## 1 Introduction  
The term 'blue nevus', which was originally introduced to the literature in 1906 by [PERSON], describes dark blue lesions of the skin and currently encompasses a group of both benign and malignant lesions composed of spindle and dendritic melanocytes [1, 2]. Benign blue nevi include the common, cellular, atypical, epithelelioid and deep-penetrating variants, while the malignant counterpart is referred to as 'blue nevus-like melanoma' or the so-called malignant blue nevus [1]. The term cellular blue nevus was introduced by [PERSON] in 1949 [3]. When features of both a common blue nevus and cellular blue nevus occur in a single lesion, it is recommended to assign the name of the predominant histopathological presentation [1]. Although the majority of blue nevi are solitary in presentation, multiple lesions could be associated with LAMB syndrome (lentigines, atrial and mucocutaneous myxomas and multiple blue nevi), NAME syndrome (blue nevi, atrial myxomas, myxoid neurofibromasand ephelides) or Carney complex (myxomas, endocrine overactivity, spotty skin pigmentation and psammomatous melanotic schwannomas) [1; 4; 5; 6; 7; 8]. Blue nevi are predominantly cutaneous lesions, although they may show a propensity to affect mucosal sites including the oral cavity [1]. Different types of cutaneous blue nevi show demographic differences. Examples are the common/dendritic blue nevus (DBN) frequently occurring in the head and neck and extremities of young adults; the scalp and buttock region of adult females commonly being affected by the cellular blue nevus (CBN); the buttocks and sacral region of young or middle-aged adults commonly affected by the atypical blue nevus (ABN) and epithelioid blue nevus (EBN) predominantly affecting young adults in the presence of Carney complex [1; 6]. Oral melanocytic nevi (OMN) are benign tumours originating from neural crest or nevus cells [9; 10; 11; 12; 13; 14; 15; 16; 17; 18]. The prevalence of OMN is unknown but could be considered a rare occurrence [11]. In support of this observation, in a series by [PERSON] et al. [14], OMN have been reported to account for 0.1% of lesions out of 90,000 biopsies received at an oral and maxillical unit during a period of 19 years. From the same study, it is reported that OMN may occur in both adults and children with a reported age distribution of 3-85 years, with no variations in distribution among different races detected [11; 14]. Different types of OMN include junctional, intra mucosal and compound nevi; blue nevi; combined nevi; Spitz nevi; dysplastic nevi and congenital nevi [9; 10; 11; 12; 13; 14; 15; 16; 17; 18]. According to the literature, the morphogenesis of junctional, intra mucosal and compound nevi is described in three phases, namely (1) proliferation of benign neoplastic melanocytes along the submucosal-mucosal junction which gives rise to a junctional nevus, (2) migration of neoplastic cells to underlying mesenchymal tissues developing into a compound nevus and (3) loss of junctional component restricting neoplastic cells in the subepithelial compartment resulting in intramucosal/subepithelial nevi [11]. The majority of OMN of the oral mucosa are believed to be acquired. A diagnosis of OMN is generally preceded by a variety of clinical diagnoses of lesions including melanotic macules, amalgam tattoos, vascular lesions such as hemangioma and, rarely, malignant melanoma. The majority of OMN are indolent lesions. However, the fact that these OMN may clinically and histopathologically mimic malignant melanoma makes it an important group of lesions to be aware of as clinicians and pathologists. There is controversy regarding whether OMN are capable of acting as precursors for oral malignant melanoma, with [PERSON] et al. [14] indicating that it is a well-known fact that melanomas may occur de novo or in pre-existing nevi such as junctional nevi, dysplastic nevi and congenital nevi. In contrast, [PERSON] et al. [11], after following up 119 OMN for more than 8 years, have shown that none of the OMN developed into melanoma.