Periodontal disease is an inflammatory disease that is common in companion animals as well as humans. It primarily affects the oral soft tissues (gingivae or gums) but will involve the bony tissues that support the teeth in its more advanced stage. The disease appears as swollen, purplish-red gums that bleed spontaneously and are painful, particularly when the animal is eating and chewing.Periodontal disease is caused by bacterial toxins and metabolic by-products that serve as irritants to the gingival tissues thereby inducing an inflammatory response. These bacterial toxins are typically released upon the death of the microorganism and the breakdown of the bacterial cell wall. Upon exposure to these toxins, the gingival tissues release white blood cells into the gingival spaces or pockets surrounding the roots of the teeth and rely upon these white blood cells to release various enzymes to destroy the bacterial toxins. Although the enzymes typically destroy the bacterial toxins, some of them also are additional irritants to the gingival tissues. Thus, there is a continual process of release of bacterial toxins and their destruction by enzymes that serves to propagate the disease and to increase its severity with the ultimate destruction of the underlying bone supporting the teeth and eventual tooth loss.

Periodontal disease begins with the accumulation of various oral bacteria on the surfaces of the teeth forming dental plaque. As the bacterial accumulation grows with time (hours) and increases in depth, the oldest bacteria in the deeper layers of the dental plaque complete their life cycle and die resulting in the rupture of their cell walls and the emptying of their cellular components (including toxins) into the plaque fluids. These toxins irritate the gingival tissues and initiate the tissue inflammation process.

Within 24 hours after the initial formation of the dental plaque and the deaths of the older bacteria located in the deeper layers of the plaque, the deeper layers of the plaque begin to calcify forming dental calculus (tartar). Due to the presence of some of the bacterial cell components, the tartar that forms is porous and contains a variety of bacterial remnants as well as toxins. Thus, the calculus serves as a continuous reservoir of the materials that causes inflammation of the gingival tissues. In addition, build-up of dental calculus often serves as a physical irritant to the adjacent gingival tissues and it is an excellent substrate for additional plaque formation. Dental calculus is virtually always covered with dental plaque.

With continuous irritation of the gingival tissues caused by bacterial toxins and defense enzymes, the inflammation process causes a reddening and swelling of the gingival around the teeth, changes in the contour of the gingival edge from knife-edged to a rolled-edge, and a change in the consistency of the gingival tissue. This tissue often bleeds when exposed to modest forces such as eating or tooth brushing. Typically, small areas of the gingival tissue involving only 2 or 3 teeth are afflicted. This condition is known as gingivitis.

An increase in the presence and the extent of the inflamed tissues (gingivitis) causes the gingiva to become even more swollen and puffy. Tissue color changes from bright red to deep, purplish red, larger areas and greater numbers of teeth become affected, and gingival tissue attached to the tooth recedes. The condition is often associated with spontaneous bleeding, even without agitation or pressure. This condition is referred to as periodontitis.

Chronic progression of periodontitis, as well as continued recession of the gingival attachment to the tooth surface, results in the development of “periodontal pockets” or spaces between the gingiva and the root surface of the tooth. These pockets harbor bacteria that promote the inflammatory disease process and continue to become deeper — pockets that are 6-9 mm (¼ to ⅓ inch) deep are common. These pockets, which are filled with bacteria, cellular debris, subgingival calculus, bacterial toxins and materials that irritate the tissues, cause recession of the bone that supports the adjacent teeth, ultimately resulting in the loss of those teeth. When the condition includes deep periodontal pockets and the loss of alveolar bone supporting the teeth, it is referred to as periodontal disease. This condition may include severe gingivitis with spontaneous gingival bleeding.

In summary, the periodontal disease process begins with the formation of dental plaque (which calcifies to form tartar) and the inflammatory progression of conditions from gingivitis, to periodontitis, to periodontal disease.

Periodontal disease must be treated by a veterinarian. Treatment involves a thorough dental prophylaxis to remove accumulated dental plaque, calculus, and diseased tissue and debris from the periodontal pockets. Antibiotics are also necessary to control oral bacteria. Antibiotics are most effective when they are placed directly in the periodontal pockets. These procedures should be repeated at 2-3 month intervals until the disease has been controlled and preventive measures have been implemented.

Regular removal of dental plaque prevents the development of calculus, gingivitis and periodontal disease. This may be accomplished by meticulously brushing the animal’s teeth on a regular basis (at least 3 times per week). Although this is the most effective means for preventing periodontal disease, relatively few pet owners are willing or able to regularly brush their pet`s teeth.

Alternative measures of reducing the formation of dental plaque and tartar include:

• Dry diets (as opposed to moist/canned or semi-moist diets), which facilitate the removal of dental plaque during mastication;
• Rawhide or other similar chew-type products that require significant mastication;
• Diets or treats that contain additives (antimicrobial agents and/or agents that sequester calcium and form soluble complexes) that have been clinically proven to reduce the formation of dental plaque and/or dental calculus.

Literature references citing published clinical trials of measures to prevent the formation of dental plaque and calculus can be provided for further review.