logoPROFESSIONAL VERSION

Oral Inflammatory and Ulcerative Disease in Small Animals

ByBrenda L. Mulherin, BS, DVM, Diplomate AVDC
Reviewed/Revised Nov 2024

Inflammation of the oral tissues can be either primary or secondary. Inflammation in the oral cavity may affect a variety of tissues:

  • gingiva (see gingivitis image)

  • nongingival tissues of the periodontium (see periodontitis image)

  • alveolar mucosa (alveolar mucositis)

  • sublingual mucosa (sublingual mucositis)

  • lip and cheek mucosa (labial and buccal mucositis)

  • lip (cheilitis)

  • widespread oral mucosa (see gingivostomatitis image)

  • mucosa of the dorsal or ventral tongue surface (glossitis)

  • mucosa of the caudal oral cavity (caudal mucositis)

  • mucosa on the palatoglossal folds (faucitis)

  • mucosa of the palate (palatitis)

  • palatine tonsil (tonsillitis)

  • mucosa of the pharynx (pharyngitis)

The nature and severity of lesions vary greatly depending on the etiology and duration of disease.

Contact mucositis and contact mucosal ulceration are lesions in susceptible animals that are secondary to mucosal contact, with a tooth surface bearing the responsible irritant, allergen, or antigen. They have also been called kissing lesions, contact ulcers, and kissing ulcers (see contact mucositis images).

Stomatitis is inflammation of the mucosal lining of any structure in the oral cavity (see gingivostomatitis caudal aspect image). In clinical use, the term stomatitis should be reserved to describe widespread oral inflammation (beyond gingivitis and periodontitis) that may also extend into submucosal tissues (eg, marked caudal mucositis extending into submucosal tissues may be termed caudal stomatitis). Tissue can be proliferative, ulcerative, or both. It extends around the teeth and may also surround the oropharyngeal opening, making intubation difficult.

Periodontal disease, including gingivitis and periodontitis, is the most common oral problem in small animals. Up to 70% of cats and 80% of dogs have been reported to have periodontal disease by 3 years old.

Gingivitis is an inflammatory response to bacterial plaque on an adjacent tooth surface.

Periodontitis is inflammation of the hard and soft tissues of the periodontium (ie, periodontal ligament, cementum, gingiva, and alveolar bone); it results from the combination of bacterial periodontopathogens and the host's immune response that together destroy tooth-supporting tissues.

When inflammation or loss of any of the structures comprising the periodontium is present, some level of periodontal disease exists.

Periapical disease (granuloma, abscess, or cyst) is usually caused by endodontic disease—ie, the spread of infection and inflammation from within an injured tooth through the apical foramina into periapical tissues. A draining sinus tract, or parulis (see parulis image), may develop that manifests as a circular raised area of inflamed granulation tissue with a central draining fistula that opens near the mucogingival junction into the oral cavity or through the skin externally. The tract can potentially be traced back to the primary periodontal or periapical lesion and the etiology resolved. A parulis is a true periodontal abscess (ie, an encapsulated mucopurulent lesion within a periodontal pocket).

Other causes of oral inflammation include the following:

  • immunopathy (eg, autoimmune disease, immune deficiency)

  • chemical agents

  • infectious disease

  • trauma

  • metabolic disease

  • developmental anomalies or conformational anatomy that predisposes to irritation or inflammation

  • burns (see electrical burn image)

  • radiotherapy

  • neoplasia

Infectious agents that have been associated with oral inflammation, glossitis, stomatitis, and oral ulcerations include feline herpesvirus, feline calicivirus, feline leukemia virus, feline immunodeficiency virus, canine distemper virus, Bartonella henselae, and certain Leptospira serovars.

Stomatitis may occur after oral exposure to plant material (embedded plant awns) or fiberglass insulation. When chewed, plants of the species Dieffenbachia may also cause oral inflammation and ulceration. Contact with processionary caterpillars may cause severe glossitis.

Thallium is the major heavy metal responsible for oral lesions, although incidence of thallium toxicosis is low. Uremia can cause stomatitis and oral ulcers. Recurrent oral ulcerations are also observed in gray Collies with cyclic hematopoiesis.

Clinical signs vary widely, depending on the cause and extent of inflammation:

  • Anorexia may occur, especially in cats experiencing marked discomfort.

  • Halitosis and drooling are common with caudal stomatitis (see gingivostomatitis oral discharge image) and glossitis.

