The endodontic-periodontal lesion: a rational

approach to treatment
C Solomon, H Chalfin, M Kellert and P Weseley
J Am Dent Assoc 1995;126;473-479

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THE ENDODONTICmPERIODONTAL LESION:
A RATIONAL APPROACH TO TREATMENT
CHARLES SOLOMON, D.D.S.; HENRY CHALFIN, D.D.S.; MITCHELL KELLERT, D.D.S.;
PAUL WESELEY, D.D.S.
Qince 1964, when Simring and Goldberg'
first described the relationship between
periodontal and endodontic disease, the
term endo-perio has become an integral
part ofthe dental vocabulary. Unfortunate-
ly, this term has been indiscriminately
used to categorize
disease of either
periodontal or endo-
When a periapical lesion com- dontic etiology, with
municates with a deep perio- or without
dontal pocket, the etiology can
secondary involve-
ment of the other, as
be either endodontic or perio- well as true
dontal. This article clarifies combined lesions. It
the relationship between pulp-
conveniently
provides a blanket
al and periodontal disease and diagnosis for any
presents a systematic such lesion, regard-
approach to the diagnosis and
less of the primary
etiology. Without
management of endodontic- information about
periodontal lesions. It also the primary etiology,
presents a case that demon-
however, a clinician
can perform appro-
strates the successful treat- priate treatment
ment of teeth that appear to only by chance. An
be hopelessly diseased.
in-depth
understanding of the
mechanisms by
which these two disease processes
interact, together with a thorough
diagnostic examination, usually will help
direct the proper course of treatment.
The relationship between pulpal and
periodontal disease can be traced to
embryological development, since the
pulp and the periodontium are derived
from a common mesodermal source.2 The
developing tooth bud pinches off a portion
of mesoderm that becomes pulp, while the
A
'Ii
remaining mesoderm develops into
periodontium. In the course of root de-
velopment, strands of mesodermal tissue
may get trapped and later become lateral
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and accessory canals. These offshoots
also may result from dentin formation
around existing blood vessels or a loss of
continuity of Hertwig's root sheath dur-
ing dentin formation. In time, most of
these communications are sealed by ce-
mentum or secondary dentin, leaving the
pulp basically dependent on the apical
foramen for metabolic exchange (and
thus forming a low-compliance system).
Some of these portals of communication
remain patent, however, and these-in
addition to the apical foramen and den-
tinal tubules-are pathways through
which etiologic agents may pass between
the pulp and the periodontium (Figure 1).
The relationship of pulpal and
periodontal disease. While the del-
eterious effects of pulpal disease on the
periodontium are well documented,34" the
converse effect of periodontal disease on
the pulp remains unclear. Some authors
have reported a strong correlation be-
tween periodontal disease and inflam-
matory and degenerative changes in the
pulp,56'7 while others have found no such
correlation.89 Langeland and others'0
found that the pulp succumbed only
when periodontal lesions involved the
apical foramen; otherwise, only minor
changes occurred in the pulp.
The clinical symptoms of pulpitis
commonly seen in periodontal patients
are related more closely to the treatment
than to the disease. Vigorous root planing
may remove cementum and expose
numerous dentinal tubules through
JADA, Vol. 126, April 1995 473
CUINICAL PRACTICE

pulp generally will not succumb

to periodontal lesions that do
not involve the apical foramen'0;
however, it must be remem-
bered that the effects of a life-
time of caries, operative proced-
ures, periodontal disease and
treatment are cumulative, with
the pulp losing some of its recu-
perative power with each added
insult. Periodontal disease,
therefore, can contribute to pulp-
al inflammation even when the
apical foramen is not involved. In
any case, these effects are cer-
tainly less dramatic than the

