Zijing He1,2, Meixi Liu3, Qiang Zhang1,2, Yihong Tian1,4, Lingzhi Wang1,2, Xiao Yan1,2, Dapeng Ren1,2, Xiao Yuan1,2. 1. Department of Orthodontics II, The Affiliated Hospital of Qingdao University, Qingdao, China. 2. School of Stomatology of Qingdao University, Qingdao, China. 3. The Center of Stomatology, Qingdao Municipal Hospital Affiliated to Qingdao University, Qingdao, Shandong, China. 4. State Key Laboratory of Oral Diseases and National Clinical Research Center for Oral Diseases Department of Orthodontics West China Hospital of Stomatology, Sichuan University, Chengdu, China.
Abstract
Objective: To explore the role of Wnt/β-catenin signaling pathway in the pathogenesis and progression of temporomandibular joint osteoarthritis (TMJ OA) caused by overloaded force. Materials and methods: We generated a rat model of forward mandibular extension device to induce TMJ OA by overloaded force. Condylar cartilage samples were collected at 2wk, 4wk, and 8wk after appliances were installed. Changes of the condylar cartilage and subchondral bone were evaluated by hematoxylin and eosin (HE), Safranin O and Fast Green staining (SO&FG), micro-CT, tartrate resistant acid phosphatase (TRAP) staining. The expression levels of β-catenin, COL-2, MMP3 and sclerostin (SOST) were detected by immunohistochemistry (IHC) and PCR. Results: HE, SO&FG, micro-CT, OARSI and Mankin scores showed that the condyle cartilage layer was significantly thinner and proteoglycan loss in the overloded group. TRAP staining exhibited that the number of positive osteoclasts increased and OPG level decreased in the overload group. IHC, PCR showed that the expression of COL2 and SOST decreased, while MMP3 and β-catenin increased in the overload group. Conclusion: Wnt/β-catenin signaling pathway is activated in the progress of mandibular condylar cartilage degeneration and subchondral bone loss induced by overloaded functional orthopedic force (OFOF).
Objective: To explore the role of Wnt/β-catenin signaling pathway in the pathogenesis and progression of temporomandibular joint osteoarthritis (TMJ OA) caused by overloaded force. Materials and methods: We generated a rat model of forward mandibular extension device to induce TMJ OA by overloaded force. Condylar cartilage samples were collected at 2wk, 4wk, and 8wk after appliances were installed. Changes of the condylar cartilage and subchondral bone were evaluated by hematoxylin and eosin (HE), Safranin O and Fast Green staining (SO&FG), micro-CT, tartrate resistant acid phosphatase (TRAP) staining. The expression levels of β-catenin, COL-2, MMP3 and sclerostin (SOST) were detected by immunohistochemistry (IHC) and PCR. Results: HE, SO&FG, micro-CT, OARSI and Mankin scores showed that the condyle cartilage layer was significantly thinner and proteoglycan loss in the overloded group. TRAP staining exhibited that the number of positive osteoclasts increased and OPG level decreased in the overload group. IHC, PCR showed that the expression of COL2 and SOST decreased, while MMP3 and β-catenin increased in the overload group. Conclusion: Wnt/β-catenin signaling pathway is activated in the progress of mandibular condylar cartilage degeneration and subchondral bone loss induced by overloaded functional orthopedic force (OFOF).
Authors: Daniel J Leong; Xiang I Gu; Yonghui Li; Jonathan Y Lee; Damien M Laudier; Robert J Majeska; Mitchell B Schaffler; Luis Cardoso; Hui B Sun Journal: Matrix Biol Date: 2010-02-12 Impact factor: 11.583
Authors: Mei Zhu; Dezhi Tang; Qiuqian Wu; Suyang Hao; Mo Chen; Chao Xie; Randy N Rosier; Regis J O'Keefe; Michael Zuscik; Di Chen Journal: J Bone Miner Res Date: 2009-01 Impact factor: 6.741