8 Heidi B. Lobprise Main Street Veterinary Dental Clinic, Flower Mound, TX, USA Oral pathology is considered present when a departure from normal occurs that is sufficient to cause signs or symptoms. Symptoms are the abnormalities detected by the patient or owner, while signs are those noted by the clinician. A syndrome is a defined group of signs or symptoms, but not always resulting from the same specifically defined cause. Etiology is the theory of the cause of the disease, though when there is no acceptable theory as to the etiology available, it is called idiopathic. This chapter will cover those conditions of the oral cavity other than certain dental lesions, congenital and developmental issues, traumatic lesions, and tumors/cysts, which are covered in other chapters. Each specific region/category will be addressed, with those conditions, lesions, and diseases that affect them. While some lesions in the oral cavity will affect multiple surfaces and tissues, some affect distinct or focal regions. Though the diagnosis of inflammation should be determined histopathologically, physical exam findings (swelling, redness, ulceration) can often lead to a reasonable description, based on the tissue involved (seeTable 8.1). The American Veterinary Dental College (AVDC) is an excellent resource for terminology and nomenclature (https://www.avdc.org/Nomenclature). Diseases and conditions that affect the oral cavity in general will first be discussed and then distinct regions/tissues will be covered. Table 8.1 Terms – oral and oropharyngeal inflammation. Though an inflammatory response is expected in the typical pathogenesis of periodontal disease, there are many factors that can contribute to excessive levels of inflammation. Infectious agents, such as bacteria, viruses, protozoans, and fungi can elicit tremendous response from healthy individuals, and in hyperresponsive or immunosuppressed animals, even normally innocuous agents may elicit substantial soft tissue changes. Necrotizing ulcerative gingivitis (NUG) in people occurs when spirochetes and Prevotella intermedia, normally opportunistic oral flora, synergistically act in the presence of physical or emotional stress as well as a decreased resistance to infection, nutritional defects, or debilitating disease [1]. The classic initial lesion is ulceration of the interdental papillae or marginal gingiva with spirochetes that may be found in the exudates and epithelium, but seldom penetrating into the connective tissue [2]. As the process continues, the surface epithelium is replaced by fibrin, necrotic epithelial cells, and neutrophils, termed a pseudomembrane [1]. In immunocompromised patients, NUG can progress to a more aggressive course and lead to necrotizing ulcerative periodontitis (NUP), with destruction of underlying periodontium, including bone [1]. Vincent’s angina affects the throat, larynx, and even the middle ear with a fusospirochetal infection. Treatment with metronidazole can be optimal to help avoid yeast overgrowth (candidiasis). Systemic bacterial infections, which are considered to be more of an exogenous type of infection as related to the oral cavity, may also exhibit lesions. Oral lesions from Leptospira spp. infections are likely to be secondary to more generalized conditions such as vasculitis, which can result in injected mucous membranes, petechiae, and ecchymosis. Severe renal involvement due to leptospirosis may result in oral ulceration secondary to uremia [3]. In cats, infection with Mycobacterium lepraemurium, or feline leprosy, can cause one or more raised, plaque‐like lesions on the lips and/or the tongue, but are generally not painful. Granulomatous lesions on the mucous membrane of the tongue [4] and oral cavity [5] may be an uncommon presentation of canine visceral leishmaniasis that often must be biopsied to be differentiated from other oral lesions [6]. In atopic dogs, Malassezia pachydermatis has been isolated in 33% of the oral cavities of patients studied, though no oral lesions were mentioned. Its presence is likely to be due more to cross‐contamination of a secondary overgrowth with an alteration of the cutaneous microhabitat [7]. In 34 dogs with symptoms of gingivostomatitis, 11.8% had Candida albicans, an opportunistic yeast, cultured from their mouths [8]. While considered a normal part of the microbiota, if cultured repeatedly, as a result of overgrowth in immunocompromised patients or those treated extensively with antibiotics, this should be treated with the appropriate medication, systemically or topically. Mycotic stomatitis may be initiated in the presence of immunodeficiency (thrush mouth in HIV patients), systemic disease, or antibiotic administration [9]. Primarily seen on the tongue and at the mucocutaneous margins, the ulcers can also be seen throughout the oropharynx, coated with a white plaque. Occasionally, extension of a nasal aspergillosis infection through the nasopalatine ducts may lead to hyperemia or ulceration at the incisive papilla [10]. The tongue or even mucosa and underlying bone can rarely be the site of lesions