Why is it happening: BOP, swelling, pocketing, and bone loss?

We see the classic signs of gingivitis and periodontitis every day in clinical practice.

Richard H. Nagelberg, DDS

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We see the classic signs of gingivitis and periodontitis every day in clinical practice. In fact, they are so common that perhaps clinicians have become desensitized to them. We are inundated with the daily demands of patient care, administrative tasks, journal articles to read, seminars to attend, new technologies to master, and so on. Pausing to consider the reasons why something we encounter daily occurs is a luxury we do not have. However, despite our time limitations, it is important for us to understand the reasons why the body consistently responds to levels of bacteria it cannot handle and employs the mechanisms it does.

We now know that periodontal tissue destruction is the result of a chronic inflammatory response to biofilm bacteria. A healthy immune system can deal with bacteria up to a point, as is the case in many organ systems, including the lungs, GI tract, and oral cavity. But when the bacterial load becomes too much to bear, tissue breakdown occurs.

Periodontally healthy patients have high levels of favorable bacteria and low levels of pathogenic bacteria. When the bacterial levels increase and the ratio of favorable to pathological bacteria starts to shift, the immune system reacts to these changes.

The primary physical properties of the early inflammatory response are blood vessel dilation and the development of gaps in the blood vessel walls. This vasodilation and increased vascular permeability are designed to increase blood flow to the infected gingival tissues. This happens at the capillary level.

The perio pathogens get inside the gingival epithelial cells and migrate from cell to cell and reach the underlying connective tissue. The gaps in the blood vessel walls result in blood flowing out of the blood vessel into the gingival tissue, because this is where the action is.

The inflammatory mediators that combat the bacterial infection are carried into the tissue by this blood flow. The net loss of plasma from the circulation into the gum tissue increases the fluid volume in the gingiva.

On a clinical level, this is the reason why gingivitis patients have swelling, redness, and bleeding upon probing. If the acute inflammatory response fails to resolve the infection, chronic inflammation sets in, resulting in additional tissue damage.

Very specific parameters must be in place for gingivitis to progress to periodontitis. Gingivitis, in fact, is not really an early form of periodontitis; it is the gatekeeper to it. We know this from several lines of evidence. On a clinical level, we know that progression from gingivitis to periodontitis is not automatic, does not occur in every patient, and does not occur in every site.

On a tissue level, we know gingivitis is primarily mediated by T cells, and periodontitis is primarily a B cell and plasma cell response. On a hereditary level, not everyone is genetically susceptible to periodontitis. If they are, gingivitis switches on the patient's DNA and periodontitis ultimately results.

Periodontal bone loss occurs as a result of the inflammatory response. When the bone-building osteoblast cells and the bone-destroying osteoclasts are in balance, bone loss does not occur. The inflammatory response that occurs during gingivitis favors the maturation of osteoclasts, leading to bone loss.

Clinically, the early inflammatory response occurs in the gingival soft tissue rather than the alveolar bone. The inflammatory response will physically travel through the gingiva.

If it reaches the underlying bone, or very close to it, the attachment apparatus will be destroyed, pocket depths will increase, and bone resorption will occur, thus establishing periodontitis. So, failure to confine the inflammatory response within the gingival tissue may lead to periodontitis.

The periodontal pathogens also release toxins, metabolites, and enzymes that can cause tissue destruction. This direct bacterial effect is, however, the minor cause of periodontal tissue destruction.

The majority of periodontal tissue destruction and the clinical signs and symptoms we see on a daily basis occur as a result of the chronic inflammatory response. In other words, the body is doing it to itself.

Understanding the processes and mechanisms that occur in common clinical conditions brings them into sharper focus. A heightened awareness of gingivitis and the importance of preventing progression to full-blown periodontal disease are among the most impactful things we can do for our patients.

Dr. Richard Nagelberg has practiced general dentistry in suburban Philadelphia for more than 27 years. He is a speaker, advisory board member, consultant, and key opinion leader for several dental companies and organizations. He lectures extensively on many topics centered on understanding the impact dental professionals have beyond the oral cavity. Contact him at gr82th@aol.com.


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