Structure and Function

The physiologically normal oral mucosa is smooth, shiny, and pink. It is composed of variably keratinizing, stratified squamous epithelium (mucous membranes). In animals in which the oral mucosa is heavily pigmented (melanosis), assessment of circulatory function (capillary refill time) and color as an indicator of red blood cell concentration (packed cell volume) can be difficult. In these cases, examination of conjunctiva, rectal, and urogenital mucosa can be substituted. The oral cavity is where ingested materials are masticated; mixed with digestive enzymes, such as those in saliva; and passed on through the oropharynx to the esophagus.

Defense Mechanisms

Defense mechanisms of the oral cavity include the stratified epithelial surface that is resistant to trauma and some irritants; taste buds, which reject potentially toxic materials based on taste and tongue feel; an indigenous bacterial flora that occupy attachment sites that would otherwise be available to pathogens; and saliva (Box 7-3). Saliva provides a flushing action so potential pathogens are cleared from the oropharynx and swallowed. Saliva also forms a protective coating of the mucosa and contains antimicrobial lysozyme in the zymogen granules of serous cells and immunoglobulins, especially immunoglobulin A (IgA), in a manner analogous to cryptal enterocytes of the intestine, through the production of a secretory component. Migration through the alimentary tract, including the oral cavity, eliminates neutrophils at the end of their lifespan. In their absence, stomatitis results.

Developmental Anomalies

There are a wide variety of developmental abnormalities in the oral cavity. Some are incompatible with life unless surgically corrected. Only a few of these congenital lesions have a proven hereditary component. Most are idiopathic. Thorough physical examination of neonates must include examination of the oral cavity for these defects.

Palatoschisis, or cleft palate, and cheiloschisis, or cleft lip, are among the most common developmental abnormalities of the oral cavity. Cheiloschisis is sometimes referred to as hare lip because this is a normal feature of the rabbit. It is a failure of fusion of the upper lip along the midline or philtrum. Palatoschisis can be genetic or toxic in origin. It results from a failure of fusion of the lateral palatine processes. It can be caused by steroid administration during pregnancy in primates, including humans. Depending on the size of the defect, which may involve only the soft palate or both the soft and hard palates (Fig. 7-1), the lesion may be surgically correctable. It is a matter of some ethical concern whether to correct such defects without also sterilizing the patient because of the potential for cleft palate to have a genetic cause. Important sequelae to the host from cleft palate are starvation, as the result of the inability of the nursing animal to create a negative pressure in the mouth with a resultant failure to suckle, and aspiration pneumonia, since no effective separation is present between the oral and nasal cavities.

Stomatitis and Gingivitis

Stomatitis and gingivitis refer to inflammation of the mucous membranes of the oral cavity and gingiva, respectively. Because the oral cavity is constantly bombarded with ingested substances that are moved around by the tongue, the final result of a variety of insults to the lining of the oral cavity is a loss of mucosa—erosions, ulcerations, and necrosis. Thus, although inflammation is apparent, clues as to the initiating process may be absent. Lesions may be at different stages and are commonly classified as macules, papules, vesicles, erosions, abscesses, granulomas, and ulcers. These lesions can be caused by infectious agents, particularly viruses; chemical injury; trauma; intoxicants; or autoimmune or systemic disease. They often result in anorexia caused by painful mastication. Hypersalivation (ptyalism) is also apparent, whether from overproduction or a failure to swallow. In the cat, gingivitis is the first and most consistent sign of feline immunodeficiency virus (FIV) infection (immune system failure) associated with a reduction in CD4 lymphocytes, thymic atrophy, and lymph node atrophy.

