Feline gingivostomatitis, also known as lymphocytic plasmacytic stomatitis, is one of the most frustrating oral diseases seen in veterinary practice. Affected cats exhibit a variety of clinical signs including partial to complete anorexia (with a predilection for canned vs. dry food), ptyalism, halitosis, weight loss, abnormal swallowing movements and oral pain.
Orofacial examination reveals gingivitis, stomatitis and possibly palatitis, glossitis, cheilitis, pharyngitis and mandibular lymphadenopathy. Oral inflammation is often extensive and affected tissues are typically ulcerated, edematous, hyperemic, and proliferative (Figure 1). All breeds can be affected at any age.
The oral lesions associated with feline gingivostomatitis are often mistaken for an oral infection; however, inflammation, rather than infection, is the problem, with infiltrates of plasma cells and lymphocytes.
The inflammatory lesions associated with feline gingivostomatitis are thought to be the result of a highly reactive immune system. The specific antigen(s) causing the aberrant immune response are unknown.1,2 Since a specific antigen has not been identified, the etiology may be be multifactorial.
Bartonella has received recognition as a possible etiologic agent, but Bartonella positive PCR status does not appear to be correlated with the presence of gingivostomatitis.3 Gingivostomatitis improves when plaque reduction efforts are made (tooth extraction being the ultimate form of plaque reduction), which suggests involvement of an antigen that is intimately associated with the teeth (i.e. plaque bacteria).
FIGURE 2: Even after having all teeth and roots removed, about 20 percent of patients with feline gingivostomatitis will continue to experience clinically relevant signs of oral inflammation.
Differential diagnoses for oral inflammation in cats include: feline gingivostomatitis, periodontal disease, inflammation secondary to feline tooth resorption, viral diseases (feline herpesvirus and calicivirus), eosinophilic granuloma, autoimmune disease, immune-mediated disease, oral ulceration secondary to uremia, other rare oral inflammatory conditions, and neoplasia.
A complete patient evaluation is paramount in making a correct diagnosis and determining appropriate treatment.
Plaque control is key to controlling gingivostomatitis. A professional dental cleaning will transiently remove plaque, but toothbrushing is necessary to prevent daily accumulation. Unfortunately, most cats with stomatitis are unwilling to allow daily toothbrushing.
Antibiotics provide transient improvements by decreasing bacterial plaque burden, but long-term use promotes resistance.
Currently available medical treatments include either drugs with poor chances of long-term success or drugs with undesirable or serious side effects (e.g. high-dose corticosteroids).
Many drugs have been used to treat feline gingivostomatitis with varying degrees of failure. One of the most effective drugs is methylprednisolone acetate given at a dosage of 20 mg/cat subcutaneously every three weeks as needed.
Other corticosteroids, such as oral prednisolone, have been used to successfully control feline gingivostomatitis. Long-term corticosteroid treatment is not ideal because cats can develop serious side effects, including diabetes and iatrogenic hyperadrenocorticism. Avoiding corticosteroids is especially important when treating cats with diabetes, feline leukemia virus or feline immunodeficiency virus.
FIGURE 3: Appearance of ablated areas immediately after CO2 laser ablation. Ablation of the inflamed oral tissue has been shown to be effective in some cases of refractory stomatitis. Scar tissue in laser-treated areas has a reduced blood supply and may be less likely to become inflamed.
Non-steroidal drugs that have been used with some success include recombinant human interferon, cyclosporine, bovine lactoferrin, piroxicam, meloxicam, chlorambucil, azathioprine and gold salts. Many of these drugs are not labeled for use in cats and may have marked side effects or require close monitoring. Recombinant feline omega interferon is commonly in use in Europe and has shown promise for refractory cases.
The authors often see cases presenting where medical therapy has been attempted for years but ultimately the disease progresses and patients require extractions. Some veterinary dentists feel that partial or full-mouth extractions may be more likely to provide a cure if performed earlier in the disease process.
Extracting all teeth (or sometimes just the premolars and molars) has been shown to be effective in curing feline gingivostomatitis. In one study, 60 percent of patients treated with extraction of all (or most) teeth were clinically cured, and an additional 20 percent were significantly improved, not requiring further medication.4
This procedure is labor-intensive and will not be successful if tooth or root fragments are not completely removed. In some patients, areas of abnormally appearing alveolar and perialveolar bone may also need to be removed. These cases are commonly referred to veterinary dental specialists.
When extracting teeth to treat feline gingivostomatitis, the question arises whether to extract the canine and incisor teeth.
A suggested approach is to extract canine and incisor teeth if they are diseased or if the surrounding tissues are markedly inflamed. If the canines and incisors are sound and inflammation is limited to the caudal portion of the oral cavity, these teeth may be spared. If extraction of premolars and molars does not provide a cure, extraction of canines and incisors may be considered in an attempt to remove every possible plaque retentive surface.
| Key Points
Even after having all teeth and roots removed, approximately 20 percent of patients will continue to experience clinically relevant signs of oral inflammation requiring further treatment (Figure 2). The goal of treatment is to reduce or eliminate oral discomfort to a degree where appetite is consistently good and patient body weight is maintained.
A first step in treatment of refractory stomatitis is to perform a radiographic re-examination of the dental arches to rule out the possibility of retained tooth roots. In some cases of refractory stomatitis, NSAIDS such as piroxicam or meloxicam provide relief. Side effects of NSAIDS include gastrointestinal ulceration and renal compromise.
Avoid combining NSAIDS with corticosteroids due to the likelihood of severe gastrointestinal ulceration. Immunosuppressive and immunomodulatory drugs such as corticoster- oids, cyclosporine, interferon4, chlorambucil and azathioprine can be used to reduce oral inflammation, though the response varies and can take weeks to get favorable results.
Of these drugs, cyclosporine seems to show the most promise. The starting dose for Neoral solution is 2.5 mg/kg every 12 hours.
Appropriate patient monitoring is critical when using any of these drugs to avoid serious or potentially fatal side effects.
Laser ablation of the inflamed oral tissue is another adjunctive treatment that can be effective in some cases of refractory stomatitis. Treatment of inflamed tissue with a CO2 laser is thought to result in the formation of scar tissue, which may be less likely to become inflamed. A recent case report in the Journal of Veterinary Dentistry details the use of C02 laser as an adjunctive treatment for caudal stomatitis in a cat (Figure 3).5
Laser treatment is not considered by the authors to be an alternative to extractions but rather an adjunctive treatment in those cats with proliferative disease not responding to extractions. <HOME>
Dr. Daniel T. Carmichael practices at Veterinary Medical Center in West Islip, N.Y. Dr. Lewis is an assistant professor of dentistry and oral surgery at the University of Pennsylvania’s Matthew J. Ryan Veterinary Hospital and president-elect of the American Veterinary Dental Society.
*Photos courtesy of Dr. Daniel T. Carmichael
1. Quimby JM, et al. Evaluation of the association of Bartonella species, feline herpesvirus 1, feline calicivirus, feline leukemia virus, and feline immunodeficiency virus with chronic feline gingivostomatitis. J Feline Med. Surg. 2008. Feb; 10 (1): 66-72.