  • Saliva may be blood-tinged.

  • The animal may paw at its mouth and resent any attempted oral cavity examination because of pain.

  • Regional lymphadenopathy may occur.

Feline Stomatitis

Feline stomatitis is a serious condition in which affected cats develop progressively worsening inflammation of oral mucosal tissues (particularly the gingiva, alveolar mucosa, labial and buccal mucosa, sublingual mucosa, and mucosa of the caudal oral cavity) and increasing levels of discomfort. Also known as chronic gingivostomatitis or chronic lymphocytic plasmacytic stomatitis complex, feline stomatitis is distinct from more general forms of stomatitis (ie, mucosal inflammation from uremia, ingestion of caustic material, electrical burns, irritants, or other causes).

Etiology

In affected cats, feline stomatitis is suspected to be an immune-mediated disease or result from an inappropriate inflammatory response to one or more antigens. This disease is posited to be a hyperimmune response to plaque bacteria within the oral cavity, on plaque-retentive surfaces (teeth) or on the periodontal ligament.

Infectious agents associated with feline stomatitis include feline herpesvirus, feline calicivirus, feline leukemia virus, feline immunodeficiency virus, and certain bacteria, such as Bartonella henselae. A high percentage of affected cats (up to 100% in some studies) are chronic carriers of feline calicivirus.

Clinical Signs

In cases of feline stomatitis, often the mucosa in the caudal oral cavity, at and lateral to the palatoglossal folds, is severely ulcerated, friable, inflamed, and proliferative (see stomatitis image), making opening the mouth, chewing, and swallowing painful.

The most immediate clinical sign is severe pain when opening the mouth. Cats may vocalize and jump when they yawn or open their mouths to eat. Halitosis, ptyalism, and dysphagia may be noted.

Hungry cats often show approach-avoidance behavior as they approach their food, then hiss and run off in anticipation of discomfort. If the condition is severe and chronic, weight loss may be evident.

The disease is slowly progressive and may not be recognized until lesions have become severe. Mandibular lymphadenopathy may be present.

Pain often prevents adequate examination of the oral cavity without sedation or anesthesia.

Diagnosis

  • Oral examination

  • Virus isolation, retroviral tests, and evaluation for systemic disease

The hallmark clinical sign for diagnosing feline stomatitis is mucosal inflammation in the caudal oral cavity (see gingivostomatitis image). If inflammation is confined to the gingiva surrounding the teeth, gingivitis or periodontitis, rather than gingivostomatitis, is the more likely diagnosis. 

During oral examination, there may be mucosal inflammation bilaterally in the caudal oral cavity, at or lateral to the palatoglossal folds. In advanced cases, the cat will strongly object to opening its mouth due to severe discomfort.

Additional tests may include virus isolation (eg, calicivirus and herpesvirus), retroviral tests, and evaluation for systemic disease (eg, renal failure).

In atypical cases (unilateral involvement, usually proliferative focal lesion), biopsy and histological evaluation are required to exclude oral neoplasia or other specific oral disorders. Most biopsy samples of chronic inflammatory or ulcerated lesions reveal a predominance of lymphocytes and plasma cells, indicating the chronic inflammatory nature of the lesion without elucidating the primary etiology.

Treatment

  • Addressing inflammation

  • Relieving pain

The main goals in treating stomatitis are elimination of inflammation and cessation of pain, frequently requiring a combination of medical and surgical intervention.

By eliminating plaque-retentive surfaces, partial-mouth extraction (removal of all premolars and molars) or full-mouth extraction (removal of all teeth) and debridement of associated soft and hard tissues is the only treatment to provide lasting improvement and aid in overall longterm control. When full-mouth extractions are performed early in the disease course, and postextraction radiographs confirm that no retained tooth roots or fragments are left within alveolar bone, 60–80% of affected cats appear to be cured or, at minimum, dramatically improved.

Chronically affected cats treated medically for many months have a poorer prognosis postoperatively.

Full-mouth radiographs are imperative for verifying that no retained tooth roots are present in areas where teeth are either missing or have been extracted previously. Any retained root fragments must be removed because they will prevent improvement and potentially resolution of disease (see full-mouth extraction, postop image).

Pearls & Pitfalls

  • Full-mouth radiographs are imperative for verifying that no retained tooth roots are present in areas where teeth are either missing or have been extracted previously.

Postoperatively, medical treatment focuses on controlling inflammation, infection, and pain.

