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BACKGROUND: Growth differentiation factor 5, a member of the transforming growth factor-β superfamily and bone morphogenetic protein family, plays an important role in articular cartilage injury repair, bone regeneration, improvement of intervertebral disc degeneration, tendon healing, and neurodevelopment. OBJECTIVE: To review the research progress of growth differentiation factor 5 in inducing chondrocytes, nucleus pulposus-like cells, tendon cell differentiation, as well as inducing bone formation and neurodevelopment. METHODS: The search terms “growth differentiation factor 5, articular cartilage, bone, nucleus pulposus cells, tendon, nerve regeneration” were used in CNKI, WanFang and PubMed. According to the inclusion and exclusion criteria, the articles not related to the subject matter were excluded and 69 articles related to growth differentiation factor 5 were included. RESULTS AND CONCLUSION: (1) Growth differentiation factor 5 can induce chondrogenic and osteoblastic differentiation of mesenchymal stem cells, but the concentration boundary of growth differentiation factor 5 to induce chondrogenic or osteoblastic differentiation remains unclear. (2) Growth differentiation factor 5 can induce mesenchymal stem cells to differentiate into nucleus pulposus cells, which may play a role in the treatment of intervertebral disc degeneration. (3) Growth differentiation factor 5 can induce mesenchymal stem cells to differentiate into tendon cells and play an important role in tendon repair and prevention of postoperative tendon adhesion. (4) Growth differentiation factor 5 can induce neurodevelopment and promote nerve regeneration. [ABSTRACT FROM AUTHOR]

BACKGROUND: Growth differentiation factor 5 is a member of the transforming growth factor superfamily and one of the earliest markers of joint development. Growth differentiation factor 5 has an important role in cartilage repair. OBJECTIVE: To explore the action mechanism of growth differentiation factor 5-induced chondrogenic differentiation of bone marrow mesenchymal stem cells. METHODS: Rabbit bone marrow mesenchymal stem cells were isolated and cultured. CCK-8 assay was used to detect the effect of different mass concentrations of growth differentiation factor 5 on the proliferation activity of bone marrow mesenchymal stem cells. RT-PCR was utilized to detect the expression of genes related to chondrogenic differentiation of bone marrow mesenchymal stem cells induced by different mass concentrations of growth differentiation factor 5. To further investigate the action mechanism of growth differentiation factor 5-induced chondrogenic differentiation of bone marrow mesenchymal stem cells, we added inhibitor XAV-939 and activator Laduviglusib of Wnt/β-catenin signaling pathways to induce cell culture for 14 days. RT-PCR and western blot assay were performed to detect the expression of cartilage-related genes and Wnt/β-catenin signaling pathway proteins. RESULTS AND CONCLUSION: (1) CCK-8 results showed no significant effect of growth differentiation factor 5 on the proliferation of bone marrow mesenchymal stem cells. (2) Growth differentiation factor 5 promoted the expression of cartilage-related genes type II collagen, aggrecan and Sox9, among which growth differentiation factor 5 induced a significant upregulation of cartilage-related genes in the 50 ng/mL group. (3) Addition of Laduviglusib, an activator of Wnt/ β-catenin signaling pathway, upregulated Sox9, β-catenin and type II collagen expression (P < 0.05). Addition of XAV939, an inhibitor of Wnt/β-catenin signaling pathway, down-regulated Sox9, β-catenin and type II collagen expression (P < 0.05). (4) Taken together, growth differentiation factor 5-induced chondrogenic differentiation of bone marrow mesenchymal stem cells may be associated with the activation of the Wnt/β-catenin signaling pathway. [ABSTRACT FROM AUTHOR]

OBJECTIVE: To explore the role of growth differentiation factor 5 in osteoarthritis and some existing problems, attempting to provide a theoretical basis for the treatment of osteoarthritis. METHODS: Literature related to the role and mechanism of growth differentiation factor 5 in osteoarthritis was searched in CNKI, WanFang, and PubMed databases with “growth differentiation factor 5, articular cartilage, cell migration, cell proliferation, subchondral bone, inflammation, osteoarthritis, rheumatoid arthritis” as Chinese and English search terms, respectively. RESULTS AND CONCLUSION: Growth differentiation factor 5 promotes the differentiation of mesenchymal stem cells into chondrocytes, expresses type II collagen and proteoglycans, and maintains the characteristics of chondrocytes. Growth differentiation factor 5 promotes the hypertrophic differentiation of chondrocytes, but some studies have shown that the expression of chondrocyte hypertrophy markers is reduced after induction with growth differentiation factor 5, indicating that growth differentiation factor 5 is more beneficial than harmful to cartilage repair. Growth differentiation factor 5 can promote steogenesis, increase the mineralization density of subchondral bone, and indirectly promote the repair of cartilage through the repair of subchondral bone. Inflammatory factors are one of the factors that promote the occurrence and development of osteoarthritis. Growth differentiation factor 5 can inhibit the expression of inflammatory factors, thereby protecting against osteoarthritis. As a “multifunctional” inducer, growth differentiation factor 5 has certain effects on cartilage, subchondral bone and inflammation. However, its mechanism of action is still unclear and needs further studies. Overall, growth differentiation factor 5 is expected to be an osteoarthritis-treating drug in the future. [ABSTRACT FROM AUTHOR]

