White Lesions
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Table of Contents
- Actinic cheilitis
- Candidiasis
- Fordyce’s Granules
- Geographic tongue
- Hairy leukoplakia
- Hairy tongue
- Leukoedema
- Leukoplakia
- Proliferative Verrucous Leukoplakia (PVL)
- Lichen Planus (Wickham striae)
- Drug-induced lichen planus (Lichenoid drug eruptions)
- Morsicatio (cheek or lip chewing)
- Smokeless tobacco keratosis
- White Sponge Nevus
ACTINIC CHEILITIS
Actinic cheilitis (solar cheilitis or actinic cheilosis) is a precancerous condition that can create rough, scaly patches on the vermillion border of the patient’s lips. Sometimes known as “farmer’s lip” or “sailor’s lip”, solar cheilitis is caused by excessive exposure to solar (UV) radiation. Fair-skinned individuals are more likely to be affected. If left untreated, actinic cheilitis may transform into cutaneous actinic keratosis and/or squamous cell carcinoma. The common clinical presentation includes:
- Pale irregularly keratotic surface with red (atrophic) regions.
- Mature lesions can appear scaly, crusted and indurated.
- Ulcerations or erosions strongly indicate progression to malignancy.
Diagnosis is based on the lesion history, clinical presentation and microscopic findings, which may include:
- Hyperkeratosis (increased thickness of the stratum corneum).
- Epithelial atrophy with variable degrees of epithelial dysplasia.
- Telangiectasia (small, widened blood vessels on the skin).
Your differential diagnosis should include:
- Exfoliative cheilitis.
- Squamous cell carcinoma.
Treatment options include:
- Sunscreens and reduced UV exposure to prevent further damage.
- Excisional biopsy that confirms diagnosis and prevents progression.
- CO2 laser vermilionectomy.
- Topical 5-fluorouracil.
The prognosis for actinic cheilosis is relatively good. Around 10% develop into squamous cell carcinoma, which grows slowly and metastasis occurs late.
CANDIDIASIS
Candidiasis is an often painless fungal infection caused by a yeast of the Candida species. Candida albicans is an opportunistic pathogenic yeast commonly found as part of the human gut flora of adults. In health candidiasis is rare. Infection is usually associated with predisposing factors such as immunosuppression, diabetes mellitus, antibiotic or steroid use, or xerostomia. Infections may be acute or chronic. The common clinical presentation includes:
Acute:
- Pseudomembranous candidiasis (thrush) is characterized by extensive white plaques consisting of desquamated epithelial cells, fibrin, and fungal hyphae.
- Erythematous candidiasis (atrophic) is the only form of candidiasis associated with pain and has been known as ‘antibiotic sore mouth’ due to its association with prolonged use of broad-spectrum antibiotics. Acute atrophic candidiasis appears as red lesions and is usually seen on the dorsum of the tongue in persons taking long term corticosteroids or antibiotics (depapillated areas).
Chronic:
- Erythematous candidiasis (atrophic) is the only form of candidiasis associated with pain. Chronic atrophic candidiasis is more strongly associated with old, poor fitting dentures or poor oral hygiene practices (denture sore mouth).
- Hyperplastic candidiasis is also termed “plaque-like candidiasis” or “nodular candidiasis”, presenting with rough or nodular texture.
- Median rhomboid glossitis is a variation of hyperplastic candidiasis seen on midline dorsum of tongue anterior to circumvallate papillae.
- Angular cheilitis (Perlèche or angular cheilosis) is a superficial inflammatory condition of the labial commissure which is strongly associated with candidiasis.
Diagnosis is based on the lesion history, clinical presentation and microscopic findings, which may include:
- Positive indication of hyphae or fungal growth from a potassium hydroxide preparation, periodic acid–Schiff (PAS) stain, or culture on proper medium (Sabouraud’s, corn meal, potato agar etc.).
- Direct microscopic examination of samples (e.g., oral swabs, vaginal secretions) to identify Candida cells.
