Oral mucosa covers and protects tissues beneath it and conveys sensory information from the surface.
Normal function is required for mastication, deglutition, chemosensory function, and phonation.
Impaired oral mucosal health causes pain, malnutrition, infection, compromised immune function, and exacerbations of medical disorders.
Diseases of the Lips ICD-9: 528.5 ° ICD-10: K13.0
Angular Cheilitis (Perlèche)
Associated with increased moisture at commissures, salivation (at sleep).
Predisposing factors: thumb sucking in children; sagging face and loss of teeth in older persons; candidiasis in immunocompromised persons; Staphylococcus aureus in atopic dermatitis and isotretinoin treatment.
Findings: erythema and maceration at commissures (see Fig. 33-1); white candidal colony.
Diagnosis: KOH for candidiasis; culture for S. aureus, Candida.
Management: Identify and treat causes.
Figure 33-1. Angular cheilitis Mild erythema and scaling in bilateral commissures. (Courtesy of Dr. Nathaniel Treister.)
Actinic/solar keratoses, usually of the lower lip. Rule out squamous cell carcinoma in situ (SCCIN) or invasive if papule or nodule or ulcer occurs. (See “Solar Keratosis” in Section 10.)
Conditions of the Tongue, Palate, and Mandible ICD-9: 528.6, 528.7, 529 ° ICD-10: K14
Normal variant in up to 11% of population. Asymptomatic.
Findings: Multiple folds with anterior-posterior orientation on the dorsal surface of the tongue (Figs. 33-2 and 33-3).
Associated disorders: Psoriasis, Down syndrome, acromegaly, Sjögren syndrome.
Synonyms: Lingua fissurata, lingua plicata, scrotal tongue, grooved tongue, furrowed tongue.
Figure 33-2. Fissured tongue Deep furrows on the dorsum of the tongue are asymptomatic.
Figure 33-3. Hairy tongue Defective desquamation of filiform papilla noted in posterior aspect of tongue. Tongue has a white surface due to retained keratin. (Courtesy of Dr. Nathaniel Treister.)
Black or White Hairy Tongue
Pathogenesis: Defective desquamation of filiform papillae resulting in hair-like projections on the dorsum of the tongue.
Associations: Heavy tobacco use, mouth breathing, systemic antibiotic therapy, poor oral hygiene, general debilitation, radiation therapy, chronic use of bismuth-containing antacids, lack of dietary roughage.
Symptoms: Gagging sensation, altered taste, halitosis, cosmetic disfigurement.
Findings: Furry plaques on dorsal tongue (Fig. 33-3). Chromogenic bacteria or exogenous pigment stain tongue: white, yellow, green, brown, black. Candidiasis may occur secondarily.
Management: Eliminate predisposing factors; good oral hygiene.
Synonym: Lingua villosa (nigra).
Oral Hairy Leukoplakia (See Section 27)
Pathogenesis: Epstein–Barr virus infection; low CD4 cell counts.
Findings: White corrugated plaques on lateral aspects of tongue (see Fig. 27-66). Does not occur in successfully treated HIV/AIDS.
Migratory Glossitis ICD-9: 529.1 ° ICD-10: K14.1
Irregular areas of dekeratinized and desquamated filiform papillae (red in color) are surrounded by elevated whitish or yellow margins (Fig. 33-4).
Etiology: unknown; possible link with psoriasis. Incidence: common; usually asymptomatic.
Synonym: Geographic tongue.
Figure 33-4. Migratory glossitis Areas of hyperkeratosis alternate with areas of normal pink epithelium, creating a geographic pattern in a female with psoriasis.
Palate and Mandibular Torus
Pathogenesis: genetic predisposition, ? autosomal dominant in some series, more common in females, Native Americans, Eskimos (torus palatini); local stressors (mandibular and palatal tori), bony protrusions
Symptoms: may be complicated by ulceration; usually asymptomatic
Findings: palatal tori are usually in midline of palate and less than 2 cm, but can vary in size through life; mandibular tori found usually near premolars; rarely bilateral. They are smooth, nodular protrusions (Figure 34-5).
Management: not needed; if create ulcerations or complicate dental prosthesis, surgery can be done. Have been used as autogenous bone grafts.
