Contemporary approaches for identifying individual risk for periodontitis.

Key breakthroughs in our understanding of the etiology and principles of predictable treatment of patients with chronic periodontitis first emerged in the late 1960s and carried on into the mid-1980s. Unfortunately, some generalizations of the evidence led many to believe that periodontitis was a predictable result of exposure to bacterial plaque accumulations over time. For a brief period, the initial plaque concept was translated by some to implicate specific bacterial infections, with both concepts (plaque exposure and specific infection) being false assumptions that led to clinical outcomes which were frustrating to both the clinician and the patient. The primary misconceptions were that every individual was equally susceptible to periodontitis, that disease severity was a simple function of magnitude of bacterial exposure over time, and that all patients would respond predictably if treated based on the key principles of bacterial reduction and regular maintenance care. We now know that although bacteria are an essential initiating factor, the clinical severity of periodontitis is a complex multifactorial host response to the microbial challenge. The complexity comes from the permutations of different factors that may interact to alter a single individual's host response to challenge, inflammation resolution and repair, and overall outcome to therapy. Fortunately, although there are many permutations that may influence host response and repair, the pathophysiology of chronic periodontitis is generally limited to mild periodontitis with isolated moderate disease in most individuals. However, approximately 20%-25% of individuals will develop generalized severe periodontitis and probably require more intensive bacterial reduction and different approaches to host modulation of the inflammatory outcomes. This latter group may also have serious systemic implications of their periodontitis. The time appears to be appropriate to use what we know and currently understand to change our approach to clinical care. Our goal would be to increase our likelihood of identifying those patients who have a more biologically disruptive response combined with a more impactful microbial dysbiosis. Current evidence, albeit limited, indicates that for those individuals we should prevent and treat more intensively. This paper discusses what we know and how we might use that information to start individualizing risk and treat some of our patients in a more targeted manner. In my opinion, we are further along than many realize, but we have a great lack of prospective clinical evidence that must be accumulated while we continue to unravel the contributions of specific mechanisms.