- Culture of samples on specific media to isolate and identify Candida species.
- Blood cultures for diagnosing invasive candidiasis, although these can take up to four weeks.
- Non-culture methods such as antigen and antibody detection, beta-D-glucan assay, and the T2Candida panel for rapid diagnosis.
- Molecular diagnostic methods like Polymerase Chain Reaction (PCR) for early detection of invasive candidiasis.
Your differential diagnosis should include:
- Allergic contact stomatitis.
- Atrophic lichen planus.
Treatment options include:
- Addressing predisposing factors.
- Antifungal medications, with azoles (e.g., fluconazole) being the most commonly used drugs for both oral and systemic infections.
- Echinocandins, recommended for candidemia and invasive candidiasis.
- Topical antifungals such as nystatin, miconazole nitrate, or clotrimazole creams for cutaneous candidiasis.
The prognosis for candidiasis varies depending on the type and severity of the infection, as well as the patient’s overall health. Superficial infections like oral thrush or vaginal candidiasis generally respond well to treatment. However, invasive candidiasis can be life-threatening, particularly in individuals with compromised immune systems
FORDYCE'S GRANULES
Fordyce’s Granules are painless small pimple-like structures caused by the presence of ectopic sebaceous glands within the oral mucosa and vermilion portion of the lips. The common clinical presentation includes:
- Bilateral areas scattered with yellowish-to-pink maculopapular granules.
- Usually located on the buccal mucosa, but may also be found on the vermilion of lips.
- Spots ranging from 1 to 5 millimeters in diameter.
- Appearance as solitary lesions or in clusters, often numbering between 50 to 100 spots.
- More pronounced visibility when the skin is stretched
-
Asymptomatic nature, causing no pain, itching, or discomfort.
Diagnosis is usually based on the lesion history and clinical presentation alone. If a biopsy is indicated, microscopic findings may include:
- Normal sebaceous glands.
- Lack of hair follicles.
Your differential diagnosis should include:
- Sexually transmitted infections (STIs) such as genital warts or molluscum contagiosum.
- Sebaceous hyperplasia, involving the enlargement of sebaceous glands on the face.
- Epidermoid cysts, which are benign cysts filled with keratin.
- Genital lichen planus, an inflammatory condition causing flat-topped, violaceous papules.
- Candidiasis.
No treatment is required and the lesions are simply monitored. The prognosis for Fordyce’s granules is excellent. They are benign and asymptomatic, posing no health risks or requiring medical treatment. However, some individuals may seek treatment for cosmetic reasons.
GEOGRAPHIC TONGUE
Geographic tongue (migratory glossitis, erythema migrans) is a distinct condition appearing as a map-like pattern on the dorsum of the patient’s tongue. It is caused by the loss of dorsal papillae, but the reason for depapillation is not well understood. The common clinical presentation includes:
- Focal red depapillated areas bordered by yellowish margins.
- Areas of depapillation may migrate over time.
- Can be associated with fissured (scrotal) tongue.
- Primarily affects the dorsum (top) and lateral borders of the tongue, but can occasionally appear on other mucosal sites, such as the floor of the mouth and cheek mucosa.
- Some individuals may experience mild discomfort or a burning sensation, particularly when consuming spicy, acidic, or hot foods.
- Many cases are asymptomatic, with individuals only becoming aware of the condition during routine dental or medical examinations.
Diagnosis is usually based on the lesion history and clinical presentation alone. Your differential diagnosis should include:
- Lichen planus.
- Lupus erythematosus.
- Candidiasis.
- Psoriasis.
The condition is benign and self-limiting. Topical corticosteroids may be appropriate if the lesion is symptomatic.
HAIRY LEUKOPLAKIA
Hairy leukoplakia is a distinct inflammatory reaction of the tongue strongly associated with an Epstein-Barr virus infection. It is most often seen in patients who are immunocompromised (e.g. AIDS) and could be a herald for an undiagnosed systemic condition. The common clinical presentation includes:
- A characteristic corrugated or shaggy appearance on the lateral border of the tongue.