Diseases of the Gingiva, Periodontium, and Mucous Membranes ICD-9: 523 ICD-10: K06
Gingivitis and Periodontitis
Gingivitis: Erythema, edema, blunting of interdental papillae without bone loss. Predisposing factors: poor oral hygiene, tobacco use, diabetes.
Periodontitis: Chronic infection of connective tissue, periodontal ligament, and alveolar bone; most common cause of tooth loss in adults.
Course: Accumulation of subgingival calculus (calcified plaque) and Actinobacillus actinomycetemcomitans infection results in painless soft tissue edema, insidious alveolar bone resorption, deepening periodontal pockets, and tooth loss.
Reaction pattern associated with viral infection, autoimmunity, lichen planus (LP), erythema multiforme, pemphigus, cicatricial pemphigoid. Findings: Erythema, desquamation, and edema of gingivae. Other mucocutaneous sites may be affected.
Findings: Reticulated white plaques and painful erosions on mucosal surfaces.
Etiology: LP, drugs (NSAIDs, antihypertensive agents), allergic contact dermatitis, graft-versus-host disease.
Figure 33-5. (A) Torus palatinus Bony protrusion in the midline, upper palate. (B) Mandibular torus Unilateral protrusion near premolars, above the mylohyoid muscle insertion into the mandible. (Courtesy of Dr. Nathaniel Treister.)
Incidence: 40-60% of individuals with LP have oropharyngeal involvement.
Wickham striae: Reticulate (netlike) patterns of lacy-white hyperkeratosis [buccal mucosa (Fig. 33-6), lips, tongue, and gingivae].
Hypertrophic LP—leukoplakia with Wickham striae usually on the buccal mucosa.
Atrophic LP—shiny plaque often with Wickham striae in surrounding mucosa.
Erosive/ulcerative LP—superficial erosions with overlying fibrin clots that are seen on the tongue and buccal mucosa; can be painful (Fig. 33-6).
Bullous LP—intact blisters (rupture and result in erosive LP).
Desquamative gingivitis—bright red gingiva (Fig. 33-7).
Figure 33-6. Lichen planus: Wickham striae Poorly defined violaceous plaque with lacy, white pattern on the buccal mucosa.
Figure 33-7. Lichen planus: desquamative gingivitis The gingival margins are erythematous, edematous, and retracted. The lesions were painful, making dental hygiene difficult, resulting in plaque formation on the teeth.
Acute Necrotizing Ulcerative Gingivitis
Precipitating factors: Poor oral hygiene, HIV/AIDS, immunosuppression, alcohol and tobacco use, nutritional deficiency.
Findings (Fig. 33-8): Punched-out ulcers of the interdental papillae. Gingival hemorrhage, severe pain, foul odor/halitosis, fever, lymphadenopathy; alveolar bone destruction.
Etiologic agents: Bacteroides fusiformis, Prevotella intermedia, Borrelia vincentii, Treponema.
Management: Systemic antibiotics such as clindamycin, metronidazole, amoxicillin. Dental hygiene.
Synonyms: Trench mouth, Vincent disease.
Figure 33-8. Acute necrotizing ulcerative gingivitis (ANUG) Very painful gingivitis with necrosis on marginal gingiva, edema, purulence, and halitosis in a 35-year-old female with advanced HIV disease. ANUG resolved with oral clindamycin.
Findings: Hypertrophy of both the free and attached gingivae, particularly the interdental papillae (Fig. 33-9).
Inflammatory enlargement: Most common cause of gingival enlargement. Caused by edema and infective cellular infiltration caused by prolonged exposure to bacterial plaque; fibrosis occurs if untreated.
Drug-induced fibrous hyperplasia of gingivae: May cover the teeth and is associated with:
Anticonvulsants: phenytoin, succinimides, valproic acid.
Calcium channel blockers: nifedipine, verapamil.
Pregnancy, puberty, vitamin C deficiency, glycogen storage disease.
Chronic myelomonocytic leukemia (Fig. 33-9).
Figure 33-9. Gingival hyperplasia: acute monocytic leukemia The gingivae show hyperplasia due to infiltration with leukemic monocytes.
