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題 名 | 骨性關節炎基礎醫學之探討(2):生化學, 免疫學, 細胞學之觀點 |
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作 者 | 楊卿潔; 林永福; | 書刊名 | 中華民國物理治療學會雜誌 |
卷 期 | 16:1 1991.03[民80.03] |
頁 次 | 頁8-18 |
專 輯 | 膝部骨性關節炎專題討論 |
分類號 | 416.61 |
關鍵詞 | 生化學; 免疫學; 骨性; 基礎醫學; 探討; 細胞學; 關節炎; 觀點; |
語 文 | 中文(Chinese) |
中文摘要 | 骨性關節主要侵犯關節軟骨,是人類最常見的關節病變。了解正常關節 軟骨的生化學,免疫學及細胞學是獲知病因,治療及預防方法的不二法門。 過去認為骨性關節炎是一種單純的機械性磨損的現象,而且認為骨性關節炎是年 老過程中必然的現象。然而現在我們知道老化與骨性關節炎之間仍存有相當大的 差異;對於骨性關節炎也將它視為一個關節面損害與修補的平衡。過去因為關節 面軟骨特殊地處於與外界隔絕的環境而認為免疫系統與骨性關節炎的致病機轉 無關;但現在則認為免疫系統中,體液免疫與細胞免疫的合作在骨性關節炎的病 理發生上扮演了一個重要的角色。 近來細胞學的研究顯示骨性關節炎中的軟骨細地已起了基因上的變化,變得比較 趨向於軟骨母細胞的性質。多醣蛋白更迭率的增加及流失量的增加均是骨性關節 炎中軟骨基質常見的現象,而此現象據信乃由軟骨細胞所控制。第一類白血球間 質素(Interleukin-I)及其它細胞激素(Cytokine)可以控制包括軟骨細胞在內的許多細 胞的生長分化,因而被認為和軟骨細胞新陳代謝的加速有關。多醣蛋白的流失 量,更迭率的增加及軟骨細胞受傷後發生的惡性循環都與細胞激素有關。 軟骨細胞的培養技術,骨性關節炎的標誌(marker)的發現,單株抗體的應用使得 我們深信在幾年內對於骨性關節炎的細胞生物學及其致病機轉必有更透澈的瞭 解。 |
英文摘要 | Osteoarthritis involves mainly the articular cartilage and is the most common of various articular disorder affecting man. Understanding the biochemistry , immunology andcytology of normal articular cartilage is thekey to discover the etiology, to develop methods of treatment and to pave ways for prevention of osteoarthritis. It was once held that osteoarthritis is a phenomenon of passive wear and tear and is almost an inevitable consequence of aging.However, we now come into that there aresome differences between cartilages of osteoarthritis and aging and that osteoarthritisshould be considered as a balance between'destnictions' and' repairs' of the cartilage. For many years, immune mechanism was believed to be unrelated to the etiology of osteoarthri tis for the isolated environment of cartilage. However, reports have revealed that cartilage is immunogenic and that synergism between cellular and humoral immunity plays signifi cant roles in the pathogenesis of osteoarthritis. It has been shown in advanced cytological studies that chondrocytes, in osteoarthritic car tilages, have undergone genetic changes andbeen changed into a more osteoblastic state.Increased turn-over rate of proteoglycans andincreased loss of proteoglycans from matrixcan be demonstrated in osteoarthritic cartilagesand is proved to be controlled by chondrocytes. Interleukin-I, tumor necrotic factor andother cytokines constitude "a polypeptidemediator network" and appear to "regulategrowth, differentiation, and function ofmesenchymal cells as well as cells involvedin immunity, imflammation, and hematopoiesis". These cytokines, released from cells ofsynovial lining as a consequence of cartilage damage, promote the metabolic function of chondrocyte that are deleterious to the matrix and perpetuate a vicious cycle for further articular cartilage damage. The technique of chondrocytes culture, identification of possible markers for os teoarthritis and the application of monclonal antibodies as probes make greater understand ing of the cell biology of osteoarthritis and its mechanism possbile in the next few years. (JPTA ROC 1990; 3: 8-18) |
本系統中英文摘要資訊取自各篇刊載內容。