Chronic Gingivitis/Stomatitis (CGS)

Gingivitis/stomatitis in the cat is the cause of a lot of heartache for both the practitioner and the client. Often, cats present in severe pain, with ptyalism, dysphagia, and marked weight loss.

Histologically, it is characterised by an infiltration of plasma cells and lymphocytes, possibly in response to polyclonal B-cell activators in oral bacteria. Other cofactors, such as viruses and proteins, have also been incriminated. Immunologically, the disease is associated with raised levels of cytokines, especially interleukin 6 (mimics the situation seen in chronic periodontitis in man), as well as high levels of immunoglobulins in the blood. Pure-breed cats (Siamese, Persians) may have more severe disease than other cats.

Aetiology

 Aetiology unknown, multifactorial disease?

 Viral? – Chronic calicivirus infection, herpesvirus, coronavirus

 May be due to chronic antigenic stimulation and an inability to moderate the host response: polyclonal B-cell activation

 Can see hyper/hypo response of immune system to plaque bacteria, other antigens such as food additives (cinnaminase, benzoin), viruses

 Cats with CGS seem to be "plaque intolerant," suggesting that periodontal disease plays a part in the disease

 Organ-specific autoimmune disease

 Bartonellosis (flea vector)

Similarities Between CGS and IBD

CGS shows similarities with inflammatory bowel disease in cats (IBD). In both diseases, it is suspected that there is a breakdown in mucosal tolerance to antigenic stimulation. This is a key feature in IBD. In IBD, the resident bacterial flora is implicated as essential in driving mucosal inflammation. Oral periodontal pathogens are suspected as a possible aetiologic factor in CGS. Modulation of the enteric microenvironment has been shown to reduce proinflammatory mucosal cytokines in Crohn's disease (a disease in man similar to IBD in animals). This may explain why tooth extraction with the subsequent reduction in bacterial reservoirs has some degree of success in CGS.

Diagnosis of FCGS

A complete oral examination is normally performed under general anaesthesia due to the painful nature of the disease. A haematological workup including viral assays is necessary to rule out FIV, FeLV, and other possible causes.

Biopsies may be required especially where lesions are asymmetrical (need to rule out tumours and autoimmune diseases), and viral culture of lesions may be of benefit to rule out calicivirus infection. Bacterial culture and sensitivity testing may also be required if there is a poor response to empirically chosen antibiotics.

Typically, cats with CGS show a widespread and dramatic inflammation of the oral tissues - often spreading into the oropharynx and along the mucosa of the hard palate.

Management of CGS

 No one treatment is successful. Owner education: Prepare the owner for a long battle.

 Professional scaling/cleaning and meticulous homecare with extraction of teeth with poor prognosis should be your starting point.

 Any root fragments need to be removed. Never leave fractured root tips behind in these cases. Intraoral dental radiographs are essential when evaluating for retained roots.

 Often lack of permanent response to meticulous oral hygiene, professional scaling.

 Antimicrobials

 Doxycycline, amoxicillin/clavulanate, metronidazole, clindamycin, Stomorgyl

 Anti-inflammatories

 20 mg IM methylprednisolone every 2–4 weeks or 2–4 mg/kg prednisolone daily, then ADT (caution re: excessive weight gain and diabetes mellitus)

 Immunosuppressant drugs

 Azathioprine (1.5–3 mg/cat/every 48 hours) - rarely used in cats

 Immunomodulators

 Interferon (Virbagen Omega) antiviral/immunomodulator

 Preferably injected into lesions 1–2 million units total dose

 Repeated 3 times every two weeks at junction between healthy and inflamed tissue (5 or 10 MU vial)

 Oral cyclosporine 5 mg/kg/day for 6–8 weeks, then ADT

 Neoral - May be of benefit instead of long-term steroids: 10 ml (100 mg/ml) of a Neoral® suspension in 40 ml of corn oil base; i.e., 50 ml = 20 mg/ml. Give 20 mg (1 ml) SID to 4 kg cat for approximately 6 weeks

 Protopic - Apply topically: tacrolimus ointment 50 g 0.1%

 Sodium aurothiomalate (Myocrisin - Rhone - Poulenc Rorer) - gold salt compound (1 mg/kg IM weekly for up to 4 months)

 Hypoallergenic diets - Novel protein diets or hydrolysed protein diets can be tried where food allergy is suspected (look for concurrent atopy).

Refractory Cases

These cases often require caudal (premolar/molar) extractions, if not the entire dentition - currently shows the highest success rates. The removal of the periodontal ligament lining the alveolus is also advisable.

