The ferroptosis is induced in degenerated temporomandibular joint osteoarthritis chondrocytes by abnor-mal biological force
10.3969/j.issn.1001-3733.2025.02.007
- VernacularTitle:异常力刺激对颞下颌关节骨关节炎退变软骨细胞铁死亡调控的初步研究
- Author:
Qinghua LI
1
;
Peinan FAN
;
Qinyu LUO
;
Yang YU
;
Hongxu YANG
Author Information
1. 710127 西安,西北大学生命科学学院
- Publication Type:Journal Article
- Keywords:
Temporomandibular joint;
Osteoarthritis;
Chondrocytes;
Ferroptosis;
Abnormal biological force
- From:
Journal of Practical Stomatology
2025;41(2):181-188
- CountryChina
- Language:Chinese
-
Abstract:
Objective:The aim of this study is to explain the key role of chondrocyte ferroptosis in TMJ OA and demonstrate that abnormal occlusion stimulation is an important causative factor of ferroptosis.Methods:We observed the morphological changes of mouse condylar cartilage in unilateral anterior crossbite(UAC,an abnormal occlusion stimulation)and bilateral anterior elevation(BAE,a proliferation occlusion stimulation)mice by HE and SO staining,and analyzed the expression of intracellular GPX4 by im-munofluorescence staining,and analyzed the changes in the content of mitochondria and reactive oxygen species by JC-1 and ROS staining.Results:The UAC caused degeneration of condylar cartilage and ferroptosis of chondrocytes in mice.The accumulation of iron ions and the dysfunction of mitochondria in chondrocytes significantly upregulated.The expression of GPX4,which is a key reg-ulator in the regulation of ferroptosis was lowered in UAC mice condyle cartilage.Moreover,in BAE model the condylar cartilage hy-perplasia was observed,but not the ferroptosis of chondrocytes.Conclusion:This study revealed that the abnormal biological force caused by abnormal occlusion could induce ferroptosis of chondrocytes,and ferroptosis is one of the main factors leading to the de-generation and thinning of condylar cartilage.GPX4 could regulate the ferroptosis of chondrocytes.