related to a systemic histoplasmosis [11] or blastomycosis infection. Feline Calicivirus (FCV) replicates primarily in the oropharynx, and it is likely that it has a role in chronic gingivostomatitis and caudal mucositis [12]. Lingual ulceration, in combination with nasal discharge and rhinitis is a common oral sign. Feline herpes virus (FHV) typically affects the respiratory system and eyes, with less frequent oral lesions [13]. Calicivirus in the dog presents primarily as an enteric disease, though glossitis has been described [14]. Other viruses in the cat that are more systemic and affect the immune system, such as feline leukemia virus (FeLV) and feline immunodeficiency virus (FIV) may predispose the individual to secondary oral infections (see Chapter 20 – Domestic Feline Oral and Dental Diseases). Distinct, wart‐like growths on the buccal mucosa, lips, and tongue are generally a self‐limiting lesion in dogs caused by exposure to the papillomavirus. There are many means by which an abnormality in the body’s immune system can have an effect on the oral cavity. While certain viruses, stress, and corticosteroids may lead to a decreased immune response that predisposes an individual to opportunistic infections, in other individuals the immune response may be an exaggerated one to relatively normal stimuli. An increase in IgG and immune complex deposition in a syndrome of ulcerative stomatitis in Maltese dogs, particularly males, may explain an excessive host response (increased gingival index) in the presence of minimal stimuli (low plaque and calculus indices). Other breeds may show similar syndromes, such as Cavalier King Charles Spaniels (CKCS) [15]. There may be marked ulceration of buccal mucosa that contact a tooth/calculus surface, known as contact mucositis or contact mucosal ulceration (“kissing lesions”). These animals appear to develop a plaque intolerance with the consequence of an excessive immune response to any accumulation. The condition is typically in localized areas of the canine and carnassial teeth initially, but may progress to a more general condition throughout the mouth. If effective plaque control cannot be maintained, and as anti‐inflammatory medications provide only a transitory relief, often extractions are necessary. Additionally, selective extractions customarily only provide temporary relief as the condition tends to recur at new sites, adjacent to other teeth. While distinct autoimmune syndromes such as pemphigus foliaceous have dermal lesions primarily (with rare oral lesions), up to 90% of patients with pemphigus vulgaris (PV) will have oral lesions, frequently at the mucocutaneous junctions, with some mucous membrane ulceration [16]. With early detection in the oral cavity, some patients with PV can be treated before the disease becomes generalized [17]. Pemphigus vegitans (PVeg) has been described as a proliferative variation of PV in humans, with one similar case in a dog [18], though other cases do not exhibit oral involvement. A newer identification of mucous membrane pemphigoid (MMP) as part of a group of AISBD (autoimmune subepidermal blistering disease) includes cases that were likely to be previously classified as bullous pemphigoid (BP) [19]. Immunohistochemistry may be needed to distinguish BP and MMP from the more severe, ulcerative epidermolysis bullosa acquista, described most frequently in Great Danes, characterized with epithelial sloughing and a poor prognosis [19, 20]. With any vesiculobulbous disorder, it is best to biopsy a fresh “blister,” which often occurs first on oral mucous membranes. Even less common in the dog, oral sequelae of systemic lupus erythematosus (SLE) may appear as ulceration of mucocutaneous junctions and oral mucosa [21]. Discoid lupus erythematosus (DLE), considered a benign variant of SLE, primarily affects the nasal planum, face, and ears, but the lips can be involved with depigmentation [21]. Another blistering and ulcerative syndrome, erythema multiforme (EM), is uncommon and self‐limiting if mild, with likely immune‐mediated factors involved [22]. Oral lesions have been seen in up to 31.8% of the cases, but oral‐only presentations have not been described [23]. Apoptosis of keratinocytes have been attributed to EM lesions associated with everything from canine parvovirus infection [24], a moderate form of drug‐induced reactions [25], and even a paraneoplastic disorder associated with thymoma in a dog [26]. Immunohistochemistry and clonality testing may be necessary to distinguish EM from epitheliotropic T‐cell lymphoma (ETCL) [22]. The immune system also plays a part in acute hypersensitivity reactions to drugs (adverse drug reaction – ADR) such as trimethoprim sulfonamides and others [27]. What can be a simple dermal lesion (fixed drug eruption) may also present as ulceration with dermal and oral lesions (drug‐induced EM) or even a severe, life‐threatening syndrome with full thickness epidermal peeling and necrosis (toxic epidermal necrolysis – TEN) [25, 28]. With the tremendous vascularity, high cell turnover, and potential for external