Apoptosis in glucocorticoid-induced bone disease

Current Opinion in Endocrinology and Diabetes

Volumn 12, Issue 3, 2005, Pages 219-223

  Weinstein, Robert S ^a,b   Manolagas, Stavros C ^a  

^a UNIVERSITY OF ARKANSAS FOR MEDICAL SCIENCES   (United States)

^b UNIVERSITY OF ARKANSAS FOR MEDICAL SCIENCES   (United States)

Author keywords

Apoptosis; Bone strength; Glucocorticoid induced osteoporosis; Glucocorticoids; Osteoblasts; Osteoclasts; Osteocytes; Osteonecrosis

Indexed keywords

BISPHOSPHONIC ACID DERIVATIVE; GLUCOCORTICOID; PARATHYROID HORMONE;

APOPTOSIS; BONE CELL; BONE DISEASE; BONE NECROSIS; BONE STRENGTH; CELL DEATH; CELL SURVIVAL; CORTICOSTEROID INDUCED OSTEOPOROSIS; DISEASE MODEL; DRUG MECHANISM; HORMONE ACTION; HUMAN; NONHUMAN; OSTEOBLAST; OSTEOCLAST; OSTEOCYTE; OSTEOLYSIS; PATHOGENESIS; REVIEW;

EID: 20444377738     PISSN: 10683097     EISSN: None     Source Type: Journal    
DOI: 10.1097/01.med.0000162075.95591.9b     Document Type: Review

References (22)

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9. Rosen CJ. What's new with PTH in osteoporosis: where are we and where are we headed? Trends Endocrinol Metab 2004; 15:229-233. This article reviews recent findings on PTH signaling in bone and persistent questions about the use of PTH in the treatment of osteoporosis including GIO.
10. Pearce G, Tabensky DA, Delmas PD, et al. Corticosteroid-induced bone loss in men. J Clin Endocrinol Metab 1998; 83:801-806.
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13. Weinstein RS, Jia D, Powers CC, et al. The skeletal effects of glucocorticoid excess override those of orchidectomy in mice. Endocrinology 2004; 145: 1980-1987. This study showed that using well-established murine models of sex-steroid deficiency and of GIO, hypogonadism does not occur in or contribute to glucocorticoid-induced osteoporosis and that the adverse skeletal effects of glucocorticoid excess override those of orchidectomy. These findings demonstrate that the adverse effects of sex steroid withdrawal on bone are mediated by osteoblastic cells and are obviated by constraints on osteoblastogenesis, whether genetically defective or acquired because of glucocorticoid excess.
14. Weinstein RS, Jilka RL, Parfitt AM, Manolagas SC. Inhibition of osteoblastogenesis and promotion of apoptosis of osteoblasts and osteocytes by glucocorticoids: potential mechanisms of the deleterious effects on bone. J Clin Invest 1998; 102:274-282.
15. Weinstein RS, Chen JR, Powers CC, et al. Promotion of osteoclast survival and antagonism of bisphosphonate-induced osteoclast apoptosis by glucocorticoids. J Clin Invest 2002; 109:1041-1048.
16. Plotkin LI, Weinstein RS, Parfitt AM, et al. Prevention of osteocyte and osteoblast apoptosis by bisphosphonates and calcitonin. J Clin Invest 1999; 104:1363-1374.
17. O'Brien CA, Jia D, Plotkin LI, et al. Glucocorticoids act directly on osteoblasts and osteocytes to induce their apoptosis and reduce bone formation and strength. Endocrinology 2004; 145:1835-1841. This investigation uses the OG2-11β-HSD2 transgenic mouse to demonstrate the direct effects of glucocorticoids on bone-forming cells in vivo. In addition, the results suggest that glucocorticoid-induced loss of bone strength results in part from increased death of osteocytes, independently of bone loss.
18. Weinstein RS. Perspective: true strength. J Bone Miner Res 2000; 15:621-625.
19. Weinstein RS, Manolagas SC. Apoptosis and osteoporosis. Am J Med 2000; 108:153-164.
20. Weinstein RS, Nicholas RW, Manolagas SC. Apoptosis of osteocytes in glucocorticoid-induced osteonecrosis of the hip. J Clin Endocrinol Metab 2000; 85:2907-2912.
21. Jilka RL, Weinstein RS, Bellido T, et al. Increased bone formation by prevention of osteoblast apoptosis with PTH. J Clin Invest 1999; 104:439-446.
22. Bellido T, Ali AA, Plotkin LI, et al. Proteasomal degradation of Runx2 shortens PTH-induced anti-apoptotic signaling in osteoblasts: a putative explanation for why intermittent administration is needed for bone anabolism. J Biol Chem 2003; 278:50259-50272.