Wilson M
Department of Microbiology, Eastman Dental Institute for Oral Health Care Sciences, University of London, UK.
Sci Prog. 1995;78 ( Pt 1):19-34.
Chronic periodontitis is a major cause of tooth loss in adults and is a consequence of the colonisation of the subgingival region by organisms such as Porphyromonas gingivalis, Prevotella intermedia and Fusobacterium nucleatum. Lipopolysaccharide (LPS) is a constituent of the cell walls of all of these bacteria and is found in large quantities on the surfaces of periodontally-diseased teeth. LPS from oral bacteria has a marked effect on most types of cell found in the periodontal tissues including macrophages, lymphocytes, fibroblasts and osteoblasts. Fibroblasts and macrophages respond to oral LPS by secreting a range of cytokines, and other effector molecules, with inflammatory, immunomodulatory and tissue-destroying capabilities. Lymphocytes are stimulated by LPS to produce a wide range of antibodies with different specificities, hence exacerbating the inflammatory response. By its actions on bone cells, LPS can stimulate bone resorption and inhibit bone formation resulting in erosion of the tooth-supporting alveolar bone. There is, therefore, considerable evidence implicating LPS in the pathogenesis of chronic periodontitis. However, the possible involvement of other biologically-active bacterial components must not be overlooked.
慢性牙周炎是成年人牙齿缺失的主要原因，是牙龈卟啉单胞菌、中间普氏菌和具核梭杆菌等微生物在龈下区域定植的结果。脂多糖（LPS）是所有这些细菌细胞壁的组成成分，在患牙周病的牙齿表面大量存在。来自口腔细菌的LPS对牙周组织中发现的大多数细胞类型都有显著影响，包括巨噬细胞、淋巴细胞、成纤维细胞和成骨细胞。成纤维细胞和巨噬细胞通过分泌一系列具有炎症、免疫调节和组织破坏能力的细胞因子及其他效应分子来响应口腔LPS。LPS刺激淋巴细胞产生具有不同特异性的多种抗体，从而加剧炎症反应。通过对骨细胞的作用，LPS可刺激骨吸收并抑制骨形成，导致支持牙齿的牙槽骨侵蚀。因此，有大量证据表明LPS与慢性牙周炎的发病机制有关。然而，其他生物活性细菌成分的可能参与也不容忽视。
