Feline necrotising sialometaplasia: A report of two cases

Abstract

Unilateral swelling of submandibular salivary gland in two cats was diagnosed as necrotising sialometaplasia. Histological features that differentiate the disease from other salivary gland lesions, particularly neoplasia are: lobular necrosis of salivary tissue; squamous metaplasia conforming to duct and/or acinar outlines; preservation of salivary lobular morphology; and variable inflammation and granulation tissue.

In humans, necrotising sialometaplasia is an ischaemic disease of salivary glands that has histological features that may be confused with neoplasia (Abrams et al., 1973; Batsakis and Manning, 1987; Brannon et al., 1991). A similar disease has been described in dogs (Brooks et al., 1995; Kelly et al., 1979a) and represented about 6% (9/160) of cases of canine salivary gland disease reported in a review by Spangler and Culbertson (1991). In the same review, salivary gland infarction in cats represented about 13% (11/85) of cases of feline salivary gland disease. Despite that relatively high incidence there appear to have been no detailed descriptions of the disease in cats; this paper describes two such cases, of feline necrotising sialometaplasia.

As part of a study of salivary gland diseases, archival material was reviewed from a total of 42 cases of feline salivary disease from the Comparative Pathology Laboratory, University of Bristol Veterinary School. There were 35 tumours, two cases of chronic inflammation, three cases of idiopathic enlargement (sialadenosis) and the two cases described here that were identified as necrotising sialometaplasia. Clinical information was limited to that included on submission forms requesting histopathological investigation.

Case 1

A 10-year-old entire male, domestic short haired cat presented with an ovoid submandibular swelling, about 2 × 0.75 × 0.5 cm, on the left side of the neck; it had developed over the previous 2 months. The mass was excised at surgery and submitted for histopathological examination; lymphoma was a possible diagnosis considered by the referring veterinary surgeon. There was no recurrence of salivary gland disease in the 6 months following surgery during which follow-up was available.

Case 2

A 7½-year-old neutered female, domestic short haired cat presented with a sudden onset swelling on the side of the neck. It was explored surgically and a 3 cm diameter mass was removed and submitted for histopathological examination. The submission form did not suggest that a salivary gland lesion was suspected. There was no recurrence of salivary gland disease in the subsequent two years, for which follow-up information was available).

Tissue samples were fixed in formalin and embedded in paraffin wax. Similar features were present in haematoxylin and eosin stained sections of both cats. There were portions of normal submandibular salivary gland tissue confirming the anatomical site of the lesion. Outlines of lobular architecture were preserved but there were extensive areas of lobular necrosis of salivary tissue with variable infiltration by neutrophils and macrophages. At the periphery of the lesion there were lobules in which granulation tissue was forming and evidence of squamous metaplasia conforming to duct and/or acinar outlines (Fig. 1). The metaplasia resulted in a pseudocarcinomatous appearance but there were no signs of neoplasia.

Figure 1

Lobules of normal salivary gland tissue (top) adjacent to lobules composed of clusters of metaplastic epithelial cells, conforming to ductal and acinar outlines, are separated by loose interstitial connective tissue containing mixed inflammatory cells. Case 2, ×20 Haematoxylin and Eosin stain.

In humans, four histological features of necrotising have been identified that differentiate the disease from other salivary gland lesions (Batsakis and Manning, 1987): lobular necrosis of salivary tissue; squamous metaplasia conforming to duct and/or acinar outlines; preservation of salivary lobular morphology; variable inflammation and granulation tissue.

The characteristic histopathological features necrotising sialometaplasia in dogs were also described (Kelly et al., 1979a). More recently, the literature was reviewed by Brooks et al. (1995). Those authors indicate that the disease has been reported in six small breeds of dog, five of which were terriers; Spangler and Culbertson (1991)mention nine further cases without giving details. The only details given by Spangler and Culbertson (1991) of the 11 cats with necrotising sialometaplasia was the sex (five males and four females with two cases not specified); the cases described here were one male and one female, both neutered.

In dogs (Brooks et al., 1995; Spangler and Culbertson, 1991), as in the eleven cats described by Spangler and Culbertson (1991) and the two cats described here, the mandibular salivary glands are affected and most cases are unilateral. In humans, although any gland may be affected, the palatine glands are involved most often; most cases are unilateral (Brannon et al., 1991). There are differences also in the clinical signs shown by dogs and humans. In dogs there is usually extreme pain, anorexia, gagging and vomiting (Brooks et al., 1995; Kelly et al., 1979b). In humans palatine lesions are usually associated with only mild discomfort and resolve spontaneously in a few weeks (Imbery and Edwards, 1996); recovery from surgery in the two cats reported here was uneventful. Brooks et al. (1995) suggest that treatment of the disease in dogs should involve surgical excision followed by short term administration of anticonvulsants for their analgesic properties. The milder disease in humans is self-limiting; in some cases there is more extensive facial or pharyngeal pain (Sneige and Batsakis, 1992).

The underlying cause of the necrosis in necrotising sialometaplasia in dogs, and cats, is unknown; it is assumed to be ischaemia and vasculitis and thrombosis are reported in many cases (Brooks et al., 1995; Kelly et al., 1979b; Mawby et al., 1991). In humans most cases follow surgical procedures and are assumed to be a result of damage to the vasculature (Imbery and Edwards, 1996); Shigematsu et al. (1996) have recently implicated local anaesthetic injections. In one dog with bilateral lesions (Mawby et al., 1991) immunoglobulin and complement were demonstrated immunohistochemically, suggesting an immune-mediated mechanism but trauma and infection or other causes of vascular injury may be involved. There was no evidence of vascular damage in the cats described here and neither vascular lesions nor necrotising sialometaplasia were reported as a complication of various surgical procedures on salivary glands in cats including experimental salivary mucoceles (Harrison and Garrett, 1975); details of the arterial blood supply to the salivary glands of the cat have been described (Mia and Sis, 1970). The changes in the salivary gland in the case of necrotising sialometaplasia reported here differ from those resulting from ductal obstruction (Harrison and Garrett, 1976).

Necrotising sialometaplasia appears to be a significant, but uncommon, cause of unilateral salivary gland disease in the cat. Spangler and Culbertson (1991) report an incidence of 13% (11/85) among cases of feline salivary gland disease while the cases reported here represent about 5% (2/42). It needs to be distinguished clinically and histopathologically from neoplasia. Although the precise aetiology remains unclear, a vascular lesion seems likely and the prognosis following surgical excision appears favourable.