This PP T is all about how to treat Endo Perio cases

1. Copyright NSU College of Dental Medicine.
Materials provided herein are protected under
United States copyright laws and are for the
explicit use of the College of Dental Medicine.

2.  Tooth and periodontium form a biologic
unit, an organ; disease in one affects the
other.
 Periodontic-Endodontic lesions are found
simultaneously in both the peri- and
endodontic spaces.
Periodontic-Endodontic Lesions

3.  Lesions of the periodontal ligament and
adjacent alveolar bone may originate from
infections of the periodontium (Periodontitis)
or tissues of the dental pulp.
Periodontic-Endodontic Lesions

4. Anatomical Pathways
Connecting
Endodontic & Periodontal Tissues
 Apical Foramina
 Accessory Canal
 Exposure of Dentinal tubules
 Enamel-cementum disjunction,
periodontal diseases, SRP

5. 8.8 %
1.6 %
17 %
Frequency of Accessory Canals
 Accessory canals were found
in approximately 27% with
the highest prevalence on the
apical third.
 28.4% of the teeth exhibited
patent accessory canals in
the “furcation region”
(29.4% mand / 27.4% max).
De Deus, 1975

6. Accessory Canals
 The inflammatory process is not always
circumscribed at the apex. It may appear
along the lateral aspect of the root or furcal
area.
 This process is induced and maintained by
bacterial byproducts
that could reach the
periodontium through
accessory canals.

7. Dentinal Tubules
 The ability of the pulp and
periodontium to
communicate via dentinal
tubules is possible, specially
where cementum was
denuded (after repeated S&RP).
 Many authors have
suggested that an
interrelationship does exists
once the integrity of the
dentinal tubules is violated.

8. Dentinal Tubules Vs. Accessory Canals
Dentinal
Tubules
Accessory
Canal

9. Furcation Foramina

10.  Simon provided a classification for
periodontic-endodontic lesions based
on possible etiology, diagnosis, and
prognosis.
 Theoretically delineates five types of
lesion formation that are interrelated.
Simon et al (1972)
Classification

11. ENDODONTIC
LESIONS
PERIODONTIC
LESIONS
Endodontic lesions with
secondary periodontic
involvement
COMBINED LESIONS
(“True” combined lesions)
Periodontic lesions with
secondary endodontic
involvement
Simon et al (1972)

12. Primary Endodontic Lesion
Characterized by:
 Necrotic pulp
 Localized osseous destruction.
 Pulp necrosis and secondary periradicular
disease may produce destruction of
periodontal tissues with formation of a
sinus-like tract through the periodontium.
 Fistulation through the apex or a lateral
canal may cause furcation involvement.
 Excellent prognosis for re-attachment.

14. Drainage of endodontic abscess into
the sulcus follows one or two routes:
Extraosseous fistulation
Periodontal
ligament
fistulation

16. Effect of Pulpal Disease on the
Periodontium
 Pulp disease can cause periradicular
pathosis (inflammation)
 Bone loss and/or drainage through
sulcus can mimic periodontal
disease

17. Periodontal ligament
Fistulation

18. Primary Endodontic Lesion w/Secondary
Periodontal Involvement
 Existing endodontic
lesion with secondary
periodontal
involvement due to
plaque and calculus
accumulation
beginning at the
cervical area.

19. Calculus
If this lesion was considered for endodontic
treatment – it is necessary to complete “closed” root
planing if there is to be any osseous regeneration

20. Retrograde Periodontitis
 Pulpal infection may cause
a tissue destructive process
that proceeds from the
apical or furcal region of a
tooth toward the gingival
margin, as opposed to
marginal periodontitis in
which infection spreads
from the gingival margin
toward the root apex.

