Lymphoplasmacytic gingivitis in a cat

Abstract

A 12-year-old male neutered short haired cat was presented due to difficulty eating and pawing at the face. Examination revealed severe gingivitis and stomatitis throughout the oral cavity. Gingival biopsy provided a diagnosis of lymphoplasmacytic stomatitis. Extraction of all premolars and molars resulted in elimination of all clinical signs.

A 12-year-old, neutered male, domestic shorthair was presented due to difficulty in eating, pawing at the face, and weight loss. Three years earlier, the cat had undergone a dental prophylaxis for mild gingivitis and tartar accumulation. On physical examination (day 1), mild dental tartar, severe gingivitis, and stomatitis involving the caudal part of the dental arcades, the commisures of the lips, and under the tongue on both sides were apparent. A complete blood (cell) count (CBC) and serum biochemical profile revealed mild decreases in albumin and alanine aminotransferase (ALT). An enzyme-linked immunosorbent assay (ELISA) (SNAP FeLV/FIV antigen test; IDEXX, Toronto, Ontario) was negative. Treatment consisted of administering dexamethasone (Dexamethasone 2; Vetoquinol, Lavaltrie, Quebec), 0.07 mg/kg bodyweight (BW), IM, and penicillin G benzathene/penicillin G procaine (Longisil; Vetoquinol) 15 000 IU/kg BW, IM, and then clindamycin (Antirobe aquadrops; Pharmacia, Orangeville, Ontario) 3.3 mg/kg BW, PO, q12h until surgery.

On the day of surgery, the cat was premedicated, IM, with a combination of butorphanol (Torbugesic; Wyeth, Guelph, Ontario), 0.2 mg/kg BW; acepromazine (Atravet; Wyeth), 0.11 mg/kg BW; glycopyrrolate (Robinul; Wyeth), 0.011 mg/kg BW; ketamine (Ketaset; Wyeth), 2.0 mg/kg BW; and midazolam (Versed; Roche, Mississauga, Ontario), 0.01 mg/kg BW, and then general anesthesia was induced by using a combination of ketamine, 6 mg/kg BW, and diazepam (Valium; Roche), 0.2 mg/kg BW, IV. The cat was maintained under general anesthesia with isoflurane (Isoflurane; Vetoquinol) in order to perform a dental scaling and gingival biopsy. A complete scaling and polishing was performed on all of the teeth. Two teeth, numbers 309 and 409, were extracted. Although teeth numbers 107, 108, 207, 208, 308, and 408 were not removed at this time, a note was made to examine the gingiva around these teeth biannually for a worsening or improvement of the current clinical presentation. Two 5-mm by 5-mm biopsies were taken from an area of gingival hyperplasia in the right ventral quadrant. The biopsy samples were preserved in 10% buffered solution and sent for histopathologic examination (Histovet, Guelph, Ontario). Histological examination of these samples revealed marked hyperplasia of the gingival epithelium with severe inflammation of the lamina propria. Some areas of each biopsy contained a predominantly lymphoplasmacytic infiltrate, while others showed significant eosinophilic inflammation. Focal areas of epithelial dysplasia were evident, as well as suppurative lesions associated with gingival ulceration. The lesions were considered consistent with the syndrome known as lymphoplasmacytic stomatitis (LPS). Eosinophilic inflammation is not only suggestive of hypersensitivity disease, but in combination with the epithelial dysplasia, it has been shown to predispose to subsequent development of carcinoma.

Treatment for the LPS began on day 12 and consisted of dexamethasone (Dextab; Vetoquinol), 0.03 mg/kg BW, PO, q24h for 5 d, and then 0.02 mg/kg BW, PO, q24h. Fourteen days post surgery (day 22), the owner reported that the cat was pawing at his face when eating. On physical examination, it appeared that although the inflammation had decreased somewhat, it was still severe. The dose of dexamethasone was increased to 0.07 mg/kg BW, PO, q12h for 4 d, then to 0.07 mg/kg BW, PO, q24h; amoxicillin (Amoxil; Pfizer, Kirkland, Quebec), 7.0 mg/kg BW, PO, q12h, was also prescribed. By day 35, the gingival inflammation had subsided somewhat, but the owner reported that the cat was not tolerating the treatment well and was becoming quite aggressive. At this time, it was suggested that all of the check teeth be removed.

On day 42, the cat was premedicated and anesthesia was induced by using the same preanesthetic and anesthetic protcol as used during the earlier dental scaling and extraction. All of the premolars and molars (106, 107, 108 109, 206, 207, 208, 209, 307, 308, 407, and 408) were extracted. The roots of teeth numbers 107, 208, 307, 308, 407, and 408 were ankylosed to the underlying bone and had to be drilled out. The extraction sites were flushed with penicillin G benzathine (Crystiben; Solvay, Markham, Ontario). During extraction, a feline osteoclatic resorptive lesion (FLORS) was found in tooth number 109. At the end of the procedure, hydromorphone (Hydromorphone hydrochloride; Sabex, Boucherville, Quebec), 0.05 mg/kg BW, IM, was administered and a 2.5-mg fentanyl analgesic patch (Duragesic; Jaansen, Toronto, Ontario) patch was placed on the dorsal part of the neck. The cat was then treated with dexamethasone (Dexamethasone 2), 0.2 mg/kg BW, IM, and penicillin (Penicillin G Potassium U.S.P; Vetoquinol), 28 000 IU/kg BW, IM. An additional 0.025 mg/kg BW of hydromorphone was given 8 h postsurgery. Treatment was to be continued, starting on day 43, consisting of dexamethasone (Dextabs; Vetoquinol), 0.07 mg/kg BW, PO, q24h, and amoxicillin (Amoxil), 14 mg/kg BW, PO, q12h. The fetanyl patch was to be removed on day 45.

