad-
vanced periodontal disease associated with an ad-
jacent tooth.
O Developmental grooves. A developmental groove
commonly breaks down as a narrow sinus tract
probing. The probing contours may change with
time, particularly if an acute infection develops in
the periodontal defect.
O Fused roots of posterior teeth. A fusion line may
result in a periodontal defect similar to that which
occurs along a developmental groove.
O Incomplete coronal fractures (cracked tooth)
which extend into the root of a tooth. Incomplete
coronal fractures almost exclusively occur in pos-
terior teeth.
O Crownroot fractures.
O Spontaneous vertical root fractures. Vertical root
fractures have been identied in molars with vital
pulps in Chinese patients.
O Enamel spurs. An extension of enamel into a fur-
cation often breaks down as a periodontal defect.
An enamel pearl may also result in a periodontal
defect.
O Impact trauma may result in a narrow or wide si-
nus tract probing. This more commonly occurs on
the palatal side of maxillary anterior teeth.
O Periodontal disease associated with a very narrow
root may probe with a moderately wide sinus
tract-type of probing. As an example, this may oc-
cur on the labial or lingual side of a mandibular
anterior tooth that is quite narrow in the mesial
distal dimension. It would usually probe from line
angle to line angle.
As with many things in life, there is the general rule
and then there are the exceptions. The general rule
in this case is that a narrow sinus tract-like probing
is commonly associated with a pulpless tooth and
Periodontalendodontic controversy
the exceptions are as listed above. It is obvious from
this example that a clinician must be very astute,
rst to nd the defect in the attachment and then to
determine the correct cause. An astute clinician will
know the general rule and the exceptions. It is also
obvious that any of the clinical situations listed as
exceptions could also be associated with a pulpless
tooth and could add to the complexity of identifying
the correct cause and appropriate treatment.
The terminology currently used in our literature
adds to the confusion of accurate identication of
various lesions resulting in defects that can be
probed. Recently a new classication for periodontal
diseases and conditions was adopted by the Interna-
tional Workshop for a Classication of Periodontal
Diseases and Conditions and a category of Peri-
odontitis Associated With Endodontic Lesions and
a subcategory of combined periodonticendodontic
lesions was added to the classication (2). Com-
bined lesions are dened as those cases where there
is any coalescence of endodontic and periodontal
lesions. (10) This denition opens the door for a
very broad interpretation of periodontalendodon-
tic lesions. Inclusion of combined periodontic and
endodontic lesions in a periodontal classication
seems not very helpful in concept, confusing as to
which lesion has coalesced and which has not, and
certainly not helpful in diagnosis and treatment
planning. The review paper (31) written in support
of adding combined lesions to the classication is
not at all helpful in suggesting how this category will
be clinically useful. As just one of many examples,
the review paper states, vertical root fractures in
nonendodontically treated teeth can sometimes ap-
pear as combined endodontic and periodontal
lesions. (31) It is true that a spontaneous vertical
root fracture does cause inammation in the peri-
odontal ligament and often results in destruction of
the attachment to the level of the gingival sulcus. A
narrow sinus tract-type of probing in line with the
fracture is the common clinical nding. If the pulp
of the tooth remains vital, and it would be vital early
on after the root fractures as stated by the review
paper, the lesion that can be probed at that time
would more than likely be classied under the head-
ing of an acquired deformity or condition. If the pulp
of the same tooth, however, should become necrotic
from bacteria in the gingival sulcus or along the frac-
ture line gaining access to pulp tissues, the same
probeable lesion now becomes a periodontitis as-
sociated with an endodontic lesion or a combined
periodonticendodontic lesion. What is the point?
The classication is not helpful in identifying the
129
cause of the lesion that can be probed, in determin-
ing the prognosis, nor in indicating the appropriate
treatment. It seems misguided and not particularly
helpful to a clinician. If many other examples of
what might be termed as combined lesions are
examined, the same muddy concepts emerge. The
authors do believe that true combined lesions do
occur when an endodontic lesion develops and ex-
tends into an existing periodontal pocket (1, 14, 15).
It is possible that the reverse may occasionally occur.
Such combined lesions are relatively rare, and the
authors believe that such lesions can be clinically
identied (1, 14, 15). A narrower view of combined
periodontalendodontic lesions would promote
better understanding between the specialties and
help to resolve what, for many, has been an ex-
tremely confusing issue for many years.
