this lecture shows the relation between periodontal and pulpal tissues, pathways of transmission of bacteria and the different lesions of endodontic periodontal lesions.

1. -ENDODONTIC
INTER-RELATIONSHIP
Dr. Diana Mostafa Abo EL Ola

2. What causes PULPAL DISEASE!!
1. Instrumentation during periodontal, restorative
procedures, or prosthetic procedures.
2. The progression of dental caries to pulp.
3. Direct, local trauma(e.g tooth fracture)

3. P. state Symp. Pulpal
status
Percussion Palpation Periapical
radiolucency
Sinus
tract
Acute PP pain Infl. pain varies None None
Chronic PP none Non vital None None present None
Acute PA pain Infl./non
vital
Pain painful varies None
Chronic PA none Non vital None None Present present
Condensing
osteitis
none/pa
in
Infl. None None Radiopaque None
Classification of periradicular diseases

4. Anatomic pathways
Non- physiologic
pathway
-Apical foramen , accessory/lateral
canals.
-Congenital absence of cementum
-Developmental groove
-Iatrogenic root canal perforation,
root planning cause exposure of
DT.
-Vertical root fracture .
-Root caries or resorption.

5. • Pulp becomes inflamed or necrotic
• inflammatory by-products go through:
• The apex
• Lateral and accessory canals
• The dentinal tubules
Inflammatory vascular response in the periodontium

6. 1-Apical Foramen
• is the principal direct communication bet. the pulp &
periodontium.
• Bacterial & its byproducts the apical foramen break down
of PD tissues periradicular bone loss infection extension to
external mucosa sinus tract.
“Retrogarde periodontitis” apical to cervical
IF a portal of entry of infl. byproducts from deep PD pockets to
the pulp " Orthograde periodontitis” cervical to apical

7. 2-Lateral and Accessory
Canals
30-40% of all teeth have these canals & the majority
in the apical 1/3 of the root.
It leads to chronic pulpal disease  CPP
BUT
rare to have PD disease reaching pulp through it.

8. 3-Dentin Tubules
Exposed DT in areas of denuded cementum
( hypersenstivity )
as a result of PD disease & SRP root resorption surgical
procedures developmentally absence of CEJ
serve as communication pathways between the pulp & PDL
• In the root, DT extend from the pulp to the DCJ. They
range in size from 1 -3 microns in diameter (bacteria and
their toxins are smaller in size)invasion from PD pocket
pulpal irritation.

9. • The following classification system was developed by
Simon, Glick and Frank in 1972:
o Primary Endodontic Disease
o Primary Periodontal Disease
o Primary Endo w/ Secondary Perio lesion
o Primary Perio w/ Secondary Endo lesion
o True Combined Lesions
1ry endo 1ry perio 1ry endo, 2ry perio
1ry perio, 2ry endo
True combined

10. • Endodontic problem with fistulization from the apex to the
gingiva. (patient is free from PD disease)
Causes: caries-restoration-trauma(fracture)
Examination:
-Symptoms : discomfort
-Probing: Not true PD pocket but fistula along
PDL into sulcus. narrow Sinus tract can be
probed with GP.(minimum/ no local factors)
-Vitality tests:-ve
-Radiographs: apical/ lateral / furcation radiolucent
resorbed bone lesion
Treatment:- conventional RCT.
Prognosis: excellent

11. Pre-op :-periapical and furcation +
a deep narrow periodontal defect
-ve vitality test
1 year follow-up: complete healing of buccal
defect.
Radiolucency in periapical
and furcation area RCT Excellent results
Case 2
Case 1

12. Caused by PD pathogens( progression of chronic periodontitis
apically along the root)
Examination:
• Symptoms: discomfort dt PD dis.
• Probing: Frequently accumulation of plaque & calculus +
wider deep PD+ tissue infl.
• Vitality tests : normal pulpal reaction(+ve)
• Radiograph: wide lateral radiolucent lesion+
horizontal /angular bone defect
• Treatment:-
1. PD therapy
2.GTR
3.Root amputation & hemisection
• Prognosis: depends on PD therapy.

