Tojyo I, Yamaguchi A, Nitta T, Yoshida H, Fujita S, Yoshida T
Department of Oral and Maxillofacial Surgery, Wakayama Medical University, Wakayama, Japan.
Oral Dis. 2008 Jan;14(1):45-50. doi: 10.1111/j.1601-0825.2006.01344.x.
The expression of tenascin-C in the synovial membrane of the internal derangement (ID) of the temporomandibular joint (TMJ) has been reported. Hypoxia of the synovial membrane in TMJ is considered to be a cause for the pathophysiology of ID. In this study, we clarify the contribution of hypoxia and interleukin-1beta in the expression of tenascin-C in ID of TMJ.
Synovial fibroblasts and disk cells obtained from ID of TMJs were cultured and treated with interleukin-1beta under normoxia and hypoxia. A Western blot analysis and reverse transcription-polymerase chain reaction analysis were used to identify tenascin-C in cultured synovial fibroblasts and disk cells. In addition, the immunohistochemical staining of tenascin-C was carried out for the specimens of ID of TMJs and normal.
The combination of hypoxia and interleukin-1beta caused a significant increase in tenascin-C protein and mRNA of synovial fibroblasts. In contrast, the combination caused no increase in tenascin-C in disk cells. However, the immunohistochemical staining demonstrated tenascin-C to be significantly detected in both the synovial tissue and disks in ID of TMJ.
These results indicate that hypoxic conditions with inflammation modulate the tenascin-C expression in synovial fibroblasts, but not in disk cells.
已有报道颞下颌关节内紊乱（ID）患者滑膜中肌腱蛋白-C的表达情况。颞下颌关节滑膜缺氧被认为是导致内紊乱病理生理的一个原因。在本研究中，我们阐明缺氧和白细胞介素-1β在颞下颌关节内紊乱中肌腱蛋白-C表达中的作用。
从颞下颌关节内紊乱患者获取滑膜成纤维细胞和盘状细胞，在常氧和缺氧条件下用白细胞介素-1β进行培养处理。采用蛋白质免疫印迹分析和逆转录-聚合酶链反应分析来鉴定培养的滑膜成纤维细胞和盘状细胞中的肌腱蛋白-C。此外，对颞下颌关节内紊乱标本和正常标本进行肌腱蛋白-C的免疫组织化学染色。
缺氧和白细胞介素-1β共同作用使滑膜成纤维细胞中肌腱蛋白-C的蛋白质和信使核糖核酸显著增加。相比之下，二者共同作用未使盘状细胞中的肌腱蛋白-C增加。然而，免疫组织化学染色显示在颞下颌关节内紊乱的滑膜组织和盘状组织中均能显著检测到肌腱蛋白-C。
这些结果表明，伴有炎症的缺氧状态可调节滑膜成纤维细胞中肌腱蛋白-C的表达，但对盘状细胞无此作用。