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effects commonly seen in the
periodontium of endodontic
lesions-an interesting situa-
tion, as the pathways involved
are reciprocal. A closer exami-
Figure 1. Canals are pathways through which etiologic agents may nation of the two disease proc-
pass between the pulp and the periodontium.
esses is necessary to explain
this apparent discrepancy.
Periodontal disease. Perio-
dontal disease has a progressive
nature. It begins in the sulcus
and migrates to the apex as
deposits of plaque and calculus
produce inflammation, which
slowly destroys the attachment
apparatus. As a constant path-
way for drainage usually re-
mains via the gingival sulcus,
acute episodes are uncommon.
These lesions may infiltrate
lateral canals, accessory canals
or exposed dentinal tubules, but
the path of least resistance is
generally sulcular. Further-
more, healthy pulp tissue is a
Figure 2. Depiction of a retrograde periodontitis, a lesion that
highly polymerized, highly vas-
progresses In the opposite direction of a marginal periodontitis and cular tissue that is quite resist-
has none of the basic characteristics of periodontal disease. ant to infection. As long as the
vascular supply is maintained
which etiologic agents may has been shown to dissolve as through the apical foramen, the
enter and inflame the pulp.4"' early as one week after surgery, pulp usually resists attack via
Furthermore, these exposed resulting in a return of dentin these other pathways, although
tubules are subject to hypersensitivity.'3 Although this calcifications or minor degenera-
hydrodynamic stimuli.'2 This pulpitis is usually reversible, tive changes may be seen histo-
has been shown to be mitigated palliative endodontic therapy logically.10 If the periodontal
by smear layer formation,'3"4 but may be necessary in some cases. lesion, or its treatment, ultimately
unfortunately, this smear layer As previously stated, the compromises the vascular supply

474 JADA, Vol. 126, April 1995


Flgure 3. Extehle periodontal destruton along the
surac that extends to the perlapical area.
Figure 4. Almost complete repair was achlved six months aftr surgery.
through the apical foramen,
pulpal necrosis will occur and
fuither exacerbate the peri-
odontal breakdown. While the
prognosis for such a tooth
basically depends on the nature of
the periodontal lesion, endodontic
therapy must be performed first
because pulpal irritants otherwise
would preclude repair.
Pulpal disease. Unlike
periodontal disease, pulpal dis-
ease commonly exhibits both
chronic and acute phases. When
chronic, pulpal degeneration
may occur rather slowly; the
C[INICAl PRACIIC[
highly polymerized nature of the
pulp makes it quite resistant to
enzymatic degradation. Pulpal
inflammation, in a low-com-
pliance system, is accompanied
by an increase in intrapulpal
pressure. Areas of infarction
and coagulation necrosis result
as the pulp succumbs incre-
mentally.
With this increase in intra-
pulpal pressure, toxic agents may
be expressed through patent
channels,' including the apical
foramen and lateral and acces-
sory canals. Corresponding
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lesions in the adjacent periodon-
tium may eventually coalesce.
While any endodontic lesion may
drain along the periodontal
ligament and form fistulas that
penetrate the gingival sulcus,
lesions in close proximity to the
gingival margn- such as those
associated with lateral canals in
the coronal half of-the root and
accessory canals in the floor of
multirooted teeth are the most
likely to do so, forming pseudo-
pockets that simulate periodontal
disease. Termed a retrograde
periodontitis, this type of lesion
progresses in the opposite direc-
tion of a marginal periodontitis
without any ofthe basic char-
acteristics of periodontal disease
and very possibly without per-
manently damaging the cemen-
tum and its fibers (Figure 2).12
The loss of attachment produced
by these lesions may be com-
pletely reversible with endodon-
tic therapy alone; however, if not
treated early, secondary perio-
dontal involvement may progres-
sively undermine the prognosis.
DIAANOSIS
The diagnosis of pulpal-perio-
dontal lesions may be relatively
simple in a case that has been
monitored over a period of time
JADA, Vol. 126, April 1995 475
C ~CLINICAL PRACTICE
Figure 5. A mandibular right first molar with a large periapical area on
the distal root and extensive breakdown in the furcation.
Figure 6. Excellent repair was evident one year after surgery.
or for which records and radio-
graphs are obtainable. The diag-
nosis becomes more difficult
when a recent history is un-
available. A growing periapical
area with secondary formation
of a deep periodontal pocket
may be similar in clinical and
radiographic appearance to a
long-standing periodontal lesion
that has progressed to the root
apex. When available, however,
476 JADA, Vol. 126, April 1995
these divergent histories leave
little doubt as to the respective
origins of each lesion.
Unfortunately, a recent
history and/or radiographs may
not always be available or en-
lightening. It is easier to diag-
nose such cases when a vital
pulp test is obtained, because
the test results usually will rule
out an endodontic etiology. Pulp
tests may be unreliable, how-
ever, and when doubt exists, a
test cavity can be made. Fur-
thermore, in multirooted teeth,
a vital response may be ob-
tained despite complete necrosis
in one or more canals, so excep-
tional care must be taken in
making a clinical judgment.
A pulpless (nonvital or endo-
dontically treated) tooth asso-
ciated with a combined lesion
usually presents the greater
diagnostic problem, because
little can be immediately in-
ferred about whether the pulp's
status was the cause of, the re-
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sult of or incidental to the perio-
dontal condition. With an endo-
dontically treated tooth, the
adequacy of this treatment
must be considered in light of
the possibility of endodontic
failure. Endodontic treatment
that radiographically appears
inadequate often is successful.
Conversely, failures also com-
monly occur despite the pres-
ence of root canal fillings that
appear to be excellent.
When a restorative post is
present in the involved root, the
possibility of root fracture also
should be considered in the dif-
ferential diagnosis. A vertical
root fracture usually will pro-
duce periodontal breakdown
similar to through-and-through
pulpal-periodontal lesions.
Surgical exposure often will be
necessary, either to confirm the
presence of a fracture or to
perform the apicoectomy if no
fracture is present.
In teeth that have not been
treated endodontically, the pres-
ence of extensive caries or of
deep restorations certainly
suggests endodontic etiology,
although either of these might
be only incidental findings in a
tooth with periodontal involve-
ment. Pulpal disease also is a
distinct possibility in any tooth

