AUTHOR AND EDITOR INFORMATION

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• Introduction
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• Differentials
• Workup
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• Follow-up
• Miscellaneous
• Multimedia
• References

INTRODUCTION

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Background

Nevi are benign proliferations of nevus cells either in the epithelium or in the subepithelial stroma. They are best categorized as hamartomas rather than true neoplasms. Nevi of the oral cavity are usually called mucosal melanocytic nevi or intramucosal nevi. In 1943, Ackermann and Field may have reported the first documented case of an oral nevus. Comerford and his coworkers were the first to propose the term intralamina propria nevus. King et al adopted the less anatomically specific term, intramucosal nevus, which clinicians more easily understand.

White adults have 10-40 cutaneous nevi on average, but intraoral lesions are rare.

On the basis of the histologic location of the nevus cells, cutaneous nevi can be classified into 3 categories. The first category, junctional nevus, is when nevus cells are limited to the basal cell layer of the epithelium. The second category, compound nevus, is used if the cells are in the epidermis and dermis. The third category, intradermal nevus, is when nests of nevus cells are entirely in the dermis. Oral nevi follow the same classification; however, the term intradermal is replaced by intramucosal.

Nevi may also be classified as congenital or acquired (see Histologic Findings). Oral acquired melanocytic nevi evolve through stages similar to those of nevi on the skin. Junctional nevi that are first noted in infants, children, and young adults typically mature into compound nevi. Then, during later adulthood, the lesions mature into intramucosal nevi. By far, the most common mucosal type is the intramucosal nevus, which accounts for more than one half of all reported oral nevi.

The common blue nevus is the second most common type found in the oral cavity. The proportion of total nevi that are blue nevi is greater in the mouth than in the skin; blue nevi account for 25-36% of all oral nevi, according to different studies. Junctional and compound nevi account for only 3-6% of all oral nevi, and only a few cases of congenital nevi, cellular blue nevi, Spitz nevi, and combined nevi have been reported. With the probable exception of halo and dysplastic nevi, all of the cutaneous subtypes of nevi have been found in the oral mucosa.

The term nevus is used in reference to many other hamartomatous or neoplastic entities that are not composed of nevus cells or melanocytes. These entities include white sponge nevus, epidermal nevus syndrome (nevus unius lateris), nevus sebaceous, blue rubber-bleb nevus syndrome, nevoid basal cell carcinoma syndrome, and widespread intramucosal nevus associated with hypertrophy of the oral mucosa and alveolar bone. This article reviews only true melanocytic nevi.

Pathophysiology

Although little doubt exists that nevus cells arise from the neural crest, whether the cells represent true melanocytes or a closely related but distinct cell type is debatable. Melanocytes of the oral epithelium are localized to primarily the tips of the rete ridges. They have a small, regular nucleus along the basal cell layer and a dendritic cytoplasm that contains melanosomes. Melanocytes transfer melanosomes to neighboring keratinocytes.

Supporting their distinction from melanocytes, nevus cells have rounded cytoplasms and lack the dendritic processes typical of melanocytes. Nevus cells have similar nuclear morphologic features, but their cytoplasm is ovoid, rounded, or spindle shaped. In addition, nevus cells have no contact inhibition and are able to form nests and clusters of cells. Normally, melanosomes are retained by nevus cells and not transferred to adjacent keratinocytes. Nevus cells also have the ability to migrate from the basal cell layer into the underlying submucosa.

Melanocytic cells derived from the neural crest migrate to the skin and oral mucous membranes during embryogenesis, and both locations are characterized by melanin production in the epithelial component. Nevus cell formation probably begins with the proliferation of melanocytes along the basal cell layer, and it 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 a nest or thèque. On the skin, this process usually results in the formation of a flat tan-to-brown junctional nevus measuring less than 0.5 mm in diameter.

Nevus cells probably continue to proliferate in the basal cell layer and then protrude into the submucosa. Eventually, they separate from the epidermis. Junctional nests are lost later, and nevus cells become confined to the submucosa. As the nevus cells penetrate into the submucosa, their pigmentation diminishes; approximately 15% of intramucosal nevi are nonpigmented. Melanocytic nevi can be present at birth, they may appear shortly after birth, or they may develop during childhood and early adulthood. Most cutaneous nevi develop in patients younger than 35 years. In studies of oral nevi, 85% of lesions are found in patients younger than 40 years.

