ource of RANKL in the bone resorptive lesions of periodontal disease. An active periodontal lesion is characterized by the prominent infiltration of B cells and T cells, both of which are major immune lymphocytes. Specifically, the occupancy of 50-60% of such cellular infiltrates by plasma cells (ultimately, differentiated B cells) makes periodontal disease very distinct from other chronic infectious diseases. B cells are known to produce a weapon (antibody) that normally attacks bacteria and protects our body from bacterial infection. As a consequence of dense infiltration of B cells found in the gum, periodontally diseased patients mount significantly elevated antibody levels to bacteria colonizing around gum tissues. However, the fact that periodontal disease continues to progress, even though B cells produce a weapon to fight off the bacteria, raised an important and interesting question. To answer this question, Dr. Kawai's group found that RANKL expressed on the T and B cells in the patient's gingival tissues were functionally sufficiently potent to induce bone destructive cells (osteoclasts) in a laboratory culture system, in spite of the elevated presence of B and T lymphocytes. Since it has never been reported that any bacteria per se invade and resorb bone independent of osteoclast activation, RANKL expression by T cells and B cells proves to be one of the major stimuli of osteoclast precursor cells and, hence, bone loss through periodontal disease.

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Source:Forsyth Institute


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