Hirsch R S, Clarke N G
Department of Dentistry, University of Adelaide, South Australia.
Int Endod J. 1993 Nov;26(6):362-8. doi: 10.1111/j.1365-2591.1993.tb00770.x.
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.
目前认为，牙周炎的进展发生在活动期，随后是缓解期，在此期间可能会出现愈合。这一概念与过去的假说形成对比，过去认为牙周炎在一生中持续但缓慢地进展。目前，没有证据支持传统的（微生物学）假说，该假说认为特定部位的细菌在附着丧失发作的起始中起主要作用。本文提出了另一种假说，该假说通过独立于菌斑的途径来解释牙周附着丧失。由牙髓病变（根尖周炎和逆行性牙周炎）引起的严重牙周组织病变已知可在牙周组织的任何水平形成，而不仅仅是在根尖。当这些病变导致牙槽嵴处的牙周组织破坏，并且同时存在菌斑、牙石和牙龈炎时，很少怀疑其牙髓源性。本文提出了三种途径来解释牙髓疾病导致的局限性牙周附着丧失的发展。这一假说解释了在定期检查下牙周部位的突然恶化、牙槽骨缺损的严格定位（紧邻正常牙槽骨）、特定部位细菌（深牙周袋的继发性定植菌）的存在（当转移到健康部位时不会致病）以及针对它们的抗体反应。
