Oral Nevi


Background

In 1943, Field and Ackermann described the features characteristic of intraoral nevi. [1Oral melanocytic nevi are benign proliferations of nevus cells in the epithelial layer, the submucosal layer, or both. As such, they are classified as junctional, intramucosal, and compound nevi. Nevi may also be classified as congenital or acquired. Unlike their cutaneous counterparts, oral melanocytic nevi are rare.

Intramucosal nevi are typically light brown and dome-shaped. These are the most common type, accounting for 64% of all reported oral nevi. [2Note the image below.

Intramucosal nevus on the lower lip. This brown paIntramucosal nevus on the lower lip. This brown papule measured 0.6 cm in diameter and was only slightly raised. Melanotic macules are invariably flat.

The common blue nevus is the second most common type found in the oral cavity, accounting for 16.5-36% of all oral nevi. [3Note the image below.

Blue nevus on the gingiva. This 1-cm saucer-shapedBlue nevus on the gingiva. This 1-cm saucer-shaped tan macule on the gingiva has histologic features consistent with those of a blue nevus, which is the second most common type of oral nevus. This location is atypical because most blue nevi occur on the palate.

Junctional and compound nevi are uncommon, accounting for only 3-6% and 5.9-16.5%, respectively. [245]

Rarer types include Spitz nevi, cellular blue nevi, congenital nevi, combined nevi, balloon cell nevi, epithelioid blue nevi, plaque-type blue nevi, halo nevi, and neurotized nevi. [6789101112131415161718192021222324252627Dysplastic nevi have not been reported in the oral mucosa.

Pathophysiology

Nevus cells are derived from the neural crest. These cells migrate to the skin and oral mucous membranes during embryogenesis. Nevus cell formation probably begins with the proliferation of melanocytes along the basal cell layer and is possibly associated with elongation of the rete ridges. Nevus cells either lack contact inhibition or lose it shortly after the proliferation process begins. They retain melanin pigment and form nests or thèques.

Nevus cells have the ability to migrate from the basal cell layer into the underlying submucosa. Eventually, they may separate from the epidermis. Junctional nests may be lost later, and nevus cells may be confined to the submucosa. As the nevus cells penetrate into the submucosa, their pigmentation diminishes.

Genetic analysis has revealed V600E point BRAF mutation in both oral benign and malignant melanocytic lesions. [28]

Epidemiology

Frequency

The incidence is 0.1-1.15% in the United States. [2930Lesions may be underreported because they often go undetected.

Race

Oral nevi may occur in persons of all races. They are reported more frequently in white patients (55%) than in black patients (23%). [29The apparent predominance of oral nevi in whites over Asians (14%) and Hispanics (7%) may be due to the over-representation of this group among patients who underwent biopsies. [31]

Sex

Oral mucosal nevi have a slight female predominance (1.5:1 female-to-male ratio), except for the blue nevi type, which occurs equally in both sexes. [4]

Age

The average age at diagnosis is 35 years (range, 3-85 y). [4Male patients tend to be a few years older than female patients. Patients with junctional and compound nevi are relatively younger, with an average age at diagnosis of 22 and 24 years, respectively.

Prognosis

Reports mainly based on case reports and case series have shown that the prognosis for oral melanocytic nevi is excellent. [32Only one case of recurrence, in a compound nevus, has been reported. [33No documented cases of malignant transformation were reported in a cohort of intraoral nevi with up to 2-8 years of follow-up. [213234However, histologic sampling is essential in all oral melanocytic nevi, especially when located in the palate, the most common site of oral melanoma, to exclude and presumably prevent such transformation.

Patient Education

Patients should be instructed to observe and report any lesion in the oral cavity, especially those that change in size, that change in color, have nodularity, bleed, and/or ulcerate.

CLINICAL PRESENTATION


History

Most oral nevi are solitary and asymptomatic. Congenital melanocytic nevi are present at birth or appear shortly after. Acquired melanocytic nevi begin to appear in early childhood. The lesions are usually detected as an incidental finding on routine dental examination.

Of patients with recorded complaints, 22% described a mass, growth, or pigmented spot. [35A minority of patients complained of soreness or pain related to another cause, such as an ill-fitting denture. Less than 1 in 10 patients were aware of evolving lesions. Most patients could only speculate about the duration of their condition.