Frequency

United States

Literature from the early 1950s suggested that primary melanoma of the oral mucosa was more common than intramucosal nevi. At that time, oral melanomas were reported far more commonly than oral nevi. King and associates investigated this observation by performing a prospective study to determine the incidence of oral nevi. In 4,191 patients examined, 3 nevi were found. None of the nevi were found in white patients. The study population had a black-to-white ratio of 2.3:1, indicating that both races were well represented. One white patient had what clinically appeared to be an oral nevus, but biopsy was deferred because of the patient's comorbidities.

According to the data of King et al, the estimated incidence of oral nevi in black patients in the United States is 3 cases per 2,912 patients (rate, 0.1%). This incidence is probably similar in the white population, because 1,279 white patients were examined, and one probable nevus was found.

In 1979, Buchner and Hansen determined the incidence of oral nevi by reviewing accession diagnoses from a large oral pathology service. They found 32 cases among 20,731 surgical specimens (rate, 0.15%); this finding again suggested that nevi are rare in the oral cavity relative to those in the skin.

One potential reason for the relative scarcity of oral nevi may be that they are too small to be easily detected (see Physical).

International

Racial differences are found in the incidences of cutaneous nevi, with whites having more lesions than Asians or blacks. No such racial differences have been found with oral nevi.

Mortality/Morbidity

Numerous references support the association between melanocytic nevi of the skin and malignant melanoma. However, no case of melanoma arising in or around an oral melanocytic nevus has been described.

• Residual nevus components are contiguous with cutaneous malignant melanoma in 18-72% of cases, depending on the study. Similarly, 18-85% of patients with melanoma have a history of a nevus at the site of a primary melanoma. In contrast, the literature on oral conditions is devoid of references that document an oral nevus in association with a mucosal melanoma.
• Although approximately one third of mucosal melanomas are associated with mucosal melanosis in patients in whom biopsy was performed, the lesion was more frequently believed to arise from atypical melanocytic hyperplasia.
• In a few documented cases, associated pigmentation consisted of completely benign mucosal melanosis.

Race

Oral nevi are found in persons of all races.

• Oral nevi are reported more frequently in whites, in whom 55% of reported oral nevi occurred. Approximately 23% of oral nevi reported in the literature occurred in black patients.
• In the largest study of race and mucosal nevi, Asians represented 14% of the patients with oral nevi and 7% of patients were Hispanic. This study was conducted in an area with a large population of Asians, blacks, and Hispanics. The apparent predominance of oral nevi in whites is likely due to the over-representation of this group among patients who underwent biopsies.
• No objective evidence confirms that oral nevi are more common in whites than in others, and the data from King et al suggest that the incidences are similar among black patients and white patients.

Sex

• Most studies have revealed that oral mucosal nevi are slightly predominant in women rather than men.
• One large study had a female-to-male ratio of 1.5:1. The intramucosal type of nevus was especially common; 64% of these lesions occurred in females. Blue nevi occurred almost equally among male patients and female patients.

Age

In one large study of patients with oral nevi, the patients were aged 3-85 years. The mean age of all patients was 35 years, but male patients tended to be a few years older than the female patients.

• Patients with junctional or compound nevi were relatively young; they were aged 22 and 24 years, respectively, whereas the mean age of patients with intramucosal nevi was 35 years.
• The average age of patients with blue nevi was 38 years.
• The incidence of oral nevi was highest in patients aged 20-40 years, who accounted for almost one half of the patients.

CLINICAL

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History

• Most oral nevi are asymptomatic, and the lesions are usually detected as an incidental finding on routine dental examination.
• In one study, the chief complaint of 107 patients with biopsy-proven oral nevi was reviewed.
• • Of those patients, 80% had no complaint and were typically unaware of their lesion.
  • Of patients with recorded complaints, 22% described a mass, growth, or pigmented spot. Fewer than 1 in 10 patients were aware of enlargement of the lesion.
  • Most lesions in question were in the anterior segments of the mouth or the lips.
  • Most patients could only speculate about the duration of their condition.
  • A few patients indicated that the lesion was present at birth.
  • A minority of patients complained of soreness or pain. Usually, pain was related to another cause, such as an ill-fitting denture.
  • Rarely, patients complained of multifocal lesions.

