Mechanisms of disease: is osteoporosis the obesity of bone?
Osteoporosis and obesity, two disorders of body composition, are growing in prevalence. Interestingly, these diseases share several features including a genetic predisposition and a common progenitor cell. With aging, the composition of bone marrow shifts to favor the presence of adipocytes, osteoclast activity increases, and osteoblast function declines, resulting in osteoporosis. Secondary causes of osteoporosis, including diabetes mellitus, glucocorticoids and immobility, are associated with bone-marrow adiposity. In this review, we ask a provocative question: does fat infiltration in the bone marrow cause low bone mass or is it a result of bone loss? Unraveling the interface between bone and fat at a molecular and cellular level is likely to lead to a better understanding of several diseases, and to the development of drugs for both osteoporosis and obesity.
Rosen
Clifford J
CJ
The Jackson Laboratory in Bar Harbor, ME 04401, USA. rofe@aol.com
Bouxsein
Mary L
ML
D017667:Adipocytes / Q000502:physiology; D000273:Adipose Tissue / Q000503:physiopathology; D000375:Aging / Q000502:physiology; D000818:Animals; D001823:Body Composition / Q000502:physiology; D015519:Bone Density / Q000502:physiology; D001853:Bone Marrow / Q000503:physiopathology; D001842:Bone and Bones / Q000503:physiopathology; D002454:Cell Differentiation / Q000502:physiology; D006801:Humans; D020738:Leptin / Q000502:physiology; D008279:Magnetic Resonance Imaging; D009765:Obesity / Q000503:physiopathology*; D010024:Osteoporosis / Q000503:physiopathology*; D047495:PPAR gamma / Q000502:physiology
D020738:Leptin; D047495:PPAR gamma