Page R C, Schroeder H E
Lab Invest. 1976 Mar;34(3):235-49.
Chronic periodontitis, a common disease of microbial origin, is the major cause of tooth loss in adult humans. The disease serves as a convenient experimental model for analysis of many aspects of chronic inflammation. A consideration of currently available data has permitted the formulation of a new concept of the pathogenesis of this disease. The gingival tissues respond within 2 to 4 days to a beginning accumlation of microbial plaque with a classic acute exudative vasculitis which we have termed the initial lesion. This response, which includes loss of perivascular collagen, is comparable to that elicited in most other tissues subjected to acute injury and may be a consequence of the elaboration and release of chemotactic and antigenic substances by microbial plaque. Within 4 to 10 days, the early lesion develops. It is characterized by a dense infiltrate of lymphocytes and other mononuclear cells, pathologic alteration of fibroblasts, and continuing loss of the connective tissue substance. The structural features of the early lesion are consistent with those expected in some form of cellular hypersensitivity, and a mechanism of this kind may be important in the pathogenesis. The early lesion is followed by the established lesion which develops within 2 to 3 weeks and is distinguished by a predominance of plasma cells in the absence of significant bone loss. The established lesion, which is extremely widespread in humans and in animals, may remain stable for years or decades, or it may become converted into a progressive destructive lesion. Factors causing this conversion are not understood. In the advanced lesion, plasma cells continue to predominate although loss of the alveolar bone and periodontal ligament, and disruption of the tissue architecture with fibrosis are also important characteristics. The initial, early, and established lesions are sequential stages in gingivitis and they, rather than the advanced lesion which is manifest clinically as periodontitis, make up the major portion of inflammatory gingival and periodontal disease in humans.
慢性牙周炎是一种常见的微生物源性疾病,是成年人类牙齿缺失的主要原因。该疾病是分析慢性炎症诸多方面的便利实验模型。对现有数据的考量使得人们能够形成关于这种疾病发病机制的新概念。牙龈组织在2至4天内对微生物菌斑开始积聚做出反应,出现典型的急性渗出性血管炎,我们将其称为初期病损。这种反应包括血管周围胶原蛋白的丧失,与大多数遭受急性损伤的其他组织所引发的反应类似,可能是微生物菌斑产生和释放趋化物质及抗原物质的结果。在4至10天内,早期病损形成。其特征为淋巴细胞和其他单核细胞的密集浸润、成纤维细胞的病理改变以及结缔组织物质的持续丧失。早期病损的结构特征与某种形式的细胞超敏反应所预期的特征一致,这种机制在发病过程中可能很重要。早期病损之后是确立期病损,它在2至3周内形成,其特点是浆细胞占优势且无明显骨质丧失。确立期病损在人类和动物中极为普遍,可能数年或数十年保持稳定,也可能转变为进行性破坏性病变。导致这种转变的因素尚不清楚。在晚期病损中,浆细胞继续占主导地位,尽管牙槽骨和牙周韧带丧失以及组织结构因纤维化而破坏也是重要特征。初期、早期和确立期病损是牙龈炎的连续阶段,它们而非临床上表现为牙周炎的晚期病损,构成了人类炎症性牙龈和牙周疾病的主要部分。