MMP3 and TIMP1 variants contribute to chronic periodontitis and may be implicated in disease progression.
MMP3 and TIMP1 variants contribute to chronic periodontitis and may be implicated in disease progression.
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DOI：
10.1111/j.1600-051x.2012.01902.x
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发表时间：
2012-08
影响因子：
6.7
通讯作者：
Vieira AR
中科院分区：
文献类型：
--
作者：
Letra A;Silva RM;Rylands RJ;Silveira EM;de Souza AP;Wendell SK;Garlet GP;Vieira AR
基质金属蛋白酶（MMPs）在慢性牙周炎的组织破坏中起关键作用。本研究的目的是调查两个人群中MMP和TIMP多态性与慢性牙周炎的关系。在401名巴西人（99例慢性牙周炎患者和302例对照）和274名美国人（70例和204例对照）中，对12个MMP和2个TIMP基因的34个多态性进行了基因分型。如果在两个不同象限中至少有三颗牙齿表现出临床附着缺失≥5mm的位置，则视为病例。对照组的特点是没有临床附着丧失，没有探测深度为bbb3mm的部位。检测健康和病变牙周组织中MMP3和TIMP1 mRNA的表达。TIMP1在巴西人群中显示与慢性牙周炎相关（rss5906435， P=0.0004），而MMP3在美国人群（rs679620， P=0.0003; rs650108， P=0.002）和巴西人群（rs639752， P=0.005）中显示相关。MMP3和TIMP1 mRNA在病变组织中的表达明显高于对照组织。我们的研究结果进一步支持MMP3变异在慢性牙周炎中的作用，并报告了与TIMP1的新关联。这些基因可能被认为是慢性牙周炎的额外候选基因。
Matrix metalloproteinases (MMPs) play a key role in the tissue destruction characteristic of chronic periodontitis. The purpose of this study was to investigate the association of MMP and TIMP polymorphisms with chronic periodontitis in two populations. Thirty-four polymorphisms spanning 12 MMP and 2 TIMP genes were genotyped in 401 individuals from Brazil (99 cases with chronic periodontitis and 302 controls), and 274 individuals from the US (70 cases and 204 controls). Individuals were considered cases if presenting at least three teeth exhibiting sites of clinical attachment loss ≥5mm in two different quadrants. Controls were characterized by absence of clinical attachment loss and no sites with probing depth >3mm. MMP3 and TIMP1 mRNA expression was evaluated in healthy and diseased periodontal tissues. TIMP1 showed association with chronic periodontitis in the Brazilian population (for rs5906435, P=0.0004), whereas MMP3 showed association in the US population (for rs679620, P=0.0003; and rs650108, P=0.002) and in the Brazilian population (for rs639752, P=0.005). MMP3 and TIMP1 mRNA expression was significantly higher in diseased tissues when compared to control tissues. Our results further support a role for variations in MMP3 in chronic periodontitis and report a novel association with TIMP1. These genes may be considered additional candidate genes for chronic periodontitis.