exposure, examination of the soft tissue of the oral cavity will often reveal things about the entire patient. A change in mucosal color may indicate anemia (pale), shock (white), cyanosis (blue), bleeding disorders (petechiation), or uremic ulcers. There are many systemic conditions that will manifest themselves in the oral cavity. With uremic ulceration, as ammonia levels in the saliva rise, it can cause irritation and dehydration [29]. Clotting abnormalities can occur and the hemorrhagic ulceration of the dorsum of the tongue can lead to necrosis and sloughing. Vasculitis and xerostomia seen with diabetes mellitus can enhance the progression of periodontitis if untreated. The decreased calcium in hypoparathyroidism can contribute to ectodermal disorders, including enamel calcification, delayed eruption, and disruption in root development if severe [30]. In people, hypothyroidism can hinder the development and eruption of teeth, as well as causing macroglossia and thick lips (cretinism) [31]. Although not caused by any known systemic problem, the idiopathic deposition of amorphous calcified tissue, or calcinosis circumscripta may be identified by the white, chalky, gritty nodules in the tongue and buccal mucosa. These are typically found in young, large breed dogs and can progress to shallow ulceration. Hematological disorders also may have oral symptoms, such as anemia due to blood loss, shock or an iron deficiency causing pale mucous membranes that are slow to heal. If the pallor is accompanied by gingival bleeding, petechiae, purpura, or ulcers with a surrounding erythema, thrombocyte irregularities should be considered. Neutropenia, in addition to other systemic signs, may include large, deep, irregular mucosal irritation that can be painful and become necrotic. There are many things that can contribute to a neutropenia, including viral diseases, chemotherapy or radiation treatment, estrogens, chloramphenicol, or phenylbutazone toxicity. Dogs with cyclic neutropenia, or Gray Collie Syndrome, a simple recessive autosomal problem, present with lethargy, fever, joint swelling and many systemic issues, as well as gingivitis, ulceration, and malocclusions of permanent teeth [32]. Leukemia and other myeloproliferative disease can cause non‐specific signs. Petechial or ecchymotic hemorrhage, gingival bleeding, or ulceration can be some of the initial manifestations of the disease [33]. In myelocytic leukemia, gingival enlargement, bleeding, and ulcerations are the most common oral symptoms [33]. Systemic treatments may give rise to oral lesions, as stated previously. Chemotherapy may result in ulcers that are large, irregular and foul smelling, at times with concurrent anemia, as evident with the pale mucous membranes. The most common sequela to radiation therapy, mucositis, can be minimized with advanced therapy systems [34]. With radiation treatment, there may also be a reduction in salivary flow, an increase in its viscosity, or xerostomia, which can contribute to periodontal disease and caries formation [35]. Severe damage by radiation may lead to a later osteoradionecrosis (ORN), particularly with post‐treatment trauma or infection [34]. Chrysotherapy may result in a secondary stomatitis with a peripheral eosinophilia, especially during the initial treatment [36]. Ingestion of warfarin and indandione may lead to various degrees of clotting abnormalities, while doses of thallium can cause erythema and inflammation of the oral epithelium and lips, as well as other tissues. Horseshoe or linear ulcers on the tongue and/or palate can be seen after ingestion of caustic chemicals. Nutritional deficiencies or excesses should be fairly uncommon, given the opportunities for well formulated pet diets. However, clients may try less traditional options without realizing that their pet’s nutritional needs may not be well served. Since the oral cavity has a high rate of cell turnover, initial signs may occur there [37]. A protein‐calorie malnutrition, as can be seen in a protein‐losing enteropathy or a nephropathy, contributes to a decrease in cell‐mediated immunity and can result in a linear ulceration on the dorsum of the tongue [38]. Chronic niacin deficiency has been associated with pellagra in humans and “black tongue” in dogs [39]. Biotin deficiency, while rare, can lead to skin lesion, anorexia, and glossitis [39], and riboflavin deficiency may cause an angular stomatitis (CDC, riboflavin: http://www.cdc.gov/mmwr/preview/mmwrhtml/mm5714a3.htm). Deficiencies of vitamin C lead to scurvy lesions in animals unable to store the nutrient, mainly humans and guinea pigs. Vitamin C is an important component in maintaining the health of the gingiva and mucous membranes. Low calcium intake can directly affect the periodontium and all calcified tissues during formative stages. More importantly, if a decreased calcium intake leads to a secondary hyperparathyroidism (or due to renal causes), there will be resorption of calcium from alveolar bone, leaving it soft and contributing to tooth mobility and “rubber jaw” [40]. One nutrient in particular that