Periodontal Disease Overview

Periodontal disease is the number one health problem in small animal patients. By two years of age, 70% of cats and 80% of dogs have some form of periodontal disease. However, there are generally little to no outward clinical signs, and therefore therapy typically comes very late in the disease. Consequently, periodontal disease may also the most undertreated disease in our patients.

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 (periodontal ligament and alveolar bone) 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). Although bone loss is irreversible, it is possible to arrest its progression. However, it is more difficult to maintain periodontally diseased teeth in comparison to healthy teeth. Additionally, periodontal attachment loss may be present with or without active inflammation.

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 (between the gingiva and the teeth or alveolar bone), it is called subgingival plaque.

Supragingival plaque likely affects the pathogenicity of the subgingival plaque in the early stages of periodontal disease. However, 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 bacteria in the subgingival plaque secrete toxins as well as metabolic products. This creates inflammation which damages 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. The end stage of periodontal disease is tooth loss; however, the disease has created significant problems prior to tooth exfoliation.

Clinical Features

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.

The first obvious clinical sign of gingivitis is erythema followed by edema of the gingiva. However, it is now known that the first evidence of gingivitis is bleeding during brushing, probing, or after chewing hard/rough toys. Therefore, it is important to realize that normal appearing teeth/gums can actually be infected. If the first stages of gingivitis are not treated, it will progress into edema, spontaneous bleeding, 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 non-pathogenic. 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. In other words, the periodontal attachment to the tooth migrates apically. 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. In other cases, the gingiva remains at the same height while the area of attachment moves apically, thus creating a periodontal pocket.

Severe Local Consequences

The most common severe local consequence of periodontal disease is an oral-nasal fistula (ONF). ONFs are typically seen in older, small breed dogs; 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). Appropriate treatment of an ONF requires extraction of the tooth and closure of the defect with a mucogingival flap. However, if a deep periodontal pocket is discovered prior to development of a fistula, periodontal surgery with guided tissue regeneration can be performed to save the tooth.

Another potential severe consequence of periodontal disease can be seen in multi-rooted teeth, and is called a class II perio-endo abscess. This occurs when the periodontal loss progresses apically and gains access to the endodontic system through the apical blood supply, thereby causing endodontic disease via bacterial contamination. The endodontic infection subsequently spreads though the tooth via the common pulp chamber and causes periapical infection 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. Pathologic fractures carry a guarded prognosis for several reasons including: lack of remaining bone, low oxygen tension in the area, and difficulty in rigidly fixating the caudal mandible.

Regardless of the method of fixation, the periodontally diseased root (s) must be extracted.

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. In this way, periodontal inflammation acts as a ‘promoter” of cancer, similar to the chronic inflammation from smoking increases the incidence of lung cancer.

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

Systemic ramifications of periodontal disease are also well documented. The inflammation of the gingiva and periodontal tissues that allows the body’s defenses to attack the invaders also allows these bacteria to gain access to the body. It is important to note that just established gingivitis (i.e. no attachment loss) is enough to create these systemic effects. In humans, the periodontal surface area comprises a surface area the size of the palm of your hand. This is a large area of infection for the body to deal with. However, if you consider the size of the mouth and teeth of a small breed dog in relation to their body, there is actually a far greater level of infection affecting these patients.

There is a plethora of studies both in the human and veterinary literature which document a link between periodontal inflammation and organ dysfunction. Affected organs include the kidneys and liver, leading to decrease in function of these vital organs over time.

Most critically, periodontal disease is now associated with early mortality. In other words, humans with bad periodontal disease die earlier than those in good periodontal health. In fact, periodontal disease is now viewed as a higher risk factor for early death than smoking!

Conversely, proper therapy of periodontal disease has been shown to have beneficial effects on systemic maladies. The kidney, liver, and heart function have all been shown to improve when periodontal disease is properly treated. Further, glycemic control is increased in patients with good periodontal health.