The pain induced by oral administration of glucocorticoids, such as prednisolone, makes oral steroid treatment less effective than injections of steroids such as methylprednisolone (10–20 mg/cat, IM or SC, weekly as indicated). Prednisolone also can be administered transdermally (2.5 mg/cat, applied to the pinna of the ear, every 24 hours); however, longterm use of transdermal corticosteroids can result in atrophy of pinna cartilage.

In refractory cases, interferon omega can be administered transmucosally. Oral administration of 100,000 units per cat per day is recommended for 90 days (extralabel). However, this medication can be expensive and difficult to acquire. In addition, results appear to be inconsistent.

Antimicrobials commonly used to treat feline stomatitis include amoxicillin-clavulanate (62.5 mg/cat, PO, every 12 hours) and clindamycin (11–33 mg/kg, PO or SC, every 24 hours); however, treatment may be ineffective or only transiently effective. Culture and susceptibility testing of lesions is rarely indicated, even with chronic or recurrent infections.

Doxycycline (5–10 mg/kg, PO, every 12–24 hours, until all oral cavity inflammation has resolved or no further improvement occurs) appears to have both efficacy against oral cavity bacteria and immunomodulating effects to decrease inflammation. The dose is decreased to the lowest effective dose. If all inflammation resolves, treatment can be discontinued. This can take up to 3–5 months after full-mouth extractions. Some patients need to remain on doxycycline indefinitely. Oral administration of doxycycline capsules and tablets should be followed by administration of 5–6 mL of water to decrease the risk of esophageal erosion in cats.

Pain control with one of the following medications may be considered:

  • meloxicam (0.1 mg/kg, PO, initially, followed by 0.05 mg/kg, PO, every 24 hours for 2–3 days, then decreased to the lowest effective dosage, PO, every 24 hours)

  • robenacoxib (1 mg/kg, PO, every 24 hours for up to 3 days)

  • buprenorphine (0.05 mg/kg, in the cheek pouch, every 8 hours, or 2.7–6.7 mg/kg, transdermally, once)

  • transdermal fentanyl patch (25-mcg patch/cat, applied every 4–5 days)

  • gabapentin (10 mg/kg, PO, every 12 hours)

Gabapentin, along with any of the other listed pain relief medications, should be considered for a multimodal approach to treat the patient's discomfort.

Dietary changes (hypoallergenic, soft, palatable foods) and administration of topical antiseptics (eg, dilute chlorhexidine or zinc ascorbate) should also be considered. A feeding tube for nutritional support may be considered in chronic cases that do not respond to treatment (eg, debilitated cats with severe weight loss and dehydration).

Many other treatments for feline stomatitis, including good at-home oral hygiene, frequent dental cleanings, periodontal debridement, cyclosporine (2.5 mg/kg, PO, every 12 hours; use is extralabel), bovine lactoferrin, laser treatment, and stem cell treatment, have been reported. An unapproved medication—purported to contain a fluoroquinolone antimicrobial and a Janus kinase (JAK; an enzyme that plays a critical role in the immune system) inhibitor—has been promoted as a remedy for gingivostomatitis; however, evidence for safety and efficacy is lacking, so the medication cannot be recommended.

Glucocorticoid administration alone to modulate the excessive inflammatory response usually results in substantial and immediate clinical improvement. However, without surgery (ie, tooth extraction), repeated use of glucocorticoids becomes progressively less effective and eventually completely ineffective. Cats that have received repeated glucocorticoid treatments also have a poorer prognosis once teeth are extracted. Longterm glucocorticoid administration is also associated with other comorbidities, such as diabetes mellitus.

Juvenile-Onset Periodontitis in Small Animals

Juvenile-onset periodontitis, which produces clinical signs similar to those of feline gingivostomatitis, affects cats less than 2 years old.

Etiology and Pathogenesis

The exact etiology of juvenile-onset periodontitis is unknown. It is thought to be a hyperimmune inflammatory response to exfoliation of the deciduous teeth and eruption of the permanent teeth, as well as to viral infections. Intense gingival inflammation appears to occur as the teeth are erupting into the oral cavity (see juvenile-onset periodontitis image).

In juvenile-onset periodontitis, inflammation extends into deeper tissues, causing attachment loss of the gingiva (gingival recession), loss of the periodontal ligament (tooth mobility), and loss of alveolar bone (periodontal pocketing and furcation exposure). Unlike in feline gingivostomatitis, inflammation does not appear to extend into the caudal oral cavity (see juvenile-onset periodontitis, caudal aspect image).

