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Introduction The mouth is the beginning of the aerodigestive tract and an extension of the skin barrier The oral mucosa, salivary glands, jawbones, and teeth are frequently the site of primary inflammatory or neoplastic disease However, the oral cavity may present with manifestations of systemic disease and in some cases, oral findings may precede systemic signs and symptoms by months or years Fitzpatrick’s dermatology of general medicine. 8 th ed. New York: Mcgraw-Hill 2012:

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Outline Introduction Evaluation of the patients Normal anatomic structures Ulcerative conditions White lesions Bullous disorders/red lesions Pigmented lesions Disorder of the lips Tongue lesions Introduction The mouth is the beginning of the aerodigestive tract and an extension of the skin barrier The oral mucosa, salivary glands, jawbones, and teeth are frequently the site of primary inflammatory or neoplastic disease However, the oral cavity may present with manifestations of systemic disease and in some cases, oral findings may precede systemic signs and symptoms by months or years Fitzpatricks dermatology of general medicine. 8 th ed. New York: Mcgraw-Hill 2012: Evaluation of the patients Taking note of where the lesions are located, and in particular, whether they are on the keratinized or nonkeratinized sites The presence or absence of saliva in the floor of mouth and whether the saliva is of the usual watery consistency or whether it is ropey The dentition and whether there are grossly carious teeth Evaluation of the patients The use of a removable prosthesis; this is particularly important for some mucosal diseases caused by denture trauma and for the diagnosis and treatment of candidiasis since the denture acts as a fomite Fordyce granules These are sebaceous glands that present as painless yellow papules, 12 mm in diameter located in a bilateral symmetric fashion on the posterior buccal mucosa, and lips (usually vermilion) Linea alba This is a linear keratosis located on the buccal mucosa bilaterally where the upper and lower teeth meet Palatal and mandibular tori These are benign, usually symmetric exostoses that are present in the midline of the hard palate or bilaterally on the lingual aspect of the mandible Fitzpatricks dermatology of general medicine. 8 th ed. New York: Mcgraw-Hill 2012: Ulcerative conditions Recurrent aphthous ulcers/stomatitis (Canker sores) Recurrent aphthous ulcers/stomatitis T-cell-mediated disorder and tumor necrosis factor (TNF)- Significant association with a number of HLA- haplotypes Stress, systemic illness, and local trauma predisposes to their occurrence in susceptible individuals Recurrent aphthous ulcers/stomatitis Clinical findings Idiopathic RAU occurs in 15%20% of the population Second decade of life and over the age of 50 Sensation of a small nodule beneath the epithelium before the ulcer appears The painful yellowwhite ulcers are surrounded by an erythematous halo Idiopathic RAU are almost always confined to the nonkeratinized mucosa Recurrent aphthous ulcers/stomatitis Clinical findings There are four clinical forms of RAU and these are always painful 1. Minor ulcers (1 cm lasting several weeks and healing with scarring) 3. Herpetiform ulcers ( 10 clustered ulcers at each episode, lasting 12 weeks) 4. Severe aphthous ulcers Recurrent aphthous ulcers/stomatitis DDx Related to a systemic disorder: Behcets disease An inflammatory disorder: EM, fixed drug eruption Traumatic lesions: mastication Herpetic ulcers: keratinized mucosa of the gingival margin and the palate Recurrent aphthous ulcers/stomatitis Lab Culture and biopsy are indicated in such patients Recurrent aphthous ulcers/stomatitis Management Bolognia JL, et al. Dermatology 3 rd ed. Elsevier 2012: Recurrent aphthous ulcers/stomatitis Management Since low-level laser therapy (LLLT) modulates inflammatory responses, and promotes pain reduction and cellular biostimulation LLLT can be suggested as an alternative for RAU treatment Scientific World Journal 2015: White lesions White sponge nevus Reactive white lesions Infectious lesions Oral lichen planus Contact stomatitis Leukoplakia and erythroplakia Oral squamous cell carcinoma White sponge nevus Extremely rare condition Autosomal dominant Affects the oral and genital mucosa, usually in a symmetric and often multifocal pattern Mutation in keratin K4 or K13 Usually within the first two decades of life White sponge nevus Patients develop poorly demarcated, diffuse, painless white plaques on the oral mucosa, usually the buccal mucosa and tongue White sponge nevus Biopsy or exfoliative cytology is always indicated and shows perinuclear eosinophilic condensations (representing abnormal keratin aggregation) There is no treatment, although some have reported resolution with antibiotics, in particular tetracycline Reactive white lesions Leukoedema Contact desquamation Morsicatio mucosae oris (pathominia mucosae oris, chronic