Genetic predisposition to persistent apical periodontitis.
Genetic predisposition to persistent apical periodontitis.
复制标题
DOI：
10.1016/j.joen.2011.01.009
复制
发表时间：
2011-04
影响因子：
4.2
通讯作者：
Mickel A
中科院分区：
文献类型：
--
作者：
Morsani JM;Aminoshariae A;Han YW;Montagnese TA;Mickel A
促炎细胞因子白细胞介素（IL）-1是宿主对微生物感染反应的关键调节因子，也是细胞外基质分解和骨吸收的主要调节因子。IL-1b的等位基因2与IL-1β产生的四倍增加相关。本病例对照研究旨在探讨IL-1β基因多态性在牙髓病发病机制中的作用。我们推测IL-1β基因多态性（等位基因2）可能影响宿主反应，增强炎症反应，从而诱发持续性根尖周炎（PAP）。回顾根管治疗后至少随访1年的受试者。应用入选和排除标准，纳入了34例具有PAP体征/症状且其他方面可接受RCT的受试者。61例对照显示愈合，RCT可接受。采用聚合酶链反应-限制性片段长度多态性（PCR-RFLP）技术对口腔颊粘膜组织基因组DNA进行扩增，以区分IL-1β基因多态性的等位基因。病例组和对照组的多态性基因型分布差异有显著性（P <0.001，Pearson χ2）。这些发现表明，与IL-1β产生增加相关的特定遗传标记可能有助于增加对PAP的易感性。
The proinflammatory cytokine interleukin (IL)-1 is a key regulator of host responses to microbial infection and a major modulator of extracellular matrix catabolism and bone resorption. Allele2 of IL-1b is associated with a four-fold increase in IL-1β production. The aim of this case-control study was to evaluate the gene polymorphism of IL-1β in the pathogenesis of endodontic failure. We hypothesized that the gene polymorphism (allele2 of IL-1β) would influence host response and enhance inflammatory reactions predisposing to persistent apical periodontitis (PAP). Subjects with at least 1 year of follow-up after root canal therapy (RCT) were recalled. Inclusion and exclusion criteria were applied, and 34 subjects with signs/symptoms of PAP with otherwise acceptable RCT were included. Sixty-one controls showed healing with acceptable RCT. Genomic DNA from buccal mucosa was amplified by polymerase chain reaction followed by restriction fragment length polymorphism to distinguish the alleles of IL-1β gene polymorphism. A significant difference in the distribution of the polymorphic genotype among cases (70.6%) and controls (24.6%) (P < .001, Pearson χ2) was shown. These findings suggest that specific genetic markers associated with increased IL-1β production may contribute to increased susceptibility to PAP.