If substantial inflammation exists in the caudal oropharynx in a cat less than 2 years old, both juvenile periodontitis and feline gingivostomatitis may be present.

Epidemiology

Juvenile-onset periodontitis is typically first diagnosed in cats 6–12 months old. While a breed predilection exists for this condition among purebred cats, any cat can be affected. Breeds demonstrating an increased incidence include Abyssinian, Maine Coon, Persian, Siamese and Somali.

Clinical Signs

Frequently, cats with juvenile-onset periodontitis will develop clinical signs of gingival and mucosal inflammation surrounding the teeth, along with halitosis, oral pain, and discomfort. Clinical evidence of gingival enlargement and periodontal disease is frequently observed in affected patients, as is tooth resorption (1, 2).

Diagnosis

Substantial inflammation within the oral cavity can trigger increased risk for tooth resorption; therefore, radiographic evaluation of the entire oral cavity is necessary for assessing and treating affected teeth. Radiographic evaluation demonstrates that horizontal bone loss is frequently observed in affected cats, with many patients also showing furcation involvement and exposure.

Biopsies of affected tissues may be warranted to rule out other inflammatory diseases.

Treatment

Management of juvenile periodontitis is aimed at keeping the oral cavity clean and supporting the immune system to decrease systemic inflammation. Treatment includes an anesthetized dental cleaning, including scaling and polishing, every 3–6 months or as needed after diagnosis.

In addition, areas of gingival enlargement should be resected to the normal contour of the tooth to decrease development of pseudopockets and reduce the surface area on which inflammation could occur. Teeth with evidence of attachment loss should be evaluated for extraction if necessary. Teeth with clinical and radiographic evidence of tooth resorption should be extracted.

If patients are amenable to an oral health home care regimen, daily brushing with soft-bristle brushes and rinsing with oral chlorhexidine can help decrease oral bacteria.

The systemic inflammatory response can be lessened with NSAIDs such as meloxicam (0.1 mg/kg, PO, initial dose, then 0.05 mg/kg, PO, every 24 hours for 2–3 days, then decrease to lowest effective dose) or robenacoxib (1 mg/kg, PO, every 24 hours for up to 3 days).

As with feline gingivostomatitis, doxycycline can be used for its antimicrobial and anti-inflammatory affects in a decreasing dosing regimen (5 mg/kg, PO, every 12 hours, or 10 mg/kg every 24 hours, for a minimum of 1–2 months until inflammation resolves or reaches an equilibrium in which it is static; then reduce by 50% every 2–3 weeks until lowest effective dose is reached).

Gabapentin is also a good longterm choice for reducing pain and discomfort. Transmucosal administration of opioids such as buprenorphine (up to 0.05 mg/kg, in the cheek pouch, every 8 hours) as needed for flare-ups of discomfort is also warranted.

Juvenile periodontitis is unique in that many cats will outgrow it once they reach 2 years old. If owners are diligent regarding frequent dental cleanings, home care, and medication administration, many cats can continue to grow and maintain their dentition.

Extracting teeth is recommended only as necessary when the amount of attachment loss or evidence of tooth resorption warrants extraction. Full-mouth extractions are not recommended unless inflammation persists well after the cat is 2 years old or there is extensive inflammation in the caudal oral cavity.

Canine Chronic Ulcerative Stomatitis

Canine chronic ulcerative stomatitis (CCUS), also known as canine stomatitis, is a painful condition in which oral mucosal ulcers develop.

CCUS is a specific clinical entity distinct from more general forms of stomatitis (ie, mucosal inflammation from uremia, ingestion of caustic material, electrical burns, irritants, or other causes).

Etiology

The etiology of CCUS remains unknown. The underlying cause of CCUS is thought to be an immunopathology resulting in an aberrant local inflammatory response to antigens in dental plaque. An immune-mediated pathogenesis involving leukocytes has been suspected. Autoantibodies are not found with canine stomatitis, and thus it is not an autoimmune condition.

Epidemiology

Canine stomatitis has been noted in Maltese, Miniature Schnauzers, Labrador Retrievers, Greyhounds, and other breeds.

