Effect of rheumatoid arthritis on volumetric bone mineral density and bone geometry, assessed by peripheral quantitative computed tomography in postmenopausal women treated with bisphosphonates.

OBJECTIVE: To investigate the effect of rheumatoid arthritis (RA) on volumetric bone mineral density (vBMD) and bone geometry in postmenopausal women treated with bisphosphonates. METHODS: Fifty-three postmenopausal women with RA and 87 control subjects, comparable in terms of age, body mass index, and years since menopause, underwent peripheral quantitative computed tomography (pQCT) of the nondominant tibia. RESULTS: At 4% (trabecular site), trabecular bone mineral content (BMC) and vBMD (p < 0.001) were lower in the RA group, while trabecular area was comparable. At 38% (cortical site), cortical BMC (p < 0.01), area (p < 0.05), and thickness (p < 0.001) were lower in the RA group, whereas vBMD was comparable. Endosteal circumference was higher (p < 0.05), whereas periosteal circumference was comparable, indicating cancellization of cortical bone. In the RA group, muscle area was lower (p < 0.001), while at 14% polar stress strength index was significantly lower (p < 0.01) in patients with RA, indicating impairment of bone mechanical properties. CONCLUSION: RA is associated with negative effects on both cortical and cancellous bone in postmenopausal women treated with bisphosphonates. Cortical geometric properties are also adversely affected mainly by increased endosteal circumference, whereas trabecular geometric properties are generally preserved.

Bone anabolic versus bone anticatabolic treatment of postmenopausal osteoporosis.

Increased bone fragility after menopause is commonly associated with accelerated bone loss and aggressive osteoclastic function. This is attributed to increased RANKL production and impaired osteoprotegerin synthesis. Fast bone loss leads to trabecular perforations, dramatic diminution of bone strength, and unexpected fractures. To avoid osteoporotic fractures, elimination of fast bone loss is recommended. Antiosteoclastic drugs, apart from estrogens, are the selective estrogen receptor modulators, calcitonins, and amino-bisphosphonates. These drugs increase bone mass by 1-5%, but reduce the relative risk of a vertebral fracture by 30-70%. Long-term exposure to bisphosphonates may be related to low bone turnover. In elderly and severe osteoporosis, antiosteoclastic regimens hardly correct the depressed osteoblastic function. Intermittent teriperatide stimulates osteoblastic function, improves bone geometry, and has an additional analgesic effect. While both anticatabolic and anabolic agents increase bone mass and decrease the risk of spinal fractures and occasionally of the fracture of the femoral neck, there are differences in the mode of their action. These pathophysiological differences are tentative therapeutic tools for the prevention of osteoporotic fractures. A fast bone loss, associated with increased biochemical markers, is the main indicator for anticatabolic agents, while impaired bone geometry, normal or low bone markers, and established bone architectural changes are in favor of the anabolic agents. Strontium ranelate combines the anticatabolic effect with an additional anabolic action.