Smalley J W
Department of Clinical Dental Sciences, The University of Liverpool, UK.
Adv Dent Res. 1994 Jul;8(2):320-8. doi: 10.1177/08959374940080022801.
Periodontal diseases have been considered as "infections" in which micro-organisms initiate and maintain the destructive inflammatory response. Host-mediated tissue destruction occurs via complement activation and the release of lysosomal enzymes, and connective tissue matrix metalloproteinases. Microbial enzymes may damage connective tissues directly, and, together with toxic metabolites and structural materials, are thought to disrupt the reparative activities of fibroblasts and cells of the immune defenses. The significance and relative contributions of host and microbial factors to the disease process remain unresolved. Environmental changes in the gingival sulcus and periodontal pocket and tissues, the degree of the host response and nutrient availability, concomitant with disease progression, compromise tissue metabolism and repair, and allow for enhanced or de novo expression of microbial virulence factors, such as proteases, which alter microbial pathogenicity. Proteolytic destruction of specific antibodies and complement by both viable and non-viable bacterial cells may retard phagocytic killing and removal of pathogens, thus prolonging the inflammatory response. Bacterial products may indirectly mediate tissue destruction by stimulating release of matrix metalloproteinases or by proteolytically inactivating the specific inhibitors of these enzymes.
牙周疾病被视为“感染性疾病”，其中微生物引发并维持破坏性的炎症反应。宿主介导的组织破坏通过补体激活、溶酶体酶释放以及结缔组织基质金属蛋白酶发生。微生物酶可能直接损害结缔组织，并且与有毒代谢产物和结构物质一起，被认为会破坏成纤维细胞和免疫防御细胞的修复活动。宿主和微生物因素在疾病过程中的重要性及相对作用仍未明确。随着疾病进展，牙龈沟和牙周袋及组织中的环境变化、宿主反应程度和营养可用性，会损害组织代谢和修复，并使微生物毒力因子（如蛋白酶）的表达增强或重新表达，从而改变微生物致病性。活细菌和死细菌细胞对特定抗体和补体的蛋白水解破坏可能会阻碍吞噬细胞对病原体的杀伤和清除，从而延长炎症反应。细菌产物可能通过刺激基质金属蛋白酶释放或通过蛋白水解使这些酶的特异性抑制剂失活来间接介导组织破坏。