21. Primary Periodontal Lesion
 Lesion caused by periodontal
disease. Periodontitis gradually
progresses until the apical
region is reached.
 Characterized by:
 Vital pulp
 Generalized bone loss
 Local factors present:
 Plaque, calculus
 Developmental defects (palato-
gingival groove)
 Prognosis for re-attachment
more questionable

22. Primary Periodontic Lesion
w/Secondary Endodontic Involvement
 Primary periodontal lesion
leading to exposure of a
lateral canal to the oral
environment with the
resulting pulpal infection and
necrosis.
 Could be the result of
periodontal procedures in
very deep lesions where the
vasculature (apical or lateral)
is severed by an instrument.

23. Primary Perio Lesion W/
Secondary Pulpal Disease

24. “True” Combined Lesions
 This lesions occur where
an endodontically induced
periapical lesion exists on a
tooth that is also
periodontally involved.
 Radiographically the two
entities meet and merge
somewhere along the root
surface.
 Very difficult to diagnose.

25. TRUE COMBINED

26. Pathogenesis
Pulpal
disease
Periodontal
disease
SHARED
ETIOLOGY
Microbiologic Immunologic

27. Microbiology
 Similar to periodontal disease, potential pathogens
most often associated with endodontic infections are
found in the anaerobic segment of the flora. The
microorganisms most commonly involved in the
causation of both periodontal and pulp lesions are:
Fusobacterium
Prevotella
Porphyromonas
Peptostreptococcus
Eubacterium
Capnocytophaga Lactobacillus
SPIROCHETES

28. Microbiology
 The microorganisms associated with periodontal
lesions also may be capable of producing necrosis of
pulp cells through the action of their metabolic
products, destructive enzymes, or other mechanisms.
 Porphyromonas and Prevotella species induce the
activation of macrophages which subsequently
produce interleukin-1. This mediator may enhance
bone resorption and perpetuation of the combined
pulp-periodontal lesion.

29. The following
entities or
pathways have
also been
mentioned in the
literature as
possible causes
of endo-perio
lesions
 Palato-gingival grooves
 Periodontal Therapy (S/RP)
 Root anomalies (microcracks)
 Trauma induced root resorption
 Fractures
 Perforations
 Over-instrumentations,
 Debris extrusion
Predisposing Factors that
Contribute to Endo- Perio Lesions

30. Palato-Gingival Grooves
Low incidence in
maxillary centrals and
laterals.
 43% of the grooves
extended less than 5mm
 47% extended 6-10 mm
 10% over 10mm
Kogan,1986

31. Trauma-Induced Root Resorption
 Trauma
 Necrotic pulp
 Injury to cementum
and periodontium
 Rapid root
resorption

33. Cracked Tooth
 Fracture resulting from external (occlusal) load
 Direction of fracture usually M-D

34. Vertical Root Fracture
 Fracture resulting from internal load
 Direction of fracture usually B-L

35. Vertical Root Fracture

38. Root Perforations
 During RCT and preparation for the insertion
of posts, instrumentation can accidentally
cause perforation of the root and wound the
PDL.
-  Mobility
-  Probing depth
- Loss of fibrous attachment
- Suppuration
 If undetected or unsuccessfully treated the
periodontal signs of root perforation are:

40. Endodontic Therapy
 Endodontic etiology should be taken into
account when breakdown of periodontal
tissue, specially if associated with poor
quality RCT.
 Periodontal pockets can be non-responsive
to periodontal therapy, showing retarded or
impaired healing due to periapical pathology
or failing endodontic therapy.

41. Effects of Periodontal Disease
on the Pulp
 Perio disease may irritate the pulp
 Increased secondary dentin, pulp stones, dystrophic
calcification, fibrosis and collagen resorption .
 All may be age related, or more related to the tooth's
past Hx such as caries and resultant operative
procedures.
 Perio disease is inflammatory, but does not
appear to have a direct inflammatory effect on the
pulp.
 Except when perio disease is severe enough to
compromise the root apex, then pulp necrosis and
inflammation can ensue.