13. Pre-op: alveolar bone loss + a periapical lesion, a
deep wide pocket was traced on the mesial
aspect of the root, the tooth tested vital
The tooth was extracted. Note the deep
mesial radicular developmental groove
Vitality test: Positive
Case 1
Case 2

14. It was referred for RCT. The
tooth tested vital to cold
Dentist insisted that endo be done.
However, since the etiology was PD
disease, no bony healing took place
After perio. therapy
Pre-op: periodontal Abscess
Same

15. It was referred for RCT. The
tooth tested vital to cold
Dentist insisted that RCT should be done.
However, since the etiology was PD
disease, no bony healing took place
After perio. therapyPre-op: periodontal Abscess
Same
Case 3
Case 4

16. Pulpal Periodontal
Etiology Pulp infection PD infection
Vitality Non vital Vital
Caries or
Restorative
Deep or
extensive
Not related
Plaque/
Calculus
Not related Primary cause
Pockets Deep Narrow Wide coronally
Bone loss Localized
Wider apically
Generalized(GCP)
Wider coronally
Periapical x-ray Radiolucent Not related(lateral)
Rx RCT PD Rx

17. When suppurating 1ry Endo. Dis. remains untreated, it becomes 2ry
involved with PD breakdown through the apical foramen, accessory &
lateral canals >>>>"retrograde periodontitis”
example
-Root fractures/perforations causes plaque acc.periodontitis.
Diagnosis:-
• Vitality test :-ve
• Probing: Deep wide periodontal pockets
• Radiographs: apical/lateral/furaction radiolucent lesion+
angular defect.
Treatment: RCT + PDT{root planning}.
Prognosis: depends on PD status

18. Pre-op: inter-radicular defect extends to the
apex appeared on x-ray while using GP.
After 1 yr: resolution of most of the
periradicular lesion but a bony
defect at the furcation area
remained. PDT is necessary for
complete healing.
After PDTBone loss and deep pockets After RCT
Case 1
Case 2

19. PD pocket can infect the pulp(may become necrotic) through a
lateral canal/DT/AF periapical lesion.
Examination
• Vitality test : irreversible /necrotic pulp. Intact crown
• Probing: Deep pocket formation + history of periodontitis
• Radiographs: angular bone loss
• Treatment: RCT+ PDT.
• Prognosis: depends on periodontal therapy.

20. Post-op :That lateral canal
served as a potential pathway
for bacteria.
Pre-op: Bone loss + periapical
radiolucency. The crown was intact,
but –ve vitality test.

21. • When an endo. Dis. progresses coronally joins with an
infected PD pocket progresses apically.(dt left untreated )
Examination :
• Symptoms: pain
• Vitality : -ve
• Probing: Deep pockets
• Radiograph :two lesions joined together
Treatment: repair and regeneration -extraction/root
resection.
The prognosis : depend on PD state but it is poor, esp.
for single or multiple rooted teeth????

22. After GTR proceduresFlap retraction was done as there was minimal improvement
After RCTFurcation inv. & facial pocket in non vital tooth Pocket detection by GP

23. How to Diagnose!
• Most important considerations:
• Patient symptoms( reversiblepulpitis:general sensitivity- irreversiblepulpitis sever
spontaneous throbbing pain - pulp necrosis, abscess feels tooth is elevatedfrom socket)
• Coronal integrity (restoration, caries, preparation )
• Shape and size of radiographic lesion and use of GP.
• Periodontal probing
• Tooth vitality
• Percussion , palpation and sinus tracking
• Cracked tooth testing: transillumination, tooth-slooth, MB staining.

24. The management of acute PD abscess:
• Drainage via PD pocket+ subgingival root planning
+curettage
• If it is large & fluctuant→ surgical flap/incision
• If extensive bone loss>>>hopeless → extraction
• Pulpectomy + Ca hydroxide /incision
The management of pericapical abscess:
Antibiotics indication:
Fever- Cellulitis- Systemic disease –Immunocompromised
patients
Penicillin /amoxicillin + metronidazole…..the common choice
Clindaymicin……..excellent
NSAD…….for controlling pain