- Early lesion – fine white vertical streaks.
- Mature lesion – may be thickened to be plaque-like.
- Extensive lesions may involve the dorsum of tongue and buccal mucosa.
Diagnosis is based on the lesion history, clinical presentation and microscopic findings, which may include characteristic EBV nuclear inclusions within the superficial keratinocytes. Your differential diagnosis should include:
- Frictional hyperkeratosis.
- Lichen planus.
- Hyperplastic candidiasis.
Treatment is not necessary, but antiviral therapies (acyclovir) may be appropriate to improve aesthetics.
HAIRY TONGUE
Hairy tongue describes an abnormal pigmented coating of the dorsal surface of the tongue, caused by elongated/hypertrophied filiform papillae. Hairy tongue may be linked to poor oral hygiene, soft diet, heavy smoking, radiation therapy, xerostomia, or medications including antipsychotics, methyldopa, lansoprazole, interferon, antidepressants, antineoplastics, and antibiotics (cephalosporins, penicillins, tetracyclines, and clarithromycin). The common clinical presentation includes:
- A furry or hairy appearance with dark/black pigmentation.
- Yellow, green, and blue appearances have also been reported.
- Asymptomatic, but may cause gagging or a tickling sensation.
Diagnosis is usually based on the lesion history and clinical presentation alone. The distinct clinical presentation likely means there is no differential diagnosis. Treatment options include:
- Daily physical debridement.
- Topical podophyllin (resin made from the roots of the American mandrake).
- Elimination of cause.
LEUKOEDEMA
Leukoedema is an asymptomatic lesion commonly seen on buccal oral mucosa and usually found incidentally during a routine oral examination. The appearance may be due to intracellular edema and/or the retention of superficial parakeratin. Leukoedema is common and may in fact be a variation of the normal tissue appearance rather than a disease. It may be more commonly seen in patients who smoke or who are of African-American descent. The common clinical presentation includes:
- White or whitish-gray edematous lesion of the buccal (or labial) oral mucosa.
- Wrinkled surface when tissue is at rest but slowly disappears when stretching the mucosa.
- Symmetrical distribution.
Diagnosis is usually based on the lesion history and clinical presentation alone. Your differential diagnosis should include:
- Cheek chewing (Morsicatio, traumatic hyperkeratosis).
- Leukoplakia.
- Hereditary benign intraepithelial dyskeratosis.
- White sponge nevus.
- Lichen planus.
- Candidiasis.
No treatment is required and lesions are simply monitored.
LEUKOPLAKIA
Leukoplakia describes a potentially malignant disorder that appears as an idiopathic white plaque. It is usually the diagnostic term used when other specific conditions have been ruled out. The most important biological element of oral leukoplakia involves its malignant potential. Leukoplakia is analogous to the term erythroplakia (red patches). The common clinical presentation includes:
- White or gray patches are most common, but can present as white-red (erythroleukoplakia).
- Usually seen on the lip, gingiva, and buccal mucosa.
- Increased risk of dysplasia/carcinoma when seen on the tongue, floor of the mouth, or vermilion portion of the lip.
- Clinical subsets include homogeneous leukoplakia, verrucous leukoplakia, speckled leukoplakia, and proliferative verrucous leukoplakia.
- Dynamic lesions that may advance or regress unpredictably.
- Dysplasia or malignancy may occur with little or no change in clinical appearance.
A biopsy is mandatory. Multiple biopsies of large lesions are needed due to the microscopic heterogeneity within a single lesion. Diagnosis is based on the lesion history, clinical presentation and microscopic findings, which may include:
- Hyperkeratosis and acanthosis of the epithelium.
- Chronic inflammatory infiltrates within the lamina propria.
- Various degrees of epithelial dysplasia, which may include:
- loss of basal cell polarity.
- increased nuclear-cytoplasmic ratio.
- irregular epithelial stratification.
- increased number of abnormal mitotic figures.
- cellular and nuclear pleomorphism.
- keratinization of single cell groups.