In summary, it is the view of the authors that the
varying physical contours of lesions in the attach-
ment can be positively identied by careful probing.
By identifying such contours and accurately inter-
preting pulp test responses, it can be determined
which probeable defects can be resolved by root ca-
nal treatment and which cannot (14, 15). Present ter-
minology and classications simply confuse diag-
noses that are commonly straightforward but oc-
casionally complex. It is time to start anew.
References
1. Ammons WF, Harrington GW. The periodontic-endodontic
continuum. In: Newman, MG, Takei, HH, Carranza, FA,
editors. Carranzas Clinical Periodontology, 9th edn. Phila-
delphia: W.B. Saunders Co., 2002: 840850.
2. Armitage GC. Development of a classication system for
periodontal diseases and conditions. Ann Periodontol
1999: 4: 16.
3. Basten CHJ, Ammons WF, Persson R. Long-term evalu-
ation of root resected molars: a retrospective study. Int J
Periodont Restorative Dent 1996: 16: 207219.
4. Bergenholtz G, Nyman S. Endodontic complications fol-
lowing periodontal and prosthetic treatment of patients
with advanced periodontal disease. J Periodontol 1984: 55:
6368.
5. Blomlf L, Jansson L, Applegren R, Ehnevid H, Lindskog
S. Prognosis and mortality of root-resected molars. Int J
Periodont Restorative Dent 1997: 17: 191201.
6. Buhler H. Survival rates of hemisected teeth: An attempt
to compare them with survival rates of alloplastic im-
plants. Int J Periodont Restorative Dent 1994: 14: 537543.
7. Carnevale G, DiFebo G, Tonelli MP, Marin C, Fuzzi M. A
retrospective analysis of the periodontal-prosthetic treat-
ment of molars with interradicular lesions. Int J Periodont
Restorative Dent 1991: 11: 188205.
8. Carnevale G, Pontoriero R, Lindhe J. Treatment of fur-
cation-involved teeth. In: Lindhe, J, Karring, T, Lang, NP,
editors. Clinical Periodontology and Implant Dentistry, 3rd
edn. Copenhagen: Munksgaard, 1997: 682710.
Harrington et al.
9. Chen SY, Wang HL, Glickman GN. The inuence of endo-
dontic treatment upon periodontal wound healing. J Clin
Periodontol 1997: 24: 449456.
10. Consensus report. Periodontic-endodontic lesions. Ann
Periodontol 1999: 4: 90.
11. Czarnecki RT, Schilder H. A histological evaluation of the
human pulp in teeth with varying degrees of periodontal
disease. J Endodont 1979: 5: 242253.
12. Ehnevid H, Jansson L, Lindskog S, Blomlf L. Periodontal
healing in teeth with periapical lesions. A clinical retro-
spective study. J Clin Periodontol 1993: 20: 254258.
13. Ehnevid H, Jansson LE, Lindskog SF, Blomlf LB. Peri-
odontal healing in relation to radiographic attachment
and endodontic infection. J Periodontol 1993: 64: 1199
1204.
14. Harrington GW. The perio-endo question: differential di-
agnosis. Dent Clin North Am 1979: 23: 673690.
15. Harrington GW, Steiner DR. Periodontal-endodontic con-
siderations. In: Walton, RE, Torabinejad, M, editors. Prin-
ciples and Practice of Endodontics, 3rd edn. Philadelphia:
W.B. Saunders Co., 2002: 466484.
16. Haskell EW, Stanley H, Goldman S. A new approach to
vital root resection. J Periodontol 1980: 51: 217224.
17. Jansson L, Ehnevid H, Lindskog S, Blomlf L. Relationship
between periapical and periodontal status. A clinical
retrospective study. J Clin Periodontol 1993: 20: 117123.
18. Jansson L, Ehnevid H, Lindskog S, Blomlf LB. Radio-
graphic attachment in periodontitis-prone teeth with en-
dodontic infection. J Periodontol 1993: 64: 947953.
19. Jansson L, Ehnevid H, Lindskog S, Blomlf L. The inu-
ence of endodontic infection on progression of marginal
bone loss in periodontitis. J Clin Periodontol 1995: 22:
729734.
