Histopathology Of Canine Ulcerative Stomatitis: A Review Of 65 Cases
Jamie G. Anderson, RDH, DVM, MS, DipAVDC
Colin E. Harvey, BVSc, FRCVS, DipACVS, DipAVDC
University of Pennsylvania
School of Veterinary Medicine
3900 Delancey Street
Philadelphia, PA 19104-6010
Telephone: (215) 8983350
Telefax: (215) 898-9937
To date, the clinical and histopathologic features of canine ulcerative stomatitis have been described in veterinary textbooks and in a limited number of journal articles1,2. The increasing importance of oral medicine and dentistry to the veterinary practitioner requires better characterization of the relatively common canine ulcerative lesions.
The purpose of this retrospective study was to better define ulcerative lesions as to particular histopathologic characteristics, infiltrating cell types and etiologic agents.
MATERIALS AND METHODS
Sixty-five cases of canine ulcerative stomatitis were evaluated by the biopsy service of the University of Pennsylvania, School of Veterinary Medicine. Where appropriate, in order to make a definitive diagnosis, extraoral tissues and additional oral biopsies were taken to include the interface of ulcerated and non-ulcerated tissue.
The ulcerative lesion most often seen in older animals associated with dental calculus is described as a large area of central ulceration with a smaller peripheral zone; the ulcerated area is covered by a fibrinous exudate, with an underlying bed of fairly mature granulation tissue with a modest infiltration of neutrophils. No underlying etiology is typically identified.
The histopathologically suggested etiologies for ulcerative lesions of the canine oral cavity include: plaque and calculus association, trauma, autoimmune, infectious, inflammatory, salivary hypersensitivity reaction, allergic, eosinophilic granuloma complex, and idiopathic. No etiology could be identified for 45% of the lesions. Table I describes the number of cases assigned to each suggested etiology.
A fibrinonecrotic exudate was found overlying 32% of the ulcers. In 42% of the cases where a fibrinonecrotic exudate was found, no underlying etiology was detected. Table II describes the correlation of the presence of a fibrinonecrotic exudate overlying the lesion and the final histopathologic assessment.
The cell types infiltrating the submucosal tissues primarily consisted of neutrophils, or lymphocytes and plasma cells. Macrophages and eosinophils were identified less frequently. The degree of infiltration (mild, moderate, severe) and the responsible cell type are depicted in Table III.
In six cases, extra-oral biopsies were also evaluated; skin (4), testicles/epididymis (1), small intestine (1). In only one case did the extra-oral diagnosis shed light on the etiopathogenesis of the oral ulceration; pathology seen in the oral cavity was felt to be secondary to sepsis associated with parvovirus infection. Table IV describes the histopathologic diagnosis for cases where oral and extra-oral tissues were biopsied.
Twelve percent of the lesions were felt to be autoimmune in etiology based on histopathologic evidence of some degree of separation at the level of the basal lamina. In 50% of these cases, a second oral biopsy was requested to include the interface of the ulcerated and non-ulcerated tissue so that a definitive diagnosis could be made. None of these lesions were assigned a definitive diagnosis of autoimmune disease on oral histopathology.
Of the 65 cases evaluated histopathologically, only 3 lesions (4.6%) were felt to be plaque/calculus associated. The prognosis was reported as good for these lesions.
When no etiologic agent was identified, the conclusion was made in 17% of cases that the lesion was probably traumatic in origin. The value of a detailed clinical history submitted with oral biopsies is emphasized.
There was no evidence of tumor in any of the oral ulcerative lesions. Neoplasia should be placed low on the list of differentials for patients presenting with ulcerative stomatitis.
A Type III hypersensitivity reaction to saliva was noted in three cases. These lesions were characterized by an infiltration of eosinophils. Eosinophilic granuloma complex, usually only seen in Arctic dogs was observed in a Huskie with ulcerative lesions. Histopathologic differentiation of eosinophilic granuloma complex from saliva hypersensitivity reaction is based on collagen degeneration in the former. The one lesion with an allergic component was characterized by an infiltration of both eosinophils and mast cells.
The fibrinonecrotic exudate found overlying 32% of the ulcers was not significantly related to a specific final diagnosis.
In the eight cases (12%) where autoimmune disease was suspected, a second biopsy was requested to include the interface of ulcerated and non-ulcerated tissue in an attempt to make a definitive diagnosis. The antinuclear antibody (ANA) status was not evaluated.
Because twenty-nine cases (45%) had no identifiable etiology, other diagnostic modalities including immunofluorescence assays, virus isolation, and microbiologic culturing should be considered to more clearly define the etiopathogenesis of canine ulcerative stomatitis.
Like canine ulcerative stomatitis, histopathology of the human ulcerative stomatitis lesions are non-diagnostic. As well, routine serum ANA's in people are generally negative. In 1990, a new association was made for human chronic ulcerative stomatitis utilizing immunofluorescence assays 3. Chronic oral ulceration was associated with a stratified epithelium-specific antibody (SES-ANA) that reacts predominantly with the basal layer of the epithelium 4-6. Description of a specific immunologic marker (SES-ANA) for canine ulcerative stomatitis has not been made. Immunofluorescence evaluation of canine ulcerative lesions is in progress (Anderson, JG) with the hope that better definition of the lesion will allow for more specific therapy.
TABLE I Suggested Etiologies for Ulcerative Lesions of Oral Cavity
# cases/% of total
# cases/% of total
TABLE II Correlation of fibrinonecrotic exudate overlaying lesion and final histopathologic assessment
Suggested Etiologies for Oral Ulcerative Lesions
# with fibrinonecrotic exudate/% of total
Salivary hypersensitivity reaction
Eosinophilic granuloma complex
TABLE III Number of cases, Degree and Cell Type Infiltrating Submucosal Tissue
TABLE IV Etiopathogenesis of Biopsies from Extra Oral and Oral Ulcerative Lesions