Because of the variability in appearance there are many visually similar lesions. Your differential diagnosis should include:
- Lichen planus or lichenoid lesions.
- Frictional keratosis.
- Hyperplastic candidiasis.
- White sponge nevus.
- Dyskeratosis.
Treatment options include:
- Excision modalities (surgery, laser ablation, cryosurgery).
- Photodynamic therapy.
- Topical cytotoxic drugs like bleomycin (glycopeptide antibiotic).
Unfortunately, recurrence is common following apparent complete excision and the long term prognosis is guarded.
PROLIFERATIVE VERRUCOUS LEUKOPLAKIA (PVL)
Proliferative Verrucous Leukoplakia (PVL) is a rare but particularly aggressive clinical variant of oral leukoplakia. It is associated with a high probability of recurrence and a malignant transformation rate exceeding 70%. Tobacco use does not seem to have a significant influence on the appearance or progression of PVL, with the condition seen in both smokers and nonsmokers. There may be a link with human papillomavirus (HPV 16 and 18). The common clinical presentation includes:
- Slow progression and persistence.
- Early lesion – flat white plaque appearing as hyperkeratosis.
- Mature lesion – a multifocal, exophytic and proliferative lesion.
- Surface may be friable.
Diagnosis is based on the lesion history, clinical presentation and microscopic findings, which may include:
- Epithelial hyperplasia and hyperkeratosis.
- Atypical papillary-verrucal proliferation.
- Less differentiated oral squamous cell carcinoma.
Your differential diagnosis should include:
- Idiopathic leukoplakia.
- Oral warts or condyloma.
- Verrucous squamous cell carcinoma.
Treatment options include:
- Mucosal stripping or excision for immature lesions.
- Surgical excision with wide margins for advanced lesions.
- Laser ablation for benign or atypical lesions.
- Systemic retinoids to control keratosis.
Prognosis is poor for this seemingly harmless-appearing white lesion since it frequently progresses to carcinoma.
LICHEN PLANUS
Lichen Planus (Wickham striae) is a chronic inflammatory autoimmune disease that can affect the skin, nails, hair and mucous membranes. Oral lichen planus affects 3-4% of the population and is typically characterized by the presence of distinct reticular white lesions. The cause is not well understood but thought to involve the targeting of basal keratinocytes by activated T Cells. Clinical variations include erosive/ulcerative, papular, plaque-like, atrophic and bullous lesions. Multiple types may be found in the same patient and even in the same lesion. The common clinical presentation includes:
- Asymptomatic reticular lace-like patterns is the most common appearance.
- Most often located on the buccal mucosa, then tongue, gingiva and lips.
- Bilateral, often symmetrical distribution.
- Erosive or atrophic pattern can present with symptoms (pain or burning)
- Extra-oral lichen planus may accompany oral presentation (planar (flat-topped), purple, polygonal, pruritic, papules, and plaques).
- Higher incidence in white females and more likely in the fourth to eighth decade.
Diagnosis is based on the lesion history, clinical presentation and microscopic findings, which may include:
- Hyperkeratosis.
- Liquefactive degeneration of the basal layer of the epithelium.
- Presence of Civatte bodies (apoptotic keratinocytes).
- Band-like appearance of inflammatory infiltrate (lymphocytes) in the mucous membranes beneath the epithelium.
- No epithelial dysplasia.
- Saw tooth rete ridges.
Your differential diagnosis should include:
- Lichenoid drug reactions.
- Lupus erythematosus.
- Mucous membrane pemphigoid.
- Erythema multiforme.
- Contact stomatitis.
Reticular oral lichen planus does not require treatment and does not progress to a more serious disease. For symptomatic lesions, immune-suppressing agents can be utilized. Treatment options include:
- Topical corticosteroids for mild to moderate cases.
- Systemic prednisone for more severe cases.
- Topical tacrolimus ointment.
Though treatment does not provide a cure, long term control can be established. The prognosis is generally good with very rare malignant transformation.
