Healthy Gum Tissue -------------> Early Periodontitis
Moderate Periodontitis -----> Advanced Periodontitis
Periodontal disease results from the host’s reaction to the growth of anaerobic bacteria in the subgingival plaque. These bacteria are called anaerobes because they grow in the absence of oxygen. This came as a great surprise when about 40 years ago it was discovered that most bacteria in the mouth, and especially those that grow between the gingival tissue (gums) and the teeth, are killed by the oxygen that is present in the very air that we breath. This seeming contradiction comes about because the depression between the teeth and the gums is actually quite removed from the inhaled air under normal breathing situations. Nasal breathing is the norm and when there is mouth breathing there often is a gingivitis about the front teeth. So anaerobes dominate in the dental plaque, especially in the subgingival plaque that causes periodontal disease. See Figure.
The bacteria in the subgingival plaque produce enzymes, lipopolysaccharides, and waste products such as hydrogen sulfide, butyric acid, etc., that elicit an inflammatory response in the adjacent periodontal tissue. This inflammation can result in the loss of the attachment fibers that hold the tooth in place in the jawbone. If unchecked, this process can eventually result in the loosening of the teeth followed by tooth loss. Clinical studies have shown that the bacteria that cause these inflammatory reactions can be kept at low levels by cleaning or debriding the roots of the teeth by a dental procedure known as scaling. This procedure has to be repeated several times during the year in a patient with periodontal pockets. ( A pocket is just what is sounds like, a pocket or space forms between the tooth and the gums that becomes a secure place for the germs to multiply forming the subgingival plaque. This plaque may harden and is now called calculus or tartar).
This treatment approach is nonspecific in nature as it is directed to physically reducing the numbers of all types of germs that are in the plaque. This is the traditional approach based upon 19th century clinical observations that concluded that dental diseases were due to a dirty mouth resulting from poor patient oral hygiene. This debridement approach was a colossal failure in the control of dental decay and its value in the treatment of periodontal disease needs to be re-assessed in the light of studies showing that most forms of periodontal disease are treatable anaerobic infections. A treatment approach based upon infection would be aimed towards the reduction and/or elimination of certain specific germs in the plaque and would employ both chemical antimicrobial agents and debridement to control and/or to eliminate the infection. Both the dirty mouth approach and he infection of these approaches are summarized below.
The Nonspecific Plaque Hypothesis (Treatment of a Dirty Mouth)
Traditionally the non-specific plaque hypothesis (NSPH) has formed the basis for the treatment of periodontal disease. According to the NSPH, the accumulation of plaque on the tooth surfaces is the sole cause of periodontal disease. The goal of treatment is to keep the amount of plaque below a certain threshold in order to maintain periodontal health. This can be done by meticulous oral hygiene, which includes brushing, flossing, use of interdental cleaning aids sucah as a Stim-u-dent™ (McNeil-PPC Inc.) and visits to the dentists for tooth cleanings. If the individual’s oral hygiene is inadequate then plaque accumulates causing gingival inflammation (gingivitis). If this situation is not corrected, then the inflammation can lead to pocket formation which with time, can extend to the periodontal ligament which holds the teeth to the underlying jaw bone. If the plaque accumulations are hidden from the patient in pockets about the teeth, then the inflammatory process can often proceed unnoticed by the individual.
This inflammatory condition can usually be detected by the dentist or dental hygienist, and can be treated by him/her through debriding the tooth surfaces, so as to get plaque amounts below the threshold level, thereby restoring gingival health. If the pockets are 6 mm or deeper, then debridement is difficult to achieve, and the clinician often uses a surgical procedure to gain access to the inaccessible plaque and calculus deposits. This treatment approach reportedly is successful in about 80 to 85% of patients with advanced forms of periodontal disease, but evidence from double blind clinical trials is not available. The success of treatment is reduced if the patient is a current smoker, or has a systemic disease, such as diabetes. When the debridement approach fails, as in the so-called refractory patient, these individuals often are given systemic antibiotics.
The surgical approach can be painful sometimes requiring medication prior to, during and after treatment. It can be expensive, and is not covered by many insurance plans, nor by Medicare and Medicaid. Periodontal surgery has been associated with a slight, but significant loss over time of periodontal attachment about the least diseased teeth in the mouth, and in some cases with radiographic evidence of bone loss. Because of these problems, it would be desirable to have an alternate treatment approach for advances forms of periodontal disease that is more user friendly,
In the illustration above, the gingival margin (gum line seen at the right of the figure) serves to differentiate two types of plaque: the supragingival plaque seen at the top and the subgingival plaque seen at the bottom of the pocket. Note that the kinds of bacteria (germs) in the two types of plaque are different, with worm-like spirochetes and gram negative rods (G-R) dominating the subgingival plaque. It is these spirochetes and gram negative rods that contribute to periodontal disease, as they release toxins into the gingival (gum) tissue, with a few even penetrating into the tissue, where they are destroyed by host inflammatory cells. Host inflammatory cells are represented in the figure as T cells (T with circle, T-lymphocytes), B cells (B with circle, B-lymphocytes), M cells (M with circle, monocytes/ macrophages) and polymorphonuclear cells (circles with the curved black C-like structure inside).
