April 17, 2006
When oral bacteria invade our gums and initiate periodontal disease, a battle ensues between the bacteria and our immune cells. The bacteria modify their protein production to assist their growth and survival, and our immune cells release various biochemicals to allow them to communicate, respond, and hopefully control the infection. As researchers over the years have attempted to define this swirl of biochemical activity more precisely, they have focused primarily on the bacteria and/or our innate immune system, our inherited, front-line defense against disease. Less well studied are the components of our acquired, or learned, immune system. In the April issue of the journal Infection and Immunity, 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, which is 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 called fibroblasts, all of which are common features of periodontal disease. As 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.” Read more about this paper by Leone, Graves, et. al. Interestingly, these NIDCR grantees also recently reported in the American Journal of Pathology that diabetes appears to enhance the death of critical 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 Porphyromonas gingivalis. Read more about this paper by Liu, Graves, et. al.