Expression of collagenase and collagenase inhibitors mRNA in periodontitisaffected human gingival tissue.

牙周炎的胶原溶解被认为是由三个基因的表达调节的，胶原酶，金属蛋白酶组织抑制剂-1和-2 （TIMP-1和2）。我们通过逆转录聚合酶链反应（RT- PCR）评估牙周炎患者和健康受试者牙龈样品中TIMP-1、TIMP-2和胶原酶mRNA水平的可能差异。这种技术允许从非常小的样本量中检测转录本。实验表明，患病组的TIMP-1和胶原酶转录物相对于β -肌动蛋白的水平显著高于健康对照组（TIMP-1为8.11*0.83比1.38*0.28%，胶原为0.50*0.10比0.0075*0.0024%）。两组间TIMP-2差异无统计学意义（2.91*0.46 vs 1.84*0.87%）。因此，宿主会通过优先产生TIMP-1来对抗组织破坏，从而对胶原酶水平的增加做出反应。在我们的研究中，TIMP-1和TIMP-2的差异基因表达可能解释了TIMP-1和-2在体内的不同遗传调控。

Collagenolysis in periodontitis is thought to be modulated by the expression of three genes, collagenase, tissue inhibitors of metalloproteinases-1 and -2 (TIMP-1 and-2). We assessed the possible difference in TIMP-1, TIMP-2 and collagenase mRNA levels between gingival samples from patients with periodontitis and those from healthy subjects by reverse transcription-polymerase chain reaction (RT- PCR). This technique allows detection of transcripts from a very small sample quantity. The experiments showed that levels of TIMP-1 and collagenase transcripts relative to beta-actin are significantly higher in the diseased group than in health controls (8.11*0.83 versus 1.38*0.28% for TIMP-1 and 0.50*0.10 versus 0.0075*0.0024% for collagenas, respectively). The difference in TIMP-2 between the two groups(2.91*0.46 versus 1.84*0.87%) did not differ. Therefore, the host would have responded to the increase in collagenase level by preferentially producing TIMP-1 against tissue destruction. The differential gene expression of TIMP-1 and TIMP-2 in our study may account for a distinct genetic regulation of TIMP-1 and -2 in vivo.