By day 53, 11 d postsurgery, the cat was doing well. He was no longer pawing at his face and the gingival inflammation had subsided considerably. The amoxicillin was discontinued and the dexamethasone was decreased to 0.035 mg/kg BW, PO, q24h for 1 wk, then 0.0175 mg/kg BW, PO, q24h for the following week. By day 67, the gingival inflammation had completely resolved.

Feline gingivostomatitis (FGS, also known as lymphoplasmacytic stomatitis) is a common condition in cats that is probably of multifactorial etiology (1,2). Bacteria, Feline calicivirus (FCV), and immonosuppression, subsequent to infection with Feline leukemia virus (FeLV) or Feline immunodeficiency virus (FIV) have all been hypothesized to cause FGS (1–4). Gingivitis in the cat has been associated with an increased number of gram-negative anaerobic bacteria; however, it has been widely accepted for a number of years that antibiotic therapy alone will not cure FGS (3). Feline calicivirus has also been suggested to play a role in the development of FGS; however, it is unknown whether FCV is present as an inciting factor or an opportunistic infection (1,3). Acquired immune deficiency, such as in FeLV or FIV infection, has been associated with feline dental disease, and stomatitis is commonly reported as a prevalent sign in such infections (3,6,7). An immune-mediated component to FGS also exists (1). In the oral mucosa of a nondiseased animal, a predominantly T-helper 1 (Th 1) cytokine profile is found, probably in response to the constant barrage of minor bacterial invasions by the normal bacterial flora of the oral cavity (4). In cats with FGS, however, biopsies of lesions show a cytokine response that is a mix of Th 1 and Th 2 cytokines. Such information can be important in determining a treatment protocol for FGS.

In this case, the cause of the FGS remained unclear. Calicivirus was not tested for, due to a lack of clinical signs commonly associated with calicivirus and the uncharacteristic distribution of lesions in the oral cavity. The owner did not report any sneezing, and no nasal discharge was noted on physical examination or in the history (8). Although gingival ulcerative lesions were reported histologically, no ulcers were found on the tongue, hard palate, or nose (8). Considering the lack of clinical signs and the cat’s up-to-date vaccination status, calicivirus infection was not placed high on the list of differential diagnoses. Antibiotics were tried for a period of time and although they were not used for a sufficient amount of time to properly judge the response, the positive response to the steroid therapy helped to negate a bacterial cause in this case (2). The negative results of the ELISAs ruled out a viral-induced immunosuppression.

The goals of treatment in FGS are to control dental plaque, which, in turn, will help to decrease the bacterial challenge, as well as decrease the inflammatory and immunologic responses (9). Several protocols have been reported with varied success, including antibiotics, corticosteroids, megesterol acetate, aurothiomalate, dental scaling, tooth extraction, thalidomide, and lactoferrin (1,2). Some studies have reported the most significant results with corticosteroids (2,3); however, FGS frequently becomes refractory to treatment (1). The use of thalidomide has been studied recently due to its suppression of the Th 2 response, allowing a more favorable Th 1 response (1). Thalidomide has also been reported to inhibit some proinflammatory cytokine responses (1). Lactoferrin has also been suggested as a treatment, due in part to its antiviral activity, as well as its capacity to bind iron and make it unavailable for bacterial growth (1). Dental scaling can be helpful for a period of time, but in severe cases, extraction is often the only option.

In this case, after trying different treatment protocols, the owner opted to have all cheek teeth removed, leaving only the canines and incisors. Although the dexamethasone tablets helped to control the inflammation for a period, the cat quickly became resentful of the treatment and not only aggressive towards the owner during medicating, but also quite uncharacteristically antisocial. This is not an uncommon occurrence in cats affected with FGS, and aggressiveness toward other pets or persons has frequently been reported (9). Cats with severe stomatitis are often unable to be treated orally, reducing the treatment options drastically (1,2). Perhaps, if this cat had been more compliant with his treatment, other pharmacologic options could have been pursued. In this particular case, the extraction of the premolars and molars appears to have significantly reduced the gingival lesions and inflammation, and the cat is currently off all medications. The owner has reported that the cat is very happy and comfortable and has become his old, socialself once again.

Research into LPS still has a long way to go. No single treatment works for every cat, supporting the hypothesis that this disease is of multifactorial etiology. Clinicians must consider the pain associated with stomatitis, when oral medications are to be administered to patients and when developing a treatment protocol.