Center for Oral and Systemic Diseases, University of North Carolina at Chapel Hill, Durham, 27709, USA.
J Dent Res. 2010 Feb;89(2):133-7. doi: 10.1177/0022034509356512. Epub 2009 Dec 30.
Levels of prostaglandin E(2) and the prostaglandin-endoperoxide synthase-2 (PTGS2, or COX-2) increase in actively progressing periodontal lesions, but decrease in chronic disease. We hypothesized that chronic inflammation is associated with altered DNA methylation levels within the PTGS2 promoter, with effects on COX-2 mRNA expression. PTGS2 promoter methylation levels from periodontally inflamed gingival biopsies showed a 5.06-fold increase as compared with non-inflamed samples (p = 0.03), and the odds of methylation in a CpG site in the inflamed gingival group is 4.46 times higher than in the same site in the non-inflamed group (p = 0.016). The level of methylation at -458 bp was inversely associated with transcriptional levels of PTGS2 (RT-PCR) (p = 0.01). Analysis of the data suggests that, in chronically inflamed tissues, there is a hypermethylation pattern of the PTGS2 promoter in association with a lower level of PTGS2 transcription, consistent with a dampening of COX-2 expression in chronic periodontitis. These findings suggest that the chronic persistence of the biofilm and inflammation may be associated with epigenetic changes in local tissues at the biofilm-gingival interface.
前列腺素 E(2) 水平和前列腺素内过氧化物合酶-2(PTGS2,或 COX-2)在进展中的牙周病病变中增加,但在慢性疾病中减少。我们假设慢性炎症与 PTGS2 启动子内的 DNA 甲基化水平改变有关,从而影响 COX-2 mRNA 的表达。与非炎症样本相比,牙周炎牙龈活检中的 PTGS2 启动子甲基化水平增加了 5.06 倍(p = 0.03),炎症牙龈组中 CpG 位点的甲基化几率是非炎症组中同一位点的 4.46 倍(p = 0.016)。-458 bp 处的甲基化水平与 PTGS2(RT-PCR)的转录水平呈负相关(p = 0.01)。数据分析表明,在慢性炎症组织中,PTGS2 启动子存在过度甲基化模式,与 PTGS2 转录水平较低有关,这与慢性牙周炎中 COX-2 表达的抑制一致。这些发现表明,生物膜和炎症的慢性持续存在可能与生物膜-牙龈界面局部组织的表观遗传变化有关。