Figure 7. Probing of the distal root surface, which communicated with
the periapical area, revealed a purulent discharge.
Figure 8. One year after surgery, probing depths remained at the
previous levels.
that has had a full cast restor-
ation, as such a tooth usually
has been subjected to numerous
operative procedures before the
crown preparation itself.
Furthermore, varying degrees
of occlusal trauma are common
with cast restorations, adding
further insult to already
compromised pulps. Since these
effects are cumulative, pulpal
necrosis is fairly common in
crowned teeth.
The mere presence of a deep
filling or cast restoration is not
sufficient basis for a diagnosis of
endodontic etiology; however,
such a diagnosis is reasonable in
C[INICAL PRACTICE
a mouth that is otherwise free of
similar periodontal lesions and
when the architecture of the
lesion is consistent with endo-
dontic lesions. Inherently, a
periodontal lesion will usually
be broader at its point of origin,
the cervix dentis, than at the
apex. The reverse would be true
for an endodontic lesion. Careful
probing of the lesion usually will
provide information about the
progression of the disease and
the presence or absence of cal-
culus on the root surface. When
a clear pattern is evident, the
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diagnosis may be fairly routine.
The absence of a definitive
diagnosis. When a clinician
cannot make a definitive diag-
nosis, it may be prudent for him
or her to initiate endodontic thera-
py and hope for repair. After
complete instrumentation, cal-
cium hydroxide should be used
as an intracanal medicament. It
is an excellent medicament in
general, because it is bactericid-
al, anti-inflammatory and pro-
teolytic; it inhibits resorption;
and it favors repair.13 It is es-
pecially effective in endo-perio
cases because its temporary ob-
turating action will inhibit
periodontal contamination of
the instrumented canals via
patent channels of communica-
tion. When the etiology is pure-
ly endodontic, this regimen
usually will resolve the pseudo-
pocket within a few weeks.
Figure 3 shows a radiograph
of a mandibular left second mo-
lar with extensive periodontal
destruction along the distal root
surface extending to the peri-
apical area. A distal periodontal
pocket could be probed directly to
the apex. The tooth was restored
with a rather ill-fitting crown
that had overhanging margins.
Thermal pulp tests were nega-
tive, however, and after a test
JADA, Vol. 126, April 1995 477
CLINICAL PRACTICE