Physical

Certain classic clinical features can help clinicians in making the correct diagnosis. Nevi are often mistaken for melanotic macules, amalgam tattoos, physiologic ethnic pigmentation, smoker's melanosis, or other vascular or pigmented lesions.

An important consideration is that melanotic 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 most often occurs in women who smoke and take oral contraceptives. Vascular lesions can be mistaken for melanocytic proliferations; the former usually blanche with compression, and aspiration may be helpful in differentiating a nevus from a vascular process. Malignant melanoma is frequently associated with diffuse areas of pigmentation, possible ulceration, nodularity, variegation in color, and an irregular outline.

• Approximately 85% of oral nevi are pigmented. Pigmentation usually varies from brown to black or blue. Some lesions are variegated. Almost 100% of blue nevi are pigmented.
• Nonpigmented nevi account for approximately 15% of oral nevi. Many amelanocytic lesions appear as sessile growths that resemble fibromas or papillomas. Approximately 15% of nevi are amelanotic.
• Typically, nevi are well circumscribed, round, or oval, and they are raised or slightly raised in 65-80% of cases. Unlike their cutaneous counterparts, oral nevi are usually smooth and rarely have a papillated or rough surface.
• Oral nevi most commonly occur on the hard palate, with almost 40% presenting in that location.
• • The second most common location is the buccal mucosa (20% of cases).
  • Other common locations include the vermillion border of the lip and the labial mucosa. Roughly 10% of all types of oral nevi are found on the gingiva. Only one mucosal nevus has been reported on the tongue or floor of the mouth.
  • Often, oral nevi are located in the posterior aspects of the oral cavity and are hard to visualize.
• The distribution varies depending on the histologic type of the nevus.
• • The hard palate is the most common location for blue nevi with almost two thirds being present in that location.
  • Intramucosal nevi are distributed almost equally between the hard palate and buccal mucosa, with almost 25% in each location. Approximately 17% of intramucosal nevi are on the gingiva, 12% on the vermillion border of the lip, and almost 9% on the labial mucosa.
• Clinically, oral melanocytic nevi can be indistinguishable from melanotic macules and melanocytic hyperplasia; therefore, maintaining a heightened clinical suspicion of oral pigmented lesions is important.
• • Biopsy and histologic examination should be performed to assess suspicious nevi of the oral cavity.
  • Early diagnosis may improve the extremely poor prognosis associated with melanoma of the oral cavity.
• In one of Buchner's studies, lesions were 0.1-3.0 cm (Buchner, Oral Surg Oral Med Oral Pathol, Jun 1987).
• • The average size was 0.5 cm, and almost one half of the lesions were 0.1-0.3 cm. About 75% of the nevi were smaller than 0.6 cm. Nevi larger than 1.3 cm were present in only about 5% of the cases.
  • In general, the larger nevi were more likely considered to be congenital.
  • Blue nevi usually were smaller than intramucosal nevi, and almost 90% were 0.1-0.6 cm.
• One potential reason for the relative scarcity of oral nevi may be that they are too small to be easily detected.
• In the prospective study by King et al, the average oral nevus was 0.3 cm in diameter.

Causes

See Pathophysiology.

DIFFERENTIALS

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Other Problems to be Considered

For pigmented oral nevi, the differential diagnosis includes melanotic macule (focal benign melanosis), smoker's melanosis, physiologic or ethnic pigmentation, and amalgam tattoo. When lesions are more purple or blue, hemangioma or another vascular anomaly should be considered. Lentigo, malignant melanoma, and mucocele with hemorrhage must also be considered.

For nonpigmented lesions, the differential diagnosis primarily includes fibroma, fibrous hyperplasia, and papilloma.

WORKUP

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Lab Studies

• As with cutaneous nevi, a histologic evaluation of the cytologic and architectural features of oral nevi is important.
• The cytogenetic makeup of precursor melanocytic lesions or melanomas can be studied.
• Loss of heterozygosity is frequently found in cutaneous melanomas, and molecular studies have led to a discovery of several cutaneous melanoma susceptibility genes.
• The same tests are available for the assessment of mucosal lesions if concern exists after histologic analysis.