should be avoided in excessive amounts is vitamin A, found in large amounts in organ meats such as liver. Most signs of excess vitamin A are related to a deforming cervical spondylosis, but it can depress bone growth at very high levels [41]. Moderate increases have not been shown to impact bone growth in the dog [42]. Many conditions previously described in the general oral pathology portion of this chapter apply to the palate and palatal mucosa (infectious, immune‐mediated, metabolic, nutrition, etc.) A significant consideration for the palate (hard and soft) involves cleft defects in the developing dog or cat (see Chapter 4 – Developmental Pathology and Pedodontology) Another topic with prevalent palatal involvement is that of oral trauma (see Chapter 6 – Traumatic Dentoalveolar Injuries – and Chapter 13 – Oral Surgery – Fracture and Trauma Repair). Particular attention is paid to the palate in specific diseases or cases, such as that of infiltrative aspergillosis [10] or acute corrosion of the palatal mucosa due to the ingestion of Multicolored Asian Lady Beetles (Harmonia axyridis) that embed in the soft tissue, causing a chemical‐like burn [43]. In cats, hemorrhage from the oral cavity should always instigate a thorough evaluation of the palatal mucosa, particularly in the region of the palatal arteries. It is thought that cats with atopy or other dermatological conditions can damage the mucosa covering this vasculature and while the source may be sometimes difficult to identify, the amount of hemorrhage can be significant. As a primary divider of the oral and nasal cavities, the palate’s integrity is important to maintain their separation. Any cause, from trauma to extension of periodontal disease, can contribute to oronasal or oroantral fistulation that requires repair, to keep the cavities from communicating. The pharynx is described as the region where the digestive and respiratory systems share a common, intersecting pathway, and is divided into the nasopharyngeal, oropharyngeal, and laryngopharyngeal regions [44]. The oropharynx is that section located between the tonsils and the base of the tongue, and while the oral mucosal epithelium lining the region extends beyond the tonsils into the laryngopharynx and further, the oral cavity is considered to extend only to the level of the tonsils. The close association of this region, and even the hard and soft palates that separate the oral and nasal cavities, with the respiratory tract and associated structures, results in syndromes that may affect each other. In a study of 67 dogs with pharyngeal disorders, 7 of those involved the oropharynx (10.5%) with 20 having soft palate disorders that affected the laryngopharynx. Of the oropharyngeal lesions, there were four soft palate granulomas with fistulation, one tonsillar abscess, one soft/hard palate neoplasia, and one mucocele [44]. In a study of 53 cats with nasopharyngeal disorders, classification included 49% with lymphosarcoma and 28% with polyps [45]. Swallowing disorders may include diseases impacting the oropharyngeal phase of swallowing, related to the voluntary prehension and mastication of food and passage of the formed bolus into the pharynx, followed by the involuntary phase of swallowing [46]. The patient can at times adjust to oral dysphagia, while intervention may be needed with pharyngeal and cricopharyngeal dysphagia [46]. With brachycephalic airway obstruction syndrome (BAOS), up to 94% of affected dogs have an elongated soft palate, along with stenotic nares, everted laryngeal saccules, and even everted tonsils (56%) [47]. Another study showed an increase in the thickness of the soft palate (not an increase in length), but this was in anesthetized, intubated dogs, and in humans, inspiratory efforts increase the length of the soft palate [48]. Dysplasia of the soft palate has also been associated with nasopharyngeal stenosis [49, 50]. Though less common in cats, an enlongated soft palate in a brachycephalic individual that was overlying the epiglottis and causing airway obstruction resulted in pulmonary edema [51]. Several Dachshunds have been diagnosed with a congenital nasopharyngeal stenosis with thickened palatopharyngeal muscles, dyspnea (expiratory cheek puff), dysphagia, and even macroglossia [52]. The brachycephalic conformation of CKCS with increased soft palate thickness, decreased nasopharyngeal aperture, and possible auditory tube dysfunction may be associated with the high incidence of otitis media with effusion (OME) in the breed [41]. Whether determined radiographically or by clinical signs, there are numerous reports of the association of palatal defects, both cleft palates [53, 54] and soft palate hypoplasia [55, 56], with middle ear disease. The palatal dysfunction is probably just one of multiple predisposing factors to the otitis, as the palate abnormalities are likely to be congenital with the otitis occurring more often later in life [56]. Ventral displacement of the caudal soft palate may result from the presence of a retropharyngeal abscess, tumor, large retained developmental cyst [57], or even a nasopharyngeal polyp. The latter, seen usually in young cats that demonstrate dysphagia and nasal discharge, are protruding, pedunculated growths from the mucous membranes of the auditory canal caused by a response to chronic inflammation. While not a distinct oral process, it is part of a differential diagnoses list, a factor to be ruled out. Often the soft palate must be gently retracted to visualize a polyp, and its treatment sometimes requires a ventral tympanic bullae osteotomy in addition to the polyp removal [58, 59]. Infectious components such as blastomycosis [60] can be found in the pharyngeal region, as well as other agents described in the general oral cavity portion of this chapter. The pharynx can often be involved with foreign body ingestion or injury, and the severity of the lesion may depend on the extent of damage to the respiratory tract, which may include cervical emphysema [61, 62]. Distinct objects such as teeth with intrusion back into the pharynx due to periodontal disease [63] or trichobezoars [64] may be successfully removed when identified. Detection of non‐radiopaque objects may be challenging with standard radiography, but may be more likely to be successful with magnetic resonance imaging (MRI) [65]. Located at the back of the pharynx on either side, the tonsils will often not be visible in their crypts, though the presence of everted tonsils is a frequent observation in brachycephalic airway obstruction syndrome (BAOS) [47]. As a component of the lymphatic system (MALT – mucosa associated lymphoid tissue), enlargement may be due to any type of immune response, such as inflammatory or infective processes (Figure 8.1). Any lesion that does not respond well to conservative therapy such as antibiotics should be biopsied, as both primary and secondary neoplastic cells may be present. A biopsy can help distinguish neoplasia from lesions of cystic formation, lymphangiomatous polyp [66], or an enlargement of the tonsils as part of a non‐specific respiratory syndrome seen in racing Greyhounds [67] (see Chapter 7 – Oral and Maxillofacial Tumors, Cysts, and Tumor‐Like Lesions – for further discussion). Figure 8.1 Inflamed tonsil visible beyond the crypt edges. Source: Copyright® AVDC®, used with permission. Like the palate, many problems of the tongue are extensions of generalized oral problems such as ulcerative stomatitis. Due to the high cell turnover rate of the lingual mucosa, the tongue may exhibit changes more quickly than elsewhere in the oral cavity, especially with nutritional causes. In a study looking at histopathology samples of tongue biopsies (0.8% of all biopsies submitted), 54% were neoplastic (64% malignant but only 2–4% of all oral neoplasia), 33.2% were due to glossitis (pyogranolomatous, foreign body 10%, etc.), and 12.2% other, including 3% calcinosis circumscripta and 3% eosinophilic granuloma complex [68]. Infectious agents that have a particular predilection for the tongue include calicivirus, herpes virus, and rhinotracheitis virus in the cat with ulceration, and a vesicular glossitis associated with calicivirus in the dog [69]. Leptospira canicola leads to severe congestion with a glossitis related to uremia that can eventually necrose the tongue tip. Opportunistic infections of acute necrotizing ulcerative gingivitis (ANUG) may exhibit necrotic bleeding ulcers, while candidiasis stimulates a diffuse inflammation with a whitish plaque coating of the surface. Leishmaniasis, while usually manifested by fever, lymphadenopathy, weight loss, lameness, and skin lesions, can also cause the formation of nodular lesions on the tongue. Caused by a flagellate protozoa transmitted by sand flies, diagnosis of one case was confirmed by identifying the presence of amastigotes in a biopsy of the lingual lesion [4]. In canine oral papillomatosis, single to multiple or coalescing white to tan hyperkeratotic, pedunculated nodules are virally induced and often spontaneously regress [70]. If extensive, surgical removal can be utilized to debulk the masses, while interferon with or without azithromycin have also been suggested as treatment options [71]. Other tumors and masses are covered in Chapter 7 – Oral and Maxillofacial Tumors, Cysts, and Tumor‐Like Lesions. Metabolic uremia as described earlier demonstrates distinct lingual signs, including hemorrhagic, brownish ulcers of the dorsal tongue with potential necrosis and sloughing. Hypothyroidism in earlier stages of development may result in a macroglossia, while hypoparathyroidism can contribute to ulceration and necrosis of the tongue tip. In an adult Dalmatian, acromegaly and insulin resistance due to growth hormone hypersecretion (somatroph adenoma of the pituitary gland) had signs of enlargement of the tongue and thickening of the skin noticed by the owner [72]. A case of atypical mucosal xanthoma associated with hyperlipidemia has been reported, characterized by granular plaques and nodules with a foamy cell, where the lipid content is similar to oral verruciform xanthomas in humans [73]. Calcinosis circumscripta refers to the idiopathic