Aphthous Ulceration ICD-9: 528.2 ° ICD-10: K12.0
Recurrent painful mucosal lesions.
Most common cause of oral ulcerations; incidence up to 30% of otherwise healthy persons.
May be associated with systemic diseases such as HIV/AIDS and Behçet disease.
Etiology. Idiopathic. Can arise at the site of minor mucosal injury, e.g., bite.
Pathogenesis. Cell-mediated immune reaction pattern.
Age at Onset. Any age; often during second decade, persisting into adulthood, and becoming less frequent with advancing age.
• Simple versus complex aphthosis based on clinical course.
• Simple: 1-3 oral ulcers that recur 1-3 times per year.
• Complex: Continuous ulcers and associated with systemic disease or genital ulcers.
• Major aphthous ulcers (AU) may persist for ≥6 weeks, healing with scarring.
• Behçet disease should be considered in patients with persistent oropharyngeal AU, with or without anogenital AU, associated with systemic findings (eye, nervous system). See Section 14.
Symptoms. Even though small, AU can be quite painful, which may impair nutrition. A burning or tingling sensation may be felt before ulceration. In persons with severe AU, weight loss may be associated with persistent pain.
• At times, small, painful red macule or papule before ulceration.
• More commonly, ulcer(s) <1 cm (Figs. 33-10 and 33-11), covered with fibrin (gray-white), with sharp, discrete, and at times edematous borders. White-gray base with an erythematous rim.
• Most commonly single; at times, multiple or numerous small, shallow, grouped—i.e., herpetiform AU (HAU). Major AU (MaAU) may heal with white, depressed scars.
• Number of ulcers: Minor AU (MiAU), 1-5; MaAU, 1-10: HAU, up to 100.
• Distribution: Oropharyngeal, anogenital, any site in the GI tract. Oral lesions most commonly on the buccal and labial mucosa, less commonly on tongue, sulci, floor of mouth. MiAU rarely occur on the palate or gums. MaAU often occur on soft palate and pharynx. Also, esophagus, upper and lower GI tract, and anogenital epithelium.
Figure 33-10. Aphthous ulcers: minor Multiple, very painful, gray-based ulcers with erythematous halos on the labial mucosa.
Figure 33-11. Aphthous ulcers: major Two large painful deep ulcers on the lateral tongue are seen in a patient with HIV/AIDS. Ulcers resolved with intralesional triamcinolone injection.
General Findings. With MaAU, occasionally tender cervical lymphadenopathy.
Associated Disorders. Behçet disease, cyclic neutropenia [acute HIV, AIDS (large chronic AU), reactive arthritis; periodic fever, aphthous stomatitis, Crohn disease, pharyngitis, and adenitis (PFAPA; occurs in young children with associated high fever occurring periodically every 3-5 weeks with AU, pharyngitis, and/or lymphadenitis).
Primary herpetic gingivostomatitis, hand-foot-and-mouth disease, herpangina, primary HIV/AIDS infection, Behçet disease, squamous cell carcinoma (SCC), bullous disease, lichen planus, Reiter syndrome, adverse drug reaction.
Dermatopathology. Nondiagnostic. Rule out specific cause of ulcer, i.e., infection (syphilitic chancre, histoplasmosis), inflammatory disorders (lichen planus), or cancers (SCC).
Usually made on clinical findings, ruling out other causes.
Tend to recur during adulthood. Uncommonly, may be almost constant in the oropharynx or anogenitalia, referred to as complex aphthosis.
Intralesional Triamcinolone. 3-10 mg/mL in lidocaine very effective for immediate relief of pain and resolution of ulcers. Amlexanox 5% can be applied topically four times a day (after meals and before bedtime). Viscous lidocaine 2% should only be used for brief, immediate control of pain.
• Prednisone: In persons with large, persistent, painful AU interfering with nutrition, a brief course of prednisone is effective (70 mg, tapered by 10 or 5 mg/d).
• Tetracycline syrup and minocycline 100 mg po BID, reported with variable success.
• Thalidomide: Effective in HIV/AIDS, Behçet disease, large painful AU. Adverse effects: peripheral sensory neuropathy. Teratogenesis. Tumor necrosis factor- a inhibitor: Adalimumab and infliximab reported to be effective.
