Maintenance of a healthy periodontium requires correct tooth alignment, systemic health and a nutritionally adequate diet that provides effective tooth cleansing by chewing (or other effective oral hygiene).

Periodontal disease is caused by accumulation of bacterial plaque on the teeth. Periodontal disease includes gingivitis (inflammation of the gingival soft tissues) and periodontitis (inflammation and resorption of the bone supporting the tooth, with eventual loss of the tooth). It is a progressive, usually non-regenerative and incurable disease if plaque accumulation is not controlled, but is preventable and is treatable with appropriate techniques.

Periodontal disease is the most common disease occurring in dogs and cats. Age, body weight, head-shape and chewing behavior affect prevalence. There is general agreement that more than half of the companion animal dog population has some measurable periodontal disease, with increasing prevalence and severity with age. It is more common and more severe in small dogs compared with medium or large dogs.

Dental Plaque

Plaque adheres to the surface of the teeth. It is composed of bacteria in a matrix of salivary glycoproteins. It is impossible to simply rinse plaque away with water; it must be removed by the chewing or other oral hygiene aids.

Initially the bacteria that adhere are largely aerobic gram-positive cocci. After a day or two of undisturbed growth, the plaque thickens and depletes the locally available oxygen supply, favoring growth of anaerobic organisms. It is the anaerobes (particularly Porphyomonas spp.) that are considered to be organisms responsible for the pathological changes that lead to periodontal tissue destruction and loss of periodontal attachment. Spirochetes are very common in mature plaque.

Calculus

Dental plaque undergoes mineralization from calcium salts in salivary fluids to form calculus (tartar). The heaviest supragingival calculus deposits are found on the buccal surfaces of maxillary fourth premolar and first molar teeth in dogs and fourth premolar teeth in cats.

Calculus promotes gingivitis because it provides a rough surface for accumulation and maturation of plaque. It is the bacteria-laden plaque that is the main irritant to the periodontium.

Pathogenesis of Periodontal Diseases

Periodontal disease begins as infiltration of bacteria and bacterial by-products through the thin epithelium of the gingival sulcus. Initially, the marginal gingiva becomes inflamed (gingivitis). There may be spontaneous gingival bleeding or bleeding on exploration of the pocket with a periodontal probe. Neutrophils that die following bacterial engulfment burst, littering the site with cytokines that initiate tissue-destructive effects such as osteoclast migration and activation (periodontitis). Like a zipper with its locking tab not closed, the underlying alveolar bone and periodontal ligament are exposed. Periodontitis can cause a significant increase in depth of the pocket (space between the tooth and the gingiva) where plaque and calculus can accumulate in a protected space. In other cases, gingival recession occurs at a rate similar to that of bone loss and no pocket is formed.

Furcation involvement is present when the bone between the roots in multi-rooted teeth is resorbed. The furcation involvement may be incomplete (a periodontal probe can enter the furcation but not pass completely through) or complete. Furcation involvements are clinically significant because they permit food debris and plaque to accumulate in areas that are very difficult for the animal or owner to cleanse.

The loss of supporting bone results in loosening and eventual loss of the tooth. In some dogs there may not be clinically obvious severe oral pain or other disabling effects. Severe periodontal disease in cats often is more painful.

Gingival hyperplasia often occurs associated with plaque-induced periodontal disease or is seen as a separate (often concurrent) abnormality in medium-large middle aged dogs.

Clinical Stages of Periodontal Disease

 Normal (PD 0): Clinically normal - no gingival inflammation or periodontitis clinically evident

 Stage 1 (PD 1): Gingivitis only without attachment loss. The height and architecture of the alveolar margin are normal.

 Stage 2 (PD 2): Early periodontitis - less than 25% of attachment loss or at most, there is a stage 1 furcation involvement in multirooted teeth. There are early radiologic signs of periodontitis. The loss of periodontal attachment is less than 25% as measured either by probing of the clinical attachment level, or radiographic determination of the distance of the alveolar margin from the cemento-enamel junction relative to the length of the root.

 Stage 3 (PD 3): Moderate periodontitis - 25–50% of attachment loss as measured either by probing of the clinical attachment level, radiographic determination of the distance of the alveolar margin from the cemento-enamel junction relative to the length of the root, or there is a stage 2 furcation involvement in multirooted teeth.

 Stage 4 (PD 4): Advanced periodontitis - more than 50% of attachment loss as measured either by probing of the clinical attachment level, or radiographic determination of the distance of the alveolar margin from the cemento-enamel junction relative to the length of the root, or there is a stage 3 furcation involvement in multirooted teeth.

Following loss of the tooth and healing of the empty alveolus, inflammation recedes and a smooth epithelium-covered jaw surface is present. The result of healing may be an oronasal fistula in the maxilla. In toy breed dogs, the mandible at the first molar tooth level may fracture.

Periodontal Disease in Cats

The general cause and effects of periodontal disease in cats are the same as in dogs. The teeth are smaller and providing good oral hygiene is more challenging. A dry food diet results in improved gingival health compared to a soft food diet, and 'dental diets' are even more effective. Stomatitis and dental resorptive lesions make periodontal disease in cats more difficult and frustrating to treat. These abnormalities are described in a later session.