Vesicular Stomatitides

Although vesicular stomatitis correctly refers to oral vesicles and blisters, the term is generally reserved for those lesions caused by epitheliotropic viruses. The vesicular stomatitides are listed in Table 7-1. Their genesis is from virus-induced epithelial cytolysis attended by fluid accumulation and subsequent rupture of the resultant vesicle. Blistering or vesiculation of the oral epithelium is present early in the course of these diseases. All of these diseases are virus-induced, and all have identical appearances at gross and histopathologic examination. None of these conditions is fatal. They produce great economic loss because of poor weight gain in affected animals and sometimes abortions in gravid females. The exact cause of the abortions is unknown, but it is probably related to the stress induced by the painful oral, cutaneous, and pedal (hoof or foot) lesions. Secondary bacterial invaders, both Gram-negative and Gram-positive, of these lesions can result in endotoxemia. Several diseases, such as foot-and-mouth disease and vesicular exanthema, affect the coronary bands of the digits and interdigital clefts, resulting in lameness. Some of these diseases (foot-and-mouth disease, vesicular exanthema, and swine vesicular disease) are exotic to the United States (US) and thus are reportable to state or federal authorities, or both, if the clinician or pathologist suspects the disease. This requirement is due to the great expense involved in eradicating these diseases from the US and their potential use as agents of agroterrorism. Nontariff export/import barriers designed to prevent the introduction of highly contagious agents, such as foot-and-mouth disease, into animal populations of countries with which we trade are often put in place.

The gross lesions of the vesicular stomatitides are epithelial. Fluid-filled vesicles are present in the oral cavity, lips, rostral palate, and tongue (Fig. 7-2, A). Entry of virus in these cases is most likely oral into areas of temporary loss of mucosa as the result of normal mastication and trauma. The viruses are cytolytic, and the resultant release of virus from cells infects neighboring cells. The lesions enlarge centripetally, forming vesicles. Bullae result from coalescence resulting in erosions and ulcers. These ulcers are typically hyperemic (Fig. 7-2, B). Viremia, often transient, sometimes occurs.

Similar vesicular lesions occur in the nasal mucosa, particularly in pigs with vesicular exanthema and in the proximal epithelium of the alimentary system (esophagus and rumen) of cattle with foot-and-mouth disease. Some animals have conjunctivitis and vesicular dermatitis of the teats and vulva. Microscopically, the lesions of these four diseases (foot-and-mouth disease, vesicular stomatitis, vesicular exanthema, and swine vesicular disease) are similar. Virus-induced, intracellular edema progresses to swelling of the cells of the stratum spinosum, cell lysis and intercellular edema, and resultant vesicles. The epithelium overlying the virus-rich vesicular fluid is thin, and even slight friction can rupture vesicles and bullae, creating an ulcer. Healing of the ulcer progresses from the usual fibrin and/or neutrophil-rich acute stages (scab) to the more chronic stages of granulation.

Lesions and signs of the vesicular stomatitides include vesicles, bullae, and detachment of patches of epithelium with resultant raw ulcers, ptyalism, lameness, fever, and anorexia. Besides the lesions that develop from the initially infected cells, the virus spreads centripetally to adjacent susceptible epithelium, causing repeated episodes of this infectious, lytic cycle. The vesicular stomatitides are tentatively diagnosed based on the clinical signs and lesions resulting from oral and nasal ulceration, conjunctivitis, and ulceration of the genitalia and mammary glands. Lameness is secondary to hoof involvement that is focused at the coronary band. Definitive diagnosis is important and performed at federal laboratories equipped to rapidly respond to suspected outbreaks. Federal quarantine of infected herds is an important control mechanism, followed by eradication, slaughter, and carcass disposal.

