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American Society for Bone and Mineral Research, Sept. 12-15

The American Society for Bone and Mineral Research Annual Meeting

The annual meeting of the American Society for Bone and Mineral Research was held from Sept. 12 to 15 in Houston and attracted approximately 4,000 participants from around the world, including basic research scientists and clinical investigators in bone and mineral metabolism, as well as physicians and other health care practitioners. The conference focused on the latest advances in bone and mineral research as well as the translation of research into clinical practice.

During the conference, Mary B. Goldring, M.D., of the Hospital for Special Surgery in New York City, led a symposium focused on bone and inflammation. In a talk presented during the symposium, Georg Schett, M.D., of the St. Vincent Hospital in Vienna, reviewed several of the novel mechanisms involved in pathologic bone loss in rheumatoid arthritis, including the unique role of anti-citrullinated protein antibodies (ACPAs) and rheumatoid factors, in directly regulating osteoclastogenesis.

"Schett highlighted that targeting inflammation with disease modifying therapies can block or attenuate local articular as well as systemic bone resorption. He also pointed out that therapies that directly target osteoclastogenesis and/or osteoclast-mediated bone resorption can inhibit articular bone erosions even in the absence of effects on inflammation," said Goldring.

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In another talk during the symposium, Ellen M. Gravallese, M.D., of the University of Massachusetts Medical School in Boston, began with an overview of anti-tumor necrosis factor agents, comparing their structures and their efficacy against inflammation and bone destruction, the role of methotrexate, and why the search for other biologicals has continued (one reason: the persistence of non-responders).

"Gravallese then summarized the biological therapies targeting other cytokines, signaling molecules, different immune cell types, or the bone-resorbing cells themselves, which are available, in development, or in clinical trials," said Goldring. "She pointed out that autoantibodies (including ACPAs) can be detected over 10 years before the onset of clinical symptoms of rheumatoid arthritis."

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In addition, Nancy E. Lane, M.D., of the University of California Davis Medical Center in Sacramento, highlighted recent work on the use of mesenchymal stem cells, which have anti-inflammatory properties, in animal models of inflammatory arthritis.

"Targeting inflammation early can prevent or attenuate articular and systemic bone loss in inflammatory arthritis, but the treatments are not effective in all individuals. Targeting osteoclast formation or activity also may result in new and effective therapies," said Goldring. "All three presenters are rheumatologists who are active in patient care and research. They are translating laboratory studies of preclinical models to clinical care of patients with inflammatory arthritis and other autoimmune diseases that result in bone loss and remodeling, contributing to significant disability."

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During another symposium, led by Ann V. Schwartz, Ph.D., M.P.H., of the University of California in San Francisco, presenters discussed the effects of diabetes and disordered energy metabolism on skeletal health. Patients with type 2 diabetes have higher bone density and an increased fracture risk. Presenters during the discussion provided insight into how fracture risk assessment scores commonly underestimate fracture risk in this patient population. However, there is a correction factor that can be incorporated into assessment scores to better assist in assessing fracture risk in this patient population.

The key take away point from the symposium, according to Schwartz, was that clinical practitioners should be aware that patients with type 2 diabetes are at a higher risk of fracture and that current assessment algorithms may underestimate the risk.

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