Imaging Studies

• Periapical radiography often helps in differentiating an amalgam tattoo from a nevus. In approximately 25% of tattoos, dental radiographs demonstrate minute opaque particles.
• Angiography can be performed to exclude vascular anomalies in highly suspicious lesions, especially those involving the palate.
• Other imaging studies are typically not indicated.

Other Tests

• Usually, compression causes a vascular lesion to blanch, and aspiration can be used as well.

Procedures

• Incisional or excisional biopsy of oral lesions is often required to confirm benignancy or malignancy.
• The primary diagnostic procedure is excisional biopsy.
• Incisional biopsy may be performed in nevi larger than 1-2 cm. The incision should be made in the nodular areas, if they exist, and the incisions should start from the center, not from the periphery of the lesion.
• Biopsy should be performed in all pigmented lesions that are in high-risk areas of the oral cavity, such as the palate or maxillary gingiva. In fact, biopsy and histologic examination should be performed to assess any suspicious nevi of the oral cavity.
• Lesions at other sites should be similarly examined if they are not clearly defined areas of physiologic melanin pigmentation or confirmed amalgam tattoos.
• If the initial biopsy reveals benign melanotic macules, the lesions should be closely monitored, and biopsy should be repeated if they recur or enlarge.

Histologic Findings

As previously described in Background, oral nevi are classified as junctional, compound, or intramucosal (intralamina propria nevus) nevi, according to the location of the nevus cell nests.

Nevi may also be classified as congenital or acquired. However, congenital nevi in the mouth are difficult to diagnose. Lesions larger than 1.25 cm and/or those that penetrate deep into the connective tissue layer and involve muscle, split collagen bundles, and/or salivary gland tissue are likely to be congenital nevi. Nevi with a definite history of being present at birth also fit into this category, but few examples have been reported. Whether oral congenital nevi have an increased risk of a malignant transformation is unknown.

Oral nevi are composed of 4 main types of nevus cells. Type A cells are found in the superficial portion of the nevus and are larger, rounded cells that often contain melanin. These cells are epithelioid and contain abundant pink cytoplasm and a large round or oval nucleus. Type B cells are smaller and resemble lymphocytes and are usually found in the mid portion of nevi. Type C cells resemble fibroblasts and are primarily found in the lower portions of the lesions. Type D cells are nevus giant cells that are multinucleated, and these cells are often scattered throughout the lesion. In oral nevi, type A and B cells are more common than type C cells. In nonpigmented nevi, type A cells are often absent.

TREATMENT

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Medical Care

Regular and thorough oral examinations should be performed; the goal is to find and remove all suspicious pigmented lesions.

• If the pigmentation is diffuse, identifying lesions as innocuous smoker's melanosis, as ethnic pigmentation, or as more challenging lesions such as benign mucosal melanosis or atypical or malignant proliferations is important.
• Even areas of benign mucosal melanosis must be carefully monitored because these lesions can transform into a malignant melanoma.

Surgical Care

Incisional or excisional biopsy of oral lesions is often required to confirm benignancy or malignancy (see Procedures).

• Biopsy is indicated for benign mucosal lesions that recur.
• Repeat biopsy is necessary for any lesion that spreads or changes clinically.

Consultations

• Consultation may be required if the clinician is unsure of the nature of the oral pigmentation and/or lesion or if he or she is unfamiliar with biopsy techniques.
• If the clinician is unfamiliar with the oral cavity and/or the various pigmented lesions that can affect it, the patient should be referred to an oral medicine and/or oral pathology specialist.

FOLLOW-UP

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Deterrence/Prevention

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

Complications

• Complications may be related to treatment by means of simple excision.
• • These complications may be minor.
  • Only one case of recurrent nevus in the oral cavity is reported.