deposition of calcified (hydroxyapatite or amorphous calcium phosphate), chalky nodules on the surface of the tongue or in the sublingual area. The etiology is unknown and is not due to the degeneration of an apocrine gland, as once thought [74]. Young (74% < 2 year, 88% < 4 year), large breed dogs (28.6% German Shepherd dog (GSD), 13% Rottweiler, 9% Labrador) are most commonly affected, and dermal lesions may also be present [75]. Three types have been identified with the dystrophic or idiopathic being most common in animals and the metastatic form being more common in humans [75]. The use of von Kossa or Alizarin red stains on cytological smears from fine needle aspiration can confirm the calcified nature of the lesion without biopsy [76]. If clinical signs are present, the lesions may be resected, but they are benign and not locally progressive. One report of an atypical case described lesions found in a 10 month old Shih Tzu, where whitish masses with amorphous calcium salts were accompanied by a slight nutritional myopathy, possibly due to vitamin E and/or selenium deficiency [77]. Most of the immune‐mediated diseases described for the general oral cavity can have lingual lesions. An uncommon finding, reactive histiocytosis of the sublingual region, was described in an eight year old Miniature Pinscher that responded to tetracycline and niacinamide administration over a period of eight months [78]. Traumatic lesions to the tongue may be related to the primary damage or secondary insult due to infection, such as a glossitis secondary to bite wounds contaminated with Pasteurella multocida [79]. The sublingual area can be swollen or distended due to a number of reasons. Unilaterally, a soft, fluctuant swelling may be indicative of a leakage of saliva into the area, also known as a ranula [70]. Sublingual edema may be secondary to venous obstruction in the pharyngeal region due to abscessation or surgery. Proliferative or hyperplastic tissue in the sublingual region or buccal mucosa can be seen due to chronic, recurrent self‐trauma of the tissues. These “gum‐chewers” lesions should be biopsied for a definitive diagnosis, and excess tissue can be surgically removed if trauma is severe or tissue is severely hyperplastic. Other lingual lesions may include a condition called “hairy tongue,” where filiform papillae are elongated to resemble hairs and are often stained darkly. This is typically an incidental finding during oral examination. Rarely will a glossitis be present and debridement of impacted material is seldom necessary. Tongue atrophy as a part of an atypical polymyositis has been described in Pembroke Welsh Corgis in Japan, with marked myofiber loss and mixed mononuclear infiltrate on histopathology [80, 81]. Dysphagia and hypersalivation were the presenting signs of one case that progressed to aspiration pneumonia and eventual death. A congenital atresion of a salivary duct or absence of one gland is unlikely to make a difference due to the presence of the other glands. Ptyalism, (excessive drooling) has been seen in cases with congenitally enlarged parotid ducts, but these are rare primary salivary gland abnormalities and can be managed well by ligating the duct. Sialadenitis, of probable immune‐ mediated causes, was described in a young Golden Retriever presented for epiphora and facial swelling extending from the inflamed submucosal glands. The condition responded to anti‐inflammatory treatment [82]. The overall incidence of salivary gland disease in dogs and cats has been reported as very low (0.3%) [83]. Malignancies accounted for only 30% of this overall low rate and epithelial malignancies accounted for approximately 85% of salivary gland tumors, but lymphoma, fibrosarcoma, and mast cell tumors have involved the salivary glands through invasion or direct extension from surrounding tissues [84] (see Chapter 7 – Oral and Maxillofacial Tumors, Cysts, and Tumor‐Like Lesions). Sialadenitis composed 26% of the overall incidence rate of salivary disease, both as primary and secondary disease (Figure 8.2a–c). It presents as inflammation and enlargement of the salivary gland, often with formation of a sialocele. Possible causes include injury, infection (local, systemic, or secondary to regional), or immune‐mediated disease. One study of 11 dogs with zygomatic sialadenitis compared clinical signs and diagnostic imaging with 20 control dogs [85]. Most were medium to large breed dogs with unilateral disease, and signs of retrobulbar disease and sialoceles were present in seven cases. Visualization of the lesion and adjacent structures was excellent with MRI and computed tomography (CT), while ultrasonography was useful for sample collection [85]. Another reported case described necrotizing sialadenitis of the mandibular salivary glands, likely due to immune‐mediated cause (responded to corticosteroids), with zygomatic gland enlargement and sialoceles [86]. Hypersalivation in the absence of gastrointestinal signs, exophthalmus, and pain on opening the mouth were some presenting symptoms, with possible epileptic activity.
