Apoptosis and osteoporosis.
During normal bone remodeling, the rate of supply of new osteoblasts and osteoclasts and the timing of the death of osteoclasts, osteoblasts, and osteocytes by apoptosis are critical determinants of the initiation of new BMUs and the extension or reduction of the lifetime of existing ones. Disruption of the fine balance among these processes may be an important mechanism behind the deranged bone turnover found in most metabolic disorders of the adult skeleton. Like most armies, the amount 5 of work done by bone cells is far more dependent on numbers than vigor. Therapeutic agents that alter the prevalence of apoptosis of osteoblasts and osteoclasts can correct the imbalance in cell numbers that is the basis of the diminished bone mass and increased risk of fractures in osteoporosis.
Weinstein
R S
RS
Department of Internal Medicine, Center for Osteoporosis and Metabolic Bone Diseases, and the Central Arkansas Veterans Healthcare System, University of Arkansas for Medical Sciences, Little Rock, USA.
Manolagas
S C
SC
D000305:Adrenal Cortex Hormones / Q000009:adverse effects; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000009:adverse effects; D017209:Apoptosis; D001861:Bone Regeneration / Q000187:drug effects; D016723:Bone Remodeling / Q000187:drug effects; D006801:Humans; D010020:Osteonecrosis / Q000139:chemically induced; D010024:Osteoporosis / Q000188:drug therapy / Q000209:etiology / Q000473:pathology* / Q000517:prevention & control; D015663:Osteoporosis, Postmenopausal / Q000473:pathology; D011241:Prednisone / Q000009:adverse effects
D000305:Adrenal Cortex Hormones; D000893:Anti-Inflammatory Agents; D011241:Prednisone