Specific Vesicular Diseases

Foot-and-mouth disease is an extremely important disease and disease threat of arteriodactyls worldwide but has not appeared in US livestock since 1929, when it was eradicated after an outbreak in California. Virus spreads rapidly and principally by aerosol. The disease is characterized in its early stages by vesicles in the planum nasale, in the oral cavity, and tongue. The picornavirus of foot-and-mouth disease attaches to susceptible cells via integrins on the cell surface. Fluid from ruptured vesicles spreads to areas of abraded skin, for example, skin of a mammary gland. When coronary bands and hooves are affected, coronary band vesiculation may eventually lead to sloughing of the hoof. Although this disease is not fatal, the pain and accompanying inappetence lead to weight loss. If allowed to heal, the hoof will regrow into a ball-like structure. Young animals with foot-and-mouth disease frequently have a viral myocarditis without other signs. Vaccination is short-lived (6 months) and takes time to become effective in individual animals; thus immediate protection is not provided. Persistent infections occur in water buffalo and infected cattle that have been previously vaccinated.

Vesicular stomatitis is common in calves, pigs, and some wildlife species but does not occur in sheep or goats. It is the only vesicular disease to which horses are susceptible. In northern latitudes, it is generally a warm weather disease, suggesting that insects act as vectors. As the name implies, vesicles in the oral cavity characterize the disease. Clinically the disease is often recognized by inappetence in the affected animal, accompanied by ptyalism.

Vesicular exanthema is a specific disease of pigs that is indistinguishable clinically and pathologically from foot-and-mouth disease. This disease is uniquely American and was believed eradicated from pigs in 1956 through enactment of federal laws requiring the cooking of garbage fed to pigs. The evidence indicates that vesicular exanthema of swine serovars are variants of San Miguel sea lion virus. This latter marine calicivirus occurs in coastal sea lion and fur seal populations from California to Alaska (Web Fig. 7-1).

Swine vesicular disease is indistinguishable from the other vesicular diseases and is exotic to the US. Efforts are underway to develop DNA microarrays to facilitate rapid identification of specific vesicular diseases from a single sample.

Erosive and Ulcerative Stomatitides

Erosions are defined by a loss of part of the thickness of the surface epithelium, whereas ulcers are full-thickness epithelial losses exposing the basement membrane. Thus erosions may progress to ulcers, which in hollow organs may become perforating ulcers. Erosive and ulcerative stomatitis can have a variety of causes. Agents responsible include the viruses of bovine viral diarrhea (BVD) (Fig. 7-3), rinderpest, malignant catarrhal fever (Fig. 7-4), feline calicivirus, and bluetongue, and in equids, nonsteroidal antiinflammatory drugs (NSAIDs). Other causes include uremia (Fig. 7-5); ingested foreign bodies, such as foxtail awns; the feline eosinophilic granuloma complex; and vitamin C deficiency in primates and guinea pigs (Web Fig. 7-2). Often, the oral lesions must be evaluated in the context of the clinical signs, together with histopathologic findings and ancillary testing, to arrive at a definitive diagnosis. Additionally, the vesicular stomatitides can progress to ulceration secondary to abrasion to the point that they cannot be distinguished from the ulcerative stomatitides.

Parapox Stomatitides

The two major diseases in this category, bovine papular stomatitis and contagious ecthyma, are zoonotic. Bovine papular stomatitis is recognized by papules on the nares, muzzle, gingiva, buccal cavity, palate, and tongue (Fig. 7-6). Lesions also occur in the esophagus, rumen, and omasum. Microscopically, acantholysis is responsible for the macule and ballooning degeneration of these cells, which may contain intracytoplasmic eosinophilic parapoxvirus inclusions at a later stage (Fig. 7-7; also see Fig. 1-12). Erosion of the infected cells accompanied by a neutrophilic infiltrate heals readily from the unaffected basal epithelium. The disease is more common in immunosuppressed animals such as those persistently infected with BVD virus. In humans, the disease is called milker’s nodules and is characterized by papules of the hands and arms.