Clinical Signs

Characteristics of CCUS, which often manifests as contact mucositis and contact mucosal ulceration, include the following:

  • severe gingivitis

  • gingival recession

  • periodontitis

  • ulceration of lingual, alveolar, labial, and buccal mucosae that are in contact with teeth (see CCUS tongue image)

Diagnosis

  • Clinical evaluation

  • Biopsy and histological examination

Diagnosis of canine stomatitis is by clinical observation of oral lesions after excluding other etiologies (eg, uremic stomatitis, caustic stomatitis, and specific infectious agents; see image of CCUS lesions).

Biopsy and histological examination of lesions helps differentiate CCUS from eosinophilic granuloma, autoimmune diseases (pemphigus vulgaris, bullous pemphigoid, lupus erythematosus), erythema multiforme, and neoplasia.

The characteristic lesion of canine stomatitis is a contact ulcer that develops where the lip or cheek mucosa contacts the tooth surface, most commonly on the inner surface of the upper lip and cheek adjacent to the maxillary canine and fourth premolar teeth. These lesions have also been termed “kissing ulcers” or "kissing lesions" because they commonly develop where the mucosa “kisses” the tooth surface (see CCUS buccal mucosa image).

Biopsy is recommended for a histological diagnosis and elimination of other ulcerative conditions.

Treatment

  • Professional cleaning

  • Tooth extraction

  • Home oral hygiene

The main goals of treatment of canine stomatitis are elimination of inflammation and cessation of pain, which are accomplished by a combination of medical and surgical interventions.

Eliminating, or at least minimizing, plaque deposition through professional dental cleaning, extraction of teeth with gingival recession and periodontitis, and meticulous home oral hygiene (twice-daily toothbrushing) may resolve the problem. However, even slight residual plaque on tooth surfaces will perpetuate inflammation and ulceration.

Supplemental antimicrobial measures with topical chlorhexidine gluconate rinses or gels and antimicrobial treatment with the following drugs should be considered:

  • amoxicillin-clavulanate (13.75 mg/kg, PO, every 12 hours)

  • clindamycin (5.5–33 mg/kg, PO, every 12 hours)

  • metronidazole (15–20 mg/kg, PO, every 12–24 hours)

  • doxycycline (5–10 mg/kg, PO, every 12–24 hours)

Anti-inflammatory and immunosuppressive medications are also indicated.

Discomfort caused by ulcers complicates efforts to brush the teeth and administer oral medications. In cases in which discomfort is severe and owners are unable or unwilling to brush the teeth, analgesic medications, such as gabapentin (10–20 mg/kg, PO, every 8–12 hours), and NSAIDs, such as carprofen (2.2 mg/kg, PO, every 12 hours) or meloxicam (0.2 mg/kg, PO, initial dose, followed by 0.1 mg/kg, PO, every 24 hours), should be added.

Extraction of otherwise healthy teeth associated with ulcers may be necessary to remove contact surfaces on which plaque accumulates and contributes to the formation of ulcers. Although extraction can help control lesions, it is not curative, because plaque also forms on oral mucosal surfaces, including the tongue. In some cases in which full-mouth extractions have been performed, dogs continue to develop lesions due to a hyperimmune response to plaque on the remaining oral surfaces.

Lip Fold Dermatitis and Cheilitis in Small Animals

Lip fold dermatitis is a chronic moist dermatitis that occurs most commonly in breeds that have pendulous lower lips (abnormal lip conformation; eg, English Bulldogs, Saint Bernards) and lateral lower lip folds (eg, Cocker Spaniels, Labrador Retrievers) that have prolonged contact with saliva. The lesions can be exacerbated when poor oral hygiene results in increased salivary bacterial levels. Lower lip folds can become very malodorous, inflamed, uncomfortable, and swollen.

Lip wounds, resulting from fights or chewing on sharp objects, are common and vary widely in severity. Thorns, grass awns, plant burrs, and fishhooks can embed in the lips and cause marked irritation or severe wounds. Irritants such as plastic or plant material can also inflame the lips.

Lip infections may develop secondary to wounds or foreign bodies or can be associated with inflammation of adjacent areas. Direct extension of severe periodontal disease or stomatitis can produce cheilitis, or lip inflammation (see cheilitis image). Licking areas of bacterial dermatitis or infected wounds can spread infection to the lips and lip folds.

Other causes of inflammation of the lips include parasitic infections, autoimmune skin diseases, and neoplasia.

Clinical Findings and Diagnosis

  • Clinical examination

  • Histological evaluation

Lip fold dermatitis and cheilitis are diagnosed by a combination of clinical examination of affected sites and histological evaluation of biopsied tissues.