bite injury) Benign Alveolar Ridge Keratosis (BARK, oral lichen simplex chronicus) Nicotine stomatitis Reactive white lesions Leukoedema Occurs in 20%70% with habits such as using tobacco, coca, marijuana Usually bilateral on the buccal mucosa or ventral tongue Painless, fine grayish white, opalescent reticulations Reactive white lesions Leukoedema A biopsy shows typical findings of keratinocyte edema or hydropic degeneration No treatment, advice on smoking cessation Reactive white lesions Contact desquamation The injury to the tissue is slightly more severe than in leukoedema The offending agents are mouthwashes and toothpastes that are caustic Painless sloughs of desquamated tissue Reactive white lesions Contact desquamation A biopsy shows desquamating strips of surface keratinocytes Discontinue the use of the offending dentrifrice Reactive white lesions Morsicatio mucosae oris (pathominia mucosae oris, chronic bite injury) Chewing habit It occurs in 3% of the population White papules and plaques on either side of the linea alba on the buccal mucosa Reactive white lesions Benign Alveolar Ridge Keratosis (BARK, oral lichen simplex chronicus) It occurs primarily on the keratinized mucosa of the gingiva and hard palate as a reaction to frictional trauma Poorly demarcated, painless white papules and plaques A biopsy shows typical features of LSC No treatment is necessary Reactive white lesions Nicotine stomatitis Not caused by nicotine By heat, usually from pipe smoking The palate: most site affected Diffusely white with red, punctuate areas Reactive white lesions Nicotine stomatitis A biopsy shows hyperkeratosis with benign epithelial changes Lesions may resolve if the habit is discontinued Infectious lesions Candidiasis The most common causative agent is Candida albicans In immumnocompromised hosts, other species such as C. tropicalis, C. dubliniensis, C. glabrata, and C. kruseii should also be considered Predisposing factors include hyposalivation, immunocompromise, topical steroid therapy, and antibiotic therapy Infectious lesions Fitzpatricks dermatology of general medicine. 8 th ed. New York: Mcgraw-Hill 2012: Infectious lesions Candidiasis A potassium hydroxide preparation using scrapings from oral lesions Infectious lesions Hairy leukoplakia EpsteinBarr virus (EBV) infections (infectious mononucleosis) Painless, white plaque Lateral border of the tongue Immunocompromised patients, HIV/AIDS Infectious lesions Hairy leukoplakia Both cytologic smears and biopsies show characteristic findings and the presence of EBV can be confirmed by in situ hybridization In HIV/AIDS usually associated with a low CD4 count and high viral load Treatment with antiretroviral therapy results in resolution Infectious lesions Hairy leukoplakia Podophyllin with acyclovir cream was found to be effective, causing regression of lesions with no recurrences World J Clin Cases 2014 Jul 16; 2(7): Oral lichen planus Immune-mediated disorder T-cell destruction of the basal cells of the epithelium Interferon- production is thought to mediate lesions involving the oral cavity only while TNF- may mediate systemic disease Medications implicated in the development of oral LP include antihypertensive agents (especially hydrochlorthiazide), some hypoglycemic agents, allopurinol, sulfasalazine, carbamazepine Oral lichen planus Clinical findings Three clinical forms are noted: keratotic/reticular, erythematous/erosive, and ulcerative The most recognizable is the keratotic/reticular form (Wickham striae) Oral lichen planus Lab Diagnostic histopathologic findings for oral LP, are squamatization of basal cells and a lymphocytic band at the interface Direct immunofluorescence studies show shaggy fibrinogen and often IgM at the interface and IgM staining of colloid bodies Oral lichen planus Management Pain control Topical steroids Anti-inflammatory agents It appears that topical tacrolimus is an effective alternative to topical clobetasol and may be considered as a first-line therapy in the management of OLP Int J Dermatol 2015 Jul 23. Contact stomatitis Cinnamon flavoring and dental amalgam (silver- containing filling material) may cause lichenoid changes of the oral mucosa Red, white or mixed lesions are seen, with varying degrees of erosion, ulceration or striae formation Lesions may be located where the offending agent contacts the mucosa for a prolonged period of time Contact stomatitis Bolognia JL, et al. Dermatology 3 rd ed. Elsevier 2012: Contact stomatitis Contact stomatitis from dental amalgam occurs mainly at sites adjacent to amalgam restorations, such as the posterior buccal mucosa The lesions may be white or erythematous, with or without peripheral striae Contact stomatitis Biopsy specimens of contact stomatitis from dental amalgam or cinnamon flavoring often demonstrate a lichenoid mucositis When contact stomatitis secondary to amalgam is suspected, patch testing is recommended and should include organic and inorganic mercury as well as amalgam and the other dental