• Congenital and dysplastic nevi have an increased risk for transformation to cutaneous malignant melanoma, but these nevi are rare or absent in the mouth.
• • In one study, Buchner described 2 oral lesions that were suggestive of congenital nevi (Buchner, Refuat Hashinayim, 1990).
  • At least 2 additional case reports have described congenital nevi in the mouth. Some of the nevi were large and certainly of concern, yet no documented case of malignant transformation has been reported.
  • No cases of dysplastic nevi were found in more than 200 reports of oral nevi in the literature. One patient with dysplastic nevus syndrome reportedly developed an oral melanoma. In this patient, the biopsy specimen demonstrated atypical melanocytic hyperplasia and not a dysplastic nevus precursor.

Prognosis

• The prognosis of oral nevi is excellent. A few patients have had multiple nevi, including multiple junctional nevi; however, to the authors' knowledge, none of the lesions have undergone malignant transformation.
• • Although congenital nevi in the oral cavity have been reported, they are extremely rare. None have been documented as having undergone malignant transformation.
  • Dysplastic nevi in the oral cavity have not been reported.
  • One patient with dysplastic nevus syndrome developed oral atypical melanocytic hyperplasia and melanoma in situ.
  • Patients with this condition should be carefully monitored with regular oral examinations.

• The definitive precursor lesion for mucosal melanoma has not been identified; however, in several patients, associated pigmentation was present prior to the development of mucosal melanoma.
• • Most often, the pigment was found to be atypical melanocytic hyperplasia, but benign pigmentation has been described in association with mucosal melanoma.
  • The lack of atypical features in the latter cases was attributed to sampling error.
  • A benign phase of melanocytic hyperplasia may precede the development of melanoma in the oral cavity.
• Early diagnosis may improve the extremely poor prognosis associated with melanoma of the oral cavity.

Patient Education

• Instruct patients to watch for pigmented lesions in the oral cavity.
• If one or more lesions are present, advise patients to watch for changes in the border outline, that is, a change from a discrete and/or round border to an irregular border.
• Patients should watch for and report increasing size, nodularity, ulceration, or changes in the color of their oral nevi.

MISCELLANEOUS

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Medical/Legal Pitfalls

• Misdiagnosis is a potential problem.
• • Because junctional nevi account for only 3% of oral nevi, that diagnosis should be made only after confirmation at biopsy.
  • At least one case initially diagnosed as an oral junctional nevus was subsequently shown to be atypical melanocytic hyperplasia. Atypical melanocytic hyperplasia may be subtle in oral lesions, and the potential exists for histologic misinterpretation of a melanoma in situ or atypical melanocytic hyperplasia as a junctional nevus. Junctional nevi are rare in the oral cavity; therefore, this diagnosis should always be reviewed.
  • A few cases of oral melanoma in situ misdiagnosed as junctional nevi have been reported. Even patients with so-called benign mucosal melanosis should be regularly observed, and repeat biopsy should be performed if the lesions change.
• Any oral pigmented lesion that recurs should be viewed with a high degree of suspicion.

Special Concerns

• Pregnancy is known to exacerbate pigmentary changes in the oral cavity.
• Patients with oral pigmented lesions should be observed during and after their pregnancy.
• If pigmentary changes progress after a pregnancy, biopsy is recommended.

MULTIMEDIA

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Media file 1:  This biopsy-proven intramucosal nevus on the gingiva is unusual because it is not raised and has an irregular outline.
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Media type:  Photo

Media file 2:  Intramucosal nevus on the lower lip. This brown papule measured 0.6 cm in diameter and was only slightly raised. Melanotic macules are invariably flat.
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Media type:  Photo

Media file 3:  Blue 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.
	View Full Size Image
Media type:  Photo