Inflammation of the lips and lip folds can be acute or chronic. Animals with cheilitis may paw, scratch, or rub at their mouth or lip; have halitosis; and occasionally salivate excessively or be anorectic. With chronic infection of the lip margins or folds, the hair in these areas is discolored, moist, and matted with thick, yellowish or brown, malodorous discharge overlying hyperemic and sometimes ulcerated skin.

Cheilitis due to extension of infection from the mouth or another area usually is detected easily because of the primary lesion.

Treatment

  • Improved hygiene

  • Antimicrobials

  • Surgical correction

The main goals of treatment are elimination of inflammation and cessation of pain, which are accomplished by a combination of medical and surgical intervention.

Medical management of lip fold dermatitis includes clipping hair, cleaning the folds every 12–24 hours with benzoyl peroxide or a mild skin cleanser, and keeping the area dry. Topical diaper rash cream applied every 24 hours may be helpful. Surgical correction (cheiloplasty) of deep lip folds is a longer-lasting remedy.

Cheilitis that is unrelated to pendulous lips or lip folds usually resolves with minimal cleansing, appropriate antimicrobials if a bacterial infection is present, and specific treatment of primary etiologies (eg, autoimmune skin disease). Lip wounds should be cleaned and sutured if necessary. Treatment of periodontal disease or stomatitis is necessary to prevent recurrence.

Infectious cheilitis that has spread from a lesion elsewhere usually improves with treatment of the primary lesion; however, local treatment is also necessary. With severe infection, hair should be clipped from the lesion and the area gently cleaned and dried. Antimicrobials are indicated if the infection is severe or systemic.

Mycotic Stomatitis in Small Animals

Mycotic stomatitis caused by overgrowth of the opportunistic yeast Candida albicans is an uncommon cause of oral inflammation in dogs and cats. It is characterized by stomatitis, halitosis, ptyalism, anorexia, oral ulceration, and bleeding from oral tissues. It is usually associated with other oral diseases, longterm antimicrobial treatment, or immunosuppression.

Diagnosis is confirmed by culture of the organism from the lesion or by histological evidence of tissue invasion.

Any existing underlying local or systemic diseases should be treated. Ketoconazole (5–10 mg/kg, PO, every 12–24 hours) or a related benzimidazole should be administered until the lesions resolve. An adequate level of nutrition should be maintained.

The prognosis is guarded if predisposing diseases cannot be adequately treated or controlled.

Acute Necrotizing Ulcerative Gingivitis in Small Animals

Acute necrotizing ulcerative gingivitis (ANUG) is a relatively uncommon disease of dogs characterized by severe gingivitis, ulceration, and necrosis of the oral mucosa.

Fusobacterium spp and spirochetes (Borrelia vincentii), normal oral cavity inhabitants, have been suggested as a cause of this disease after some predisposing factor increases their numbers or decreases local resistance of the oral mucosa. The role, if any, of these organisms in causing disease is unknown. Other potential contributing factors are stress, excess glucocorticoid administration in susceptible dogs, and poor nutrition.

In humans, Bacteroides melaninogenicus intermedius may play a more important role.

ANUG appears first as reddening and swelling of the gingival margins and interdental papillae, which are painful, bleed easily, and may progress to gingival recession. Extension to other areas of the oral mucosa is common, resulting in ulcerated, necrotic mucous membranes and exposed bone in severe cases, and ultimately osteomyelitis and osteonecrosis. Halitosis is severe, and anorexia may develop because of pain. Ptyalism sometimes occurs, and saliva may be blood tinged.

Differential diagnoses include severe periodontal disease, autoimmune skin disease, uremia, neoplasia, and other systemic disease associated with oral lesions.

Diagnosis is made by exclusion of other etiologies.

Treatment of ANUG includes the following measures:

  • treatment of periodontal disease

  • partial- or full-mouth extractions

  • debridement of lesions (removal of necrotic soft tissue and bone)

  • meticulous oral hygiene at home

  • systemic antimicrobials (amoxicillin-clavulanate, clindamycin, metronidazole, doxycycline)

  • oral antiseptics (dilute chlorhexidine solution or gel)

Glossitis in Small Animals

Glossitis, an acute or chronic inflammation of the tongue, can result from a variety of causes:

Frequently, glossitis is caused by embedded foreign material, viruses, or chemical contact. Foreign body glossitis is especially a problem in long-haired dogs that attempt to remove plant burrs from their coats. (See glossitis images showing tongue surface, edema, ulcerations, and foreign body penetration.)

