The growth plate is the cartilaginous portion of long bones where the longitudinal growth of the bone takes place. Its structure comprises chondrocytes suspended in a collagen matrix that go through several stages of maturation until they finally die, and are replaced by osteoblasts, osteoclasts, and lamellar bone. The process of endochondral ossification is coordinated by chondrocytes and a variety of humoral factors including growth hormone, parathyroid hormone, oestrogen, growth factors, cytokines, and various signalling pathways. Chondrocytes progress from a resting state to enter the phases of proliferation and hypertrophy. Under the influence of oestrogen, the proliferation of chondrocytes decreases as the resting chondrocytes are consumed. During the terminal phase of differentiation, cartilage is replaced by blood vessels and organized bone tissue, and once chondrocytes have died, the longitudinal growth of the bone ceases and the growth plate closes. The highly complex regulatory signals involved in this process are genetically determined, and genetic perturbations in any of the associated genes can result in abnormalities of bone growth. Hundreds of chondrodysplasias have been described, pointing to the complexity of the humoral control systems involved in endochondral ossification. While our knowledge of the mechanisms behind the various bone growth control systems is improving, a deeper understanding of the underlying processes could aid clinicians to better understand bone health and bone growth abnormalities. This review describes the current clinical research into the physiology of the growth plate. Cite this article: EFORT Open Rev 2020;5:498-507. DOI: 10.1302/2058-5241.5.190088
Background/aim: The treatment of posttraumatic deformities and differences in length between the extremities resulting from physeal injury remains controversial. The aims of this study were to compare the efficacy of tissue-engineered, monolayer, and allogeneic mesenchymal stem cell sheets and chondrocyte sheets for physeal arrest treatment and to investigate cell sheet technology as a novel method for cell transplantation in physeal cartilage repair. Materials and methods: A proximal tibial physeal injury was induced in New Zealand rabbits. Allogeneic mesenchymal stem cells (MSCs) and chondrocytes were cultured in temperature-responsive culture dishes and applied to the iatrogenic partial growth plate defects in single-sheet grafts (cell sheets). Treatment efficacy was determined using radiological measurements, as well as histological and immunohistochemical staining. Results: Treatment with MSCs and chondrocytes prevented endochondral ossification in the physeal plate, and bone growth resumed after treatment in both the MSC and chondrocyte cell groups. We found significant differences in radiological evaluations between preand posttreatment measurements in both MSC and chondrocyte groups. Transplanted cells were observed in the damaged area in both of the groups, which differentiated in the direction of growth plate cartilage. Conclusion: Our results support the hypothesis that MSC or chondrocyte transplantation using the cell-sheet technique described in the present study aids in the regeneration of cartilage tissue during physeal arrest after growth plate damage.
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