Huilin Guo1, Huimin Li2, Yaping Feng2, Jin Ke1, Wei Fang1, Cheng Li3, Xing Long4. 1. State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) & Key Laboratory of Oral Biomedicine Ministry of Education (KLOBM), School and Hospital of Stomatology, Wuhan University, Wuhan, China; Department of Oral and Maxillofacial Surgery, School and Hospital of Stomatology, Wuhan University, Wuhan, China. 2. State Key Laboratory Breeding Base of Basic Science of Stomatology (Hubei-MOST) & Key Laboratory of Oral Biomedicine Ministry of Education (KLOBM), School and Hospital of Stomatology, Wuhan University, Wuhan, China. 3. Department of Stomatology, Zhongnan Hospital of Wuhan University, Wuhan, China. 4. Department of Oral and Maxillofacial Surgery, School and Hospital of Stomatology, Wuhan University, Wuhan, China. Electronic address: longxing@whu.edu.cn.
Abstract
OBJECTIVE: Increasing evidence indicates an interaction between the synovium and the cartilage in the temporomandibular joint (TMJ) and other joints. We recently demonstrated that the expression of proangiogenic factors was enhanced and that of factors promoting matrix degradation was decreased in synovial fibroblasts in condylar hyperplasia (CH). The aim of this study was to explore whether CH chondrocytes can affect the expression of these factors of synovial fibroblasts in a co-culture system. STUDY DESIGN: The expressions of vascular endothelial growth factor (VEGF), cluster of differentiation 34 (CD34), fibroblast growth factor 2 (FGF-2), and tissue inhibitor of metalloproteinase 1 (TIMP1) from CH condylar tissues were observed by using immunohistochemical methods. Synovial fibroblasts of control tissues were co-cultured with the chondrocytes of CH, and protein expressions of VEGF, FGF-2, thrombospondin 1 (TSP1), matrix metalloproteinase 3 (MMP3), and TIMP1 were examined by using Western blotting. RESULTS: Positive staining for VEGF, CD34, FGF-2, and TIMP1 was found in the hypertrophic cartilage layer of CH condylar tissues. Protein expressions of VEGF, FGF-2, and TIMP1 were significantly increased in co-cultured synovial fibroblasts, but TSP1 and MMP3 expressions were decreased. CONCLUSIONS: The angiogenic factors and matrix degradation-related factors in synovial fibroblasts co-cultured with CH chondrocytes showed the same trends as those in synovial fibroblasts from CH tissue, suggesting potential cross-talk between synovial fibroblasts and chondrocytes during CH progression.
OBJECTIVE: Increasing evidence indicates an interaction between the synovium and the cartilage in the temporomandibular joint (TMJ) and other joints. We recently demonstrated that the expression of proangiogenic factors was enhanced and that of factors promoting matrix degradation was decreased in synovial fibroblasts in condylar hyperplasia (CH). The aim of this study was to explore whether CH chondrocytes can affect the expression of these factors of synovial fibroblasts in a co-culture system. STUDY DESIGN: The expressions of vascular endothelial growth factor (VEGF), cluster of differentiation 34 (CD34), fibroblast growth factor 2 (FGF-2), and tissue inhibitor of metalloproteinase 1 (TIMP1) from CH condylar tissues were observed by using immunohistochemical methods. Synovial fibroblasts of control tissues were co-cultured with the chondrocytes of CH, and protein expressions of VEGF, FGF-2, thrombospondin 1 (TSP1), matrix metalloproteinase 3 (MMP3), and TIMP1 were examined by using Western blotting. RESULTS: Positive staining for VEGF, CD34, FGF-2, and TIMP1 was found in the hypertrophic cartilage layer of CH condylar tissues. Protein expressions of VEGF, FGF-2, and TIMP1 were significantly increased in co-cultured synovial fibroblasts, but TSP1 and MMP3 expressions were decreased. CONCLUSIONS: The angiogenic factors and matrix degradation-related factors in synovial fibroblasts co-cultured with CH chondrocytes showed the same trends as those in synovial fibroblasts from CH tissue, suggesting potential cross-talk between synovial fibroblasts and chondrocytes during CH progression.