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| Title: | 牙周病嚴重程度與牙齦液胱抑素活性關係之流行病學追蹤研究-1
A Longitudinal Study of Periodontal Disease and Gingival Crevicular Fluid Cystatin Activity-1 |
| Authors: | 胡素婉
林育誼 |
| Contributors: | 中山醫學大學口腔科學研究所 |
| Keywords: | 公共衛生學;牙醫學
牙周病,半胱胺酸蛋白酶,組織蛋白酶,胱抑素,激肽
periodontal disease;cysteine proteinases;cathepsin;cystatin;kinin |
| Date: | 2015 |
| Issue Date: | 2016-07-21T07:17:02Z (UTC)
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| Abstract: | 牙周病致病菌會釋放出半胱胺酸蛋白酶，我們最近的研究發現牙周病患者牙齦液的半胱胺酸蛋白酶活性在治療後會降低。牙周病菌所引起的組織破壞， 大部份是宿主本身降解酶作用的結果。宿主的組織蛋白酶也是屬於半胱胺酸蛋白酶，在骨頭破壞上扮演重要角色，它的天然抑制物-胱抑素，存在於唾液和牙齦液中。研究指出牙周病患牙齦液中具有較高的組織蛋白酶，發炎牙齦組織胱抑素表現較低。然而有關研究仍然相當缺乏。在牙齦液中的激肽釋放酶系統也可能受到胱抑酶所調控，因為激肽的產生也是藉由半胱胺酸蛋白酶活化，我們先前研究顯示，激肽可以增加血管通透性，幫助牙周病菌進入循環系統。因此本研究的目的在探討牙周狀態和宿主半胱胺酸蛋白酶抑制能力的關連性、以及唾液和牙齦液中胱抑素的濃度，同時也將測量牙周病人的組織蛋白酶含量、激肽濃度以及牙周病菌的半胱胺酸蛋白酶水解能力。本追蹤式調查之研究對象為在牙周病科門診求診且符合研究納入條件的280位患者，參加者將接受問卷訪談，並在4或5個時間點回診(治療前後、間隔約3個月)接受口腔檢查並採集唾液和牙齦液，牙齦液將採自兩顆有最嚴重牙周病的牙齒和兩顆正常的牙齒。資料分析將包括repeated measure analysis，同時調整可能干擾因子。
Periodontitis is an inflammatory disease caused by a special group of anaerobic bacteria, the so called “Red Complex”, characterized by the release of cysteine proteinases. Previous studies suggested the proteinase activities in gingival crevicular fluid and maybe in saliva from patients with periodontitis can be used as an indicator of disease severity. Our recent study has shown a reduction in bacterial cysteine proteinase activity following periodontal treatment. The destructive process of periodontitis including alveolar bone loss, though initiated by bacterial insults, is a consequence of host degradative enzymes. Cathepsin playing an important role in bone destruction and tissue matrix damage belongs to cysteine proteinases. Its natural inhibitor, cystatin, is present in saliva and gingiva crevicular fluid. The concentration of cathepsin has been shown to elevate significantly in gingival crevicular fluid from persons with periodontitis as compared with that in healthy individuals. Inhibition of cystatin expression was also observed in inflamed gingiva and fluids. However, the studies concerning cathepsin and cystatin and their association with periodontal disease are still limited. Since cystatin is a potent physiological inhibitor of cysteine proteinases, kinin-forming pathway which is controlled by a cascade of cysteine proteinases is very likely affected in periodontal pockets by gingival concentrations of cystatin. The generation of kinin may help periodontopathogenic bacteria disseminate from sequestered oral cavity to other part of hosts. Kinin may represent a link between periodontal disease and systemic diseases, such as cardiovascular disease (CVD). Therefore, the purpose of this study is to investigate the association between periodontal status and host cysteine protease inhibition activities, especially the levels of cystatin, in saliva and gingival crevicular fluid. We will look into host cathepsin levels, host kinin contents and bacterial cysteine proteinase activities in patients with periodontal disease. This epidmiological study has a cross-sectional part and a longitudinal follow-up part. Two hundred and eighty study subjects who meet the inclusion criteria will be recruited from the department of periodontal disease at a teaching hospital. These participants will have an oral examination, an interview, and their saliva and gingival crevicular fluid samples will be collected from four tooth sites (two sites with the most severe periodontitis and two normal sites) in four (for subjects without periodontal surgery) or five (for those with periodontal surgery) occasions, about three month apart. The samples will be analyzed for host cystatin, cathepsin and kinin levels, and bacterial protease activities using ELISA and substrate chromatography. In data analysis, the repeated measurement analysis will be used to compare proteinase activities, cystatin, cathepsin, and kinin, respectively, measured in different occasions and from teeth with different severity of periodontal disease, taking into account intra-individual correlation and confounding factors. The types of periodontal treatment received by the subjects and the severity of periodontal diseases of the subjects will be considered in the analysis. The data obtained from this study will greatly improve our understanding about physiopathogenesis mechanisms of periodontal disease development. |
| URI: | https://ir.csmu.edu.tw:8080/ir/handle/310902500/15524 |
| Appears in Collections: | [口腔醫學研究所] 研究計劃
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