Glucocorticoids, osteocytes, and skeletal fragility: the role of bone vascularity.
Glucocorticoid administration is required for many inflammatory and autoimmune diseases, but use of these drugs is associated with skeletal side effects including bone loss, fractures, and osteonecrosis. Fractures often occur without a reduction in bone mineral density, strongly suggesting that glucocorticoid excess adversely affects other aspects of bone strength. Although the primary effects of glucocorticoid excess on the skeleton are directly on bone cells, a vascular connection between these cells and the loss of bone strength appears likely. This review examines this connection and how it may explain the greater decline in bone strength than loss of bone mass that occurs with glucocorticoid excess.
Weinstein
Robert S
RS
Department of Internal Medicine and the Central Arkansas Veterans Healthcare System,University of Arkansas for Medical Sciences, Little Rock, AR 72205-7199, USA. weinsteinroberts@uams.edu
D000818:Animals; D015519:Bone Density / Q000187:drug effects / Q000502:physiology; D001842:Bone and Bones / Q000098:blood supply* / Q000187:drug effects*; D005938:Glucocorticoids / Q000009:adverse effects* / Q000627:therapeutic use; D006801:Humans; D018836:Inflammation Mediators / Q000009:adverse effects / Q000627:therapeutic use; D010011:Osteocytes / Q000187:drug effects* / Q000473:pathology* / Q000502:physiology; D010024:Osteoporosis / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology
D005938:Glucocorticoids; D018836:Inflammation Mediators