Bone Mass In Rheumatoid Arthritis Research Articles

AB0333 The Risk of Osteoporotic Fractures According to the FRAX Model in Korean Patients with Rheumatoid Arthritis

BackgroundRheumatoid arthritis (RA) is a systemic inflammatory disease and is commonly associated with osteoporosis. To prevent osteoporotic fractures in patients with RA, it is important to identify the high risk...

SAT0467 Relationship of Body Composition and Abdominal Adiposity with Bone Mineral Density in Patients with Rheumatoid Arthritis

BackgroundIn general population,a high body mass index,is considered protective against osteoporosis.The relationship of body composition and abdominal adiposity with bone mineral density (BMD) in rheumatoid arthritis (RA) has not been...

AB0722 Trabecular bone score in rheumatoid arthritis and ankylosing spondylitis and changes during long term treatment with tnfa blocking agents

BackgroundInflammatory rheumatic diseases such as rheumatoid arthritis (RA) and ankylosing spondylitis (AS) are associated with osteoporosis. Bone mass in RA and AS has been well evaluated by measuring areal bone...

AB0378 Microarchitecture assessment by trabecular bone score at the spine in patients with rheumatoid arthritis and ankylosing spondylitis. Preliminary results

BackgroundInflammatory rheumatic diseases such as rheumatoid arthritis (RA) or ankylosing spondylitis (AS) are associated with osteoporosis and increased risk of fractures. This bone involvement is related to the inflammatory process,...

THU0402 Effects of Raloxifene for Prevention of Bone Loss in Rheumatoid Arthritis Women Receiving Long-Term Glucocorticoids

BackgroundThe inflammatory disease, oestrogen deficiency and glucocorticoids contribute to the generalized bone loss seen in postmenopausal rheumatoid arthritis (RA).ObjectivesThe aim of this study is to prove that raloxifene treatment is...

Tumor necrosis factor α and interleukin‐1β modulate calcium and nitric oxide signaling in mechanically stimulated osteocytes

Inflammatory diseases often coincide with reduced bone mass. Mechanoresponsive osteocytes regulate bone mass by maintaining the balance between bone formation and resorption. Despite its biologic significance, the effect of inflammation on osteocyte mechanoresponsiveness is not understood. To fill this gap, we investigated whether the inflammatory cytokines tumor necrosis factor alpha (TNFalpha) and interleukin-1beta (IL-1beta) modulate the osteocyte response to mechanical loading. MLO-Y4 osteocytes were incubated with TNFalpha (0.5-30 ng/ml) or IL-1beta (0.1-10 ng/ml) for 30 minutes or 24 hours, or with calcium inhibitors for 30 minutes. Cells were subjected to mechanical loading by pulsatile fluid flow (mean +/- amplitude 0.7 +/- 0.3 Pa, 5 Hz), and the response was quantified by measuring nitric oxide (NO) production using Griess reagent and by measuring intracellular calcium concentration ([Ca(2+)](i)) using Fluo-4/AM. Focal adhesions and filamentous actin (F-actin) were visualized by immunostaining, and apoptosis was quantified by measuring caspase 3/7 activity. Cell-generated tractions were quantified using traction force microscopy, and cytoskeletal stiffness was quantified using optical magnetic twisting cytometry. Pulsatile fluid flow increased [Ca(2+)](i) within seconds (in 13% of cells) and NO production within 5 minutes (4.7-fold). TNFalpha and IL-1beta inhibited these responses. Calcium inhibitors decreased pulsatile fluid flow-induced NO production. TNFalpha and IL-1beta affected cytoskeletal stiffness, likely because 24 hours of incubation with TNFalpha and IL-1beta decreased the amount of F-actin. Incubation with IL-1beta for 24 hours stimulated osteocyte apoptosis. Our results suggest that TNFalpha and IL-1beta inhibit mechanical loading-induced NO production by osteocytes via abrogation of pulsatile fluid flow-stimulated [Ca(2+)](i), and that IL-1beta stimulates osteocyte apoptosis. Since both NO and osteocyte apoptosis affect osteoclasts, these findings provide a mechanism by which inflammatory cytokines might contribute to bone loss and consequently affect bone mass in rheumatoid arthritis.

Biomarks in secondary osteoporosis.

The existence of a metabolic disease in rheumatoid arthritis in distant zones of the active synovitis areas, remains controversial. Indeed, the variations found, by different authors, in PTH, in alkaline phosphatase and in serum and/or in the calcium urinary values, as well as in phosphate and hydroxyproline, have not clarified this problem, despite the demonstration by histomorphometry and by densitometrical methods, of a greater loss of the bone mass in rheumatoid arthritis. At the same time, metabolic changes in sexual hormones, primary or secondary, can modulate the immune response and interfere in the clinic expression of rheumatoid arthritis and also in the bone turnover. Therefore, the purpose of this study was to compare some parameters of the bone metabolism and of the hormonal condition, in women with rheumatoid arthritis, with and without corticotherapy and in an age-related control group. In Group RA (patients), we found relatively higher levels of phosphates, alkaline phosphatase and osteocalcin, just as in the nephrogenic c'AMP and the hydroxyproline/creatinine quotient. The blood levels of calcitonin, PTH, T3, T4, cortisol and estradiol did not show significant differences between the 2 groups, although they were lower in Group RA. On the contrary, the plasma levels of testosterone, of 4-androstenedione and DHEA.S were significantly reduced in patients with rheumatoid arthritis. These results are compatible with the existence of bone metabolic hyperactivity in rheumatoid arthritis, which can be related, directly or indirectly to the reduced androgens plasma levels, since these seem to play a protective role in auto-immune diseases and also on the bone metabolism.(ABSTRACT TRUNCATED AT 250 WORDS)

Prevalence of decreased bone mass in rheumatoid arthritis. Relation to anti-inflammatory treatment.

The bone mineral content (BMC) in both forearms (highly correlated to total body calcium) was measured by photon absorptiometry in a representative sample of rheumatoid arthritis outpatients comprising 129 patients treated with either gold salts (n = 29), penicillamine (n = 61), prednisone (n = 24), or other anti-RA drugs (n = 15). The mean BMC value was 84% of normal (p less than 0.001) with the lowest mean value in the group treated with prednisone (73% of normal). The patients as a group had hypocalcaemia (p less than 0.001), raised serum alkaline phosphatase (p less than 0.001), and normal urinary excretion rates of calcium and hydroxyproline. These results indicate that RA patients have disturbances in their calcium and bone metabolism.