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  • 學位論文

乳鐵蛋白基因多形性與慢性牙周炎及侵犯性牙周炎之關係

Association of lactoferrin gene polymorphisms in chronic and aggressive periodontitis

指導教授 : 蔡吉政

摘要


背景:由小樣本數的研究發現,乳鐵蛋白基因多形性Lys/Arg基因型在局部性年輕型牙周炎與健康者有很明顯的差異,因此本研究將針對台灣居民探討乳鐵蛋白基因多形性與牙周炎的關係。   材料與方法:採取65位侵犯性牙周炎病患、278位慢性牙周炎病患及88位健康者血液之白血球,分析其乳鐵蛋白N-終端阿爾發螺旋區域,在位置29的Lys/Arg基因多形性(rs 1126478)做為研究標的。 結果:侵犯性牙周炎出現GG基因型及G-對偶基因的機率最高,其次是慢性牙周炎,最後是健康組。G-對偶基因出現的機率在侵犯性牙周炎及慢性牙周炎組明顯高於健康組(p=0.0037及0.0212)。侵犯性牙周炎之GG基因型明顯高於健康者,但在慢性牙周炎與健康組之間則未達到統計學上之差異。以對數迴歸分析,在調整過年齡、性別及吸菸狀態等變數後,乳鐵蛋白基因多形性及侵犯性牙周炎的關係依然存在(GG/AG+AA:Adj OR=2.16,95%CI=1.09-4.35,p=0.0287)。研究對象依吸菸狀態再細分兩組,在非吸菸組GG基因型仍然與侵犯性牙周炎維持其相關性(OR=2.69, p=0.018),但是在吸菸組中慢性牙周炎與健康者,或是侵犯性牙周炎與健康者間,則未達統計學上之差異了。 結論:目前的研究顯示,乳鐵蛋白A/G基因多形性可能與侵犯性牙周炎的發生有關。而台灣居民之乳鐵蛋白29 A/G基因多形性確實與侵犯性牙周炎有關,A-對偶基因可能會降低侵犯性牙周炎發生的風險。至於吸菸與乳鐵蛋白基因對牙周病的影響都各有其獨立的機制,不見有互相加成或干擾的現象,唯基因的作用會被影響力較強的吸菸因素所掩蓋,不易在吸菸組表現出來。這個基因多形性的功能影響,值得再進一步探討。

並列摘要


Background and Objective: A dramatic difference in the frequencies of the Lys/Arg single nucleotide polymorphism in the lactoferrin genotype between a small population of patients with localized juvenile periodontitis and healthy subjects has been reported. As the single nucleotide polymorphism could be associated with ethnicity, the present study aimed to investigate the association between polymorphisms of the lactoferrin gene and periodontitis. Material and Methods: Sixty-five patients with aggressive periodontitis, 278 with chronic periodontitis and 88 healthy controls were genotyped for the Lys/Arg polymorphism of the lactoferrin gene at position 29 [reference sequence (rs) 1126478] in the N-terminal alpha-helical region. Results: The frequencies of the GG genotype and the G allele were highest in the aggressive periodontitis group, followed by the chronic periodontitis group and then the healthy controls. The frequency of the G allele was significantly higher in aggressive periodontitis and chronic periodontitis groups than in healthy controls (p = 0.0037 and 0.0212). Although the difference of the GG genotype distribution between subjects with chronic periodontitis and healthy controls did not reach significance, the distribution of genotypes between aggressive periodontitis and healthy controls was significantly different. The association of the gene polymorphism and aggressive periodontitis still existed, even after adjusting for age, gender and smoking status by logistic regression analysis (GG/AG+AA: odds ratio = 2.16, 95% confidence interval = 1.09–4.35, p = 0.0287). After the study, subjects were further stratified by their smoking status; the GG genotype was still significantly associated with the risk of aggressive periodontitis in the nonsmoking group (odds ratio = 2.69, p = 0.018). However, there were no statistical differences between chronic periodontitis vs. healthy controls and aggressive periodontitis vs. healthy controls in the smoking group. Conclusion: The present study revealed that the A/G polymorphism in the lactoferrin gene might be associated with aggressive periodontitis. The A allele might reduce the risk of development of aggressive periodontitis in a Taiwanese population. Our results also support the hypothesis that lactoferrin genetic polymorphisms could play a role in the risk for periodontitis separate from the smoking factor. The functionality of this gene’s polymorphisms has to be further elucidated.

參考文獻


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