Periodontal disease is now thought by most researchers to be caused by amixed anaerobic infection, modulated by a complex interplay with local andhost factors.Pulpal infection is a polymicrobial process & is of an anerobic nature. As theinfective process proceedes, the proportion of strict anaerobic-to-facultativeorganisms & the total number of bacteria increases.An exception to this rule seems to be the microaerophilic A.actinomycetemcomitans, which has been associated with aggressiveperiodontitis (Newman & Socransky 1977).
Most of the species that have been found in infected root canals can also be present in the periodontal pocket. (Moore 1987, Sundqvist 1994) Porphyromonas endodontalis seems to be very rare in oral infections other than those of endodontic origin. (VanWinkelhoff et al. 1988) Overall, the root canal flora does not appear to be as complex as the periodontal flora of adjacent pockets. However, it is inherent problems in bacterial sampling of periodontal pockets that strains from more shallow levels of the site are harvested along with the strains at the front of the lesion.
Necrosis of the pulp, however, can result in bone resorption and theproduction of radiolucency at the apex of the tooth, in thefurcation or at points along the root.The lesion that results may be: an acute apical lesion or abscess, a more chronic peri-radicular lesion (cyst or granuloma) or a lesion associated with a lateral or accessory canal.The lesion may remain small, or it can expand sufficiently todestroy a substantial amount of the attachment of the toothand/or to communicate with a lesion of periodontitis.
Different authors have created varying nomenclatures for thesepathologies, based on either etiological or clinical criteria, or acombination of these factors.Simon et al. (1972) separated the lesions of both periodontal andpulpal tissues into the following groups: Primary endodontic lesions with secondary periodontal involvement, Primary periodontal lesions with secondary endodontic involvement, and True combined lesions.
Appropriate endodontic therapy is sufficient to result inhealing of the lesion.Occasionally an abscess of pulpal origin, through an apical orlateral canal, may establish drainage through theperiodontal ligament & erupt into the furcation or thegingival sulcus.
(A)Preoperative radiograph showing large periradicular radiolucency associated with the distal root and furcal-lucency.(B)Clinically, a deep narrow buccal periodontal defect can be probed. Note gingival swelling.(C)One year following root canal therapy, resolution of the periradicular bony radiolucency is evident.(D)Clinically, the buccal defect healed and probing is normal.
Chronic periodontitis progresses apically along theroot surface.In most cases, pulp tests indicate a clinically normalpulpal reaction.The prognosis depends upon the stage ofperiodontal disease and the efficacy of periodontaltreatment.
The progress of periodontitis is slow.The involvement of apical periodontium by the pulpal lesion mayobscure the symptoms of the periodontium.Because the apical lesion tends to be the most painful lesion,endodontic therapy is normally initiated first.Endodontic therapy results in the resolution of the endodonticlesion , but has little or no effect on the periodontal pocket, anappropriate periodontal therapy is required for a successful result.
Such lesions may present with the characteristic of bothdiseases, which may complicate diagnosis & treatmentplanning.The extent to which the periodontal lesion contributes to theloss of bone is a key consideration in diagnosis & treatmentplanning
(A) Preoperative radiograph showing periradicular radiolucencies. Pulp sensitivity tests were negative.(B) Immediate postoperative radiograph of nonsurgical endodontic treatment.(C) Six-month follow-up radiograph showing no healing. Gutta-percha cone is inserted in the buccal gingival sulcus.(D) Clinical photograph showing treatment of the root surfaces and removal of the periradicular lesion.(E) One-year follow-up radiograph demonstrating healing.