Modern Hygienist - February 2009 - (Page 25)

GENETICS | patients nuclear leukocytes). Their main job is to phagocytize the pathogens identified by the T cells. When the PMNs reach the gingiva, they squeeze out through the capillary walls, which are already more porous and leaky due to another immune reaction. Once in the tissue, they are supposed to start gobbling up pathogens—but they don’t. The pathogens deploy a range of their own immune counter-measures, nullifying the PMNs. Now the damage begins. PMNs only have a three-day life span. They’re supposed to use up all their destructive enzymes killing bacteria, but if they don’t, when they die all those enzymes are dumped onto nearby gingival cells, killing them instead. Since the pathogens are still present, the T cells continue to send urgent warnings to the thymus which ramps up the immune response mine who gets periodontal disease and how chronically and severely. A surprisingly large portion of the population has tiny mutations in one or more of the genes that produce interleukin 1 (IL-1), one of the most important and potent inflammatory cytokines (a protein that acts like a hormone or neurotransmitter). It influences almost every aspect of immune cell activity. The production of IL-1 is regulated by three genes in immune cells; two are involved in the synthesis of IL-1, and the third is an antagonist that inhibits production. Mutations in any of these genes typically result in a greater production of IL-1, amplifying the immune response. Paradoxically, in autoimmune diseases, increased IL-1 production makes the disease worse, because most of THE BOTTOM LINE Periodontal diseases actually are auto-immune diseases. Relative risk of contracting periodontal disease depends on three genetic factors: 1. Bacterial genetics: Some bacteria possess antigens that provoke an immune response. 2. Human genetics: Normal WBCs react to periodontal pathogens. Witness the 70% to 90% levels of gingivitis and periodontitis in the population. 3. Human genetic mutations: About 20% of the population has the kinds of small genetic mutations that result in abnormal (elevated) IL-1 production, and thus possess a greater response to pathogens than those with un-mutated genes. In the future, gene therapy may offer some therapeutic opportunities for preventing and cur- In the future, gene therapy may o er some therapeutic opportunities for preventing and curing periodontal disease. Right now, there’s not much we can do to modify our genetic expression. by increasing PMN cell production, thus further aggravating the damage. With increased production, the body needs a better way to get all those PMNs to the infection, so the immune system starts to build a better delivery system—i.e., more capillaries. But first, it needs more room for them. It activates collagenase (to break down collagen and connective tissue) and osteoclasts (to break down bone) to provide the physical space for a denser capillary network to deliver more inflammatory cells to the site of the infection. To no avail. Breaking down tissue to deliver even more inflammatory cells that just die in three days adds to the overall damage. That’s why periodontal diseases are so chronic. HUMAN GENETICS Human genetics matter because besides orchestrating the overall immune response, small variations in the host’s genetics deter- the damage is being caused by the immune system itself. In people with no genetic mutations in their IL-1 genes, IL-1 levels are normal, which isn’t any great comfort since even normal levels of IL-1 result in the immune cascade that eventually damages the periodontium. But in people with mutations, the risk is greater, particularly in smokers. If either of the production genes have mutations (see sidebar), IL-1 levels increase, as does cellular damage. If the antagonist gene has a mutation, even if the production genes are normal, there are no controls on the production genes and, again, IL-1 levels increase. The worst genetic scenario is when both production and antagonist genes have mutations. These unfortunates have extremely high levels of IL-1 and pathogenic bacteria provoke a stronger immune response. ing periodontal diseases. Right now, there’s not much we can do to modify our genetic expression. However, genetic tests are commercially available to detect smokers with mutated IL-1 genes. These patients can be put on more stringent home care regimens to prevent bacterial colonization and receive more frequent professional care. We can also do something about bacterial genetics by preventing pathogenic bacteria from colonizing the sulcus. The future of home care isn’t just teaching patients to floss more, but also instructing them to prevent colonization and growth of pathogenic biofilms. Periodontal disease is complicated, but our understanding of the role genetics plays is opening new diagnostic and therapeutic options. mh Bill Landers is President of OraTec, a company that manufactures products and delivers information for anti-infective periodontics. February 2009 | modern hygienist 25

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Modern Hygienist - February 2009 Contents Editor's Letter Letters News Modern Solutions Caring for Kids The DNA Difference A Healthy Perspective The Economic Impact on You How Single Moms Make it Work Ad Index Classified Economy 101

Modern Hygienist - February 2009

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