Pathogenesis

Periodontal disease is generally described in two stages, gingivitis and periodontitis. Gingivitis is the initial, reversible stage in which the inflammation is confined to the gingiva. The gingival inflammation is created by plaque bacteria and may be reversed with a thorough dental prophylaxis and consistent homecare. Periodontitis is the later stage of the disease process and is defined as an inflammatory disease of the deeper supporting structures of the tooth caused by microorganisms. The inflammation results in the progressive destruction of the periodontal tissues, leading to attachment loss. This can be seen as gingival recession, periodontal pocket formation, or both. Mild to moderate periodontal pockets may be reduced or eliminated by proper plaque and calculus removal. However, periodontal bone loss is irreversible (without regenerative surgery).

Periodontal disease is initiated by oral bacteria which adhere to the teeth in a substance called plaque. Plaque is a biofilm, which is made up almost entirely of oral bacteria, contained in a matrix composed of salivary glycoproteins and extracellular polysaccharides. Calculus (or tartar) is basically plaque which has secondarily become calcified by the minerals in saliva. Plaque on the tooth surface is known as supragingival plaque. Once it extends under the free gingival margin and into the area known as the gingival sulcus, it is called subgingival plaque. Once the periodontal pocket forms, the effect of the supragingival plaque and calculus is minimal. Therefore, control of supragingival plaque alone is ineffective in controlling the progression of periodontal disease.

The specific plaque hypothesis is based on the fact that these few species are seen in virtually all cases of chronic periodontal disease.

The bacteria in the subgingival plaque secrete toxins as well as metabolic products. Also produced are cytotoxins and bacterial endotoxins which can invade tissues on their own, and in turn cause inflammation to the gingival and periodontal tissues. This inflammation causes damage to the gingival tissues and initially results in gingivitis. Eventually, the inflammation can lead to periodontitis, i.e., the destruction of the attachment between the periodontal tissues and the teeth. The inflammation produced by the combination of the subgingival bacteria and the host response damages the soft tissue attachment of the tooth and decreases the bony support via osteoclastic activity. This causes the periodontal attachment of the tooth to move apically (towards the root tip). The end stage of periodontal disease is tooth loss; however, the disease has created significant problems prior to tooth exfoliation.

Clinical Features

It is important to be familiar with normal features in order to identify abnormal findings. Normal gingival tissues are coral pink in color (allowing for normal pigmentation), and have a thin, knife-like edge, with a smooth and regular texture. In addition, there should be no demonstrable plaque or calculus on the dentition. Normal sulcal depth in a dog is 0 to 3 mm and in a cat is 0 to 0.5 mm.

The first clinical sign of gingivitis is gingival bleeding. This is followed by erythema and edema of the gingiva and halitosis. Gingivitis is typically associated with calculus on the involved dentition, but is primarily elicited by plaque and thus can be seen in the absence of calculus. Alternatively, widespread supragingival calculus may be present with little to no gingivitis. It is critical to remember that calculus itself is essentially nonpathogenic. Therefore, the degree of gingival inflammation should be used to judge the need for professional therapy. As gingivitis progresses to periodontitis, the oral inflammatory changes intensify.

The hallmark clinical feature of established periodontitis is attachment loss. As periodontitis progresses, alveolar bone is also lost. On oral exam, there are two different presentations of attachment loss. In some cases, the apical migration results in gingival recession while the sulcal depth remains the same. Consequently, tooth roots become exposed and the disease process is easily identified on conscious exam. In other cases, the gingiva remains at the same height while the area of attachment moves apically, thus creating a periodontal pocket. As attachment loss progresses, alveolar bone loss continues, until tooth exfoliation in most cases.

Severe Local Consequences

The most common of these local consequences is an oral-nasal fistula (ONF). ONFs are typically seen in older, small breed dogs (especially chondrodystrophic breeds); however, they can occur in any breed as well as felines. ONFs are created by the progression of periodontal disease up the palatal surface of the maxillary canines; however, any maxillary tooth is a candidate. This results in a communication between the oral and nasal cavities, creating an infection (sinusitis). Clinical signs include chronic nasal discharge, sneezing, and occasionally anorexia and halitosis. Definitive diagnosis of an oronasal fistula often requires general anesthesia. The diagnosis is made by introducing a periodontal probe into the periodontal space on the palatal surface of the tooth. Interestingly, this condition can occur even when the remainder of the patient's periodontal tissues is relatively healthy. Appropriate treatment of an ONF requires extraction of the tooth and closure of the defect with a mucogingival flap.

Another potential severe consequence of periodontal disease can be seen in multirooted teeth and is called a class II perio-endo lesion. This occurs when the periodontal loss progresses apically and gains access to the endodontic system, thereby causing endodontic disease via bacterial contamination. The endodontic infection subsequently spreads through the tooth via the common pulp chamber and causes periapical ramifications on the other roots.

The third potential local consequence of severe periodontal disease is a pathologic fracture. These fractures typically occur in the mandible (especially the area of the canines and first molars), due to chronic periodontal loss, which weakens the bone in affected areas. This condition is, again, most commonly seen in small-breed dogs, mostly because their teeth (especially the mandibular first molar) are larger in proportion to their jaws as in comparison to large breed dogs. Pathologic fractures occur most commonly as a result of mild trauma, or during dental extraction procedures.

The fourth local consequence of severe periodontal disease results from inflammation close to the orbit which could potentially lead to blindness. The proximity of the tooth root apices of the maxillary molars and fourth premolars places the delicate optic tissues in jeopardy.

The fifth local consequence is described in recent studies which have linked chronic periodontal disease to oral cancer. The association in this case is likely due to the chronic inflammatory state that exists with periodontitis.

The final significant local consequence of periodontal disease is chronic osteomyelitis, which is an area of dead, infected bone. Once an area of bone is necrotic, it does not respond effectively to antibiotic therapy. Therefore, definitive therapy generally requires aggressive surgical debridement.

Severe Systemic Manifestations

Recent animal studies suggest that periodontal bacteria negatively affect the kidneys and liver, leading to decrease in function of these vital organs over time. Furthermore, it has also been suggested that these bacteria can become attached to previously damaged heart valves and cause endocarditis, which in turn can result in intermittent infections, and potentially thromboembolic disease. Other studies have linked oral bacteremias to cerebral and myocardial infarctions and other histological changes. Additional human studies have linked periodontal disease to an increased incidence of chronic respiratory disease (COPD) as well as pneumonia. There are many studies that strongly link periodontal disease to an increase in insulin resistance, resulting in poor control of diabetes mellitus as well as increased severity of diabetic complications. Additionally, it has been shown that diabetes is also a risk factor for periodontal disease. Periodontal disease and diabetes are currently viewed as having a bidirectional interrelationship where one worsens the other.

We must learn to view periodontal disease as not just a dental problem that causes bad breath and tooth loss, but as an initiator of more severe systemic consequences. As one author states, "Periodontal disease is clearly an important and potentially life threatening condition, often underestimated by health professionals and the general public." Only by thinking in these terms can we fully appreciate the scope of the disease process and discuss the problem with clients so that they can appreciate the depth of the problems their pets face. This information will significantly increase client compliance with homecare and dental prophylaxis, as well as advanced dental procedures.