Diseases of Bone and Cartilage

Elderly Women May Still Benefit From Osteoporosis Treatment

Patients with RA experience localized and generalized bone loss.2 Data have also shown that patients with well-controlled RA have significantly more bone loss than healthy individuals.4 The pathology of bone loss in RA is multifactorial and complex. The pannus, a proliferation of inflamed synovial tissue, releases several proinflammatory cytokines. Some, such as TNF-α, IL-1, IL-6, and IL-17, are osteoclastogenic and promote bone resorption, partly through upregulation of nuclear factor-kB ligand.1,3,5 They also inhibit anti-osteoclastogenic cytokines.1 Further, TNF-α upregulates proteins that inhibit the Wnt pathway, thus suppressing osteoblast activity.1,3,5 The resulting imbalance in bone remodeling, favoring bone resorption, causes bone loss and inferior bone quality. Immobility and glucocorticoid use, both common in patients with RA, also promote bone loss.1,2 Standard risk factors for bone loss may exacerbate RA-induced bone loss.5

Patients with RA experience localized and generalized bone loss.2 Data have also shown that patients with well-controlled RA have significantly more bone loss than healthy individuals.4 The pathology of bone loss in RA is multifactorial and complex. The pannus, a proliferation of inflamed synovial tissue, releases several proinflammatory cytokines. Some, such as TNF-α, IL-1, IL-6, and IL-17, are osteoclastogenic and promote bone resorption, partly through upregulation of nuclear factor-kB ligand.1,3,5 They also inhibit anti-osteoclastogenic cytokines.1 Further, TNF-α upregulates proteins that inhibit the Wnt pathway, thus suppressing osteoblast activity.1,3,5 The resulting imbalance in bone remodeling, favoring bone resorption, causes bone loss and inferior bone quality. Immobility and glucocorticoid use, both common in patients with RA, also promote bone loss.1,2 Standard risk factors for bone loss may exacerbate RA-induced bone loss.5

Late-life women with osteoporosis, including those with comorbidities, may still be drug treatment candidates to prevent future hip fracture.

HealthDay News — Late-life women with osteoporosis, including those with comorbidities, may still be drug treatment candidates to prevent future hip fracture, according to a study published online June 17 in JAMA Internal Medicine.

Kristine E. Ensrud, M.D., from the University of Minnesota in Minneapolis, and colleagues used data from 1,528 community-dwelling women (mean age, 84.1 years) living in four cities, who were identified as potential candidates for initiation of osteoporosis drug treatment. Based on disease definition criteria from the National Bone Health Alliance, participants were classified as having osteoporosis (761 women) and not having osteoporosis but having high fracture risk (767 women).

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The researchers found that during follow-up, 8.0 percent of women experienced a hip fracture and 18.8 percent died before experiencing one. Among women with osteoporosis, five-year mortality probability was 24.9 percent compared with 19.4 percent among women without osteoporosis but at high fracture risk. Similar increases were noted in mortality probability with more comorbidities and poorer prognosis between the groups. However, among women with osteoporosis, five-year hip fracture probability was 13.0 percent compared with 4.0 percent among women without osteoporosis but at high fracture risk. Among women with at least three comorbid conditions, hip fracture probability was 18.1 percent among women with osteoporosis compared with 2.5 percent among women without osteoporosis but at high fracture risk.

“Women 80 years and older with osteoporosis, including those with more comorbidities or poorer prognosis, have a high hip fracture probability despite accounting for competing mortality risk and may be the group most likely to be candidates for drug treatment to prevent hip fractures,” the authors write.

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