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Chondrocyte apoptosis in temporomandibular joint osteoarthritis promotes bone resorption by enhancing chemotaxis of osteoclast precursors.
Guo, Y N; Cui, S J; Tian, Y J; Zhao, N R; Zhang, Y D; Gan, Y H; Zhou, Y H; Wang, X D.
Afiliación
  • Guo YN; Department of Orthodontics, Peking University School and Hospital of Stomatology, Beijing, China; National Clinical Research Center for Oral Diseases & National Engineering Laboratory for Digital and Material Technology of Stomatology, Beijing, China; Beijing Key Laboratory of Digital Stomatolog
  • Cui SJ; Department of Orthodontics, Peking University School and Hospital of Stomatology, Beijing, China; National Clinical Research Center for Oral Diseases & National Engineering Laboratory for Digital and Material Technology of Stomatology, Beijing, China; Beijing Key Laboratory of Digital Stomatolog
  • Tian YJ; Department of Orthodontics, Peking University School and Hospital of Stomatology, Beijing, China; National Clinical Research Center for Oral Diseases & National Engineering Laboratory for Digital and Material Technology of Stomatology, Beijing, China; Beijing Key Laboratory of Digital Stomatolog
  • Zhao NR; Department of Orthodontics, Peking University School and Hospital of Stomatology, Beijing, China; National Clinical Research Center for Oral Diseases & National Engineering Laboratory for Digital and Material Technology of Stomatology, Beijing, China; Beijing Key Laboratory of Digital Stomatolog
  • Zhang YD; Department of Orthodontics, Peking University School and Hospital of Stomatology, Beijing, China; National Clinical Research Center for Oral Diseases & National Engineering Laboratory for Digital and Material Technology of Stomatology, Beijing, China; Beijing Key Laboratory of Digital Stomatolog
  • Gan YH; Department of Orthodontics, Peking University School and Hospital of Stomatology, Beijing, China; National Clinical Research Center for Oral Diseases & National Engineering Laboratory for Digital and Material Technology of Stomatology, Beijing, China; Beijing Key Laboratory of Digital Stomatolog
  • Zhou YH; Department of Orthodontics, Peking University School and Hospital of Stomatology, Beijing, China; National Clinical Research Center for Oral Diseases & National Engineering Laboratory for Digital and Material Technology of Stomatology, Beijing, China; Beijing Key Laboratory of Digital Stomatolog
  • Wang XD; Department of Orthodontics, Peking University School and Hospital of Stomatology, Beijing, China; National Clinical Research Center for Oral Diseases & National Engineering Laboratory for Digital and Material Technology of Stomatology, Beijing, China; Beijing Key Laboratory of Digital Stomatolog
Osteoarthritis Cartilage ; 30(8): 1140-1153, 2022 08.
Article en En | MEDLINE | ID: mdl-35513247
OBJECTIVE: This study aimed to explore the effect and mechanism of chondrocyte apoptosis on the chemotaxis of osteoclast precursors (OCPs) during bone destruction. DESIGN: The relationship between cartilage and bone destruction was verified with a rat temporomandibular joint osteoarthritis (TMJOA) model. The pan-caspase inhibitor Z-VAD-FMK (ZVAD) was applied to confirm the chemotactic effect of chondrocyte apoptosis on OCPs. Synthesis and release of the key chemokine CX3CL1 in apoptotic and non-apoptotic chondrocytes was assessed with IHC, IF, WB, and ELISA. The function of CX3CL1-CX3CR1 axis in the chemotaxis of OCPs was examined by CX3XR1 inhibitor AZD8797 (AZD) and si-CX3CL1. The regulatory effect of p38 MAPK on CX3CL1 release was verified by p38 inhibitor PH-797804. RESULTS: A temporal and spatial association between cartilage degradation and bone resorption was found in the TMJOA model. The caspase-dependent chondrocyte apoptosis promoted chemotaxis of OCPs, which can be restrained by ZVAD. CX3CL1 was significantly upregulated when chondrocytes underwent apoptosis, and it played a critical role in the recruitment of OCPs, blockage of CX3CL1-CX3CR1 axis resulted in less bone resorption in TMJOA. P38 MAPK was activated in apoptotic chondrocytes, and had a regulatory effect on the synthesis and release of CX3CL1. After inhibition of p38 by PH-797804, the chemotactic effect of apoptotic chondrocytes on OCPs was limited. CONCLUSIONS: This study indicates that apoptosis of chondrocytes in TMJOA enhances chemotaxis of OCPs toward osteoclast precursors through upregulation of the p38-CX3CL1 axis, thereby promoting the activation of local osteoclasts.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Osteoartritis / Resorción Ósea / Cartílago Articular Límite: Animals Idioma: En Revista: Osteoarthritis Cartilage Asunto de la revista: ORTOPEDIA / REUMATOLOGIA Año: 2022 Tipo del documento: Article Pais de publicación: Reino Unido
Texto completo
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Osteoartritis / Resorción Ósea / Cartílago Articular Límite: Animals Idioma: En Revista: Osteoarthritis Cartilage Asunto de la revista: ORTOPEDIA / REUMATOLOGIA Año: 2022 Tipo del documento: Article Pais de publicación: Reino Unido