Contagious ecthyma, sore mouth or infectious pustular dermatitis, is a condition of sheep and goats characterized by progression of the stages typical of pox viruses—macules, papules, vesicles, pustules, scabs, and scars in areas of skin abrasions, including the corners of the mouth (Fig. 7-8; also see Fig. 17-43), mouth, udder, teats, coronary bands, and anus. Occasionally, the mucosa of the esophagus and rumen also can be affected. The virus is quite hardy and can survive for 50 to 60 days in the summer and longer in cold weather. At room temperature, scabs containing virus can be infective after 10 years. Eosinophilic cytoplasmic inclusion bodies are visible at microscopic examination of lesions early in the course of disease. The condition in humans is called orf.

Necrotizing Stomatitides

Necrotizing stomatitis occurs in cattle, sheep, and pigs. In cattle, it is sometimes referred to as calf diphtheria (Fig. 7-9). Necrotizing stomatitis is the end-stage of all other forms of stomatitis when they are complicated by infection with Fusobacterium necrophorum, a filamentous-to-rodlike-to-coccoid, Gram-negative anaerobe. Bacterial toxins are responsible for the extensive lesions. Necrotizing stomatitis is characterized by yellow-gray, round foci surrounded by a rim of hyperemic tissue in the oral cavity, larynx, pharynx, or tongue. Well-demarcated foci of coagulation necrosis typify the histologic appearance of necrotizing stomatitis. As might be expected in foci of inflammation, there is a circumferential rim of leukocytes and hyperemia. Clinical signs include swollen cheeks, inappetence, pyrexia, and halitosis. Infection may become systemic if severe, resulting in lesions throughout the alimentary system and associated lymphoid tissue.

Noma is a severe form of oral ischemic necrosis with lesional spirochetes and fusiform bacteria. Although rare, it is seen most often in primates, including humans, and dogs. It is characterized by severe necrotizing gingivitis that can extend into adjacent bone causing osteolysis and sometimes death.

Ulcerative gingivitis (trench mouth), caused by anaerobic spirochetes, affects humans, some nonhuman primates, and rarely, puppies. In addition to Fusobacterium spp., Borrelia vincentii may be causative. Debilitated animals and those with intercurrent infections are at increased risk for these secondary invaders, which may be part of normal oral flora. Similar clinically to necrotizing stomatitis, ulcerative gingivitis is characterized by acute inflammation and necrosis, oral ulceration and pain, halitosis, a fragile oral mucosa, and ptyalism. The morphologic diagnosis is an acute, necrotizing gingivitis. Unlike the case in necrotizing stomatitis, the causative agents are readily identified by tissue smears or by culture.

Eosinophilic Stomatitides

Oral granulomas or ulcers (“rodent ulcers”) occur frequently in cats. Similar lesions occur sporadically in a variety of canine breeds. In cats, they are termed oral eosinophilic granulomas. Although the etiology of this condition is unknown, the histologic appearance of lesions suggests an immune-mediated mechanism, possibly a hypersensitivity reaction to an unknown antigen. Antibodies to intercellular material can often be demonstrated in affected cats. In the majority of cases of both dogs and cats, an increase in circulating eosinophils is present.

In cats, lip lesions are commonly visible near the philtrum and may extend through the adjacent haired skin. Oral lesions may occur anywhere in the mouth, including the gingiva, hard and soft palates, oral and nasal pharynx, tongue, and occasionally draining lymphoid tissues, excluding the tonsils, which do not have afferent lymphatic vessels (Fig. 7-10; also see Fig. 17-21, C). In dogs, eosinophilic granulomas typically are raised, fungating masses on the ventral and lateral lingual epithelium and palate. Collagenolysis (because collagen is acellular, it cannot undergo necrosis) is characteristically central in the lesion. The surrounding inflammatory tissue contains mixed inflammatory cells with increased numbers of eosinophils, mast cells, and multinucleated giant cells (see Web Fig. 3-14). Lesions grouped as the eosinophilic granuloma complex of cats include eosinophilic ulcer, linear (collagenolytic) granulomas, and eosinophilic plaques. The latter two lesions are strictly cutaneous and do not affect the oral cavity. No proven etiologic link has been established between these cutaneous conditions (linear granulomas and eosinophilic plaques) and oral eosinophilic granulomas. The cause of the canine lesions is unknown.

