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題名 | 牙周病--病因與病理=Periodontal Disease--Etiology and Pathogenesis |
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作者 | 蔡吉政; 吳逸民; 侯桂林; 王俊欽; | 書刊名 | 臺灣口腔醫學會雜誌 |
卷期 | 13:2 1997.12[民86.12] |
頁次 | 頁35-64 |
分類號 | 416.946 |
關鍵詞 | 牙周病; 牙周炎; Periodontal disease; Periodontitis; |
語文 | 中文(Chinese) |
中文摘要 | 牙菌之堆集引起牙齦發炎及產生趨化因子,這些因子進入組織內, 活化了血管 粘著因子及血中循環之炎性的與免疫的細胞。結果使不同的細胞,開始為嗜中性白血球,再 隨著為巨噬食細胞及淋巴球進入牙周組織。控制炎性的與免疫的反應,可能主要還是在牙周 組織的範圍內,各種不同的宿主來的破壞機轉可能助於炎性及傷口癒合的過程。炎性過程具 有強的組織破壞潛能。結締組織可為酵素如從嗜中性白血球或造纖維細胞來的膠原蛋白�t所 破壞。骨之破壞則可因細胞激素及炎性介質,例如,介白質 - β及前列腺素 E �砟妞﹞あ� 引起。當這些過程繼續進行時,在接合上皮之上皮細胞則向牙根尖移動,以上所言只是大略 的指出由在牙齦緣的細菌堆集能導致牙周炎。事實上,各種過程關係到一系列的複雜的交互 作用,這些作用是決定何時及如何發生病變。本文陳述牙周病的病因與病理學供大家參考 。 |
英文摘要 | Plaque accumulation initiated the gingival inflammation and produced factors which enter the tissue and activate adhesion molecules on the blood vessels and on the inflammatory and immune cells circulating in the blood. This results in sequential influx of different cell populations begining with PMNs and followed by macrophages and lymphocytes. The control of the full oxpression of the inflammatory and immune responses may be mainly in the local periodontol environment. A wide variety host-destructive mechanisms to assist in both the inflammatory and wound-healing process may be involved. The inflammatory process hase the potential to be very destructive. Connective tissue is destroyed by enzymes such as collagenase from PMNs and fibroblasts. Bone destruction is activated by cytokines and inflammatory mediators such as IL-1 β and PGE2. As these processes are continuing, the epithelial cells in the junctional epithelium are migrating in an apical direction. These are just a broad strokes of processes that bacterial accumulation at gingival margin can lead to periodontitis. Actually, each of processes involves a series of complex interactions that responsible for when and how the process acts. The present review briefly describes the etiology and pathogenesis of periodontal diseases. |
本系統之摘要資訊系依該期刊論文摘要之資訊為主。