metals Contact stomatitis Investigation of contact allergy to dental materials by patch testing Twenty patients who had undergone dental procedures with symptoms of oral lichen planus, oral stomatitis, burning mouth, and recurrent aphthosis, were included in the study Dental personnel with history of hand dermatitis were also included in the study Indian Dermatol Online J 2014 Jul-Sep; 5(3): 2826. Contact stomatitis Investigation of contact allergy to dental materials by patch testing Six patients with stomatitis, lichenoid lesions, and oral ulcers showed positive patch tests to a variety of dental materials Seven patients with ulcers had negative patch tests Seven dental personnel with hand dermatitis showed multiple allergies to various dental materials, and most had multiple positivities Indian Dermatol Online J 2014 Jul-Sep; 5(3): 2826. Contact stomatitis Investigation of contact allergy to dental materials by patch testing The patch test is a useful, simple, noninvasive method to detect contact allergies among patients and among dental personnel dealing with these products Indian Dermatol Online J 2014 Jul-Sep; 5(3): 2826. Contact stomatitis The offending restoration may be treated conservatively Alternative dental materials, such as composite (a white plastic-like material), gold or porcelain fused to metal, can be used to replace the amalgam restoration Leukoplakia Leukoplakia is the most common premalignant condition of the oral cavity Leukoplakia is strongly associated with smoking and/or alcohol ingestion Leukoplakia Painless, white plaque Common sites of involvement include the floor of the mouth, the lateral and ventral surfaces of the tongue, and the soft palate Leukoplakia Biopsy is mandatory in order to assess the degree of dysplasia and to exclude invasive SCC Leukoplakia in low-risk sites (buccal mucosa, labial mucosa, hard palate) may warrant periodic clinical evaluation, with cessation of any potentially carcinogenic habits Moderate or severely dysplastic lesions often require complete removal and continued monitoring Oral squamous cell carcinoma Risk factors include smoking cigarettes, excessive use of alcohol, a past history of cancer and/or immunosuppression, family history of cancer, exposure to high-risk forms of human papilloma virus (HPV), age, sunlight Oral squamous cell carcinoma The most common sites are the tongue and floor of mouth A nonhealing ulcer or ulcerated nodule, or a mass Oral squamous cell carcinoma A biopsy shows a proliferation of malignant epithelial cells infiltrating the stroma Most Stage I and II lesions are treated with surgical excision Stage III and IV tumors may be treated with surgery, radiation or chemoradiation Five-year survival for patients with local disease only, locoregional disease and distant metastases are 81%, 50%, and 14%, respectively Bullous disorders/red lesions Mucous membrane pemphigoid Pemphigus Lupus erythematosus Mucous membrane pemphigoid Heterogeneous group of disorders characterized by subepithelial blistering The most common presentation for mucous membrane pemphigoid is desquamative gingivitis Mucous membrane pemphigoid The presence of linear IgG, IgA, and/or C3 at the basement membrane zone on direct immunofluorescence testing Rx: topical steroid gel twice a day Prednisone and dapsone may be used if lesions are recalcitrant Azathioprine and cyclophosphamide are also effective in some cases Chronic and rarely remits completely Pemphigus The oral cavity may be involved by pemphigus vulgaris and paraneoplastic pemphigus The antigen is desmoglein 3 Patients may present with lesions in the mouth before developing skin lesions Oral lesions are denuded and erythematous, painful, and slightly depressed involves mucosal sites Pemphigus The biopsy for pemphigus vulgaris shows suprabasilar acantholysis and direct immunofluorescence studies show intercellular deposition of IgG Paraneoplastic pemphigus shows deposition of IgG and C3 both intercellularly and at the basement membrane zone Treatment for pemphigus vulgaris is with topical steroids in mild cases More severe cases: prednisone and MMF Lupus erythematosus Patients may present with erythematous and eroded mucosa, especially on the buccal mucosa and palate with a hint of white reticulations Ulcers may be present Lupus erythematosus The biopsy shows an interface stomatitis with linear IgG deposition along the basement membrane zone on direct immunofluorescence The mainstay of treatment is topical steroid therapy Pigmented lesions Amalgam tattoo Physiologic pigmentation (racial pigmentation) Postinflammatory hypermelanosis Medication-induced hyperpigmentation Nevomelanocytic nevi melanoma Amalgam tattoo Dental amalgam restorations are primarily composed of silver and mercury A discrete, nontender, slate-gray, or black macule of the oral mucosa that is usually less than 1 cm Physiologic pigmentation Dark-skinned patients Asymptomatic diffuse, even or patchy, brown to-black macular pigmentation of the oral mucosa and in particular