The differential diagnosis of leukoplakia is shown in Table 33-1.
TABLE 33-1 DIFFERENTIAL DIAGNOSIS OF LEUKOPLAKIA
Figure 33-12. Leukoedema In this variant of normal, there is bluish and whitish discoloration of mucosa that blanches when the cheek is stretched. (Courtesy of Dr. Nathaniel Treister.)
Figure 33-13. (A, B) Lichen simplex chronicus Note the white plaque in the retromolar pad (after third molar extractions). These are often seen on edentulous ridge after extractions. (Courtesy of Dr. Sook-Bin Woo.)
Figure 33-14. Chronic chewing A wedge-shaped white papule is noted on the lateral surface of the tongue. (Courtesy of Dr. Sook-Bin Woo.)
Figure 33-15. Nicotine stomatitis Posterior palate shows erythematous pinpoint papules at sites of ducts, where chemical irritation has caused chronic inflammation. (Courtesy of Dr. Sook-Bin Woo.)
Figure 33-16. Condyloma acuminatum: mucosal lip Cluster of white cauliflower-floret-like lesions on the mucosa of the lower lip.
Leukoplakia ICD-9: 528.6 ° ICD-10: K13.21
Leukoplakia is a chronic white plaque/lesion in the oropharynx.
Premalignant leukoplakia has histologic atypia.
Leukoplakia is a descriptive clinical term regarding morphology: squamous cell carcinoma, in situ and invasive, must be ruled out.
Findings: a white plaque that cannot be wiped off and cannot be diagnosed as any other distinct lesion and may be premalignant or malignant.
Definitive diagnosis should be made on clinical findings and/or histology.
When diagnosis is definitive histologically, “leukoplakia” is no longer appropriate.
Erythematous Lesions and/or Leukoplakia
Erythematous lesions ± leukoplakia appear red because of inflammation, hemorrhage, increased angiogenesis, epithelial atrophy, acantholysis, ulceration.
The differential diagnosis includes SCCIS, invasive SCC, candidiasis, migratory glossitis, radiotherapy and chemotherapy-induced mucositis, lichen planus, lupus erythematosus.
Premalignant and Malignant Neoplasms ICD-10: C14
Dysplasia and Squamous Cell Carcinoma In Situ (SCCIS)
Etiology: Tobacco-related habits [smoking moist snuff, pan (betel nut)]; human papillomavirus (HPV).
Risk factors: Tobacco use, alcohol use, oral lichen planus.
Oncogenesis: Complex, multifocal process, multiclonal field carcinogenesis, and intraepithelial clonal spread; multifocal nature of early process reduces efficacy of local treatment.
Findings: Chronic, ± solitary patch/plaque on oropharyngeal mucosa. ± Reddish velvety
appearance with either stippled or patchy regions of leukoplakia (Fig. 33-17). ± Smooth patch with minimal or no leukoplakia.
Size: Usually <2 cm. Location: Floor of mouth (men); tongue and buccal surface (women).
Course: Most dysplasias do not progress to invasive SCC; some do.
Biopsy all lesions that persist for >3 weeks without definitive diagnosis.
Figure 33-17. Squamous cell carcinoma in situ: inferolateral tongue A 72-year-old male with an asymptomatic lesion on the tongue noticed by his dentist. A 6-mm white plaque (leukoplakia) on the tongue is noted. Biopsy reported SCCIS. The lesion was excised.
Oral Invasive Squamous Cell Carcinoma (See also Section 11)
High associated morbidity and mortality, accounting for about 5% of all neoplasms in men and 2% of those in women.
Findings: Usually appears as a granulating, velvety plaque or nodule with stippled hyperkeratosis ± ulceration (Fig. 33-18) (lips, floor of the mouth, central and lateral sides of the tongue).
Biopsy all lesions that persist for >3 weeks without definitive diagnosis.
Management: Aggressive surgical intervention.
Figure 33-18. Invasive squamous cell carcinoma: palate An advanced leukoplakic tumor on the hard palate of a cigarette smoker.