Lymphoplasmacytic Stomatitis

Lymphoplasmacytic stomatitis is an idiopathic condition of the cat named on the basis of the histologic appearance of the lesions (Fig. 7-11). Associations have been hypothesized between this condition and the presence of bacteria or calicivirus associated with feline leukemia virus (FeLV) and/or FIV infection. It is a chronic condition characterized by red, inflamed gums, a fetid breath, and inappetence. The oral mucosa may be hyperplastic and ulcerated. An inefficient immune response may be responsible for the persistence of oral bacteria and the accumulation of lymphocytes and plasma cells.

Chronic Ulcerative Paradental Stomatitis

Chronic ulcerative paradental stomatitis, a condition of dogs also known as ulcerative stomatitis and lymphocytic-plasmacytic stomatitis, is caused by apposition of “kissing ulcers” to dental plaque. The condition is painful with resultant inappetence and anorexia. Affected dogs drool and have halitosis. This condition occurs in older dogs of any breed, but Maltese dogs and cavalier King Charles spaniels are particularly susceptible. The lymphocytic-plasmacytic lesions noted on histologic examination are suggestive of an inflammatory rather than infectious etiology possibly caused by mediators released from the plaque. If untreated, bone resorption may occur.

Oral Mucosal Hyperplasia and Neoplasia

Structure and Function

Molar teeth in general are designed for grinding feedstuffs, whereas incisors in ruminants (mandibular only) are for cropping forage. Canine teeth are designed for tearing flesh. Brachydont teeth consist of a crown, which is the portion above the gingiva (the neck that is slightly constricted), and just below the gingiva are the roots, which are embedded in the bony socket (alveolus) of the jaw. Enamel covers the crown, cementum covers the roots, and both cover the dentin. Besides carnivores, the incisor (lower) teeth of ruminants and porcine teeth, except the canines of the boar, are brachydontic.

Hypsodont teeth have an elongated body, but the neck and roots may form later in life. Cementum covers the tooth, and enamel is beneath the cementum. Beneath the enamel is the dentin. The cementum and enamel invaginate into the dentin, forming the infundibula. Enamel crests result from normal wear, with enamel being the hardest of the layers. The cheek teeth of ruminants and tusks of boars and the teeth of horses are hypsodont.

In simple-toothed animals, such as carnivores, the tooth root is not covered by enamel. Receding gum lines therefore expose the dentin, resulting in pain and invasion by bacteria. Domestic animal species seldom get caries, although buildup of plaque can result in gingival infections and tooth loss.

Malocclusions

Abnormal development and positioning of the teeth may affect dental function. Malocclusion refers to a failure of the upper and lower incisors to oppose properly. This feature is “normal” for some dogs, particularly the brachycephalic breeds. In the extreme, malocclusions can lead to difficulty in the prehension and mastication of food. Malocclusions are named according to the position of the mandible. Protrusion of the lower jaw is termed prognathia, whereas a short lower jaw with resultant protrusion of the upper jaw is termed brachygnathia and sometimes hypognathia (Fig. 7-16). Sometimes these terms are incorrectly used, referring to brachygnathia as superior prognathia and prognathia as superior brachygnathia.

Malocclusions result from abnormal jaw conformation or rarely from abnormal tooth eruption patterns. In some animals, such as rodents and rabbits, the teeth continue to grow throughout the animal’s lifetime. If these animals are not provided with sufficient roughage in their diets, the teeth (both incisors and cheek teeth) overgrow and either “lock” the jaw or because of a lack of occlusal grinding surfaces, prevent the animal from receiving proper nutrition (Web Fig. 7-3).

