A new study led by Brendan Boyce, M.B.Ch.B.., professor of Pathology & Laboratory Medicine and the Center for Musculoskeletal Research and Zhenqiang Yao, MD., Ph.D., assistant professor of Pathology & Laboratory Medicine suggests that age-related osteoporosis could be prevented or treated through pharmacologic stabilization of the protein, TNF receptor-associated factor 3 (TRAF3).
The collaborative study was published in Nature Communications after five years of work by Boyce and fellow URMC researchers who note the need to better understand the mechanisms through which osteoporosis occurs in order to develop new drugs that can be given to help prevent or reverse the disease.
The study notes that the process by which young, healthy peoples' bones are naturally rebuilt, deteriorates as people age or go through menopause. Increased inflammation, or inflammaging, leads to an increase in bone-degrading osteoclast cells and a reduction in bone-forming osteoblasts, resulting in osteoporosis.
Existing treatments that prevent bone destruction offer long term solutions, but many patients are reluctant to take them because they fear side effects of the drugs, while bone forming drugs can be administered only for short periods to help patients suffering from chronic osteoporosis.
The paper shows that the protein, TGF-beta, which is released in increasing amounts from bone during aging, causes breakdown of TRAF3 in osteoblast precursor mesenchymal progenitor cells. This leads to a reduction in the number of osteoblasts and less bone repair and indirectly to increased numbers of osteoclasts and more bone destruction.
By stabilizing TRAF3 levels in bone cells through new drugs, the authors provide a novel mechanism for how treatments may offer a more long-term solution for patients. This is especially crucial as more people live longer and are exposed to a greater risk of fractures and early death.