Temporomandibular joint osteoarthritis (TMJOA) is a complex inflammatory condition with multiple factors and degenerative processes co-occurring. However, its pathogenesis remains uncertain. The purpose of the study was to observe the expression of Indian hedgehog (Ihh) signal related molecules in TMJOA induced by bite-raising and to study the effect and mechanism of Ihh signaling. Our research indicated that Ihh signaling pathway can be activated in condylar cartilage induced by bite-raising. The histological analysis showed TMJOA-like structural changes of condylar cartilage in experiment groups. Ihh, Smoothened (Smo), and Gli zinc finger transcription factors-1 (Gli-1) were activated in the experimental groups, and the expression levels increased significantly over time, whereas the sham control groups showed no fluctuation. Additionally, the expression levels of matrix metalloproteinase-13 (MMP-13) and cysteinyl aspartate specific proteinase-3 (Caspase-3) in the experiment groups increased in a time-dependent manner compared with the matched sham control groups. In conclusion, our results indicated that the Ihh signaling pathway may activate the occurrence of TMJOA by mediating the hypertrophy of chondrocytes, which may be an important regulatory mechanism and potential therapeutic target in the repair of condylar cartilage.

中文翻译：

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成年大鼠咬后after突软骨中Ihh信号通路的表达。

颞下颌关节骨关节炎（TMJOA）是一种复杂的炎症性疾病，具有多种因素，并同时发生变性过程。但是，其发病机理仍不确定。该研究的目的是观察叮咬诱导的TMJOA中印度刺猬（Ihh）信号相关分子的表达，并研究Ihh信号转导的作用和机制。我们的研究表明，Ihh信号通路可以在咬人诱导的con突软骨中被激活。组织学分析显示，实验组of突软骨的结构类似TMJOA。在实验组中，Ihh，Smoothened（Smo）和Gli锌指转录因子-1（Gli-1）被激活，表达水平随时间显着增加，而假对照组则没有波动。另外，与假手术对照组相比，实验组中基质金属蛋白酶13（MMP-13）和半胱氨酸天冬氨酸特异性蛋白酶3（Caspase-3）的表达水平呈时间依赖性。总之，我们的结果表明，Ihh信号通路可能通过介导软骨细胞肥大来激活TMJOA的发生，这可能是con突软骨修复的重要调控机制和潜在治疗靶点。