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Periodontal disease

Description

An in-depth report on the causes, diagnosis, treatment, and prevention of periodontal disease.

Alternative Names

Gingivitis

Causes

Periodontal disease is marked by bacterial overgrowth. However, a persistent immune response to chronic infections in the mouth is believed to play a major role in gum destruction.

Bacterial Culprits

In the healthy mouth, more than 350 species of microorganisms have been found. Periodontal infections are linked to fewer than 5% of these species. Healthy and disease-causing bacteria can generally be grouped into two categories:

• The harmless or helpful bacteria are usually known as gram positive aerobic bacteria .
• In periodontal disease, the bacterial balance shifts over to gram negative anaerobic bacteria . Inflammatory disease and injury cannot develop without these bacteria.

Following are some of the bacteria most implicated in periodontal disease and bone loss:

• Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis. These two bacteria appear to be particularly likely to cause aggressive periodontal disease. In one study, both P. gingivalis and A. actinomycetemcomitans, along with multiple deep pockets in the gum, were associated with resistance to standard treatments for gum disease. In another study, P. gingivalis doubled the risk for serious gum disease. Particularly virulent strains of this bacterium may be responsible for periodontal disease. A 2001 study suggests that the P. gingivalis produces enzymes, such as one called arginine-specific cysteine proteinase, which may be the specific destructive factors that disrupt the immune system and lead to subsequent periodontal connective tissue destruction.
• Bacteroides forsythus is also strongly linked to periodontal disease.
• Other bacteria associated with periodontal disease are Treponema denticola, T. socranskii, and P. intermedia . These bacteria, together with P. gingivalis , are frequently present at the same sites, and are associated with deep periodontal pockets.

Some bacteria are related to gingivitis, but not plaque development. They include various streptococcal species.

The Autoimmune and Inflammatory Response

Evidence now suggests that periodontal disease is an autoimmune disorder , in which immune factors in the body attack the person's own cells and tissue -- in this case, those in the gum. It appears to work as follows:

• The bacteria that form plaque and tartar release toxins that stimulate the immune system to overproduce powerful infection-fighting factors called cytokines .
• Ordinarily, cytokines are important for healing. In excess, however, they can cause inflammation and severe damage. Cytokines of particular importance in periodontal disease are known as tumor necrosis factor-alpha (TNF-alpha) and interleukin-1beta, which are very active in the mouth, and are important in causing destructive inflammation.
• In addition, white blood cells produced by the immune response to bacteria also release a family of enzymes called matrix metalloproteinases (MMPs), which break down connective tissue.

Studies suggest that this inflammatory response may have damaging effects not only in the gums but also in organs throughout the body, including the heart.

Viral Causes

Certain herpes viruses (herpes simplex and varicella-zoster virus, the cause of chickenpox and shingles) are known causes of gingivitis. A 2000 study found that other herpes viruses (cytomegalovirus and Epstein-Barr) may play a role in the onset or progression of some types of periodontal disease, including aggressive and severe chronic periodontal disease. All herpes viruses go through an active phase followed by a latent phase and possibly reactivation.

Some experts theorize that these viruses may cause periodontal disease in different ways, including release of tissue-destructive cytokines, overgrowth of periodontal bacteria, suppressing immune factors, and initiation of other disease processes that lead to cell death.

• Review Date: 11/10/2006
• Reviewed By: Harvey Simon, MD, Associate Professor of Medicine, Harvard Medical School; Physician, Massachusetts General Hospital

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