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Tooth and Gum Disease

Dental caries result from bacterial action that gradually demineralizes enamel and underlying dentin. Decay begins when dental plaque (a film of sugar, bacteria, and other mouth debris) adheres to the teeth.

Bacterial metabolism of the trapped sugars produces acids, which dissolve the calcium salts of the teeth. Once the salts are leached out, enzymes released by the bacteria readily digest the remaining organic matrix of the tooth.
More serious than tooth decay is the effect of unremoved plaque on the gums. As dental plaque accumulates, it calcifies, forming calculus or tartar.

These stonyhard deposits disrupt the seal between gingivae and teeth, deepening the sulcus and putting the gums at risk for infection by pathogenic anaerobic bacteria. In the early stages of such an infection, called gingivitis, the gums are red, sore, swollen, and may bleed.

If gingivitis it is neglected, the bacteria eventually form pockets of infection which become inflamed. Neutrophils and immune system cells attack not only the intruders but also body tissues, carving deep pockets around the teeth, destroying the periodontal ligament, and activating osteoclasts which dissolve the bone.

This serious condition, periodontal disease or periodontitis, affects up to 95% of all people over age 35 and accounts for 80–90% of tooth loss in adults.

Periodontal disease may jeopardize more than just teeth. Some contend that it increases the risk of heart disease and stroke in at least two ways:

  • The chronic inflammation promotes atherosclerotic plaque.
  • Bacteria entering the blood from infected gums stimulate the formation of clots that clog coronary and cerebral arteries.

Tooth

Via Human Anatomy & Physiology (9th Edition) – Elaine N. Marieb – Katja N. Hoehn

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