cavity was made, endodontic
treatment was advised. The ill-
fitting crown was removed and
the canals instrumented and
treated with calcium hydroxide.
When the patient was seen again
six weeks later, the pocket no
longer could be probed. The ca-
nals were filled with gutta-
percha and the patient referred
for restorative treatment. Six
months after surgery, radiog-
raphy showed that the repair
was almost complete (Figure 4).
Figure 5 shows the radiograph
of a mandibular right first molar
treatment, it may be that the
diagnosis was incorrect, there is
a true combined lesion or there
is periodontal involvement sec-
ondary to the endodontic lesion.
This involvement may occur
when the prolonged loss of the
sulcular attachment promotes
secondary invasion of plaque
and calculus. In such cases,
either periodontal therapy or
extraction would be indicated.
CASE REPORT
Following is a description of a
purulent discharge was observed
when we probed the distal root
surface, which measured 10 mm
in depth and communicated with
the periapical area (Figure 7).
Probing depths on other surfaces
were 5 mm to 6 mm. Pulp
vitality tests were negative, and
a test cavity confirmed pulpal
necrosis. Although this finding in
a tooth with a full cast restora-
tion may suggest a pulpal
component, it could be secondary
to a primary periodontal lesion,
in which case endodontic treat-
ment would not significantly

Downloaded from jada.ada.org on December 26, 2010

with a large periapical area on
the distal root and extensive
breakdown in the furcation,
which could be probed to the
periapical area. Pulp tests were
negative. The prevalence of
accessory canals in the floor of
multirooted teeth"4'15 commonly
produces furcal lesions in teeth
with necrotic pulps. Endodontic
therapy resulted in dramatic
closure of the pocket within two
weeks. After obturation of the
canals with gutta-percha, radio-
graphs showed a rather large lat-
eral canal communicating with
the furcal area. One year after
surgery, excellent repair was
evident (Figure 6).
Because lesions of endodontic
origin usually are reversible
with endodontic treatment
alone, the temptation to per-
form invasive periodontal pro-
cedures should be resisted; such
procedures might cause further
injury to the attachment and
possibly delay healing. When
marginal lesions fail to respond
to endodontic treatment, addi-
tional instrumentation and con-
tinuation of calcium hydroxide
therapy may be necessary. Clin-
ical judgment should determine
the duration of such treatment.
If endodontic lesions persist
despite exhaustive endodontic
case in which true combined improve the prognosis.
lesions were present. Periodontal On the chance that a true
treatment was performed after combined lesion was present, we
the completion of the endodontic began endodontic treatment with
therapy. calcium hydroxide and contin-
The case involved a mandibu- ued the treatment until its ef-
lar right second molar. The fectiveness could be determined.
radiograph showed a large peri- After three weeks, suppuration
apical area extending coronally was no longer evident in the
on the distal aspect and invol- sulcus. After three months, the
ving the crest of bone. There also distal pocket no longer could be
appeared to be a vertical bony probed to the apex, although
defect between the first and probing depths of 4 mm to 6 mm
second molars, as well as hori- remained on all surfaces. The
zontal bone loss around the endodontic treatment was con-
second molar. The tooth was cluded at that time. We saw the
splinted, so it was impossible to patient again one year after sur-
assess mobility; however, radio- gery, at which time apical heal-
graphically, ing was radiographically evident
there appeared but the vertical defect between
to be little the first and second molars and
osseous support the horizontal
for this tooth. A bone loss re-
mained. Prob-
ing depths re-
Dr. Solomon is a
mained at the
clinical professor of
endodontics at the
Columbia University Dr. Kollart Is an
School of Dental and assitant clinical
Oral Surgery, New professor of endo-
York, and ls In Dr. Chalfin Is chief of dontics at the
private practice at ondodontics at Columbia University
Endodontic Asso- Brookdale Hospital School of Dental and
ciates of Greater Oral Surgery, New
New York P.C., 515
and Medical Conter,
Brooklyn, N.Y., and York, and Is In Dr. Weseley Is In
Madison Avenue, Isin private practice private practice at
:private practice at
Suite 715, New York at Endodontic As- Endodontic Asso-
:Endodontlc Asso-
10022. Addres sociates of Greater clates of Greater
reprint request to New York P.C., New Now York P.C., New
:ciates of Greater
:Nw York P.C., New
Dr. Solomon. York. York.
:York.