General Oral Pathology
8.1 Introduction
8.2 Oral Cavity – General
Gingivitis
Inflammation of gingiva
Gingival enlargement
A clinical term, referring to overgrowth or thickening of gingiva in the absence of a histological diagnosis
Gingival hyperplasia
A histological term, referring to an abnormal increase in the number of normal cells in a normal arrangement and resulting clinically in gingival enlargement
Periodontitis
Inflammation of non‐gingival periodontal tissues (i.e., the periodontal ligament and alveolar bone)
Alveolar mucositis
Inflammation of alveolar mucosa (i.e., mucosa overlying the alveolar process and extending from the mucogingival junction without obvious demarcation to the vestibular sulcus and to the floor of the mouth)
Sublingual mucositis
Inflammation of mucosa on the floor of the mouth
Labial/buccal mucositis
Inflammation of lip/cheek mucosa
Caudal mucositis
Inflammation of mucosa of the caudal oral cavity, bordered medially by the palatoglossal folds and fauces, dorsally by the hard and soft palate, and rostrally by alveolar and buccal mucosa
Contact mucositis and contact mucosal ulceration
Lesions in susceptible individuals that are secondary to mucosal contact with a tooth surface bearing the responsible irritant, allergen, or antigen. They have also been called “contact ulcers” and “kissing ulcers”
Palatitis
Inflammation of mucosa covering the hard and/or soft palate
Glossitis
Inflammation of mucosa of the dorsal and/or ventral tongue surface
Cheilitis
Inflammation of the lip (including the mucocutaneous junction area and skin of the lip)
Osteomyelitis
Inflammation of the bone and bone marrow
Stomatitis
Inflammation of the mucous lining of any of the structures in the mouth; in clinical use the term should be reserved to describe widespread oral inflammation (beyond gingivitis and periodontitis) that may also extend into submucosal tissues (e.g., marked caudal mucositis extending into submucosal tissues may be termed caudal stomatitis)
Tonsillitis
Inflammation of the palatine tonsil
Pharyngitis
Inflammation of the pharynx
8.2.1 Infectious Diseases
8.2.1.1 Bacterial
8.2.1.2 Fungal‐Mycotic Yeast
8.2.1.3 Viral
8.2.2 Immune System
8.2.2.1 Contact Mucositis
8.2.2.2 Pemphigoid and Blistering Syndromes
8.2.2.3 Hypersensitivity
8.2.3 Oral Manifestation of Systemic Diseases
8.2.3.1 Hematology
8.2.4 Systemic Therapy Adverse Reactions
8.2.5 Nutrition
8.3 Palate/Soft Palate/Oropharynx/Tonsils
8.4 Soft Palate
8.5 Tonsils
8.6 Tongue
8.6.1 Infectious Agents
8.6.2 Lingual Masses
8.6.3 Metabolic
8.6.4 Immune Mediated
8.6.5 Trauma
8.6.6 Miscellaneous
8.7 Salivary Glands
8.7.1 Congenital
8.7.2 Acquired
8.7.2.1 Sialadenitis
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