DRUG-INDUCED LICHEN PLANUS
Drug-induced lichen planus (Lichenoid drug eruptions) is caused by a hypersensitivity to medications or industrial by-products, and presents with a similar appearance to lichen planus. Common drugs linked with lichenoid reactions include sulfasalazine, carbamazepine, angiotensin converting enzyme (ACE) inhibitors, interferon alpha, antihistamines, nonsteroidal anti-inflammatory drugs, β-blockers, gold, antimalarials, proton pump inhibitors and sulfonylurea compounds. The common clinical presentation includes:
- White striae or papules.
- Possible ulceration with associated tenderness/pain.
- Most commonly seen on the buccal mucosa and attached gingiva.
Patch testing may be performed to confirm contact allergens. Diagnosis is based on the lesion history, clinical presentation and microscopic findings, which may include:
- A dense, band-like lymphocytic infiltrate in the dermis.
- Cytoplasmic vacuolization (formation of vacuoles) of basal keratinocytes.
- Apoptotic keratinocytes that degenerate into colloid bodies (Civatte bodies).
- See “lichen planus” above.
Your differential diagnosis should include:
- Lichen planus.
- Leukoplakia.
- Dysplasia or carcinoma.
Treatment options include:
- Identification and elimination of predisposing factor(s).
- Finding an alternative medication.
- Topical corticosteroid or tacrolimus application.
MORSICATIO
Morsicatio (cheek or lip chewing) is caused by chronic low-grade trauma to oral soft tissues. The common clinical presentation includes:
- White hyperkeratotic surface.
- Granular or macerated appearance.
- Lesion in an area where teeth can get to it.
Diagnosis is usually based on the lesion history and clinical presentation alone. Your differential diagnosis should include:
- Leukoedema.
- Leukoplakia.
- Lichen planus.
- Lichenoid tissue reactions.
The only treatment generally required is the elimination of the habit. Prognosis is excellent.
SMOKELESS TOBACCO KERATOSIS
Smokeless tobacco keratosis describes a keratotic change in the oral mucosa where smokeless tobacco products are placed. It is usually seen in the lower buccal vestibule or buccal mucosa (chewing tobacco). Irritant contact stomatitis can be caused by any chemical products used, including toothpastes, mouthwashes, and dental restorations. The common clinical presentation includes:
- Early lesion – filmy white to gray opalescent surface.
- Mature lesion – more keratotic white, fissured appearance and thickening of the epithelium.
Diagnosis is based on the lesion history, clinical presentation and microscopic findings, which may include:
- Hyperkeratosis with parakeratotic “chevron sign” on the surface.
- Increased vascularity.
- Hyalinization in submucosa and minor salivary glands.
- Epithelial dysplasia and carcinoma may be visible.
Your differential diagnosis should include:
- Idiopathic leukoplakia.
- Chemical or thermal burn.
- Frictional keratosis.
Treatment options include:
- Identification and elimination of predisposing factor(s).
- Excision or stripping of mucosal site if dysplasia present.
The prognosis is usually good if the patient stops the habit.
WHITE SPONGE NEVUS
White Sponge Nevus is a rare benign inherited condition characterized by the formation of white or gray diffuse patches called nevi (singular: nevus). It is caused by mutations in the cytokeratin 4 and cytokeratin 13 genes, resulting in keratin instability and tonofilament aggregation. The common clinical presentation includes:
- Lack of symptoms.
- Thickened, velvety, sponge-like tissues that do not disappear when the oral mucosa is stretched.
- Most commonly affected intraoral site is the buccal mucosa.
Diagnosis is based on the lesion history, clinical presentation and microscopic findings, which may include:
- Parakeratosis.
- Acanthosis with intracellular edema.
- Eosinophilic deposition of tonofilaments.
- Perinuclear condensation of keratin.
Your differential diagnosis should include:
- Idiopathic leukoplakia.
- Chemical or thermal burn.
- Chronic low-grade trauma (morsicatio).
No treatment is required. There is no malignant potential and the prognosis is excellent.