Anomalies of Tooth Development

In simple-toothed animals and rarely in other animals, agenesis of a tooth or teeth occurs and is generally of no clinical significance (see Fig. 17-35). Supernumerary tooth development is less common than tooth agenesis and is similarly of little clinical significance. Some animals, such as elasmobranches (sharks), continue to produce row on row of teeth as the outermost rows are lost. Dental dysgenesis may be primarily due to dysplasia of the enamel-forming organ or secondary to trauma, infection and hyperthermia, toxicosis, or other metabolic irregularities during odontogenesis.

Dentigerous cysts result from dental dysgenesis, and epithelial-lined, cystic structures in tissue, including the bone of the jaw result. Dentigerous cysts develop from abnormal proliferation of the cell rests of Malassez. They appear as variably sized, sometimes fluctuant swellings of the mandible or maxilla. In the maxilla, they sometimes invade the nasal sinuses. Although rare, dentigerous cysts are often painful, and while not usually neoplastic, they can destroy the jaw. Dentigerous cysts are epithelial-lined and may become impacted with keratin. Rudimentary, malformed teeth may be found within these cysts, and painful fistulas may develop, especially in horses. These draining tracts are seen most often rostral and ventral to the ear (ear tooth). Dentigerous cysts occur less frequently in otherwise normal, mature animals.

Segmental enamel hypoplasia occurs before eruption of the permanent teeth of dogs as a result of hyperthermia and viral infection, most often by canine distemper virus infection. Enamel is fully formed when the teeth erupt; therefore virus infection of ameloblasts must occur during enamel formation, which is before the dog is 6 months of age, if enamel hypoplasia is to occur. Canine distemper virus infection causes necrosis and disorganization of the enamel organ. After the virus is cleared, structure and function of the enamel organ return to normal. Thus segmental enamel hypoplasia results from the lack of enamel formation during the period of virus infection (Fig. 7-17). A similar condition in calves is caused by in utero BVD virus infection.

Chemicals, most notably tetracycline antibiotics ingested during the process of mineralization, can cause yellowish, permanent discoloration (see Fig. 1-58). Congenital porphyria, a defect in red blood cell production, may result in incorporation of porphyrins into dentin, resulting in pink discoloration of the teeth (pink tooth) (Web Fig. 7-4). Both tetracycline and porphyrins fluoresce under ultraviolet light, dramatically demonstrating these lesions.

Fluoride incorporation into the enamel and dentin occurs in fluoride toxicosis, particularly in cattle and sheep. A relationship exists in beef cattle between fluorosis and selenium supplementation, with selenium supplementation being protective in high fluoride areas such as those downwind from aluminum smelters or with high levels of fluoride in ground water. Excessive dietary concentrations of fluorine during odontogenesis (from 6 to 36 months of age) may result in incorporation of the fluoride in the enamel and dentin of the permanent teeth. The result is soft, chalky, discolored enamel, usually yellow, dark brown, or black (Web Fig. 7-5). Occlusal grinding of affected soft teeth against more normal enamel results in rapid dental wear to the extent that severely affected sheep may have almost completely worn down their incisors. One wonders therefore about the cumulative effect of fluoride supplementation in municipal drinking water, vitamins with added fluoride, fluoride-supplemented toothpaste, fluoride treatment of teeth, reconstituted and bottled soft drinks made with fluoridated water, and so forth. It is difficult to calculate the total fluoride load ingested by individuals or what the effects may be of that fluoride supplementation.

Lesions Caused by Attrition and Abnormal Wear

Loss of normal dental structure and function often results from rapid and irregular and/or abnormal wear of occlusal surfaces in many species of domestic animals. In those species with hypsodont teeth, attention to the dentition as the animal ages is often a major factor in overall body conditioning and health (Fig. 7-18). Aggressive treatment of occlusal surface irregularity by filing of high points in the dental arcade (floating) can notably prolong an animal’s life. Rock chewing or other compulsive oral behaviors in dogs may result in accelerated dental wear. Similarly, cribbing in horses and herbivorous animals grazing on sandy soils can cause premature dental wear. In all species, exposure of dentin or the pulp canal may lead to dental infection with serious consequences.