478 JADA, Vol. 126, April 1995

 1_Um._iW ,1jI{Xs,.I1l,fr'! |_
CLINICAL PRACTICE-

previous levels (Figure 8).
Resolution of the endodontic
component of these combined
lesions allowed the tooth to be
retained, albeit in a periodon-
tally compromised state. With
lesions of primary periodontal
etiology and secondary pulpal
necrosis (not true combined le-
sions), little or no improvement
would be seen after endodontic
treatment, leaving a very poor
and often hopeless prognosis.
With the advent of guided
tissue regeneration, however,
successful periodontal treat-
may have a favorable prognosis
if they are of endodontic origin.
As the case presented in this
article attests, a thorough diag-
nostic examination usually will
indicate the primary etiology
and, thereby, direct the proper
course of treatment. a
1. Simring M, Goldberg M. The pulpal
pocket approach: retrograde periodontitis. J
Periodontol 1964;35:22-48.
2. Bhashkar SN. Orban's oral histology and
embryology. St. Louis: Mosby; 1991.
3. Simon J, Glick D, Frank A. The relation-
ship of endodontic-periodontic lesions. J
Periodontol 1972;43:202-8.
4. Sinai IH, SoltanoffW. The transmission
of pathologic changes between the pulp and
Periodontol 1965;36:34-8.
8. Czarnecki RT, Schilder H. A histologic
evaluation of the human pulp in teeth with
varying degrees of periodontal disease. J
Endod 1979;5:242-53.
9. Mazur B, Massler M. Influence of perio-
dontal disease on the pulp. Oral Surg Oral
Med Oral Pathol 1964;17:592-603.
10. Langeland K, Rodrigues H, Dowden W.
Periodontal disease, bacteria, and pulpal
histopathology. Oral Surg Oral Med Oral
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11. Lowman JV, Burke RS, Pelleu GB. Pa-
tent accessory canals: incidence in molar
furcation region. Oral Surg Oral Med Oral
Pathol 1973;36:580-4.
12. Brannstrom M. A hydrodynamic mecha-
nism in the transmission of pain producing
stimuli through dentine. In: Andersson DJ,
ed. Sensory mechanisms in dentine. Volume
1. London: Pergamon; 1973:73-9.
13. Kerns DG, Schedit MJ, Pashley DH,
Homer JA, Strong SL, Van Dyke TE. Den-
tinal tubule occlusion and root hyper-

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ment of such lesions may now
be possible.
SUMMARY
Periodontal defects that commu-
nicate with periapical lesions
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Med Oral Pathol 1973;36:558-68.
5. Seltzer S, Bender IB, Ziontz M. Interrela-
tionship of pulp and periodontal disease. Oral
Surg Oral Med Oral Pathol 1963;16:1474-90.
6. Stallard RE. Periodontic-endodontic rela-
tionships. Oral Surg Oral Med Oral Pathol
1972;34:314-26.
7. Rubach WC, Mitchell DF. Periodontal
disease, accessory canals and pulp pathosis. J
sensitivity. J Periodontol 1991;62(7):421-8.
14. Cuenin MF, Scheidt MJ, O'Neal RB, et
al. An in vivo study of dentin sensitivity: The
relation of dentin sensitivity and the patency
of dentin tubules. J Periodontol 62:668-73.
15. Simon J, De Deus QD. Endodontic-
periodontal relations. In: Cohen S, Burns RC,
eds. Pathways of the pulp. 4th ed. St. Louis:
Mosby; 1987: 553-76.

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JADA, Vol. 126, April 1995 479