Figure 1 (above): Stage 4 periodontal disease. Local disease is obvious, with profound tartar accumulation, gingival recession, and purulent debris and plaque present in the sulcus.
Periodontal disease is plaque-induced inflammation of the supporting tissues of the teeth; it can destroy the gingiva, periodontal ligament, cementum, and alveolar bone. Associated pain results from tissue effects of inflammatory cytokines and chemokines produced by periodontal pathogens and the host's own immune system.
Systems. Generally considered a primary disease of the tissues around the teeth; however, systemic disease (eg, diabetes mellitus, Cushing's disease, FeLV, FIV, renal and hepatic insufficiency) can exacerbate primary disease, especially in states of immunocompromise.
Species. Dogs and cats are both highly susceptible to periodontal disease. Cats may have exacerbated pain due to coexisting feline tooth resorption.
Breed Predilection. Small-breed dogs are particularly susceptible. Overcrowding and malocclusions play a role in progression in many of these patients. Greyhound, Maltese, and miniature schnauzer dogs tend to have more severe manifestations of rapidly progressive and refractory periodontitis. Somali and Abyssinian cats are overrepresented.
Age and Range. Severity and discomfort generally increase with age because of the progressive nature of the condition.
- Gram-negative anaerobic bacteria incite tissue inflammation, resulting in the release of adenosine triphosphate, potassium ions, hydrogen ions, prostaglandins, bradykinin, and nerve growth factors from damaged tissue.
- Lymphocytes, monocytes, macrophages, and mast cells are attracted to the site, where they release cytokines, such as histamine, that enhance vasodilation and subsequently increase inflammation.
- Allodynia results, whereby even touch or mastication may produce a pain response at the site of periodontitis.
- Chronic inflammation may result in central sensitization and wind-up pain. In cases of chronic oral pain, neurons in the brain stem (nucleus caudalis) are chemically stimulated, enhancing the frequency and intensity of the pain signal to the brain. Glutamate and other chemicals bind to the NMDA receptor, sensitizing the postsynaptic neuron and adding to the local pain response. Specific NMDA-receptor antagonists, such as ketamine, can be used to counter this wind-up component of pain.
History. Patients commonly exhibit no systemic clinical signs that are attributed to periodontal disease. Slowly progressive behavioral changes are often recognized only after the pain associated with periodontal disease resolves following proper surgical treatment.