1. Department of Basic Medical Sciences, Neurosciences and Sense Organs, University of Bari "Aldo Moro", Piazza Giulio Cesare 11, 70124, Bari, Italy.
2. Department of Interdisciplinary Medicine, University of Bari "Aldo Moro", Piazza Giulio Cesare 11, 70124, Bari, Italy.
Int J Med Sci. 2014 May 1;11(7):674-9. doi: 10.7150/ijms.6962. eCollection 2014.
Periodontics has evolved from a simplistic model to a more complex interplay between infection and host response. Genetic factors have been a new addition to the list of risk factors for periodontal diseases. The processes leading to destruction and regeneration of the destroyed tissues are of great interest to both researchers and clinicians. The selective susceptibility of subjects for periodontitis has remained an enigma and wide varieties of risk factors have been implicated for the manifestation and progression of periodontitis. Emerging pathway models suggest that gene-environment interactions are etiologically important in disease pathogenesis. The current practical utility of genetic knowledge in periodontitis is limited. Allelic variants at multiple gene loci probably influence periodontitis susceptibility. The pro-inflammatory cytokine interleukin-1 (IL-1) is a key modulator of host responses to microbial infection and a major modulator of extracellular matrix catabolism and bone resorption, and polymorphisms in the IL-1 gene cluster have been associated with an increased risk of developing severe adult periodontitis. The aim of this study was to test if polymorphisms of genes of IL-1α(+4845) and IL-1β(+3954) were linked with periodontitis, in a case-control study population, delimited to a specific geographic area, in association with microbiological findings. The polymorphisms observed in IL-1α(+4845) and IL-1β(+3954) single nucleotide polymorphisms (SNPs), was significantly different among the study groups (healthy controls, mild, moderate and severe periodontitis with p<0.05, d.f.=1. We found a significant correlation between the severe form of periodontitis and the presence of composite genotype (p < 0.05, d.f.=1, calculated among healthy vs. severe). Furthermore a statistically significant association between the presence of bacteria and periodontitis was detected (p<0.05, d.f.=1). In the current investigation findings were concordant with literature observations.
牙周病学已经从一个简单的模型发展为感染和宿主反应之间更为复杂的相互作用。遗传因素是牙周病危险因素的新成员。导致组织破坏和再生的过程引起了研究人员和临床医生的极大兴趣。牙周炎患者的选择性易感性仍然是一个谜,并且已经涉及到广泛的危险因素来解释牙周炎的表现和进展。新兴的途径模型表明,基因-环境相互作用在疾病发病机制中具有重要的病因学意义。目前,遗传知识在牙周病中的实际应用是有限的。多个基因位点的等位变体可能影响牙周炎的易感性。促炎细胞因子白细胞介素-1(IL-1)是宿主对微生物感染反应的关键调节剂,也是细胞外基质分解代谢和骨吸收的主要调节剂,IL-1 基因簇中的多态性与发生严重成人牙周炎的风险增加有关。本研究旨在检测特定地理区域内的病例对照研究人群中白细胞介素-1α(+4845)和白细胞介素-1β(+3954)基因的多态性是否与牙周炎有关,同时还与微生物学发现相关联。在研究组(健康对照组、轻度、中度和重度牙周炎)中,观察到的白细胞介素-1α(+4845)和白细胞介素-1β(+3954)单核苷酸多态性(SNP)存在显著差异(p<0.05,d.f.=1。我们发现严重牙周炎形式与复合基因型(p < 0.05,d.f.=1,在健康对照组与严重对照组之间计算)之间存在显著相关性。此外,还检测到细菌与牙周炎之间存在统计学显著相关性(p<0.05,d.f.=1)。在当前的研究中,研究结果与文献观察结果一致。