Physical Examination

Benign oral nevi present as asymptomatic, well circumscribed, round or oval macules or papules with smooth surface that range in color from light brown to black. [36These lesions may rarely present as epulislike swelling of the gingiva and as a hamartoma on the palate, composed of nevus cells, hyperplastic salivary gland tissue, adipose tissue, nerves, and vessels. [3738Oral nevi usually occur as solitary lesions; however, one case of multiple intraoral nevi has been described in the literature. [39Intramucosal nevi and rarely Spitz nevi may be nonpigmented or amelanotic 15-22% of the time and present as sessile growths that resemble fibromas or papillomas. [73538]

The average size of an oral nevus is 0.3-0.5 cm at the largest diameter. [2930Blue nevi are smaller than intramucosal nevi. Larger nevi (>6 mm) are more likely to be congenital.

Intraoral melanocytic nevi most commonly occur on the hard palate, followed by the buccal mucosa. Rarely, the tongue, floor of the mouth, [640and pharynx may be involved. [21The distribution varies depending on the histologic type of the nevus. The hard palate is the most common location for blue nevi. [341The hard palate, buccal mucosa, gingiva, and lips are common locations for intramucosal nevi. [35See the images below.

Intramucosal nevus on the lower lip. This brown paIntramucosal nevus on the lower lip. This brown papule measured 0.6 cm in diameter and was only slightly raised. Melanotic macules are invariably flat.
Blue nevus on the gingiva. This 1-cm saucer-shapedBlue nevus on the gingiva. This 1-cm saucer-shaped tan macule on the gingiva has histologic features consistent with those of a blue nevus, which is the second most common type of oral nevus. This location is atypical because most blue nevi occur on the palate.

Oral nevi may be mistaken for other pigmented lesions in the oral cavity secondary to endogenous and exogenous causes. Certain clinical features can assist clinicians in making the correct diagnosis. [4243Melanotic macules and amalgam tattoos are usually flat and 80% of nevi are elevated. Ethnic pigmentation is nearly always symmetric and rarely affects the surface topography or disturbs the normal stippling in the gingiva. Smoker's melanosis involves only the anterior gingiva, and, of course, a history of smoking is essential. Vascular lesions usually blanch with compression and melanocytic proliferations do not. Malignant melanoma is frequently associated with diffuse areas of pigmentation, possible ulceration, nodularity, variegation in color, and an irregular outline.

DDx


Diagnostic Considerations

Oral junctional nevi, atypical melanocytic hyperplasia, and malignant melanoma may have similar clinical presentations, and lesions initially diagnosed as oral junctional nevi may subsequently be shown to be atypical melanocytic hyperplasia. [44A few cases of oral melanoma in situ misdiagnosed as junctional nevi have also been reported. [35It is imperative that the definitive diagnosis be confirmed through biopsy.

Differentials for focal pigmented lesions are as follows:

  • Melanotic macule

  • Melanoacanthoma

  • Mucosal melanoma

  • Amalgam tattoo

  • Hemangioma

  • Kaposi sarcoma

  • Varix

  • Vascular malformation

  • Thrombus Hematoma

Differentials for diffuse pigmented lesions are as follows:

  • Smoker’s melanosis

  • Physiological pigmentation

Drug-induced lesions may be caused by the following:

  • Antimalarials: Quinacrine, chloroquine, hydroxychloroquine

  • Antibiotics: Minocycline, tetracycline

  • Antifungals: Ketoconazole

  • Antimycobacterials: Clofazimine

  • Antiretrovirals: Zidovudine

  • Antineoplastics: Bleomycin, busulfan, tacrolimus, cyclophosphamide, doxorubicin, hydroxyurea

  • Cardiac drugs: Amiodarone, quinidine

  • Psychiatric drugs: Chlorpromazine

  • Estrogen: Oral contraceptives

  • Gold therapy

Post-inflammatory hyperpigmentation/hypopigmentation should be considered in the differential diagnosis.

Systemic conditions to consider in the differential diagnosis are as follows:

  • Peutz-Jeghers syndrome

  • Laugier-Hunziker syndrome

  • Addison disease

  • McCune-Albright syndrome

  • Neurofibromatosis

Non-pigmented/amelanotic lesions to consider are as follows:

  • Fibroma

  • Fibrous hyperplasia

  • Papilloma

TREATMENT & MANAGEMENT
SECTIONS

Medical Care

Regular and thorough oral examinations should be performed; the goal is to exclude malignant lesions.

Surgical Care

All melanocytic and amelanocytic lesions in the oral cavity should be viewed with suspicion. Complete excision is suggested to be the most reliable approach to oral melanocytic lesions. [51Evolving and/or recurrent lesions also necessitate excision and microscopic evaluation.

Consultations

Patients may be referred to an oral medicine and/or oral pathology specialist for questionable clinical/histological diagnosis.

Complications

Minor surgical complications may occur.

Prevention

Because oral nevi are not related to sun exposure, they are impossible to prevent.


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