Miscellaneous Dental Lesions

Infundibular Impaction

Impaction of the infundibulum, also known as infundibular necrosis or infundibular caries, may cause serious dental disease in ruminants and more rarely in horses. Incomplete infundibular cementum formation before the tooth erupts likely predisposes to infundibular impaction. The pathogenic mechanism is comparable to dental caries in simple-toothed animals, which is uncommon in domestic animals. Feed material is ground into the infundibulum, where bacteria metabolize it to form acid, which causes demineralization. Bacterial enzymes digest the organic matrix of enamel and dentin. As a result of this destruction, the pulp cavity becomes exposed and infected, resulting in pulpitis and endodontitis. Dental abscesses and fistulous tracks may develop and rupture into the paranasal sinuses. The inflamed infundibular cavities often continue to become impacted with feed, creating a vicious cycle.

Periodontal Disease

More than 200 species of bacteria and fungi have been associated with dental plaque (a film of an organic matrix, food particles, and bacteria on the tooth surface). This plaque often becomes mineralized (tartar or dental calculus). The mineralized material contributes to atrophy and inflammation of the gingival mucosa and supporting stroma by acting as a nidus for additional plaque accumulation. Bacteria resident in films on the tooth surface produce acids and enzymes that may damage their enamel substrate (cavities) and also destroy the subjacent gingival tissue and periodontal ligament (periodontal disease).

The initial site for destructive inflammation is in the gingival crevice–forming pockets where bacteria lodge. With time, this inflammation spreads distally along the tooth, resulting in gingival-epithelial attachment only on the root of the tooth, deep in the alveolar socket. Progression of inflammation may destroy the connective tissue of the periodontal ligament, resulting in loosening of the tooth. The infection can spread causing alveolar osteomyelitis and pulpitis and can result in apical abscesses and bacteremia. There is significant oral pain, reluctance to masticate, and halitosis. Periodontal disease is common in carnivores and humans. Mildly abrasive diets and brushing of the teeth of pet carnivores, combined with regular dental examination, is preventive as it is in humans.

Dental Neoplasia

Proliferative, cystic, or neoplastic diseases of the dental arcade can originate from cell rests that form from the dental lamina or the enamel organ (the cell rests of Malassez). Dental neoplasms usually arise close to the teeth, either deeply in the jaw or from the oral epithelium. There is a relatively precise method of naming dental neoplasms based on the tissue or cell of origin and the extent of differentiation and odontogenesis present within the neoplastic tissue. The histologic appearance of these neoplasms is complex; pathologists with considerable experience in differentiating these uncommon neoplasms should be consulted when a precise diagnosis is indicated.

Odontomas are hamartomas originating in the enamel organ and are usually seen in puppies and foals (Fig. 7-19). They usually contain well-recognizable dentin and enamel, as well as ameloblasts, odontoblasts, and dental pulp.

Ameloblastoma is a term applied to epithelial neoplasms of enamel organ origin. Several subtypes, distinguished histologically, are ameloblastic fibroma, ameloblastic odontoma, calcifying epithelial odontogenic tumor, peripheral odontogenic fibroma, and other rare tooth neoplasms. Ameloblastoma appears randomly in the dental arcade, usually in adult dogs. They are often osteolytic and thus are locally invasive. Histologic examination by an expert is often necessary to distinguish ameloblastoma from acanthomatous epulis (acanthomatous ameloblastoma) and squamous cell carcinoma.

Structure and Function

The palatine tonsils are pharyngeal lymphoid structures covered by stratified squamous epithelium. Their function is uncertain, although it is likely they serve in lymphocyte production and antibody formation (see Chapter 13). In carnivores, they are found in crypts or recesses at the dorsolateral aspect of the caudal oropharynx. In pigs, they are flat and recognized by tiny pores in the surface epithelium of the caudal soft palate. Equids, ruminants, and pigs have lingual tonsils in addition to palatine tonsils.

