Homeostasis and Immune System

Periodontal disease pathogenesis is a fascinating subject. The oral soft tissue barrier is unique within the human body, as it surrounds mineralized (teeth) or metal (implants) transgingival fixtures essential for mastication and speech. This distinct environment requires a highly specialized system of immune surveillance to prevent bacterial invasion to the tissues and the bloodstream. The immune system in the mucosal soft tissue barrier is continually working to keep the internal environment in a condition of homeostasis.

In the oral cavity, bacteria do not live in a planktonic state but form dental plaque, an organized biofilm community consisting of microorganisms that live in synergy to survive host defenses. This biofilm can either live symbiotically with the human host, in which case it does not cause pathogenicity. This homeostatic state of biofilm-host immune interactions is clinically referred to as “health”. Thus, it becomes apparent that health is much more than the mere absence of disease. Homeostasis is a dynamic state that cannot be defined solely by the absence of inflammatory disease signs. For instance, bleeding on probing (BOP), which is the key clinical sign of gingivitis (aka bleeding gums), is often indicative of an effective immune surveillance and homeostasis. The prevalence of gingivitis is up to 80% in adult dentate patients. BOP is part of a homeostatic mechanism to effectively protect host integrity through elimination of bacteria.

The bacteria within the biofilm are capable of initiating the gingival lesion by triggering a localized inflammatory reaction. The host immune system responds to this bacterial challenge through an array of coordinated but complex processes that are designed to eliminate the initiating agent(s) and return the site to a state of homeostasis (Figure 1). However, if this inflammatory response is not successful in resolving the bacterial trigger and perpetuates into chronic persistent gingivitis, then the risk for progressing periodontal inflammation that may lead to bone resorption increases. The severity and extent of destruction of the periodontium are often related to a combination of factors such as the virulence of the biofilm bacteria, the robustness of the immune response and the chronicity of the inflammatory lesion that will be broached in this course.

Figure 1.

Figure 1.