Centre for Clinical and Diagnostic Oral Sciences, Institute of Dentistry, Barts & The London School of Medicine and Dentistry, Queen Mary University of London, London, UK.
J Oral Pathol Med. 2012 Jul;41(6):454-62. doi: 10.1111/j.1600-0714.2012.01129.x. Epub 2012 Mar 3.
Oral submucous fibrosis (OSMF) is associated with paan chewing, altered collagen metabolism, inflammation and the upregulation of numerous cytokines. OSMF fibroblasts accumulate senescent cells at an increased rate because of increased reactive oxygen species production and DNA double-strand breaks (DDBs), generated intrinsically by damaged mitochondria. This results in a reduced replicative lifespan. However, it is still unclear which other changes are intrinsic to the fibroblasts and associated with OSMF rather than the paan chewing habit or the OSMF environment. Both the oral epithelium and the mesenchyme have elevated levels of TGF-β(1) in OSMF in vivo. However, in cultured fibroblasts, secreted levels of TGF-β(1,) other cytokines and the matrix metalloproteinases 1 and 2 showed no association with OSMF. In contrast, the tissue inhibitors of metalloproteinases, TIMP-1 and TIMP-2, were increased in 10/11 OSMF fibroblast cultures relative to normal and non-diseased paan user controls. OSMF fibroblast collagen levels were normal. TIMP levels correlated with replicative lifespan of the cultures but not with the presence of senescent cells, as senescent cell depletion in OSMF fibroblast cultures did not result in a reduction in either TIMP-1 or TIMP-2. However, the introduction of unrepairable DDBs into normal oral fibroblasts by ionizing radiation increased TIMP-1 and TIMP-2 secretion by two-fold and seven-fold, respectively, within 5 days, replicating early senescence and the elevation seen in OSMF cultures. Therefore, increased fibroblast TIMP-1/2 levels could be early disease-specific markers of OSMF onset, DDBs and ageing and may have clinical significance, as OSMF can be reversed in its early stages.
口腔黏膜下纤维性变(OSMF)与嚼槟榔、胶原蛋白代谢改变、炎症和大量细胞因子的上调有关。OSMF 成纤维细胞由于活性氧(ROS)产生和 DNA 双链断裂(DDB)增加,内在地由受损线粒体产生,以更快的速度积累衰老细胞。这导致复制寿命缩短。然而,目前尚不清楚哪些其他变化是成纤维细胞固有的,与 OSMF 相关,而不是与嚼槟榔习惯或 OSMF 环境相关。OSMF 体内的口腔上皮和间充质都有较高水平的 TGF-β(1)。然而,在培养的成纤维细胞中,TGF-β(1)、其他细胞因子和基质金属蛋白酶 1 和 2 的分泌水平与 OSMF 无关。相反,在 10/11 例 OSMF 成纤维细胞培养物中,组织金属蛋白酶抑制剂 1 和 2(TIMP-1 和 TIMP-2)的水平增加,而正常和非疾病性嚼槟榔对照者则没有。OSMF 成纤维胶原水平正常。TIMP 水平与培养物的复制寿命相关,但与衰老细胞的存在无关,因为在 OSMF 成纤维细胞培养物中耗尽衰老细胞不会导致 TIMP-1 或 TIMP-2 减少。然而,电离辐射将不可修复的 DDB 引入正常口腔成纤维细胞后,TIMP-1 和 TIMP-2 的分泌在 5 天内分别增加了两倍和七倍,复制了早期衰老和 OSMF 培养物中观察到的升高。因此,成纤维细胞 TIMP-1/2 水平的升高可能是 OSMF 发病、DDB 和衰老的早期疾病特异性标志物,可能具有临床意义,因为 OSMF 可以在早期阶段逆转。