Researchers at The Forsyth Institute have made a significant new discovery about the nature of periodontal disease. The scientific studies led by Xiaozhe Han, DDS, Ph.D., Postdoctoral Research Fellow, found that the key to bone loss in periodontal (gum) disease is tied to immune response.
This new understanding shows that gum disease is not a conventional infectious disease, but rather an inflammatory disease trigged by host response. This research offers the potential to intervene and halt bone loss to save the teeth of people suffering from periodontitis.
Periodontal disease is a chronic infection of the teeth and their supporting structures that results in soft tissue, bone destruction and tooth loss.
Previous research has examined the bacterial association with this disease. This study, published in the current issue of The Journal of Immunology, looked at the role of the host immune response in periodontal disease and found that the body's response to the bacteria is causing bone loss. Dr. Han and the team of researcher's previously found that T-cells and B-cells
(B and T lympocytes are immune cells) in human periodontal lesions bear abundant
receptor activator of NF kappa B ligand (RANKL), a protein that is a major factor in the regulation of osteoclast (bone cells that destroy bone) differentiation. The current study shows that B-cells can contribute to increased periodontal bone resorption in the absence of T-cells.
"By confirming the link between the host response to infection and periodontal bone loss at the molecular level, we are gaining an exciting new understanding of periodontal disease," said Dr. Han. "This has great future potential for saving people's teeth."
Summary of Study
The purpose of this study was to evaluate the properties of transferred bacterial responsive B lymphocytes in their level of RANKL expression and their effects on periodontal bone resorption. Congenitally athymic Rowett rats received injections of bacteria into the gingivae, and B cells from bacterial-immunized donor rats were transferred via tail vein injection. Bacterial-
specific B cells from immunized animals had greater levels of RANKL expression and induced a significantly higher level of osteoclast differentiation in vitro than did nonimmune B cells that were not Ag specific. This activity was eliminated by incubation with the RANKL decoy receptor osteoprotegerin (OPG). Specific bacterial binding (ABB), RANKL-expressing B cells were recovered from the gingival tissues of recipient rats transferred with ABB, but not from recipients of PBS nonimmune B cells or nonbinding B cells. Recipients of ABB also exhibited increased osteoclasts on the alveolar bone surface and significantly elevated periodontal bone resorption. This effect was antagonized by injection of OPG into the local gingival tissues.
Xiaozhe Han, DDS, Ph.D. a Postdoctoral Research Fellow in The Forsyth Institute Department of Immunology. This research was carried out with Martin A. Taubman DDS, Ph.D., Head of the Department of Immunology, and Dr. Toshihisa Kawai. Research in the Taubman laboratory at Forsyth is directed toward exploring the role of immunological phenomena in the two major infectious diseases of the oral cavity, dental caries and periodontal disease.
The Forsyth Institute is the world's leading independent organization dedicated to scientific research and education in oral, craniofacial and related biomedical sciences.