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First human study confirms that immune cells can be a primary cause of bone loss in gum disease

Researchers at The Forsyth Institute have confirmed in human gingival tissue that immune cells play a destructive role in periodontal disease. Although researchers had suspected the correlation between bone loss in periodontal (gum) disease and immune cells, this is the first time that this has been confirmed in human tissue samples. With this work, Forsyth scientists and colleagues hope to determine methods for intervening and halting bone loss and thus improving the health outcomes of the estimated 80 million Americans suffering from periodontal disease.

The study, led by Toshihisa Kawai, D.D.S., Ph.D., examined whether immune response to periodontal bacteria is protective or pathogenic in the context of gum disease. Periodontal disease is an infection of the teeth, and their supporting structures, which results in soft tissue and bone destruction, leading to tooth loss. Dr. Kawai and his colleagues had found that B cells (B and T lymphocytes are immune cells) can contribute to increased periodontal bone loss coordinating with activated T-cells. Both cell types had previously been found to manifest a host immune response to the bacteria causing bone loss in animal models, by his group.

"This research validates our hypothesis that immune cells are harmful in gum disease," said Dr. Kawai. "It's a groundbreaking discovery because it truly gives a new understanding of periodontal disease, while also raising interesting questions about immune cells. We hope this work will help us save people's teeth in the future."

Research Overview
RANKL is a protein that is a major factor in the regulation of osteoclasts (cells that destroy bone). Dr. Kawai's research examined the receptor activator of NF-kB ligand, (RANKL)-mediated osteoclastogeneis, and the pivotal role it plays in inflammatory bone resorption. The aim of this study, which will be published in the September issue of the American Journal of Pathology, was to identify the cellular s
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Source:Forsyth Institute


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