REFERENCES

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• Abe K, Katsuyama H, Harada T, et al. A widespread intramucosal naevus associated with hypertrophy of oral mucosa and alveolar bone. A case report. J Craniomaxillofac Surg. Nov 1989;17(8):367-70. [Medline].
• Allen CM, Pellegrini A. Probable congenital melanocytic nevus of the oral mucosa: case report. Pediatr Dermatol. Jun 1995;12(2):145-8. [Medline].
• Barker GR, Sloan P. An intraoral combined blue naevus. Br J Oral Maxillofac Surg. Apr 1988;26(2):165-8. [Medline].
• Biesbrock AR, Aguirre A. Multiple focal pigmented lesions in the maxillary tuberosity and hard palate: a unique display of intraoral junctional nevi. J Periodontol. Aug 1992;63(8):718-21. [Medline].
• Bucci E, Mignogna MD, Lo Muzio L. Primary malignant melanoma of the oral cavity: a case report. J Oral Maxillofac Surg. Jun 1989;47(6):621-2. [Medline].
• Buchner A, Hansen LS. Pigmented nevi of the oral mucosa: a clinicopathologic study of 36 new cases and review of 155 cases from the literature. Part II: Analysis of 191 cases. Oral Surg Oral Med Oral Pathol. Jun 1987;63(6):676-82. [Medline].
• Buchner A, Hansen LS. Pigmented nevi of the oral mucosa: a clinicopathologic study of 32 new cases and review of 75 cases from the literature. Part I. A clinicopathologic study of 32 new cases. Oral Surg Oral Med Oral Pathol. Aug 1979;48(2):131-42. [Medline].
• Buchner A, Hansen LS. Pigmented nevi of the oral mucosa: a clinicopathologic study of 36 new cases and review of 155 cases from the literature. Part I: A clinicopathologic study of 36 new cases. Oral Surg Oral Med Oral Pathol. May 1987;63(5):566-72. [Medline].
• Buchner A, Leider AS, Merrell PW, Carpenter WM. Melanocytic nevi of the oral mucosa: a clinicopathologic study of 130 cases from northern California. J Oral Pathol Med. May 1990;19(5):197-201. [Medline].
• Buchner A, Hansen LS. Pigmented nevi of the oral mucosa: a clinicopathologic study of 32 new cases and review of 75 cases from the literature. Part II. Analysis of 107 cases. Oral Surg Oral Med Oral Pathol. 1980;49(1):55-62. [Medline].
• Buchner A, Leider AS, Carpenter WM, Littner MM. Melanocytic nevi of the oral mucosa--a clinicopathologic study of 60 new cases. Refuat Hashinayim. Jul 1990;8(3):3-8. [Medline].
• Buchner A, Merrell PW, Carpenter WM. Relative frequency of solitary melanocytic lesions of the oral mucosa. J Oral Pathol Med. Oct 2004;33(9):550-7. [Medline].
• Chen X, Wang S, Li Y. [Benign focal melanotic lesions of the oral mucosa: a clinicopathologic study of 41 cases]. Hua Xi Kou Qiang Yi Xue Za Zhi. Aug 1997;15(3):242-3, 246. [Medline].
• Comerford TE Jr, Delapava S, Pickren JW. Nevus of the oral cavity. Oral Surg Oral Med Oral Pathol. Feb 1964;17:148-51. [Medline].
• Dyer PV, Eveson JW. Recurrent compound naevus of gingiva. J Periodontol. Aug 1993;64(8):739-41. [Medline].
• Eisen D, Voorhees JJ. Oral melanoma and other pigmented lesions of the oral cavity. J Am Acad Dermatol. Apr 1991;24(4):527-37. [Medline].
• Elder DE, Greene MH, Bondi EE, Clark WH Jr. Acquired melanocytic nevi and melanoma: the dysplastic nevus syndrome. In: Ackerman AB, ed. Pathology of Malignant Melanoma. New York: Masson Publishing;1981:185-215.
• Ficarra G, Hansen LS, Engebretsen S, Levin LS. Combined nevi of the oral mucosa. Oral Surg Oral Med Oral Pathol. Feb 1987;63(2):196-201. [Medline].
• Field HJ, Ackerman AA. Non-pigmented nevus on labial mucosa. Am J Orthodontics Oral Surg. 1943;29:180-1.
• Flaitz CM, McCandless G. Palatal blue nevus in a child. Pediatr Dent. Jul-Aug 2001;23(4):354-5. [Medline].