Oral Verrucous Carcinoma
Etiology: Oncogenic HPV types 16, 18.
Findings: Extensive hyperkeratotic white leukoplakia (Fig. 33-19).
Course: Metastasizes late but can be locally destructive. Biopsy all lesions that persist for >3 weeks without definitive diagnosis.
Management: Aggressive surgical intervention.
Figure 33-19. Verrucous carcinoma: buccal mucosa Extensive thick plaque arising on the buccal mucosa.
Oropharyngeal Melanoma (See also Section 12)
Incidence: 4% of primary oral malignancies.
For the most part, lesions are asymptomatic; often advanced when first detected.
Findings: Presents as pigmented lesion (Fig. 33-20), with variegation of color and irregular borders; rarely amelanotic. In situ lesions are macular; sites of invasion are usually raised within the in situlesion.
Distribution: 80% arise on pigmented mucosa of the palate and gingiva.
Risk factors: More deeply pigmented individuals (Africans) have higher proportional incidence rates of mucosal melanoma than whites.
Figure 33-20. Melanoma: hard palate A large, highly variegated pigmented lesion in a 63-year-old male. Lesional biopsy of a raised part showed invasive acrolentiginous melanoma.
Mucocele ICD-9: 527.6 ° ICD-10: K11.6
These arise following rupture of minor salivary gland.
Findings: Nodule with mucus-filled cavity, with a thick roof (Fig. 33-21). Chronic lesions are firm, inflamed, poorly circumscribed nodules; bluish, translucent; fluctuant.
Location: Develops at sites where minor salivary glands are easily traumatized: mucous membranes of the lip and floor of the mouth.
Course: Chronic, recurrent, and then it presents as a firm, inflamed nodule.
Figure 33-21. Mucocele A well-defined, soft bluish submucosal fluctuant nodule on the lip. Thick clear mucus drained when the lesion was incised.
Irritation Fibroma ICD-9: 528.8 ICD-10: M8810/0
This is a submucosal nodular scar, occurring at a site of recurrent trauma (Fig. 33-22).
Findings: Sessile or pedunculated, well-demarcated nodule, usually 2 cm in diameter (may be large if neglected). Normal color of the mucous membrane to pink-red; firm to hard.
Location: Buccal mucosa along bite line; tongue, gingiva, labial mucosa.
Synonym: Bite fibroma.
Figure 33-22. Irritation fibroma: lower lip A 58-year-old female with a lesion on the lip for 10 years. She frequently bites it when chewing. There is a rubbery pink nodule at the reflection of the labial mucosa.
Cutaneous Odontogenic (Dental) Abscess
A periapical dental abscess can extend into the overlying soft tissues, tracking and draining on the face (Fig. 33-23).
Figure 33-23. Cutaneous odontogenic abscess: cheek A 23-year-old healthy female notes a lesion on the cheek for 6 months. Nodule on the lower left cheek near the jawline with surrounding erythema and scar-like depression.
Cutaneous Disorders Involving the Mouth
Cutaneous disorders may present in oral mucosa; may be confined to this site for months before cutaneous involvement occurs.
Pemphigus Vulgaris (PV) (See also Section 6)
ICD-9: 694.4 ° ICD-10: L10.0
Often presents in oral mucosa; may be confined to this site for months before cutaneous bullae occur.
Findings: Blisters are very fragile, rupture easily, rarely seen. Sharply marginated erosions of the mouth (buccal mucosa, hard and soft palate, and gingiva) are presenting symptoms. Gingivitis can be a presenting sign. Erosions are extremely painful, interfering with nutrition (Fig. 33-24).
Biopsy, immunofluorescence, or antibody titers against desmogleins 1 or 3 confirm the diagnosis (see “Pemphigus Vulgaris” in Section 6).
Figure 33-24. Pemphigus vulgaris Shallow ulcers and erosions with underlying beefy erythema/dermal tissue are commonly aggravated by trauma from swallowing spicy foods or citrus.
Paraneoplastic Pemphigus (See also Section 19)
ICD-9: 694.4 ° ICD-10: L10.81
Painful mucosal erosions. Cutaneous blisters, lichenoid papules and erosions; conjunctival erythema can be prominent (see Fig. 33-25).
