The nitty-gritty of periodontitis

Periodontal tissue destruction is the result of the inflammatory response to the bacteria in biofilm. Everyone knows that. Well, everyone in dentistry. But it gets a lot fuzzier when we try to understand exactly how this happens. Dr. Richard Nagelberg gets down to the nitty-gritty of periodontitis in his latest blog, so grab your coffee; you're going to learn something.

THE BASIC FACTS OF THE MECHANISM OF PERIODONTAL TISSUE DESTRUCTIONare well established and accepted. The narrative goes like this: Periodontal tissue destruction is the result of the inflammatory response to the bacteria in biofilm. Pretty simple. LESS WELL UNDERSTOOD IS EXACTLY HOW THIS HAPPENS—specifically, which white blood cells and cytokines are operating, what determines which cytokines jump in the pool, and how did they get to the party in the first place. The inflammatory response causes periodontal tissue destruction—periodontitis—however, the patient's innate susceptibility is one of the primary determinants of the outcome of the disease process. (1)

The gingival tissue response to bacteria leads to the production of pro-inflammatory cytokines and other inflammatory mediators, such as adhesion molecules and a variety of chemokines. Blood vessels in the subjacent connective tissue develop increased permeability, and chemoattractants guide white blood cells into the gingival tissue. Neutrophils cross through the junctional epithelium into the gingival sulcus. A constellation of events ensues coordinated by a variety of dynamic factors, including the persistence of bacteria, the innate susceptibility of the individual, and the robustness of the inflammatory response, among many others.

A variety of cells—including epithelial cells, endothelial cells, and fibroblasts—respond differently than they normally do, depending on the presence of other agents during the destruction of periodontal tissue. For example, fibroblasts normally synthesize the extracellular matrix and collagen. However, in the presence of bacterial lipopolysaccharides (LPS), tumor necrosis factor-alpha (TNF-α), and prostaglandins, the fibroblast genes for collagen synthesis are switched off, resulting in the destruction of the extracellular matrix. This loosens up the tissue and provides a highway for the inflammatory cells to reach the infection site. The whole process is orchestrated by cytokines. The types of cytokines present in gum tissue are determined by T cells from the lymphocytic response. (1)

What does all this mean?

It means a number of things, including the fact that the nature of periodontal disease is incredibly complex. There are so many moving parts and variables that we currently cannot tease everything out in real time. What we can understand is what is happening at one point in time—when the periodontal evaluation, charting, and radiographs are observed—and that is important to understand. But it falls far short of revealing any of the intricacies of the disease process that occurs in periodontitis.

This brings to mind the effort to understand what is happening within atoms in a particle accelerator, where particles collide at high velocity, and then trying to sort out what is going on from the damage. It’s rather like smashing a fine wristwatch with a hammer and attempting to figure out how the watch works simply from examining the pieces. We’re not smashing anything in our case, but we are trying to discern what is happening in each of our individual patients.

So, in the end, bacteria’s role in periodontal tissue destruction is to get the ball rolling. Once that ball starts down the mountain, it’s up to us to sort out the damage.

Reference

1. Gemmell E, Yamazaki K, Seymour GJ. Destructive periodontitis lesions are determined by the nature of the lymphocytic response. Crit Rev Oral Biol Med. 2002;13(1):17-34.

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