 However, in a study of 30 cats, 7% showed no improvement after multiple extractions (Hennet 1994).

 Poor response to extraction: These cats need to be treated with anti-inflammatories or immunomodulators.

 Rare reports of dysplasia in refractory cases and conversion to SCC.

Inflammatory Tooth Resorption (TR)

Tooth resorption (TR) is a common disease of cats. The inflammatory form of the disease (see below) is seen at the cervical or neck area of the tooth and is thought to be associated with PD, although this is unproven.

At the present time, the aetiology of TR is not known.

Like periodontal disease (PD), TR may be asymptomatic, although symptoms such as dysphagia, ptyalism, face rubbing, jaw chattering, poor appetite, and weight loss may be seen.

Oral examination may show from little to abundant plaque and calculus covering the teeth, while hyperplastic gingiva may sometimes be seen extending onto the eroded tooth surface. TR can be confused with feline gingivitis/stomatitis, especially when there are retained roots in the mouth.

Prevalence of TR

Prevalence rates of 28–57% have been reported in the literature, and older cats are more likely to be affected, with the number of lesions increasing with age.

Asian shorthair cats appear to be more susceptible, although any breed/domestic cat can be affected. Some studies have shown male cats to be more susceptible to TR than females, but recent studies show no gender predilection. The disease often exists in conjunction with PD.

Clinical Appearance

Posterior teeth are more commonly affected than anterior teeth, and diagnosis is often difficult when the affected teeth are covered with plaque, calculus, or inflamed gingiva. In one study, the two most commonly affected teeth were the maxillary and mandibular fourth premolars. Lesions are more common on the buccal surface of the tooth, and they often start in the cervical area, extending both apically and coronally.

Aetiology of TR

As yet, there is no known cause, but many theories and suggestions have been put forward to explain this most perplexing disease.

Gorrel (2003) concluded that TR may be two separate disease processes - one predominantly affecting the cervical or neck area of the tooth (inflammatory process - type 1 TR), while the other process (replacement resorption - noninflammatory or type 2 TR) affects the root of the tooth and may not show any tooth loss above the alveolar bone margin. There is a type 3 resorption, which is a combination of type 1 and 2.

Some veterinarians felt that dietary or endogenous acids were the trigger in initiating the lesion. Others put forward the idea of occlusal stresses (so-called abfraction lesion) as being the cause, and still others incriminated viruses as the initiator. There may be an association with PD. Currently, there is much research being done in discovering the aetiology of TRs, with scientists now looking at hypervitaminosis D (high levels of vitamin D have been found in some pet foods) as a possible cause.

Types of Resorption

 Type 1 TR - Characterised by a normal PDL space and radiodensity of root structure (based on intraoral radiographs).

 Type 2 TR - Characterised by part of the lesion being somewhere along the root surface. There is an absence of the PDL space and extensive root replacement by alveolar bone.

 Type 3 TR - Same as type 2, but in multirooted teeth, one root has lost the PDL space, whilst the other root has a normal PDL space.

Diagnosis

Diagnosis is usually based on clinical examination with a dental explorer, but intraoral radiography is a more sensitive tool for diagnosing TR especially when the lesion is subgingival.

The disease can be classified into stages I–V, with stage I being the early lesion, stage II lesion into dentine, stage III lesion involving the pulp of the tooth, stage IV lesion involving pulp and extensive crown loss, and the endstage V lesion involving loss of the crown of the tooth but with retained roots.

Treatment of TR

 Early lesion involving cementum - topical fluoride? and monitoring

 Lesions involving dentine +/- pulp: extraction is the current treatment accepted

 Treatment - Can be very difficult extraction due to partial/complete root ankylosis (type 2/3)

 Most TR extractions require a surgical technique (type 1).

 Restoring lost tooth structure? Not recommended.

Other Treatment Options

 Crown amputation technique described by Dupont. In the original study, DuPont treated over a hundred teeth with crown amputation. Radiographs showed continued uneventful replacement resorption of the root structure with gingival healing.

 Crown amputation should only be considered based on a radiographic analysis of the tooth without the presence of endodontic disease (apical periodontitis) or severe periodontitis. On radiographs, the absence of a periodontal ligament space would indicate root replacement by bone and so the crown amputation technique would be considered the better treatment option.

It must be remembered that the gold standard for the management of TRs where extraction is indicated is the complete removal of the tooth. On intraoral radiographs, if an intact periodontal ligament space (PDL) is seen around the tooth root, then extraction of the whole root is possible. However, if radiographs of the tooth indicate resorption of the root(s) of the tooth with loss of the PDL space and replacement resorption of the root, then crown amputation is an alternative treatment.