Oral Melanoacanthoma

Updated: Feb 12, 2021
Author: Claudia C Cotca, DDS, MPH; Chief Editor: Jeff Burgess, DDS, MSD 



Melanoacanthoma is a rare condition of oral mucosa that has been reported only in the last century. The lesion is characterized by a proliferation of both melanocytes and keratinocytes that results in pigmented macular or plaquelike lesions (see image below).

Intraoral melanoacanthoma lesion on the mandibular Intraoral melanoacanthoma lesion on the mandibular gingiva.

Oral melanoacanthoma is regarded by many as a reactive condition unrelated to cutaneous melanoacanthoma, but the histologic features are similar. Cutaneous melanoacanthoma and mucosal melanoacanthoma differ in terms of patient age, patient race, and site.

Early publications

In 1927, Bloch provided the earliest known description of melanoacanthoma, which was reported in the German literature.[1] Bloch described several skin lesions, which he originally called benign nonovoid melanoepithelioma of the skin. He further subdivided his cases into two types. In the histologic samples studied, type 1 had both dendritic melanocytes and keratinocytes, whereas the histologic appearance of type 2 was similar to that of type 1, but it lacked the dendritic melanocytes.

In 1960, Mishima and Pinkus reexamined the condition and further refined the diagnostic terminology.[2] The condition that Bloch designated as type 1 is currently called melanoacanthoma, and type 2 is currently called pigmented seborrheic keratosis.[3]

Although cutaneous lesions of melanoacanthoma were reported as early as 1927, Tomich et al at the American Academy of Oral Pathology first reported oral mucosal lesions in 1978.[1] Although many authors subsequently published case reports, Goode et al published the first case report in 1983.[4] This was a retrospective review of 10 cases of oral melanoacanthoma reported in the literature.

Oral melanoacanthoma continues to be listed as a rare condition. While some studies report approximately fewer than 100 reported cases, it would be legitimate to point out that the low case published reports may be attributed to the benign nature of lesion appearance, rate and timing of manifestations, and potential differential diagnosis of amalgam tattoo, for example, which though common, are not routinely reported nor typically addressed with treatment owing to the location of the lesion and treatment options.

The cutaneous variant is also rare; however, it has been suggested it is more prevalent than the mucosal variant. This variance in observation of data may be due to differential diagnosis options and subsequent interest in case reporting, as well as by the patient motivation, with potential patient action biased by treatment selection for aesthetic considerations.


The mucosal variants of melanoacanthoma have histologic appearances similar to those of cutaneous melanoacanthoma. The lesion consists of proliferating melanocytes and keratinocytes, which result in large pigment-containing dendritic cells. The dendritic cells are present throughout the middle and upper layers of the epithelium. See the image below.

Diagram of a pigmented epithelial macule. Diagram of a pigmented epithelial macule.

Inflammation occurs almost universally in patients with mucosal lesions. The presence of inflammation and the spontaneous resolution of oral lesions are suggestive of a reactive process rather than a neoplastic process.[5] The observation of trauma and inflammation associated with oral lesions has led to the conclusion that the mucosal variant is likely the result of a reactive process rather than a neoplastic process.[6]


The role of trauma in the development of the lesion remains controversial, but any irritant must be removed. BRAF inhibitor therapy may play a role in some cases.[7] Some data suggest the close resemblance in the pattern of pathophysiological development shared with amalgam tattoos or other external or internal stimulants as reactive-induced lesions, including comorbidities, leaving the location and the rate of presentation as the first clinical differentiating factors.


US frequency

Oral melanoacanthoma is rare, with only approximately fewer than 100 cases reported since 1978,[8, 9, 10] when the lesions were first reported. The cutaneous variant is more common, but it is still relatively rare among skin lesions. Among all the cases reported, specific patterns are described with respect to the race, sex, and age of patients with cutaneous melanoacanthoma and those with mucosal melanoacanthoma.


Cutaneous lesions of melanoacanthoma are reported almost exclusively in White patients. The mucosal variant is reported almost exclusively in Black patients,[11, 12] with higher rates reported in women. Some sporadic mucosal cases are reported in Asian individuals.


The prevalence for both variants of melanoacanthoma is fairly equal in both sexes, with a slight female predominance.[13] The female-to-male ratio is approximately 3:2.


The age distributions of the two types of melanoacanthoma differ.[14] Cutaneous lesions are found in patients with a mean age of approximately 60 years. Mucosal lesions appear in patients with a mean age of approximately 25 years.


Prognosis with treatment intervention can vary, for example by blade surgical excision, laser surgery, or other treatment options. More studies are needed to differentiate optimal outcomes with a minimally invasive approach.

Initially, cutaneous lesions were suspected to be malignant, and, subsequently, the lesions were linked to a transformation to low-grade malignancy. Malignant transformation has been reported in at least two cases. However, most lesions are considered benign and should be treated conservatively. Clinical data collection supported by histopathology reports can substantiate a better prognosis.

