![]() ![]() Complement-dependent stimulation of prostaglandins synthesis and bone resorption. Raisz LG, Sandberg AL, Goodson JM, Simmons HA, Mergenhagen SE. Hypercalcemia and tumour-prostaglandins: the VX2 carcinoma model in the rabbit. Voelkel EF, Tashjian AH Jr, Franklin R, Wasserman E, Levine L. Evidence that the bone resorption stimulating factor produced by mouse fibrosarcoma cells is prostaglandin E 2: a new model for the hypercalcemia of cancer. Tashjian AH Jr, Voelkel EF, Levine L, Goldhaber P. Prostaglandins: stimulation of bone resorption in tissue culture. The effect of parathyroid hormone on the concentration of adenosine 3′, 5′-monophosphate in skeletal tissue in vitro. Thus endogenous PGs are probably important local regulators of bone turnover, and abnormalities in their production could play a role in the pathogenesis of osteoporosis.Ĭhase LR, Aurbach GD. Many other factors including mechanical forces and growth factors influence PG production in bone. Glucocorticoids probably act by a different mechanism, decreasing either arachidonic acid or PGH synthase activity. ![]() PGE 2 production and PGH synthase mRNA are increased by PTH and interleukin-1 and decreased by estrogen. A major site of regulation is at the level of the enzyme PG endoperoxide synthase (cyclooxygenase or PGH synthase). The major source appears to be cells of the osteoblast lineage. The production of PGs in bone is highly regulated. The stimulatory effect on bone formation has been demonstrated when PGs are administered exogenously, but it is not clear how endogenous PG production affects bone formation in physiological or pathologic circumstances. In osteoblastic cell lines this inhibition can be shown to occur at the level of transcription of the collagen gene. However, at high concentrations or in the presence of IGF-I, PGE 2 inhibits collagen synthesis. This increase is associated with an increase in production of insulin-like growth factor-I (IGF-I). At relatively low concentrations or in the presence of glucocorticoids, the replication and differentiation of osteoblasts is stimulated and bone formation is increased. PGs have a biphasic effect on bone formation. Stimulation of osteoclastic bone resorption may be important in mediating bone loss in response to mechanical forces and inflammation. PGs also stimulate osteoclast formation in cell culture systems. However, the major long-term effect in bone organ culture is to stimulate bone resorption by increasing the replication and differentiation of new osteoclasts. PGs have an initial, transient, direct inhibitory effect on osteoclast function. Prostaglandins (PGs), particularly PGE 2, are produced by bone and have powerful effects on bone metabolism. ![]()
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