RESUMEN
Normal bone remodeling depends of a balance between bone forming cells, osteoblasts and bone resorbing cells, the osteoclasts. In chronic arthritides and some inflammatory and autoimmune diseases such as rheumatoid arthritis, there is a great constellation of cytokines produced by pannus that impair bone formation and stimulate bone resorption by inducing osteoclast differentiation and inhibiting osteoblast maturation. Patients with chronic inflammation have multiple causes that lead to low bone mineral density, osteoporosis and a high risk of fracture including circulating cytokines, impaired mobility, chronic administration of glucocorticoids, low vitamin D levels and post-menopausal status in women, among others. Biologic agents and other therapeutic measures to reach prompt remission might ameliorate these deleterious effects. In many cases, bone acting agents need to be added to conventional treatment to reduce the risk of fractures and to preserve articular integrity and independency for daily living activities. A limited number of studies related to fractures in chronic arthritides were published, and future investigation is needed to determine the risk of fractures and the protective effects of different treatments to reduce this risk.
Asunto(s)
Artritis Reumatoide , Resorción Ósea , Fracturas Óseas , Humanos , Femenino , Osteoclastos , Huesos , Osteoblastos , CitocinasRESUMEN
Long-term glucocorticoid (GC) therapy is frequently indicated to treat autoimmune and chronic inflammatory diseases in daily clinical practice. Two of the most devastating untoward effects are bone loss and fractures. Doses as low as 2.5 mg of prednisone for more than 3 months can impair bone integrity. Population at risk is defined based on the dose and duration of GC therapy and should be stratified according to FRAX (Fracture Risk Assessment Tool), major osteoporotic fracture, prior fractures, and bone mineral density values (BMD). General measures include to prescribe the lowest dose of GC to control the underlying disease for the shortest possible time, maintain adequate vitamin D levels and calcium intake, maintain mobility, and prescribe a bone acting agent in patients at high risk of fracture. These agents include oral and intravenous bisphosphonates, denosumab, and teriparatide.
Asunto(s)
Conservadores de la Densidad Ósea , Osteoporosis , Fracturas Osteoporóticas , Densidad Ósea , Conservadores de la Densidad Ósea/efectos adversos , Glucocorticoides/efectos adversos , Humanos , Osteoporosis/inducido químicamente , Osteoporosis/tratamiento farmacológico , Fracturas Osteoporóticas/inducido químicamente , Fracturas Osteoporóticas/prevención & controlRESUMEN
Few data are available on the prevention of fracture in glucocorticoid-treated premenopausal women with autoimmune disorders such as systemic lupus erythematosus. In this setting, Okada et al. compared the effect of coadministration of alfacalcidol alone with that of alfacalcidol combined with alendronate. After 12 months of treatment, lumbar spine bone mineral density increased by 1.7% in the combination group, but decreased by 9.9% in the alfacalcidol-only group (P <0.001). Importantly, although no vertebral fractures were observed in the alendronate group, four patients in the alfacalcidol-only group experienced a vertebral fracture within 12-18 months of treatment. Although these data suggest that alendronate improves bone mineral density, we do not recommend the routine use of bisphosphonates in premenopausal women. Our reasons include the long-term skeletal retention of bisphosphonates, and the possible inhibitory effects on fetal skeletal maturation in pregnant patients. In addition, recent data suggest that premenopausal women who undergo glucocorticoid therapy have a low 10-year absolute risk of fracture.