Linjian Huang1, Xieyi Cai2, Hui Li3, Qianyang Xie4, Min Zhang5, Chi Yang6. 1. Department of Oral and Maxillofacial Surgery, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory of Stomatology, Shanghai 200011, China; Department of Oral and Maxillofacial Surgery, The Second Affiliated Hospital Zhejiang University School of Medicine, Hangzhou 310009, China. Electronic address: dshuanglinjian@126.com. 2. Department of Oral and Maxillofacial Surgery, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory of Stomatology, Shanghai 200011, China. Electronic address: caixieyi27@126.com. 3. Department of Oral and Maxillofacial Surgery, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory of Stomatology, Shanghai 200011, China. Electronic address: lihui9x@163.com. 4. Department of Oral and Maxillofacial Surgery, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory of Stomatology, Shanghai 200011, China. Electronic address: aqiang2134@126.com. 5. College of Stomatology, The Fourth Military Medical University, Xi'an 710032, Shanxi Province, China. Electronic address: zhangmin@fmmu.edu.cn. 6. Department of Oral and Maxillofacial Surgery, Ninth People's Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Key Laboratory of Stomatology, Shanghai 200011, China. Electronic address: yangchi63@hotmail.com.
Abstract
OBJECTIVE: The goal of the study was to investigate the production of collagen, type II, alpha 1 (COL2A1), SOX9, alkaline phosphatase (ALP), runt-related transcription factor 2 (Runx2), Indian hedgehog (Ihh), and periarticular cell-derived parathyroid hormone-related protein (PTHrP) in mandibular condylar chondrocytes under static pressure stimuli. METHODS: Mandibular condylar chondrocytes separated from rabbit temporomandibular joint (TMJ) were treated with a static pressure of 100kPa for 0, 1, 2, 3, and 4h by an in-house-designed pressure chamber. A CCK-8 kit was used to analyze the cell viability. The production of COL2A1, SOX9, ALP, Runx2, Ihh, and PTHrP was detected by Western blot or real-time polymerase chain reaction (PCR). Changes in cell morphology were observed by scanning electron microscopy. RESULTS: Compared with the control group (0h), the cytoplasmic processes of treated chondrocytes obviously increased and elongated, and the cell viability of pressurized chondrocytes were 91.13% (1h), 103.41% (2h), 103.47% (3h), and 104.94% (4h), respectively. The exposure of condylar chondrocytes to a static pressure of 100kPa for 3-4h resulted in a significant increase in COL2A1, SOX9, ALP, and Runx2. After a static pressure loading of 100kPa, the activation of Ihh and PTHrP was also observed. CONCLUSIONS: Mandibular condylar chondrocytes adapt to alterations of the microenvironment. Ihh and PTHrP are sensitive to static pressure. Our findings suggest that static pressure accelerated the chondrogenic and osteogenic differentiation of condylar chondrocytes, which may influence the pathological progress of temporomandibular diseases.
OBJECTIVE: The goal of the study was to investigate the production of collagen, type II, alpha 1 (COL2A1), SOX9, alkaline phosphatase (ALP), runt-related transcription factor 2 (Runx2), Indian hedgehog (Ihh), and periarticular cell-derived parathyroid hormone-related protein (PTHrP) in mandibular condylar chondrocytes under static pressure stimuli. METHODS: Mandibular condylar chondrocytes separated from rabbit temporomandibular joint (TMJ) were treated with a static pressure of 100kPa for 0, 1, 2, 3, and 4h by an in-house-designed pressure chamber. A CCK-8 kit was used to analyze the cell viability. The production of COL2A1, SOX9, ALP, Runx2, Ihh, and PTHrP was detected by Western blot or real-time polymerase chain reaction (PCR). Changes in cell morphology were observed by scanning electron microscopy. RESULTS: Compared with the control group (0h), the cytoplasmic processes of treated chondrocytes obviously increased and elongated, and the cell viability of pressurized chondrocytes were 91.13% (1h), 103.41% (2h), 103.47% (3h), and 104.94% (4h), respectively. The exposure of condylar chondrocytes to a static pressure of 100kPa for 3-4h resulted in a significant increase in COL2A1, SOX9, ALP, and Runx2. After a static pressure loading of 100kPa, the activation of Ihh and PTHrP was also observed. CONCLUSIONS: Mandibular condylar chondrocytes adapt to alterations of the microenvironment. Ihh and PTHrP are sensitive to static pressure. Our findings suggest that static pressure accelerated the chondrogenic and osteogenic differentiation of condylar chondrocytes, which may influence the pathological progress of temporomandibular diseases.