the attached gingiva The biopsy shows the presence of melanin within basal cells Postinflammatory hypermelanosis LP is often associated with postinflammatory hypermelanosis and the pigmentation underlies the reticulations of the disease No treatment is necessary Medication-induced hyperpigmentation The most common site of pigmentation caused by minocycline and antimalarial medications is the palatal mucosa A slate-gray to blue diffuse macular discoloration and asymtomatic Discontinuation of the drug may or may not result in eventual complete resolution of the lesion Nevomelanocytic nevi The most common location is the palate (40%) followed by the buccal mucosa (19%) Intramucosal and compound nevi tend to be nodular, while junctional and blue nevi tend to be macular In general, nodular lesions are excised or shaved Melanoma Fifth to seventh decades of life A male predilection Usually evolve from preexisting dysplastic melanocytic lesions The most common site is the palate or maxillary gingiva A biopsy shows an invasive proliferation of melanocytes from an intraepithelial component Melanoma Five-year survival is approximately 20%30% Excision with clear margins is the treatment of choice Surgery with radiotherapy greatly reduces local relapse and metastasis to lymph nodes Disorder of the lips Actinic cheilitis Cheilitis granulomatosa (orofacial granulomatosis) Angular cheilitis Exfoliative cheilitis Actinic cheilitis Atrophy of the lips caused by actinic damage Precancerous lesion Predominantly involving the lower lip Presents as single or multiple crusted or scabbing, slightly scaly lesions and plaques on the vermilion of the lip Lesions may be surgically excised, treated with cryotherapy or carbon dioxide laser Actinic cheilitis Photodynamic therapy is safe and has the potential to clinically and histologically treat AC, with a need for future randomized controlled trials Dermatol Surg 2015 Feb; 41(2): Cheilitis granulomatosa Noninfectious granulomatous diseases The term Melkersson Rosenthal syndrome refers to the triad of fissured tongue, facial palsy, and cheilitis granulomatosa Painless swelling of the lip Cheilitis granulomatosa Biopsy reveals the presence of nonnecrotizing granulomas without foreign material or identifiable infectious agent Rx: intralesional steroid injections Angular cheilitis In most cases, this represents a form of candidiasis Drooping of the corners of the mouth with drooling and retention of saliva in the creases leading to candidiasis, often associated with wearing of full dentures Angular cheilitis There is painful, usually bilateral maceration of the corners of the mouth with ulceration, crusting, cracking, and, in severe cases, fissuring Rx: antifungal creams with topical steroid therapy Exfoliative cheilitis A rare inflammatory condition of the lip Associated with factitial injury and lip licking The lips may also appear cracked and fissured A biopsy shows parakeratosis, acanthosis, and chronic inflammation Some patients have been at least partially successfully treated with antidepressants Other treatment modalities include mupirocin and tacrolimus Tongue lesions Atrophic glossitis Hairy tongue (black hairy tongue, coated tongue) Fissured tongue Benign migratory glossitis/stomatitis (geographic tongue) Clinical macroglossia Hyperplastic lingual tonsil Atrophic glossitis Often seen in hematinic deficiencies and in patients with prolonged hyposalivation The tongue presents with a smooth, bald appearance and papillae are atrophic Atrophic glossitis Patient should have blood work to rule out hematinic deficiencies, in particular iron and vitamins B6 and B12 deficiency Treatment is with repletion of deficient elements Topical anesthetics help to control symptoms Hairy tongue There is generally an antecedent history of illness and antibiotic use Caused by retention of keratinaceous debris on the tongue dorsum The tongue presents with a matted or coated appearance Hairy tongue Vigorous hydration and return to a normal diet with fresh fruits and vegetables generally resolve the lesions The tongue may be brushed as part of the daily oral hygiene regimen to help to dislodge loose keratin squames and reduce discoloration Fissured tongue The term Melkersson Rosenthal syndrome refers to the triad of fissured tongue, facial palsy, and cheilitis granulomatosa Asymptomatic Do not require therapy A permanent condition Geographic tongue There is an area of atrophy of the tongue dorsum leading to loss of filiform papillae and a slightly depressed erythematous area Approximately 13% of patients with psoriasis 2% viscous lidocaine may reduce symptoms Clinical macroglossia Diffuse enlargement of the tongue Aging or with some systemic conditions such as amyloidosis For patients with amyloidosis, a work-up for plasma cell dyscrasia is indicated Hyperplastic lingual tonsil The lingual tonsil is located on the posterolateral aspects of the tongue Inflammation of this tissue from trauma or URI leads to hyperplasia Excision is curative