[Local factors in bone repair]

Abstract

Besides the systemic hormones (parathyroid hormone, calcitonin...), several local factors act on bone resorption and formation. These factors are released by cells of the bone microenvironment (hematopoietic cells, fibroblasts, endothelial cells...) and also by bone cells, mainly of the osteoblastic lineage. Among the factors which increase locally bone resorption ("osteoclastic activating factors, OAF"), interleukin 1, acting alone or synergistically with tumor necrosis factor, seems to be the most potent. As parathyroid hormone, it does not act directly on osteoclasts, but stimulates cells of the osteoblastic lineage to secrete unknown factors stimulating resorption. Prostaglandins E have been thought to be among these soluble factors secreted by osteoblasts or osteoblast precursors which stimulate bone resorption directly, but it appears now that the direct effect of prostaglandins on the osteoclasts is inhibitory. Several growth factors are secreted by cells of the osteoblastic lineage and by other bone cells. They are stored in the bone matrix, from which they are released and activated during resorption. The most important are IGF-I, IGF-II, and TGF beta. These growth factors stimulate replication of the osteoblast precursors and collagen synthesis by osteoblasts, and could be responsible for the well known coupling between resorption and formation. TGF beta also seems to inhibit replication of osteoclast precursors, and could thus stop the resorption process. It seems now that estrogens and physical stress act on bone at least in part by modulating the equilibrium between these local factors which act on resorption and formation.