• Gnepp DR. Diagnostic Surgical Pathology of the Head and Neck. Philadelphia: WB Saunders Co;2001:222-4.
• Greene GW, Haynes JW, Dozier M, et al. Primary malignant melanoma of the oral mucosa. Oral Surg Oral Med Oral Pathol. 1953;6:1435-43.
• Hansen LS, Buchner A. Changing concepts of the junctional nevus and melanoma: review of the literature and report of case. J Oral Surg. Dec 1981;39(12):961-5. [Medline].
• Hickman RE, Eveson JW, Cawson RA. Nevus unius lateris and intraoral verrucous nevi. Oral Surg Oral Med Oral Pathol. Aug 1988;66(2):226-9. [Medline].
• Hicks MJ, Flaitz CM. Oral mucosal melanoma: epidemiology and pathobiology. Oral Oncol. Mar 2000;36(2):152-69. [Medline].
• Kahn MA, Weathers DR, Hoffman JG. Transformation of a benign oral pigmentation to primary oral melanoma. Oral Surg Oral Med Oral Pathol Oral Radiol Endod. Oct 2005;100(4):454-9. [Medline].
• King OH Jr, Blankenship JP, King WA, Coleman SA. The frequency of pigmented nevi in the oral cavity. Report of five cases. Oral Surg Oral Med Oral Pathol. Jan 1967;23(1):82-90. [Medline].
• Little JW. Melanoma: etiology, treatment, and dental implications. Gen Dent. Jan-Feb 2006;54(1):61-66; quiz, 67. [Medline].
• Lovas GL, Wysocki GP, Daley TD. The oral blue nevus: histogenetic implications of its ultrastructural features. Oral Surg Oral Med Oral Pathol. Feb 1983;55(2):145-50. [Medline].
• Miller CS, Craig RM Jr. White corrugated mucosa. J Am Dent Assoc. Aug 1988;117(2):345-6. [Medline].
• Moghadam BK, Gier RE. Melanin pigmentation disorders of the skin and oral mucosa. Compendium. Jan 1991;12(1):14, 16-20. [Medline].
• Morency R, Labelle H. Nevus sebaceus of Jadassohn: a rare oral presentation. Oral Surg Oral Med Oral Pathol. Oct 1987;64(4):460-2. [Medline].
• Neville BW, Damm DD, Allen CM. Epithelial pathology. In: Oral and Maxillofacial Pathology. 2nd ed. Philadelphia: WB Saunders Co;2002:330-6.
• Nikai H, Miyauchi M, Ogawa I, et al. Spitz nevus of the palate. Report of a case. Oral Surg Oral Med Oral Pathol. May 1990;69(5):603-8. [Medline].
• Rapini RP, Golitz LE, Greer RO Jr, et al. Primary malignant melanoma of the oral cavity. A review of 177 cases. Cancer. Apr 1 1985;55(7):1543-51. [Medline].
• Sagebiel RW. Diagnosis and management of premalignant melanocytic proliferations. Pathology. Apr 1985;17(2):285-90. [Medline].
• Sumi Y, Taguchi N, Kaneda T. Blue rubber bleb nevus syndrome with oral hemangiomas. Oral Surg Oral Med Oral Pathol. Jan 1991;71(1):84-6. [Medline].
• Takagi M, Ishikawa G, Mori W. Primary malignant melanoma of the oral cavity in Japan. With special reference to mucosal melanosis. Cancer. Aug 1974;34(2):358-70. [Medline].
• Takeda Y. Congenital nevocellular nevus of the oral mucosa. Ann Dent. Winter 1988;47(2):40-2. [Medline].
• Taylor CO, Lewis JS. Histologically documented transformation of benign oral melanosis into malignant melanoma: a case report. J Oral Maxillofac Surg. Jul 1990;48(7):732-4. [Medline].
• Torres Fernandez G. Pigmented lesion of the oral cavity with eight years follow-up. P R Health Sci J. Jun 2000;19(2):165-8. [Medline].
• Tremblay JF, O''Brien EA, Chauvin PJ. Melanoma in situ of the oral mucosa in an adolescent with dysplastic nevus syndrome. J Am Acad Dermatol. May 2000;42(5 Pt 1):844-6. [Medline].
• Weathers DR. Benign nevi of the oral mucosa. Arch Dermatol. Jun 1969;99(6):688-92. [Medline].
• Weathers DR, Waldron CA. Intraoral cellular nevi. Review of the literature and report of five cases. Oral Surg Oral Med Oral Pathol. Oct 1965;20(4):467-75. [Medline].

Article Last Updated: Apr 12, 2006