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Journal ArticleDOI

Markers of bone metabolism in postmenopausal women with rheumatoid arthritis. Effects of corticosteroids and hormone replacement therapy.

TLDR
Bone formation appears to be reduced, partly reflecting disease activity, whereas resorption is increased only in steroid users, and bone metabolism may be uncoupled in chronic RA.
Abstract
Objective. To investigate bone metabolism in postmenopausal women with rheumatoid arthritis (RA) treated with or not treated with corticosteroids, and the response to hormone replacement therapy (HRT). Methods. One hundred six RA patients were divided into those taking low-dose steroids (RA+; n = 35) and those not (RA–; n = 71) and randomly allocated to receive HRT or calcium for 2 years. Bone formation markers included serum osteocalcin (OC) and bone-specific alkaline phosphatase, and resorption markers included urinary deoxypyridinoline (DPyr) and CrossLaps (XL). Bone mineral density (BMD) was measured annually using dual x-ray absorptiometry. Results. OC levels were significantly lower in both the RA+ and RA– groups compared with 112 healthy control subjects (P < 0.01 and P < 0.05, respectively), but were similar in the 2 RA groups. DPyr and XL levels were elevated in the RA+ group compared with the RA– group (P < 0.05) but were similar between the RA– group and controls. OC was negatively correlated with parameters of disease activity (P < 0.05). After HRT, XL excretion decreased significantly in the overall RA group. Three-month changes in XL correlated with 2-year changes in spinal BMD (P < 0.01). Conclusion. Bone metabolism may be uncoupled in chronic RA. Bone formation appears to be reduced, partly reflecting disease activity, whereas resorption increased only in steroid users. HRT reduces resorption in RA irrespective of steroid usage, emphasizing its value in the treatment of postmenopausal women with RA.

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Journal ArticleDOI

The complex role of estrogens in inflammation

TL;DR: This review reinforces the concept that estrogens have antiinflammatory but also proinflammatory roles depending on above-mentioned criteria and explains that a uniform concept as to the action of estrogens cannot be found for all inflammatory diseases due to the enormous variable responses of immune and repair systems.
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Identification of cell types responsible for bone resorption in rheumatoid arthritis and juvenile rheumatoid arthritis.

TL;DR: The resorbing cells in RA exhibit a definitive osteoclastic phenotype, suggesting that pharmacological agents that inhibit osteoclast recruitment or activity are rational targets for blocking focal bone erosion in patients with RA and JRA.
Journal ArticleDOI

Rheumatic diseases: the effects of inflammation on bone.

TL;DR: An overview of the cell types, inflammatory mediators, and mechanisms that are implicated in bone loss and new bone formation in inflammatory joint diseases is provided.
Journal ArticleDOI

Promotion of osteoclast survival and antagonism of bisphosphonate-induced osteoclast apoptosis by glucocorticoids.

TL;DR: Results indicate that the early loss of bone with glucocorticoid excess is caused by extension of the life span of pre-existing osteoclasts, an effect not preventable by bisphosphonates, and the early beneficial effects of these agents must be due, in part, to prolonging the life spans of osteoblasts.
Journal ArticleDOI

Association between Corticosteroid Use and Vertebral Fractures in Older Men with Chronic Obstructive Pulmonary Disease

TL;DR: Data indicate that vertebral fractures are common in older men with COPD; the likelihood of these fractures is greatest in those men using continuous systemic steroids.
References
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Journal ArticleDOI

Measurement of patient outcome in arthritis.

TL;DR: A structure for representation of patient outcome is presented, together with a method for outcome measurement and validation of the technique in rheumatoid arthritis, and these techniques appear extremely useful for evaluation of long term outcome of patients with rheumatic diseases.
Journal ArticleDOI

Stimulation of bone resorption and inhibition of bone formation in vitro by human tumour necrosis factors

TL;DR: It is reported that both cytokines at 10−7 to 10−9M caused osteoclastic bone r(c)sorption and inhibited bone collagen synthesis in vitro and suggest that at least part of the bone-resorbing activity present in activated leukocyte culture supernatants may be due to these cytokines.
Journal ArticleDOI

Glucocorticoid-induced osteoporosis: pathogenesis and management.

TL;DR: Osteoporosis is common in patients requiring long-term treatment with glucocorticoids, and reasonable recommendations include the use of a glucoc Corticoid with a short half-life in the lowest dose possible, maintenance of physical activity, adequate calcium and vitamin D intake, sodium restriction and use of thiazide diuretics, and gonadal hormone replacement.
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