Chondrocyte-like apoptosis in temporomandibular joint disc internal derangement as a repair-limiting mechanism. An in vivo study
Chondrocyte-like apoptosis in temporomandibular joint disc internal derangement as a repair-limiting mechanism. An in vivo study
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DOI：
10.14670/hh-24.293
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发表时间：
2009-03-01
影响因子：
2
通讯作者：
Leonardi, R.
中科院分区：
文献类型：
--
作者：
Loreto, C.;Musumeci, G.;Leonardi, R.
颞下颌关节内部紊乱（TMJ ID）的特征是椎间盘移位和退行性组织改变，涉及活跃的细胞反应，细胞表型从成纤维细胞样转变为纤维软骨细胞样，最终转变为软骨细胞样，可能是对异常负荷的反应。然而，只有小块的软骨组织被检测到TMJ椎间盘与ID。我们决定探索这种不完全组织改变的原因，假设参与了细胞凋亡过程。从19例TMJ患者中取出21个椎间盘进行TRAIL和DR5免疫组织化学定位，并进行TUNEL试验。软骨细胞样细胞中DR5受体及其配体（TRAIL）的过表达提示程序性细胞死亡的激活，tunel阳性细胞也证实了这一点。数据表明，通过软骨样体化生对椎间盘移位的适应性反应失败。至少部分由TRAIL及其死亡受体调控的软骨细胞样细胞的凋亡性死亡似乎是椎间盘修复失败的基础，最终导致其穿孔。
Temporomandibular joint internal derangement (TMJ ID) is characterised by disc displacement and degenerative tissue changes involving an active cellular response, with cell phenotype transformation from fibroblast-like to fibrochondrocyte and, eventually, to chondrocyte-like, possibly as a response to abnormal loading. However, only small patches of chondral tissue are detected in TMJ discs with ID. We decided to explore the reasons for such incomplete tissue change, postulating an involvement of the apoptosis process.Twenty-one discs removed from 19 patients with TMJ ID were processed for TRAIL and DR5 immunohistochemical localisation, and subjected to the TUNEL assay.Overexpression of DR5 receptor and its ligand (TRAIL) in chondrocyte-like cells suggested activation of programmed cell death, as also demonstrated by TUNEL-positive cells.The data suggest a failed adaptive response to disc displacement through chondroid metaplasia. The apoptotic death of chondrocyte-like cells, which is at least partly regulated by TRAIL and its death receptor, appears to underpin the failed disc repair, eventually leading to its perforation.