Pulpal disease and bursts of periodontal attachment loss

Progression of periodontitis is currently thought to occur during bursts of activity, followed by periods of remission, when healing may occur. This concept contrasts with the older hypothesis that periodontitis was continuously, but slowly, progressive throughout life. At present, there is no proof of the conventional (microbiological) hypothesis which gives a major role to site-specific bacteria in the initiation of bursts of attachment loss. An alternative hypothesis is presented in this paper which accounts for periodontal attachment loss by pathways that are independent of plaque. Severe lesions of the periodontium caused by pulpal pathoses (apical and retrograde periodontitis) are known to form at any level of the periodontium, not only at the root apex. When these lesions cause destruction of the periodontal tissues at the alveolar crest, and when plaque, calculus and gingivitis are also present, an endodontic origin is rarely suspected. Three pathways are proposed to account for the development of localized periodontal attachment loss consequent to pulpal disease. This hypothesis accounts for the sudden deterioration of periodontal sites under regular review, the strict localization of alveolar defects with normal alveolar bone immediately adjacent, the presence of site-specific bacteria (secondary colonizers of deep pockets) which cannot cause disease when transferred to healthy sites, and the antibody responses directed against them.