Is There a Role for NFAT Inhibitors in the Prevention of Bone Destruction?


Mark S. McMahon
Department of Orthopedic Surgery, Beth Israel Deaconess Medical Center, 330 Brookline Avenue, Boston, MA
Department of Developmental Biology, Harvard SDM, Research and Education Building 413, 188 Longwood Avenue, Boston, MA

Abstract

Pathologic conditions resulting from excessive bone destruction include osteoporosis, rheumatoid arthritis, metastases, periprosthetic osteolysis, cherubism, and others. A scarcity of molecular targets in bone has thwarted the development of drugs to combat these conditions. Nuclear factor of activated T-cells (NFAT) is a master regulator of osteoclastogenesis and is induced by RANKL. The immunosuppressive drugs, Cyclosporin A and Tacrolimus, inhibit osteoclast formation by targeting the NFAT/calcineurin pathway. These NFAT inhibitors should be considered in the treatment of osteoclastic hyper-resorptive syndromes.

This article appears in HSS Journal: Volume 5, Number 2.
View the full article at springerlink.com.

About the HSS Journal

HSS Journal, an academic peer-reviewed journal, is published twice a year, February and September, and features articles by internal faculty and HSS alumni that present current research and clinical work in the field of musculoskeletal medicine performed at HSS, including research articles, surgical procedures, and case reports.


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