When oral bacteria invade the gingival tissues and initiate periodontal disease, a battle ensues between the bacteria and the host’s immune cells. The bacteria modify their protein production to assist their growth and survival, and immune cells release various biochemicals to allow them to communicate, respond, and hopefully control the infection. Over the years, researchers have attempted to precisely define this biochemical activity, focusing on the bacteria and/or the host’s innate immune system. Less well-studied are the components of the acquired immune system. In the journal Infection and Immunity (April 2006), National Institute of Dental and Craniofacial Research (NIDCR) grantees and colleagues fill in some of the blanks. Studying mice that had learned to mount an acquired immune response to the oral bacterium Porphyromonas gingivalis (strongly associated with periodontal disease), the scientists characterized the biochemical changes that occurred following inoculation with the pathogen. Among them is an increase in various immune signaling proteins that promote a more pronounced and prolonged recruitment of inflammatory cells. This, in turn, seems to produce a greater area of tissue destruction, including enhanced bone loss and increased programmed cell death of important connective tissue cells (fibroblasts), all of which are common features of periodontal disease. The authors concluded, “These results support earlier studies which indicate that the acquired immune response may play a significant role in the loss of tissue that occurs in response to periodontal pathogens. Interestingly, these NIDCR grantees also recently reported in the American Journal of Pathology that diabetes appears to enhance the death of critical, yes;” matrix-producing cells that produce connective tissue and bone. This may render people with diabetes more susceptible to damage caused by periodontal pathogens such as P. gingivalis.
(Source: NIDCR Web site, Science News in Brief, accessed April 18, 2006)