Portals of Entry

Tonsils do not possess afferent lymphatic vessels and do not serve as lymph filters. Therefore only primary (or direct) or hematogenous infections occur (tonsillitis) (Fig. 7-20), as well as primary neoplasms of either the lymphoid (lymphoma) (Fig. 7-21) or epithelial (squamous cell carcinoma) (Fig. 7-22) components. In many viremias of mammals, such as pseudorabies of pigs, virus may be isolated from the tonsils.

Structure and Function

Most salivary glands are discrete aggregates of compound tubuloalveolar tissue. Saliva is a mixture of serous and mucoid secretions. Saliva lubricates the mouth and esophagus and moistens ingesta. Saliva also dissolves water-soluble components of food so the taste buds can function. The mucus in saliva binds to masticated food and creates a bolus that is more easily swallowed. Salivary mucus also coats the epithelium of the mouth, preventing mechanical damage to the tissue. Saliva, through its flushing action, reduces bacterial populations. Saliva contains a lysozyme that lyses bacteria. Carbohydrate digestion begins in the oral cavity as a result of the presence of α-amylase, which changes starch into maltose. There are very small quantities of this enzyme in carnivores and cattle. Saliva also is an effective buffer, especially in ruminants, whose forestomachs have no glands. In carnivores, evaporation of saliva is a major mechanism of thermoregulation.

Portal of Entry

Salivary glands are generally affected by blood-borne pathogens, direct penetration by foreign objects, obstruction of the excretory ducts, or bite wounds. In humans, ascending infections from the salivary ducts occur, but there is no evidence that this occurs in domestic animals. The serous portions of the salivary glands are radiosensitive.

Response to Injury

Injury to the salivary gland is accompanied by incomplete regeneration, principally from ductular epithelium. There are often atrophy, fibrosis, and squamous metaplasia of secretory epithelium, sometimes resulting in blockage of ducts.

Inflammatory Diseases

Sialoadenitis, inflammation of a salivary gland, is relatively rare in veterinary medicine. Although diagnosis of systemic diseases is not made by examining the salivary gland, rabies and canine distemper are two very important diseases that cause inflammation of the salivary glands. Saliva is a particularly important medium of spread, by bite wounds, of the rhabdovirus that causes rabies. There are focal necrosis, mononuclear cell inflammation, and sometimes inclusions (Negri bodies) in the nuclei of ganglion cells. In the rat, a coronavirus termed sialodacryoadenitis virus is responsible for inflammation of the salivary gland and some adnexal ocular glands. Salmonella typhisuis has caused suppurative parotid sialoadenitis in pigs.

Gross lesions of sialoadenitis are subtle and include swelling and edema. Sialoadenitis can be accompanied by pain on palpation. Abscesses occasionally occur sometimes secondary to the migration of foreign bodies (grass awns) and are especially noticeable when they occur in the retrobulbar zygomatic gland where they may cause ocular protrusion (proptosis).

Miscellaneous Diseases or Conditions

Changes in the salivary glands are uncommon in domestic animal species. A ranula is a cystic saliva-filled distention of the duct of the sublingual or submaxillary salivary gland that occurs on the floor of the mouth alongside the tongue (Fig. 7-23). It is thus epithelial lined. The cause is generally unknown, although some cases are due to sialoliths. A salivary mucocele, in contrast, is a pseudocyst not lined by epithelium but filled with saliva. The cause of this lesion is also unknown, but it may occur secondary to traumatic rupture of the duct of a sublingual salivary gland with resultant leakage and encapsulation of saliva by reactive connective tissue.

Sialoliths are rare in domestic animal species. When they do occur, they are considered to be caused by inflammation of the salivary gland with sloughed cells or inflammatory exudate forming a nidus for mineral accretion (Fig. 7-24). Thus they are one cause of ranula formation.