G-protein-coupled estrogen receptor-1 facilitates chondrocyte proliferation in pubertal epiphyseal growth plate via PTHrP/Ihh regulation.

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Abstract

Conflict of interest statement: The authors report support for attending meetings and/or travel from the Regenerative Medicine and Cell Therapy Research Center, Kaohsiung Medical University (KMU-TC112A02), unrelated to this study. 11. J Musculoskelet Neuronal Interact. 2005 Jul-Sep;5(3):194-201. Bone growth in length and width: the Yin and Yang of bone stability. Rauch F(1). Author information: (1)Genetics Unit, Shriners Hospital for Children, Montreal, Canada. frauch@shriners.mcgill.ca Bone growth in length is primarily achieved through the action of chondrocytes in the proliferative and hypertrophic zones of the growth plate. Longitudinal growth is controlled by systemic, local paracrine and local mechanical factors. With regard to the latter, a feedback mechanism must exist which ensures that bone growth proceeds in the direction of the predominant mechanical forces. How this works is unknown at present. Bone growth in length is detrimental to bone stability, but this effect is counteracted by concomitant bone growth in width. This occurs through periosteal apposition, which is the responsibility of periosteal osteoblasts. The action of these cells is mainly controlled by local factors, with modulation by systemic agents. According to the mechanostat theory, periosteal apposition is regulated by mechanical requirements. An alternative model, called sizostat hypothesis, maintains that a master gene or set of genes regulate bone growth in width to reach a pre-programmed size, independent of mechanical requirements. The virtues of these two hypotheses have been the subject of much discussion, but experimental data are scarce. Future research will have to address the question how periosteal bone cells manage to integrate mechanical, hormonal and other input to shape bones that are as strong as they need to be.