Meisel P, Siegemund Annett, Dombrowa Sylke, Sawaf H, Fanghaenel Jutta, Kocher Th
Department of Pharmacology, Ernst Moritz Arndt University, Greifswald, Germany.
J Periodontol. 2002 Jan;73(1):27-32. doi: 10.1902/jop.2002.73.1.27.
Polymorphisms within the interleukin-1 cluster are known to be associated with adult periodontal disease. However, interactions of genetic with other risk factors, especially smoking, remain questionable. The aim of this cross-sectional study was to evaluate the genetic influence on periodontal variables in relation to environmental factors.
One-hundred fifty-four (154) Caucasian subjects were clinically and radiographically assessed for their periodontal status, their smoking history recorded, and their allelic pattern of IL-1alpha, IL-1beta, and IL-1RN polymorphisms determined by genotyping.
In assessing periodontitis with mean probing depth, mean attachment loss, or mean bone loss, no differences were found in allele frequencies or combined allotypes between subjects with mild or moderate versus those with severe signs of periodontitis. However, the extent of attachment loss defined as percentage of sites >4 mm was significantly associated with the composite genotype of IL-1alpha/1beta in smokers (odds ratio [OR] = 4.00; 95% confidence interval [CI] 1.03 to 16.70; P= 0.02). No differences were found in genotype negative subjects irrespective of their smoking status. They had nearly identical attachment loss as genotype positive non-smokers. Similar non-significant results were found with respect to extent of bone loss. An increased risk of more extended attachment loss was observed also in individuals carrying mutations of the combined genotype IL-1alpha/IL-1RN, again showing enhanced risk only in genotype-positive and smoking subjects.
The results provide evidence that the composite genotypes studied show interaction with smoking, the main exposition-related risk factor of periodontal disease. Non-smoking subjects are not at increased risk, even if they are genotype-positive.
白细胞介素-1基因簇内的多态性已知与成人牙周病有关。然而，基因与其他风险因素，尤其是吸烟之间的相互作用仍存在疑问。本横断面研究的目的是评估基因对牙周变量与环境因素关系的影响。
对154名白种人受试者进行临床和影像学评估，以确定其牙周状况，记录吸烟史，并通过基因分型确定白细胞介素-1α、白细胞介素-1β和白细胞介素-1受体拮抗剂（IL-1RN）多态性的等位基因模式。
在通过平均探诊深度、平均附着丧失或平均骨丧失评估牙周炎时，轻度或中度牙周炎体征的受试者与重度牙周炎体征的受试者之间，等位基因频率或组合单倍型无差异。然而，定义为>4 mm位点百分比的附着丧失程度与吸烟者白细胞介素-1α/1β的复合基因型显著相关（比值比[OR]=4.00；95%置信区间[CI]1.03至16.70；P=0.02）。无论吸烟状况如何，基因型阴性的受试者均未发现差异。他们的附着丧失情况与基因型阳性的非吸烟者几乎相同。在骨丧失程度方面也发现了类似的无显著差异的结果。携带白细胞介素-1α/白细胞介素-1RN复合基因型突变的个体也观察到附着丧失更广泛的风险增加，同样仅在基因型阳性和吸烟的受试者中显示出风险增加。
结果提供了证据表明所研究的复合基因型与吸烟存在相互作用，吸烟是牙周病主要的暴露相关风险因素。非吸烟受试者即使基因型为阳性，风险也不会增加。
