Growth factor control of bone mass.

Abstract

Bone formation is determined by the number and function of osteoblasts. Cell number is governed by factors that regulate the replication and differentiation of pre-osteoblasts and factors that regulate osteoblastic cell death. Cell function is controlled by signals acting on the mature osteoblast. Platelet-derived and fibroblast growth factors are bone cell mitogens. Bone morphogenetic proteins (BMPs) and Wnt induce the differentiation of mesenchymal cells toward osteoblasts, and insulin-like growth factor (IGF)-I stimulates the function of mature osteoblasts and prevents their death. The activity of BMP, Wnt, and IGF-I is modulated by extracellular antagonists or binding proteins. Changes in growth factor synthesis and activity may play a role in the pathogenesis of selected forms of osteoporosis, and alterations in the expression or binding of the extracellular antagonists can be associated with changes in bone mass. Current approaches to bone anabolic therapies for osteoporosis include the administration of a growth factor, such as IGF-I, or the neutralization of an antagonist. Ideally, the targeting of an anabolic agent should be specific to bone to preclude non-skeletal unwanted side effects. Clinical trials are needed to determine the long-term effectiveness and safety of novel anabolic agents for the management of osteoporosis.

• Authors: Ernesto Canalis
• Journal: Journal of cellular biochemistry (J Cell Biochem) Vol. 108 Issue 4 Pg. 769-77 (Nov 01 2009) ISSN: 1097-4644 [Electronic] United States
• PMID: 19718659 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Review)
• Copyright: (c) 2009 Wiley-Liss, Inc.

Chemical References

• Bone Morphogenetic Proteins
• Intercellular Signaling Peptides and Proteins
• Wnt Proteins
• Insulin-Like Growth Factor I

Topics

• Animals
• Bone Morphogenetic Proteins (metabolism)
• Bone and Bones (metabolism)
• Cell Differentiation
• Cell Lineage
• Humans
• Insulin-Like Growth Factor I (metabolism)
• Intercellular Signaling Peptides and Proteins (metabolism)
• Mice
• Mice, Transgenic
• Models, Biological
• Mutation
• Osteoblasts (cytology, metabolism)
• Osteoporosis (metabolism, prevention & control)
• Wnt Proteins (antagonists & inhibitors, metabolism)