Oral melanoacanthoma is a benign, reactive process and is unrelated to cutaneous melanoacanthoma. The reported age of presentation ranges from 9 to 77 years, with a mean age of 29 years [
3,
4,
12]. The lesion is most predominantly observed among black patients, though occurrences have been observed among Caucasians, Hispanics and Asians [
1,
4,
12‐
14]. Oral melanoacanthomas show a female predilection, with a male to female ratio of 2:1 [
1,
2,
14]. The etiology has been largely attributed to local irritation or even mild trauma [
3,
14]. The intra-oral site most commonly affected is the buccal mucosa but involvement of other sites such as the mucosa of the lip, palate, gingiva and alveolar mucosa has also been reported (Table
1). Clinically, the lesion is a flat or slightly raised black or brown macule and may rapidly increase in size, ranging from a few millimeters to several centimeters [
1,
12,
13]. The lesions are usually solitary and well circumscribed though a few authors have reported bilateral or multiple (Table
1) melanoacanthomas. Oral melanoacanthomas are usually asymptomatic and are not neoplastic. The other lesions to be considered in the differential diagnosis are smoker's melanosis, drug induced pigmentation, Addison's disease, melanotic macule, pigmented nevi – junctional, intramucosal, compound, Spitz nevus, postinflammatory melanosis and oral melanoma. A biopsy is mandatory to rule out melanoma and to alleviate patient apprehension. Histologically, melanocytes which are usually restricted to the basal layer are found distributed throughout the epithelium. These melanocytes exhibit prominent dendritic processes and are immunoreactive for S-100, Melan-A/Mart-1, HMB-45 and Tyrosinase [
14]. Other dendritic cells in the oral mucosa are the Langerhans' cells which are antigen presenting cells of the immune system, usually distributed in the superficial epithelium and are demonstrated on immunohistochemistry by S-100 or CD1a. The adjacent connective tissue exhibits chronic inflammatory cell infiltrate. The presence of eosinophils among the inflammatory cells is not a universal feature and may not be essential for the diagnosis of oral melanoacanthoma. Once diagnosis is established, no further treatment is required, with some cases exhibiting spontaneous regression after biopsy [
1]. It has been suggested that this entity be renamed melanoacanthosis or oral melanotic macule – reactive type, since the term melanoacanthoma is suggestive of a neoplastic process [
11].
In our patient, the etiology of the lesion may be attributed to the incident of trauma during the restorative procedure. It may be safely assumed that GIC did not contribute to the cause of the lesion since the patient has multiple restorations with the same material and the adjacent sites did not exhibit any lesion.