42. Effect of Perio Tx on the Pulp
 Unless root planing is invasive (either
significantly deep layers of dentin removed,
or severance of apical vessels), it is
doubtful perio Tx results in significant
pathologic changes in the pulp. *
 Most studies have found no pulpal changes
in presence of perio disease.**
*Bergenholtz and Lindhe,1978
**Mazur and Massler, 1964
Czarnecki and Schilder, 1979
Torabinejad and Kiger,1985

43. Effect of Endo Tx on the
Periodontium
 Iatrogenic alterations of the periodontium
 Perforations, Over-instrumentations, Debris
extrusion
 Vertical root fracture
 Cause is excessive internal force either during
obturation or post placement
 Results in narrow probing defect
 RC contents may delay healing in perio Tx

44. Diagnosis

46. Diagnostic Considerations
 Is the tooth vital?
 Is the lesion localized or generalized?
 Periodontitis usually more generalized.
 Endodontic lesion and/or endo-perio lesions more
localized.
 Is there a periodontal pocket?
 Probe prior to endo therapy to rule out vertical
fracture or developmental anomalies.
 Isolated deep pocket surrounded by a normal
sulcus is indicative of a vertical fracture.

47. Diagnostic Considerations
 Radiographic presence of severe pulpal
calcifications ?
 Pulpal pathology may be secondary to perio
pathology
 Is there apical resorption or condensing
osteitis in the radiograph?
 Suggestive of pulpal pathology
 What are the pain symptoms
 Endo: Acute, sharp
 Perio: Chronic, dull, tolerable

48. Treatment
 Therapy is directed toward the
removal of the etiologic factors
responsible for the tissue destruction.
 Essential in the prognosis is the origin
of the pathosis

49.  Treatment of perio-endo lesions is a
combination of conventional
treatment for each separate lesion:
 Root Canal Treatment
 Scaling and Root Planing
 Regenerative Procedures
 Treatment involves always
completing the endodontic therapy
before the periodontal treatment.
Treatment

50. Endodontic Lesion
Clinical Findings
 Periapical bone loss
 Drainage through the
sulcus
 Pulp test negative
 Rapid onset
 Inadequate root canal
 Periodontal probing
yields narrow, isolated
pocket
Treatment
Endodontic Treatment only

51. Endodontic Lesion with secondary
Periodontal disease
Clinical Findings
 Necrotic Pulp
 Periodontitis with plaque
and calculus
 Pulp test negative
 Increase in pocket depth
and attachment loss
 Rx evidence of pulp and
periodontal disease
Treatment
 First: Endodontic
treatment, evaluate.
 Then: Periodontal
treatment
 Initially a closed
procedure
 Revaluation 4-6 weeks
post treatment

53. Periodontal lesion
Clinical Findings
 History of disease
progression/therapy
 Deep pockets
 Attachment loss
 No evidence of pulpal
disease
 Pulp test positive
Treatment
 Periodontal treatment
only

54. Periodontal Lesion with secondary
Endodontic disease
Clinical findings
 Deep pockets
 Extensive attachment
loss
 Pulp disease:
increase pain, pulp
test negative
 Rx evidence
Treatment
 First: Endodontic
treatment, evaluate.
 Then: Periodontal
treatment
 Not very common
unless the disease
involves the main
pulpal blood supply

55. Combined Lesion
Clinical findings
 Etiologic factors present
for both conditions
 Generalized periodontal
destruction that connects
to periapical lesion
 Pulp test negative
 Root Fracture
Treatment
 Root Canal therapy
 Periodontal therapy
 Extraction?

56.  The major determinant of successful
treatment of periodontic-endodontic
lesions is the chronicity of the periodontal
component.
 Typically, bone loss of endodontic origin
has a better prognosis than periodontal
origin, because.
 Endodontic Lesions are generally acute.
 Periodontic lesions are generally chronic.
 Intact periodontium (JE and CT attachment) is the best
barrier.
Treatment

57.  The character of the clinical symptoms
may occasionally be confusing and cause
misinterpretation of their etiology.
 The clinician should, therefore be well
acquainted with the pathogenesis as well
as with available diagnostic measures
aimed at identifying disease conditions of
these tissues.
Periodontic-Endodontic Lesions