Periodontal disease, caused by plaque bacteria, is probably the most common oral inflammatory condition in cats. However, other inflammatory diseases are relatively frequent as well. A proper diagnosis is very important, because prognosis and treatment differ quite significantly.
Feline Chronic Gingivostomatitis
Feline chronic gingivostomatitis (FGCS) is a persistent inflammatory disease of the oral mucosal tissues. It affects particularly young adult cats, but may be diagnosed at any age. No sex or breed predilection has been proven. Clinically, it is characterized by inflammation and ulceration of gingival and mucosal tissues. In particular, caudal stomatitis, the inflammation of the caudal oral mucosa (lateral to the palatoglossal folds), is a key feature of the disease. The mucocutaneous junctions, palate (the mucosa of the hard palate immediately adjacent to the teeth), tongue (dorsal, lateral and ventral sides) and pharynx may also be affected in some cases. Ulcero-proliferative lesions may be seen in long-standing cases. These seem to be much more difficult to heal even after appropriate treatment.
Feline chronic gingivostomatitis is a very painful and debilitating disease, with patients often becoming depressed or aggressive, and showing clear signs of social withdrawal. Weight loss secondary to dysphagia and anorexia are also common. Other typical signs include halitosis, dehydration, poor hair coat due to limited grooming activity, mandibular lymphadenopathy, pawing at the mouth, restricted mouth opening during yawning, vocalization during feeding and grooming, oral bleeding, ptyalism and sialorrhea.
The etiology of FCGS is unclear, but is believed to be multifactorial. Viruses, bacteria, and possibly other exogenous factors may be involved. Affected individuals may also have an altered, exaggerated immune response to infectious or non-infectious antigens.
Feline immunodeficiency virus and feline leukemia virus do not seem to play an important role in the pathogenesis of the disease. Indeed, the prevalence of FIV and FeLV among cats with stomatitis is not significantly different from that of the general population.
Feline calicivirus (FCV) instead can be isolated from 85 to 100% of cats affected by FCGS, versus a prevalence of up to 20–30% in the general population. Its exact role in the disease process remains unclear. Experimental reproduction of chronic stomatitis or chronic FCV carrier status have never been demonstrated. The virus could therefore be an opportunistic agent rather than the cause of the disease. However, the detection of FCV has been shown significantly correlated to the presence of caudal stomatitis and its degree of severity.
The role of feline herpesvirus (FHV) in the disease process is still controversial. However, FHV is shed intermittently, and may be difficult to detect.
Oral bacteria are considered to play an important role in the disease process, either as complicating or causative factors, and plaque control is a key point in the treatment of FCGS.
Decreasing inflammation and eliminating any inflammatory factor from the oral cavity, controlling plaque bacteria and treating any secondary infections, and controlling oral pain and discomfort are key points in treatment.
Initially, a complete professional dental cleaning (i.e., supragingival and subgingival plaque and calculus removal, gingival curettage, and polishing), and complete (i.e., all portions of a tooth) and selective (i.e., diseased teeth) extractions of diseased teeth should be performed. Following surgery, medical treatment (e.g., antibiotics, anti-inflammatories, analgesics, immunomodulatory drugs) may be prescribed, based on the clinical situation of each patient. Home oral hygiene measures should be implemented to control or prevent plaque and calculus accumulation, but they may be very difficult to perform. A conservative approach is therefore rarely effective. In severe and refractory cases, extraction of diseased as well as healthy teeth in contact with soft tissue lesions is recommended. This often results in full-mouth or nearly full-mouth (i.e., all premolar and molar teeth) dental extraction. No other treatment regimen has been shown to obtain comparable results, with 60% of cases clinically cured and 20% of cases significantly improved at the time of follow-up. After tooth extraction, the need for medical treatment has also been demonstrated to decrease significantly. This clinical improvement is supposedly due to significant reduction of plaque bacteria, removal of diseased teeth causing discomfort and inflammation, and possibly removal of contact between the hard dental surface and the ulcero-proliferative soft tissues.
Medical treatment is always an adjunct to proper surgical management. Antibiotics, antimicrobials, anti-inflammatory, immunosuppressive and immunomodulatory drugs, and analgesics may be prescribed based on individual needs.
Prognosis of FCGS is always reserved, as it is impossible to predict treatment response for any single patient.
Juvenile Hyperplastic Gingivitis
It affects very young individuals. The disease onset usually corresponds to the time of eruption of the permanent teeth, around 6 months of age. It seems to be particularly frequent in Maine Coon cats, possibly suggesting a genetic component. There seem to be no sex predisposition.
The gingival tissues appear inflamed and enlarged to a point that sometimes the dental crowns are completely encased in soft tissues. The inflammation is usually diffuse (affecting both attached and free gingiva) and generalized (affecting the majority of the teeth), even though the premolars-molars areas seem to be more frequently and more severely affected than canines and incisors areas.
It is believed to be a plaque-induced disease. Extraction of the teeth next to the inflamed tissues is normally an effective treatment. However, a more conservative type of treatment may also be attempted if compliance of owners and animals is expected to be good. A complete periodontal and intraoral radiographic examination should be performed in affected animals. It is not infrequent to find periodontal pockets and other lesions, as chronic gingivitis may lead to alveolar bone resorption and inflammatory root resorption. Diseased teeth should be extracted, and the remaining teeth scaled and polished. Gingivectomy should be performed (and possibly histopathology examination performed) to remove excessive gingival tissues. Home care (i.e., daily tooth brushing, dry diets and use of dental treats) should then be recommended, as plaque control is necessary to keep the inflammation under control and reduce the risk of development of hyperplastic tissues. However, if home care is not properly performed, recurrence is very frequent. The disease seems to be self-limiting. In appropriately treated animals inflammation may reside around 1.5–2 years of age, or even earlier.
In humans pyogenic granulomas are described as reactive tumour-like lesions. They develop in response to a low-grade stimulus, which is often traumatic in nature. The name is a misnomer, as they are not granulomatous lesions and do not have a bacterial component.
Lesions with similar clinical and histopathological appearance have been described in cats. They seem to develop secondary to an abnormal occlusal contact between premolar and molar teeth and the vestibular mucosa on the opposite jaw.
The lesions are normally not more than 10 mm in diameter, and appear as broad-based plaques or exophytic lesions, round or irregularly elongated, from pink to deep red in colour, sometimes with yellowish discolouration, often with superficial ulceration, with a soft or friable consistency, and bleeding easily.
Two non-specific histopathological patterns have been described, defined as chronic focal lymphoplasmacytic mucositis and chronic focal fibrovascular hyperplastic mucositis. They are clinically undistinguishable and possibly represent two stages of the same lesion.
Etiopathogenesis for pyogenic granulomas in cats is still unclear. Congenital or post-traumatic malocclusion, occlusal drift of the premolar and molar teeth, buccal bone expansion, and an increased latero-lateral range of motion of the mandibles have been hypothesized as possible causes. However, lesions develop particularly following loss or extraction of large caudal teeth, possibly indicating that an acquired overbite may develop, favoring tooth-to-tissue contact.
Successful treatment entails surgical excision of the proliferation and removal of the traumatic contact (i.e., coronal reduction or extraction of the tooth/teeth in contact with the lesion).
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