Demystifying periodontal disease

March 1, 2011
Periodontal disease is a very complex disease entity with many microbial and host processes and events occurring.

by Richard H. Nagelberg, DDS

For more on this topic, go to and search using the following key words: periodontal disease, immuno-inflammatory response, Richard H. Nagelberg, DDS.

Periodontal disease is a very complex disease entity with many microbial and host processes and events occurring. The details are mind-boggling. Among the factors and events in play are: biofilm, periodontal pathogens, the immune system, inflammatory mediators, Toll-like receptors, gingival epithelium, collagen, neutrophils, cytokines, endotoxins, plasma cells, collagenase, and all of those alphabet factors such as B cells, C-reactive protein, T cells, IL-1, IL-6, TNF-α, and MMPs. The interplay of these factors and events involve details that are also mind-boggling. It is an incredibly complex, intricately choreographed battle between the host and microbial processes, with oral and general health, or the lack thereof, going to the side that prevails.

A detailed description of the development and progression of periodontal disease can be found in textbooks and journals, seminars, webinars, universities, and online. It is an evolving knowledge, but certain aspects are now universally recognized, including the bacterial beginnings and the contribution of the immuno-inflammatory response to tissue destruction.

The primary aspect that is universally recognized is how truly complicated it is. Intricately choreographed is an accurate term, since there is an incredible interplay involved in all that is going on. One small facet sums it up quite well – only one of the cell types involved, plasma cells, secrete hundreds to thousands of antibodies per second per cell.

If one plasma cell secretes one thousand antibodies per second, that would be 60,000 per minute or 3.6 million in one hour or 86.4 million antibodies per day, and they live for days to months. The multiples are incomprehensible when we try to think past one plasma cell. With this mind-numbing complexity, how do we wrap our minds around the processes and events so they have clinical relevance?

When we break it down into its most elemental form, gum tissue destruction in genetically susceptible individuals is really the story of increasing levels of many things. There is a lot of "When this increases, then that happens" going on. Nothing starts to go wrong until bacterial levels increase, especially when the perio bugs start building up on the biofilms.

That is the kickoff event. All heck breaks loose when this happens. White blood cells that are patrolling around looking for troublemakers react immediately. They don't wait around to see if more bacteria start climbing down the wall of the sulcus. They act without delay, attacking the bugs and sending out a whole constellation of signals. Capillaries proliferate, vasodilation and vascular permeability increases, inflammatory mediators and enzymes increase and pour out of these blood vessels, secreting zillions of factors. If the inflammatory process is not intercepted, the connective tissue starts to break down in just a couple of days.

In only four to seven days, 60% to 70% of the supporting collagen fibers are degraded, but clinically evident attachment loss is not present yet. If treatment is completed at this time, the early lesion will resolve. If not, the lesion becomes established and the levels of B cells and those nasty plasma cells increase considerably. Increasing levels of tissue destruction and advanced periodontal disease are not far behind if the disease process is not intercepted.

The details of periodontal disease development and progression are important to understand. Taking the long view, however, and understanding the basic concepts has value as well. In short, increasing levels of periodontal pathogens lead to increasing levels of inflammatory mediators.

If the early inflammatory response does not resolve the infection, chronic inflammation sets in, leading to increasing levels of periodontal tissue destruction in susceptible individuals. When periodontal therapy is provided, these processes reverse. Bacterial levels are reduced as a result of mechanical and chemotherapeutic intervention. The inflammatory response slows down as the level of pathogens is reduced, giving the body a fighting chance to heal.

Even though it is critically important to understand the minutiae involved in periodontal disease, the clinical relevance is minimal at this time. New treatment modalities focused on the tissue destructive inflammatory response are coming online in the foreseeable future. The minute details may hold more clinical relevance when we have them in our toolbox.

Demystifying periodontal disease is really an attempt to stand back and see the forest from the trees. It can enable us to focus on preventing and intervening to reverse the most important increasing factor – the patient's level of disease. It's always first and foremost about the patient.

Dr. Richard Nagelberg has practiced general dentistry in suburban Philadelphia for more than 28 years. He is a speaker, advisory board member, consultant, and key opinion leader for several dental companies and organizations. He lectures extensively on a variety of topics centered on understanding the impact dental professionals have beyond the oral cavity. In-office consultations are available. Contact him at [email protected].

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