Cyclooxygenase-2, Fc?? Receptor IIIb, Vitamin D Receptor, Tumor Necrosis Factor-?? 及 Lymphotoxin-?扆穧]多型性與台灣人罹患牙周炎易感性之相關性

The Association of Cyclooxygenase-2, Fc?? Receptor IIIb, Vitamin D Receptor, Tumor Necrosis Factor-?? and Lymphotoxin-?? Gene Polymorphisms with Susceptibility to Periodontitis in a Taiwanese Population

何雅萍(Ya-Ping Ho)

指導教授 ： 蔡吉政

高雄醫學大學/口腔醫學院/牙醫學研究所/博士(2008年)

https://doi.org/10.6832/KMU.2008.00123

摘要

研究目的: 探討cyclooxygenase-2-765 (COX-2), FcγRIIIb, vitamin D receptor (VDR), tumor necrosis factor-α-308(TNF-α)及lymphotoxin-α+252 (LT-α)基因多型性與國人罹患侵犯型牙周炎､慢性牙周炎易感性之相關性。
研究方法: 研究對象分成三組,分別為侵犯型牙周炎病患､慢性牙周炎病患及牙周健康者。以聚合酵素鏈鎖反應-限制酵素片段長度多型性技術測定上述基因位置之基因型。各基因型之分佈是否有組間差異是採用卡方檢定, 各基因型與疾病危險之相關性是以邏輯回歸分析,以odds ratio及95%信賴區間表示。
結果: 1. COX-2-765帶有C allele之基因型與國人罹患侵犯型牙周炎及慢性牙周炎之危險性呈負相關。2. FcγRIIIb帶有NA2之基因型與國人罹患侵犯型牙周炎之危險性呈正相關, 與罹患慢性牙周炎之危險性無關。相反地, FcγRIIIb帶有NA1之基因型會增加罹患慢性牙周炎之危險性,但與侵犯型牙周炎之危險性無關。3. VDR BsmI-RFLP帶有B allele之基因型與國人罹患慢性牙周炎及侵犯型牙周炎之危險性呈負相關, FokI-RFLP之FF基因型與國人罹患侵犯型牙周炎之危險性呈正相關, ApaI-及TaqI-RFLP則與罹患牙周炎之危險性無關。4. TNF-α-308及LT-α+252基因多型性與國人罹患牙周炎之危險性無關。
結論: COX-2-765帶有C allele之基因型､VDR BsmI-RFLP帶有B allele之基因型對國人是保護因子,可減少罹患牙周炎之危險性; FcγRIIIb帶有NA2之基因型､FokI-RFLP之FF基因型是國人罹患侵犯型牙周炎之危險因子, FcγRIIIb帶有NA1之基因型是國人罹患慢性牙周炎之危險因子; 本研究測定的其他基因多型性則與國人罹患牙周炎之危險性無關。

關鍵字

cyclooxygenase-2-765 ； FcγRIIIb ； vitamin D receptor ； tumor necrosis factor-α-308 ； lymphotoxin-α+252 ； 基因多型性 ； 侵犯型牙周炎 ； 慢性牙周炎

並列摘要

Objectives: The host-activated immunological and inflammatory reactions responding to bacterial challenge that result in destruction of periodontal tissue are under genetic control. Polymorphisms of genes may affect the function or expression of genes which in turn might affect the expression of periodontal disease. Genetic variants associated with proinflammatory cytokine production and receptor expression might alter the individual susceptibility to periodontitis. The purpose of the present study was to evaluate the association of cyclooxygenase-2-765(COX-2), FcγRIIIb, vitamin D receptor (VDR), tumor necrosis factor -α-308 (TNF-α) and lymphotoxin-α+252 (LT-α) genetic polymorphisms with susceptibility to periodontitis in Taiwanese.
Material and methods: There were three groups of study subjects: aggressive periodontitis patients, chronic periodontitis patients and periodontally healthy controls. Genotypes were determined by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). The distribution of genotypes among groups was compared by chi-square test. The risk for periodontitis associated with genotypes was calculated by logistic regression and was expressed as the odds ratio and 95% confidence interval.
Results: The genotypes distribution of COX-2-765, FcγRIIIb, BsmI-, FokI-VDR polymorphisms were significantly different among groups. The COX-2-765 genotypes carrying the C allele and the VDR BsmI-RFLP genotypes carring the B allele were associated with the reduced risk of aggressive periodontitis and chronic periodontitis. The NA2 carrier of FcγRIIIb and the VDR FokI-RFLP FF genotypes were significantly associated with the increased risk of aggressive periodontitis. On the other hand, the NA1 carrier of FcγRIIIb might increase the susceptibility for chronic periodontitis. The other genotypes determined in the present study were not associated with the risk of periodontitis.
Conclusions: The COX-2-765 C allele and the VDR BsmI-RFLP B allele might be the genetic protective factors for our study subjects against the development of periodontitis. The NA2 carrier of FcγRIIIb and the VDR FokI-RFLP FF genotypes might be the genetic risk factor for aggressive periodontitis. Susceptibility for chronic periodontitis was related to FcγRIIIb NA1 carrier.

並列關鍵字

cyclooxygenase-2-765 ； FcγRIIIb ； vitamin D receptor ； tumor necrosis factor-α-308 ； lymphotoxin-α+252 ； genetic polymorphism ； aggressive periodontitis ； chronic periodontitis

參考文獻

References

1. Löe H, Anerud A, Boysen H, Morrison E. Natural history of periodontal disease in man. Rapid, moderate and no loss of attachment of Sri Lankan laborers 14 to 46 years of age. Journal of Clinical Periodontology 1986;13:431-440.

2. Hart TC, Kornman KS. Genetic factors in the pathogenesis of periodontitis. Periodontology 2000 1997;14:202-215.

3. Shapira L, Wilensky A, Kinane DF. Effect of genetic variability on the inflammatory response to periodontal infection. Journal of Clinical Periodontology 2005;32 (suppl. 6) 72-86.

4. Lopez NJ. Clinical, laboratory, and immunological studies of a family with a high prevalence of prepubertal and juvenile periodontitis. Journal of Periodontology 1992;63:457-468.