No cases of recurrence or metastasis have been reported in either the mucosal variant or cutaneous variant. A low risk of recurrence exists. To date, no malignant oral melanoacanthoma have been reported.

Patient Education

Patient observation and regular monitoring and screening of the cutaneous and oral mucosal lesion classifications are easily established in the dermatologic and dental routine evaluation protocols. Subsequent comprehensive patient education on findings and appropriate recall can be enhanced by etiologic diagnosis of lesion, and proved by histological report.




Because the lesions of oral melanoacanthoma are not painful, medical practitioners usually discover them on routine oral examination.

Physical Examination

The clinical features of oral melanoacanthoma may mimic those of other pigmented lesions. For example, the clinical and histologic features of oral melanoacanthoma lesions can resemble those of melanoma in situ.

Cutaneous lesions

Cutaneous lesions are reported in the scalp, eyelid, ear, nose, neck, thorax, and abdomen.

Cutaneous lesions may be found on any area of the head and neck, as well as on the chest, abdomen, back, or legs.

The lesions are generally asymptomatic, flat or slightly raised, hyperpigmented areas.

The color of the lesions ranges from brown to black to blue.

Lesions are usually isolated, with no apparent precipitating factors.

Lesions are slow growing and usually are present for months before treatment is sought.

Mucosal lesions

Mucosal lesions can occur in the buccal mucosa, labial mucosa, palate, gingiva (see image below),[15] alveolar ridge, or lip.[16, 17]

Although the appearance of mucosal lesions is similar to that of cutaneous lesions, mucosal lesions have a more rapid onset and rate of growth.[18]

Mucosal lesions occur mostly on the lip,[19] buccal mucosa,[20] or palate,[21] and they are precipitated by a traumatic event.

The diameter of the mucosal lesions can range from a few millimeters to several centimeters.

Intraoral melanoacanthoma lesion on the mandibular Intraoral melanoacanthoma lesion on the mandibular gingiva.


Comorbidities are an important consideration in not only etiologic diagnosis but treatment planning options and optimal clinical outcomes.



Diagnostic Considerations

Also consider the following:

  • Melanoma in situ
  • Melanosis
  • Superficial melanoma
  • Junctional melanocytic nevus
  • Melanotic macule
  • Pigmented basal cell epithelioma
  • Nevoid eruptive keratoacanthoma [22]
  • Amalgam tattoo
  • Medication-induced reactive lesion

Differential Diagnoses



Approach Considerations

Consider the following in the diagnostic approach:

  • Clinical presentation with documentation of lesion presentation, growth rate, and parallel stimuli present
  • Comorbidities
  • Medications


The clinical features of cutaneous and mucosal lesions may mimic those of other pigmented lesions; therefore, definitive diagnosis is based on histologic examination. Incisional or excisional biopsy may be performed based on the size and anatomic location of the lesion. Insulinlike growth factor 2 mRNA-binding protein-3 has been suggested to help histologically differentiate keratoacanthoma from squamous cell carcinoma.[23]

Histologic Findings

Microscopic examination reveals a hyperplastic edematous stratified squamous epithelium with acanthosis and elongated widened rete ridges.[24] Increased melanin pigmentation is present in the basal layer (see image below). In addition, many proliferating dendritic melanocytes or clear cells extend upward into the prickle-cell layers (see images below).

Increased melanin pigmentation in the basal layer Increased melanin pigmentation in the basal layer of a melanoacanthoma (hematoxylin and eosin, original magnification X10).
Proliferating dendritic melanocytes in the prickle Proliferating dendritic melanocytes in the prickle-cell layers of a melanoacanthoma (hematoxylin and eosin, original magnification X40).

The clinical and histologic features of oral melanoacanthoma lesions can resemble those of melanoma in situ.[25] Usually, no evidence of cellular pleomorphism or abnormal mitotic activity is seen in oral melanoacanthoma, and this feature excludes malignancy.

In mucosal lesions, mixed chronic inflammatory cells and numerous melanin-laden macrophages densely infiltrate the stratum corneum. This inflammatory process may indicate the reactive rather than the neoplastic nature of the lesion.[26, 27]



Medical Care

No medical treatment for mucosal or cutaneous lesions is known. A low risk of recurrence exists. In patients with mucosal lesions, treatment may be limited to removal of the precipitating stimulus.[28] Lesions spontaneously resolve in approximately 40% of patients with oral lesions.[2]

Surgical Care

Surgical excision is the treatment of choice for both mucosal and cutaneous lesions. Because rare cases of premalignant or malignant cutaneous lesions are reported, wider resection with clear margins is recommended. In benign cutaneous melanoacanthoma, local excision or ablation of the site is adequate. If mucosal lesions do not resolve, local excision or ablation is indicated.

Cryosurgery, electrosurgery, or laser treatment[29] may be used to remove lesions; however, these modalities may jeopardize the microscopic diagnosis. Specific laser utilization must be stated on the biopsy order.


No evidence of malignant transformation has been reported. No complications arise from incisional or excisional biopsy.