20. Jansson LE, Ehnevid H. The inuence of endodontic infec-
tion on periodontal status in mandibular molars. J Peri-
odontol 1998: 69: 13921396.
21. Jaoui L, Machtou P, Ouhayoun JP. Long-term evaluation of
endodontic and periodontal treatment. Int Endodont J
1995: 28: 249254.
22. Karlsson S. A clinical evaluation of xed bridges, ten years
following insertion. J Oral Rehab 1986: 13: 423432.
23. Kirkham DB. The location and incidence of accessory pul-
pal canals in periodontal pockets. J Am Dent Assoc 1975:
91: 353356.
24. Kornman KS, Robertson PB. Fundamental principles af-
fecting the outcomes of therapy for osseous lesions. Peri-
odontol 2000 2000: 22: 2243.
25. Langeland K, Rodrigues H, Dowden W. Periodontal dis-
ease, bacteria and pulpal histopathology. Oral Surg Oral
Med Oral Path 1974: 37: 257270.
26. Mazur B, Massler M. Inuence of periodontal disease on
the dental pulp. Oral Surg Oral Med Oral Path 1964: 17:
592603.
130
27. McGuire MK. Prognosis versus actual outcome. A long-
term survey of 100 treated periodontal patients under
maintenance care. J Periodontol 1991: 62: 5158.
28. McGuire MK, Nunn ME. Prognosis versus actual outcome.
II. The effectiveness of clinical parameters in developing
an accurate prognosis. J Periodontol 1996: 67: 658665.
29. McGuire MK, Nunn ME. Prognosis versus actual outcome.
III. The effectiveness of clinical parameters in accurately
predicting tooth survival. J Periodontol 1996: 67: 666674.
30. McGuire MK. Prognosis vs. outcome: predicting tooth sur-
vival. Compend Contin Educ Dent 2000: 21: 217228.
31. Meng HX. Periodontic-endodontic lesions. Ann Peri-
odontol 1999: 4: 8489.
32. Miyashita H, Bergenholtz G, Grndahl K, Wennstrm JL.
Impact of endodontic conditions on marginal bone loss. J
Periodontol 1998: 69: 158164.
33. Nyman S, Lindhe J. A longitudinal study of combined peri-
odontal and prosthetic treatment of patients withadvanced
periodontal disease. J Periodontol 1979: 50: 163169.
34. Paul BF, Hutter JW. The endodontic-periodontal con-
tinuum revisited: new insights into etiology, diagnosis and
treatment. J Am Dent Assoc 1997: 128: 15411548.
35. Petka K. The 14 warning signs. Endodontic Prac 2001: 4:
1826.
36. Ross IF, Thompson RH. A long term study of root retention
in the treatment of maxillary molars with furcation in-
volvement. J Periodontol 1978: 49: 238244.
37. Sanders JJ, Sepe WW, Bowers GM, Koch RW, Williams JE,
Lekas JS, Mellonig JT, Pelleu GB, Gambill V. Clinical evalu-
ation of freeze-dried bone allografts in periodontal oss-
eous defects. 3. Composite freeze-dried bone allografts
with and without autogenous bone grafts. J Periodontol
1983: 54: 18.
38. Stanley HR. Design for a human pulp study. Part II. Oral
Surg Oral Med Oral Path 1968: 25: 756764.
39. Stanley HR, Weaver K. A technique for the preparation of
human pulpal tissues. In: Finn SB, editor. Biology of the
Dental Pulp Organ. A Symposium. Alabama: University of
Alabama Press, 1968: 125.
40. Swerdlow H, Stanley HR. Response of the human dental
pulp to amalgam restorations. Oral Surg Oral Med Oral
Path 1962: 15: 499508.
41. Tagger M, Smukler H. Microscopic study of the pulps of
human teeth following vital root resection. Oral Surg Oral
Med Oral Path 1977: 44: 96105.
42. Torabinejad M, Kiger RD. A histologic evaluation of dental
pulp tissue of a patient with periodontal disease. Oral Surg
Oral Med Oral Path 1985: 59: 198200.
43. Wang HL, Glickman GN. Endodontic and periodontic
interrelationships. In: Cohen, S, Burns, RC, editors. Path-
ways of the Pulp, 8th edn. St Louis: C. V. Mosby, 2002: 651
664.

You might also like