Drooling and reluctance to eat are common clinical signs associated with glossitis in cats. The source of these clinical signs may go undiscovered unless the mouth is carefully evaluated. Excess plaque accumulation on the lingual surfaces of mandibular teeth may result in reddening, swelling, and occasionally ulceration of the lateral edges and tip of the tongue.

A thread, string, or other linear foreign body may get caught under the tongue, slicing its way through the lingual frenulum and sublingual mucosa. Inflammation may be absent from the dorsal lingual surface; however, the ventral surface is painful, acutely or chronically irritated, and frequently is lacerated by the foreign body. Porcupine quills, plant material, and other foreign bodies can become embedded so deeply that they are not visible or palpable.

Pearls & Pitfalls

  • Porcupine quills, plant material, and other foreign bodies can become embedded so deeply that they are not visible or palpable.

Acute lingual swelling may be caused by insect stings and venomous animal bites.

With chronic ulcerative glossitis, thick, brown, foul-smelling discharge (occasionally with bleeding) may be present. Frequently, the patient is reluctant to allow oral examination.

Fissured, or plicated, tongue (lingua dissecta) describes a textural variation of the dorsum of the tongue with deep median or sagittal longitudinal grooves (see fissured tongue image). The fissure deepens with age and is therefore thought to be acquired from some extrinsic factor. However, it may also represent a developmental anomaly. The groove often becomes deeply filled with hairs that act as a local irritant, causing inflammation and discomfort.

Glossitis in Small Animals
Glossitis, tongue surface, dog
Glossitis, tongue surface, dog

Dog with glossitis. Note the irregular lingual surface with multiple fissures.

Courtesy of Dr. Ben Colmery III.

Glossitis with severe edema, cat
Glossitis with severe edema, cat

Cat with glossitis and severe edema. Note the swelling associated with the ventral lingual surface and the protrusion of the tongue from the oral cavity.

... read more

Courtesy of Dr. Ben Colmery III.

Glossitis, ulcerations, dog
Glossitis, ulcerations, dog

Dog with severe inflammation of the ventral and lateral aspect of the tongue. Ulcerations are present where the tongue contacts plaque on the lingual aspect of the left mandibular teeth. In this patient, glossitis was caused by excessive plaque and calculus accumulation on the lingual surface of the teeth.

... read more

Courtesy of Dr. Brenda Mulherin.

Glossitis, foreign body, dog
Glossitis, foreign body, dog

Dog with mild glossitis due to foreign body penetration. In this case, hair embedded in the tongue can act as a foreign body and cause inflammation. Treatment involves removing the hair from the tongue. Patients that excessively groom and have pronounced dermatological or behavioral conditions are predisposed to developing glossitis.

... read more

Courtesy of Dr. Brenda Mulherin.

Fissured tongue, dog
Fissured tongue, dog

Deep fissures like those on this dog's tongue can entrap hair. A thorough dermatological examination and testing should be performed to identify a cause for excessive grooming.

... read more

Courtesy of Dr. Gregg A. DuPont.

Foreign bodies or hairs should be removed and diseased teeth treated or extracted. Bacterial infectious glossitis should be managed with an appropriate systemic antimicrobial. Debridement and dilute chlorhexidine mouthwashes are beneficial in some cases. Lingual debridement is sometimes required if foreign material is embedded in the tongue.

A soft diet and parenteral fluids are administered as needed. If the patient is debilitated and unable to eat well for a prolonged period, a feeding tube for nutritional support should be considered.

Acute glossitis due to insect stings or venomous animal bites may require emergency treatment.

If glossitis is secondary to another condition, the primary disease should be treated. Lingual tissues heal rapidly after irritation and infection have been eliminated.

For More Information

References

  1. Ruhnau J. Treatment of juvenile gingivitis in cats. Paper presented at World Small Animal Veterinary Association Congress September 25–28, 2017; Copenhagen. Accessed April 18, 2023. https://www.vin.com/doc/?id=8506389

  2. Soltero-Rivera M, Vapniarsky N, Rivas IL, Arzi B. Clinical, radiographic and histopathologic features of early-onset gingivitis and periodontitis in cats (1997-2022). J Feline Med Surg. 2023;25(1). doi:10.1177/1098612X221148577

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