內毒素與牙周病的關係

脂多醣或內毒素（Lipopolysaccharides, LPS or Endotoxin）是一種發現於革蘭氏陰性細菌細胞膜的生物活性分子，此物質藉由與宿主細胞的結合而產生作用。據了解，將純化之脂多醣注入動物體內，會導致其系統性休克。至於內毒素之局部反應，同樣以發炎和免疫反應為特徵，特別是血管方面的改變。牙周炎其特徵為造成牙周組織的破壞，而革蘭氏陰性細菌已被認為是造成牙周炎及於牙周炎之進展中的一種重要的致病菌。這致病菌的毒性來自於其細胞膜的諸多成份，尤其是內毒素。內毒素可以誘發細胞產生一些炎前細胞激素（cytokine），如TNF、IL-6、IL-8及IL-1等，對參與牙周炎等發炎疾病之產生，內毒素是主要的致病介質。雖然內毒素也許不會直接作用於破骨細胞之上，但內毒素極有可能藉由激發牙齦及牙周細胞釋放許多細胞激素及前列腺素，而使組織被破壞。本文獻回顧乃探討內毒素其可能誘發的細胞激素與牙周炎之間交互作用的關係。

關鍵字

脂多醣；牙周炎；細胞激素

並列摘要

Lipopolysaccharides (LPS) is a biologically substance found in the cell walls of Gram negative bacteria. LPS exerts its effects by binding to host cells. The consequence of LPS stimulation can be severe, as injection of purified LPS into animals elicits an inflammatory response that can lead to systemic shock. Local reactions to endotoxin are also characterized by inflammatory and immune reponses. More specifically, vascular change occur, which are accompanied by recruitment of leukocytes and the subsequent release of proinflammatory mediators, such as TNF, IL-6, IL-8, and IL-1, which are the major pathological mediators of inflammatory diseases, incuding as periodontal disease. Periodontitis is characterized by the loss of tooth-supporting tissue and alveolar bone destruction. Gram-negative bacteria have been considered to be important pathogenic microorganisms in the initiation and development of periodontal disease. The virulence of this pathogen is attributed to many of its cell wall components, especially LPS. Although LPS may not directly stimulate osteoclasts, it is possible that LPS could induce osteoclast activity indirectly be first stimulating other cell types such as gingival cells, periodontal cells to release cytokines and prostaglandin. This review article discussed the relationship between LPS and cytokines derived from cells which can be divided into 6 groups, and the interaction between periodontal tissue and cytokines.

並列關鍵字

Lipopolysaccharides ； LPS ； cytokines ； periodontitis

國際替代計量

內毒素與牙周病的關係

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