Confirmed or occult malignancy (though this may precede or lag presentations by 6 months to a year). Can be associated with bronchiolitis obliterans-like obstructive pulmonary defects.
Acantholysis, keratinocyte necrosis, interface dermatitis. IgG and complement (C3) within the epidermal intercellular spaces and basement membrane seen on immunofluorescence. Circulating antibodies specific for stratified or transitional epithelium.
Figure 33-25. Paraneoplastic pemphigus Note beefy-red erosive mucositis in this patient with advanced CLL. There is also mild gingivitis. (Courtesy of Dr. Mark Lerman.)
Bullous Pemphigoid (See also Section 6)
ICD-9: 694.5 ° ICD-10: L12.0
In contrast to pemphigus vulgaris, bullous pemphigoid uncommonly affects the oropharynx.
Findings: Blisters (Fig. 33-26), which initially are tense, erupt on the buccal mucosa and the palate, rupture, and leave sharply defined erosions that
are practically indistinguishable from those of PV or cicatricial pemphigoid (see Fig. 33-24).
However, erosions less painful and less extensive than in PV.
Diagnosis, see “Bullous Pemphigoid” in Section 6.
Figure 33-26. Bullous pemphigoid In the initial stages, bullae may be seen, which invariably rupture, leaving erosions that are difficult to distinguish from cicatricial pemphigoid or pemphigus vulgaris.
Cicatricial Pemphigoid (See Section 6)
ICD-9: 694.6 ° ICD-10: L12.1
Autoimmune mucosal blistering disease that heals with scarring.
Clinical manifestations dependent on sites involved. Persistent painful erosions on mucous membranes. Desquamative gingivitis with painful erosions on tongue, buccal, and palatal mucosa (Fig. 33-27). Ocular symblepharon and corneal scarring are feared complications. May be associated with malignancy, particularly if antibodies against epiligrin are noted.
Sequelae: decreased vision/blindness; hoarseness, upper airway compromise, esophageal stenosis.
Figure 33-27. Cicatricial pemphigoid. Gingivitis is seen, which outlines the junction with teeth. Mucosal disease is similar in bullous pemphigoid. (Courtesy of Dr. Sook-Bin Woo.)
Systemic Diseases Involving the Mouth
Behçet Disease. See above and Section 14.
Adverse Drug Reactions. See Section 23.
Lupus Erythematosus (See also Section 14)
ICD-9: 710.0 ° ICD-10: M32.9
Mucosal involvement occurs in approximately 25% of those with chronic cutaneous lupus erythematosus.
Findings: Lesions: painless erythematous patches to chronic plaques, sharply marginated, irregularly scalloped white borders, radiating white striae, and telangiectasia. In older lesions: central depression, painful ulceration.
Distribution: buccal mucosa; palate (Fig. 33-28), alveolar process, tongue. Chronic plaques may also appear on the vermilion border of the lips.
In acute systemic lupus erythematosus, ulcers arise in purpuric necrotic lesions of the palate (80%), buccal mucosa, or gums.
Figure 33-28. Lupus erythematosus: hard palate Erythematous eroded plaques were associated with chronic cutaneous LE.
Stevens-Johnson Syndrome/Toxic Epidermal Necrolysis (See also Section 8)
ICD-9: 695.15 ° ICD-10: L51.2
Idiopathic reaction to medications and occasionally viral agents that lead to epidermal necrosis and desquamation. It is essential to discontinue possible culprits as soon as possible. There is a better prognosis with culprit drugs of shorter halflife.
Classification schemes depend on extent of body surface area involved, but greater than 30% involvement generally agreed to be TEN with mucosal involvement.
Most common mucosal location affected is the oropharynx. Mucosal lesions can precede cutaneous involvement by 1-3 days. In the mouth, presenting symptoms are burning sensation of the mouth and decreased oral intake. Erosions are seen in up to 90% of cases. Desquamation can follow soon thereafter (Fig. 33-29).
Figure 33-29. Toxic epidermal Necrolysis Exuberant desquamation, pyoderma, and hemorrhage accompany oral pain on swallowing, a burning sensation, and, often, dysphonia.