Periodontal diseases rankle thousands of Americans with their nagging persistence. But scientists are learning that these inflammatory conditions rankle in more ways than one. As active periodontal lesions progress, they contain increased amounts of RANKL, a much-studied messenger glycoprotein that is a key natural factor in stimulating osteoclasts to degrade and reabsorb bone. What remains unclear is which of the myriad cell types at active gingival lesions secrete RANKL, critical information in learning how to better prevent bone and tooth loss from periodontal disease. In the September 2006 issue of the American Journal of Pathology, a team of National Institute of Dental and Craniofacial Research (NIDCR) grantees offers an answer. Comparing healthy and diseased tissue from 32 patients with bone resorptive periodontitis, they found both immune T and B cells are the primary sources of RANKL. Their data show that more than 50% of lesion-infiltrating T cells and more than 90% of lesion-infiltrating B cells produced the glycoprotein. In healthy gingival tissue, less than 20% of T and B cells expressed RANKL. These findings support the idea that increased production of RANKL may be necessary to disturb the delicate balance between bone resorption and bone replacement, tipping the biochemical milieu near the affected tooth socket toward the bone loss that plagues those with severe periodontal disease.
(Source: NIDCR Web site, Science News in Brief, accessed November 16, 2006)
