Endodontics
Course Review
Enoch Ng, DDS 2014
Endo-Perio
Pulpal/Perio Communication
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Dentinal tubules
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Accessory canals
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27.4% of teeth have accessory canals
Apical area – 17%
Middle third – 8.8%
Coronal third – 1.6%
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28.4% molars (Mx and Mn) have accessory furcation canals
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Apical foramina
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Palatal groove
Pulpal Perio Disease
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Bacterial infection of the pulp system induces significant inflammatory and immune response in apical tissues
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Untreated endodontic disease may support an increase in:
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Pocket depth
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Bone loss
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Perio treatment of teeth with pulpal necrosis and ARL resulted in delayed or impaired perio healing
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If blood supply through apical foramen is intact, perio disease rarely jeopardizes vital function of pulp
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Pulpal inflammation can come from exposure of lateral canals
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Pulpal necrosis results from main apical foramen invaded by bacteria
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Potential exists for S&RP to open dentinal tubules – indirectly induce localized pulpitis
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Microorganisms found in infected root canals of caries-free teeth with advanced perio usually resemble those
found in adjacent perio pockets
Endodontic Lesions
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Endo lesions associated with inflamed/necrotic pulp with distinct etiology for pathosis
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Caries, restorations, cracks, trauma, attrition, abrasion, erosion
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Perio lesions usually associated with local factors that induce inflammation
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Bacteria, plaque, calculus
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Periodontal origin – generalized, broad lesions
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Pulpal origin – narrow coronally, isolated
Glickman’s Classification
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Grade I – engaged flutes – pocket formation into the flute of the furca, but interradicular bone intact
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Grade II – engaged roof – loss of interradicular bone, pocket formation of varying depths into furca but not
completely through (dead end, cul de sac)
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Grade III – probe thru – complete loss of interradicular bone with a pocket probable to opposite side of tooth
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Grade IV – see thru – grade III with advanced gingival tissue recession that has made furca clearly visible during
clinical Exam