The inflammatory cells cause the gums to redden, swell and bleed, in a process known as inflammation. This inflammatory condition can usually be detected by the dentist or dental hygienist. Clinical studies have shown that the bacteria that cause these inflammatory reactions can be kept at low levels by cleaning or debriding the roots of the teeth by a dental procedure known as scaling and root planing (debridement). This procedure has to be repeated several times during the year in a patient with periodontal pockets. If the pockets are 6 mm or deeper, then debridement is difficult to achieve, and the clinician usually uses a surgical procedure to gain access to the inaccessible plaque and calculus deposits. Certain teeth that are extensively involved are often extracted, as clinical experience indicates that they will not respond to the cleaning procedures. This approach reportedly is successful in about 80 to 85% of patients with advanced forms of periodontal disease, who receive treatment. When the debridement approach fails, as in the so-called refractory patient, these individuals are often given systemic antibiotics.
This treatment approach is nonspecific in nature as it is directed to physically reducing the numbers of all types of germs that are in the plaque. Because it is labor intensive and open-ended, it can become expensive. This is particularly true when periodontal surgery is recommended, as then the cost of treatment can be several thousand dollars. The debridement procedures are recommended to be given 2 to 5 times a year for a lifetime.
This nonspecific treatment approach involves three modules of treatment: scaling and root planing the teeth to remove the bacteria on the root surfaces (debridement), access surgery to debride the root surfaces hidden within the gingival pockets, and the prescription of systemic antimicrobials, usually tetracyclines, if the patient is non-responsive to the first two approaches (see figure below). Since the overgrowth of all bacteria (germs) is thought to be the cause of gum inflammation (a dirty mouth), there is no need to determine which bacteria are involved (no need to diagnose an infection).
In recent years, considerable evidence has been provided by the research community that most advanced forms of periodontal disease are associated with the overgrowth in the subgingival plaque of a finite number of germs. The germs which overgrow are usually anaerobic gram negative bacterial species, with hard to pronounce names, such as Porphyromonas gingivalis, Tannerella forsythensis and Treponema denticola, among others. This suggests that antimicrobial agents that are specific for these germs might be of value in the treatment of advanced forms of periodontal disease. In order to make an appropriate choice of an antimicrobial agent, it is necessary to make a bacterial diagnosis of which germs have actually overgrown in the subgingival plaque. You cannot rely on the NSPH rationale and say that all germs have overgrown.
The modules of treatment of a specific periodontal plaque infection would be identical to those used for the nonspecific plaque treatments, except that there would be a need to diagnose an infection, and the sequence of using the modules would be different (see illustration above). This change in sequence is extremely important, because the systemic antimicrobial (antibiotic) would be given in combination with the debridement procedures, and not held in reserve to treat patients who do not respond to the surgical procedures. In fact, when treating according to the specific plaque hypothesis, it is the surgical module that is held in reserve, only to be used about those teeth which do not respond completely to the antimicrobial approach. In the specific plaque treatment paradigm, antimicrobials are used to prevent or reduce access surgery, whereas in the nonspecific plaque treatment paradigm, access surgery is used to prevent or reduce the use of systemic antibiotics.
We have conducted four double-blind studies in which we treated patients with tooth cleanings and short term usage (one to two-weeks) of metronidazole or doxycycline to see if this treatment would result in restoration of periodontal health. In three of these studies we used as our treatment outcome (does it work?) the reduction in the need for periodontal surgery and in tooth extraction. In all four studies the antimicrobial treatment resulted in significantly better results than was obtained in our control groups who received the traditional scaling and root planing procedures. These results suggest that most forms of periodontal disease respond to antimicrobial treatments as if they were indeed specific bacterial infections.
But antimicrobial agents are not magic bullets that can be routinely used to treat a chronic infection such as periodontal disease. There is much to be learned about how to use these agents appropriately. In order to make an appropriate choice of an antimicrobial agent, it is necessary to make a bacterial diagnosis of which germs have actually overgrown in the subgingival plaque. (See section on Chairside Diagnostic for Periodontal Disease)
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