Histomorphometric profile, pathophysiology and reversibility of corticosteroid-induced osteoporosis

Bressot, C; Meunier, Pierre J.; Chapuy, M. C.; Lejeune, E; Edouard, C.; Darby, A. J.

doi:10.1016/0221-8747(79)90024-9

Cited by 297 publications

(101 citation statements)

References 26 publications

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“…Glucocorticoids decrease bone formation and stimulate bone resorption, the latter partly secondary to reduced intestinal calcium absorption (1). In accord, histomorphometric studies in steroid-induced osteopenia have shown decreased bone formation rate and signs of increased bone resorption (2)(3)(4). Bone mineral content (BMC) and density (BMD) are markedly decreased in untreated CS, with significant improvement following treatment (5)(6)(7)(8).…”

Section: Introductionmentioning

confidence: 53%

Decreased bone area, bone mineral content, formative markers, and increased bone resorptive markers in endogenous Cushing's syndrome

Godang

Ueland

Bollerslev

1999

European Journal of Endocrinology

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It is well established that chronic excess of glucocorticoids has negative effects on bone and collagen turnover, and that secondary osteoporosis is a known clinical complication of endogenous Cushing's syndrome (CS). The aim of the present study was to evaluate bone dimension and bone mineral content in relation to biochemical markers of bone and collagen turnover, in a consecutive series of 23 patients with endogenous CS (18 with pituitary adenoma and 5 with adrenal tumor; 17 women, 6 men; mean age 39.7 Ϯ 2.8 (S.E.M.) and 44.3 Ϯ 3.1 years respectively), compared with 23 age-, sex-and body mass index-matched healthy controls.Bone mineral densities were uniformly reduced in the different regions analyzed: lumbar spine (16.1%, P < 0.001), femoral neck (15.2%, P < 0.001), total body (11.5%, P < 0.001), and the subregions of arms (8.4%, P < 0.05), legs (10.1%, P < 0.05) and trunk (15.8%, P < 0.001). Similar results were observed for bone mineral content, although these were less prominent. The calculated area was significantly decreased in trunk (13.8%, P < 0.01) and total body (11.6%, P < 0.05).Serum levels of osteocalcin were significantly decreased (28%, P < 0.03) in patients with CS. No significant differences were observed for the formative markers carboxyterminal propeptide of type I procollagen and aminoterminal propeptide of type I procollagen. Markers of bone resorption, serum Crosslaps and carboxyterminal cross-linked telopeptide of type I collagen were increased in patients compared with controls, although only significantly for Crosslaps (P < 0.02). No correlations between formative and resorptive markers were found in the patients, but in controls, the formative markers were positively correlated with resorptive markers.In conclusion, bone dimension and bone mineral content of the entire skeleton are found to be decreased in endogenous CS. As judged by biochemical markers of bone remodeling, this is caused by decreased bone formation and an increased bone resorption.

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Section: Introductionmentioning

confidence: 53%

Decreased bone area, bone mineral content, formative markers, and increased bone resorptive markers in endogenous Cushing's syndrome

Godang

Ueland

Bollerslev

1999

European Journal of Endocrinology

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“…In this study, PICP levels increased with treatment. This may be a consequence of either the removal of the known suppressive effect of high-dose corticosteroid on osteoblasts (34,39) or a reduction of systemic inflammation on bone turnover. In animal models (1.5) and in other inflammatory diseases (38), there is evidence of osteoblast suppression by systemic inflammation.…”

Section: Discussionmentioning

confidence: 99%

Effects of inflammation and treatment on bone turnover and bone mass in polymyalgia rheumatica

Dolan

Moniz

Dasgupta

et al. 1997

Arthritis & Rheumatism

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Objective. Polymyalgia rheumatica (PMR) has an abrupt onset of inflammatory symptoms, making it a useful model for studying the effects of inflammation in bone. PMR requires corticosteroid treatment, which may itself have a detrimental effect on bone. This study used serially measured biochemical markers of bone turnover and bone density to address the relative contributions of systemic inflammation and corticosteroid therapy to bone loss.Methods. Fifty untreated patients with PMR were randomized to receive oral prednisolone or intramuscular methylprednisolone. Biochemical bone markers (pyridinoline [PYR] , deoxypyridinoline [DPYR] , procollagen type I carboxy-terminal peptide [PICP]) and bone mineral density (BMD) were measured at baseline and at 6, 12, and 24 months.Results. The median disease duration at presentation was 12 weeks (range 5-32 weeks). Levels of urinary crosslinks were increased in patients with untreated PMR compared with controls (PYR 74.9 f 30.0 nmoledmmole creatinine, DPYR 14.6 2 6.4 nmoles/ mmole creatinine [mean f SD]; P = 0.0001); the PICP level was normal (115.0 2 39.0 pg/liter). With treatment, the crosslinks levels fell and PICP levels rose within 6 months (P = 0.01). Bone resorption (PYR) correlated with untreated disease activity (erythrocyte sedimentation rate [ESR]) (r = 0.5, P = 0.003) and with interleukin-6 levels (r = 0.48, P = 0.05). There was Conclusion. Inflammation in PMR increases bone resorption and appears to have a more detrimental effect on bone than does low-dose corticosteroid. If corticosteroids can be tapered and discontinued, bone loss in PMR can be a transient phenomenon.

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“…A study of 17 patients found that whereas patients with active Cushing's syndrome have a substantially reduced BMD, previously cured patients had normal BMD [114]. A morphometric analysis in two cured Cushing's patients found a dramatic renewal of osteoblastic activity, with extended osteoid surfaces and normal appositional rate [115].…”

Section: Offset Of Skeletal Effectsmentioning

confidence: 99%

The Epidemiology of Corticosteroid-Induced Osteoporosis: a Meta-analysis

Staa

Leufkens

Cooper

2002

Osteoporosis International

1,027

272

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Abstract. Studies of oral corticosteroid dose and loss of bone mineral density have reported inconsistent results. In this meta-analysis, we used information from 66 papers on bone density and 23 papers on fractures to examine the effects of oral corticosteroids on bone mineral density and risk of fracture. Strong correlations were found between cumulative dose and loss of bone mineral density and between daily dose and risk of fracture. The risk of fracture was found to increase rapidly after the start of oral corticosteroid therapy (within 3 to 6 months) and decrease after stopping therapy. The risk remained independent of underlying disease, age and gender. We conclude that oral corticosteroid treatment using more than 5 mg (of prednisolone or equivalent) daily leads to a reduction in bone mineral density and a rapid increase in the risk of fracture during the treatment period. Early use of preventive measures against corticosteroid-induced osteoporosis is recommended.

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Histomorphometric profile, pathophysiology and reversibility of corticosteroid-induced osteoporosis

Cited by 297 publications

References 26 publications

Decreased bone area, bone mineral content, formative markers, and increased bone resorptive markers in endogenous Cushing's syndrome

Decreased bone area, bone mineral content, formative markers, and increased bone resorptive markers in endogenous Cushing's syndrome

Effects of inflammation and treatment on bone turnover and bone mass in polymyalgia rheumatica

The Epidemiology of Corticosteroid-Induced Osteoporosis: a Meta-analysis

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