A Deeper Look at Plaque and Pockets

Periodontitis is not simply about plaque and pockets. Furthermore, periodontal treatment is much more than just reducing pockets. You can no longer simply take a plaque score and tell your patient, "Mrs. Jones, you have too much plaque." The paradigm for periodontal disease has changed dramatically over the last decade. The classical model of periodontitis is based upon an accumulation of bacterial debris and calculus around the gingival sulcus. If allowed to stay unaltered, this accumulation will lead to the formation of gingivitis. Eventually, pockets would form and this would lead to alveolar bone loss. In this issue of The Perio Letter, I will point out some of the most important changes that have recently occurred in our understanding of periodontitis.

All people are not similarly affected by periodontitis. There are huge differences between individuals with regard to their susceptibility to disease.

We now know that heredity alone may account for nearly 50 % of the risk for developing adult periodontitis. Furthermore, various types of patients with severe periodontitis have been shown to correlate with a combination of two IL-1 gene polymorphisms. In contrast, several studies point to populations of periodontitis resistant patients having poor oral hygiene levels and no disease. This underscores why you may see patients in your practice with similar amounts of plaque, but unequal amounts of disease damage.

Certain other risk factors can also affect an individual's susceptibility to disease and their response to therapy.

The risk factors may be innate, acquired, or environmental. Numerous studies evaluating smoking and periodontitis show a strong positive correlation. Stress may also play an important role in decreasing host resistance. These are examples of factors that can be modified during the course of periodontal treatment. Additionally, diabetic patients have an increased risk for disease due to impaired neutrophil functions. We see countless examples of patients with poor gylcemic controls having exaggerated responses to periodontitis. In many cases glycemic control can be improved by treating the periodontal infection.

Periodontitis progresses in episodes or bursts of activity of attachment loss rather than moving in a straight linear manner. The "asynchronous multiple burst model" of periodontitis demonstrated that multiple sites can experience a rapid loss of attachment then remain in a period of remission for variable lengths of time. Later, either an individual site or multiple sites can reactivate and resume their destruction resulting in greater pocket depths and more bone loss. The bursts of activity depend upon the equilibrium state between the host immune response and the bacterial challenge presented. Many times a patient asks us during consultation, "how long have I had this problem before my dentist sent me?" The description of the burst theory always provides the true and proper answer.

The etiologic agents of periodontitis are specific bacteria in bacterial complexes or biofilms. A biofilm is a living dynamic community of microbes. It is attached to an inert or living surface that is enclosed within and protected by a polymeric matrix of secreted components. These characteristics explain why periodontal pathogens are not eliminated by our host immune response or by antibiotic therapy. Additionally, many factors affect the inhabitants of the community. Biofilm constituents such as Porphyromonas gingivalis and Bacteriodes forsythus are pathogens that are strongly associated with periodontitis. The constant immunologic insult produced by the biofilm is responsible for the host-mediated response that results in tissue damage (described below) and may provide the basis for the systemic disease correlations we are now evaluating.

Tissue destruction such as bone and collagen loss is mostly due to our own inflammatory response.

The biofilm stimulates macrophages to secrete cytokines to attract other immune cells and activate multiple inflammatory pathways. The list of cytokines that play a role in tissue destruction is long and no doubt will continue to grow. They stimulate bone resorption, cause apotosis and destroy collagen. This hot area of research will no doubt lead to more breakthroughs in attacking periodontitis medically. Periostat is an example of a therapeutic directed at interrupting an inflammatory pathway.

Periodontitis maybe a risk factor for systemic disorders such as cardiovascular disease, diabetes, and preterm low birth weight babies.

Correlations have been established, but so far cause and effect has not been proven. I have already discussed this at length in a prior article, but suffice it to say that we simply cannot ignore periodontitis as a risk to the general health and well being of our patients.

Why is all of this so important?

It is changing the way we evaluate and treat the perio patient. Pockets and radiographic evidence of bone loss are historical parameters. They do not tell us much about what is currently happening with our patient. We continue to employ root planing and surgery to eliminate the etiologic agents and to restore periodontal health. We now look for activity in individual sites during maintenance and direct specific therapy toward that activity. We employ risk reduction techniques to improve host resistance (glycemic control in diabetics, smoking cessation and oral hygiene training). Periodontitis is a complex disease process and if we use what we know, we can attack it and control it with a variety of new and novel approaches that will improve the periodontal and systemic health of our patients.