BACKGROUND: The main pathological change of osteoarthritis is cartilage degeneration. The current means of treatment of osteoarthritis is very limited. With the development of interdisciplinary science in recent years, tissue engineering brings new hope for the repair and reconstruction of cartilage degeneration. Nerve growth factor plays an important role in the physiological and pathological processes of multiple systems and organs in the body. In recent years, it has been found that nerve growth factor is closely related to the occurrence and development of osteoarthritis. OBJECTIVE: To explore the research progress of nerve growth factor in osteoarthritis in recent years from the aspects of nerve growth factor’s effects on cartilage, subchondral bone, synovium, and pain. It was envisaged that nerve growth factor could be used as a bioactive factor or cytokine in tissue engineering to repair bone and cartilage, providing new thoughts and ideas for the treatment of osteoarthritis. METHODS: In PubMed, Web of Science, CNKI, and WanFang databases, search terms used were “nerve growth factor, TrkA, osteoarthritis, chondrocyte, cartilage degeneration, subchondral bone, synovium, pain” in English and Chinese. Basic and clinical studies on the mechanisms of nerve growth factor in osteoarthritis were searched from January 1, 2010 to July 1, 2021. RESULTS AND CONCLUSION: Nerve growth factor promoted the differentiation of stem cells, maintained the phenotype of chondrocytes, and promoted the expression of chondrocytes to maintain the characteristics of cartilage. Nerve growth factor promoted osteogenic expression in a variety of ways, inducing or aggravating the occurrence and development of osteoarthritis, but some studies suggest that subchondral bone repair is beneficial to cartilage repair. Synovium promoted nerve growth factor expression and participated in the pain of osteoarthritis. Synovium also indirectly promoted the expression of cartilage degradation protein under the stimulation of inflammatory factors. Nerve growth factor is the main signal factor causing pain. The use of nerve growth factor antibody has a good and definite effect on the pain of osteoarthritis, but its use is limited by serious side effects, and the mechanism of its occurrence is explored. It may still become the most potential analgesic drugs in the future. [ABSTRACT FROM AUTHOR]

BACKGROUND: Repair of osteochondral defects is a major challenge that orthopedic surgeons face today, because current treatments fail to achieve satisfactory results. With the development of tissue engineering in recent years, new hope has been brought for the repair of osteochondral defects. Bone morphogenetic protein 2 is an important factor involved in bone growth, development, and repair, with good osteoinductive effects. In recent years, it has been found that bone morphogenetic protein 2 also has an effect on cartilage development. OBJECTIVE: To investigate the research progress of bone morphogenetic protein 2 in the repair of osteochondral defects in recent years and to provide new ideas and strategies for the treatment of osteochondral defects by summarizing the application of bone morphogenetic protein 2 in the repair of various types of bone defects. METHODS: WanFang, CNKI, and PubMed databases were searched for literature regarding the mechanism of bone morphogenetic protein 2 in the repair of osteochondral defects and its application in osteochondral tissue engineering published between January 1, 2012 and July 1, 2022. The search terms were “Bone morphogenetic protein 2, Chondrocytes, Cartilage defects, Bone defects, Mesenchymal stem cells, MSC, Signaling pathways” in Chinese and English. RESULTS AND CONCLUSION: Bone morphogenetic protein 2 promotes chondrogenic differentiation of mesenchymal stem cells and can maintain the chondrocyte phenotype to maintain cartilage properties. Bone morphogenetic protein 2 controls chondrogenesis by regulating chondrocyte glucose metabolism. Bone morphogenetic protein 2 acts on osteogenesis through the classical Smad 1/5/8 signaling pathway, but the mechanism of chondrogenesis is not clear. The current research and application of bone morphogenetic protein 2 in tissue engineering mainly focus on the field of bone defect repair, and less is reported on cartilage defect repair. How to prevent bone morphogenetic protein 2 from promoting the transformation of chondrocytes to hypertrophic chondrocytes will be the focus of future research. [ABSTRACT FROM AUTHOR]