Year : 2020 | Volume
: 7 | Issue : 4 | Page : 228--231
Pigmented lesions of the oral cavity – A brief review
Department of Oral Pathology and Microbiology, Dr. B.R. Ambedkar Institute of Dental Sciences and Hospital, Patna, Bihar, India
Department of Oral Pathology and Microbiology, Dr. B.R. Ambedkar Institute of Dental Sciences and Hospital, Patna, Bihar
Pigmentation is a common clinical finding of an oral cavity, but a proper diagnosis of the lesions is very challenging. Pigmentation can be focal, multifocal, associated with systemic/genetic disorder, or due to exogenous agents. Pigmented lesions are either melanocytic or nonmelanocytic. Pigmented lesions of the oral cavity have a broad spectrum of diversity. They present as racial pigmentation, innocuous lesions (amalgam tattoo, oral melanotic macule), benign nevi, and life-threatening malignant melanoma, and they can also produce a diagnostic dilemma. Thus, a proper diagnosis of a pigmented lesion in an early stage is very important for the accurate treatment plan. In this review, pigmented lesions of the oral cavity are briefly discussed.
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Mukherjee D. Pigmented lesions of the oral cavity – A brief review.J Dent Res Rev 2020;7:228-231
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Mukherjee D. Pigmented lesions of the oral cavity – A brief review. J Dent Res Rev [serial online] 2020 [cited 2021 Feb 24 ];7:228-231
Available from: https://www.jdrr.org/text.asp?2020/7/4/228/302048
Pigmentations usually occur due to increased melanin production, increased number of melanocytes (melanocytosis), or accidental deposition of exogenous materials. Oral pigmented lesions are both physiologic and pathologic. Depending on the nature of the causative agent, pathologic pigmentations can be classified into exogenous and endogenous. Pathologic pigmentations due to exogenous agents including drugs, tobacco smoking, amalgam tattoo, and heavy metals. Melanin, hemoglobin, hemosiderin, and carotene are endogenous pigments., Melanocytes (nonkeratinocytes in oral epithelium) produce melanin which is eventually transported to adjacent keratinocytes by melanosomes. Nevus cells (derived from the neural crest) can also synthesize melanin which is found in the skin and mucosa. Due to increased melanin deposition, pigmented lesions may appear as black, brown, or gray, which is usually determined by the location and amount of melanin in the tissue. Endogenous pigmentation is usually associated with endocrine disorders, syndromes, infections, chronic irritation, and reactive and neoplastic lesions. Correct diagnosis is of utmost importance for proper treatment plan. Several clinical parameters, i.e., color, duration, localization, distribution, and medical history are useful for proper diagnosis. Histopathological evaluations are necessary to exclude neoplasia. Herein, I have briefly discussed various oral pigmented lesions that can be categorized under melanocytic and nonmelanocytic lesions.
Racial pigmentation occurs due to increased melanin production by the melanocyte rather than an increased number of melanocytes. Pigmentation (from light brown to dark brown) may involve attached gingiva, buccal mucosa, hard palate, lips, and tongue. It presents as a persistent, symmetrical, dark brown band frequently involving the attached gingiva. In other affected sites, it appears as brown patches with ill-defined borders. No treatment is required for asymptomatic physiologic pigmentation.
Nearly 25%–31% of tobacco product consumers are affected by smoker's melanosis due to the increased production of melanin. It appears as brown-black lesions involving the anterior attached mandibular gingiva, interdental papillae, palate, or buccal mucosa. Females are most commonly affected, suggesting a strong influence of estrogens. It usually disappears without any treatment after cessation of smoking habit.,
Oral Melanotic Macules
Oral melanotic macules (brown, black, blue, or gray) are well-circumscribed, flat lesions. The common site of occurrence is the vermillion border of lip, palate, gingival, and buccal mucosa, and females are more affected than males., They occur due to increased melanin production by the melanocyte rather than an increased number of melanocytes. Oral melanotic macules are HMB-45 negative. Surgical excision and histopathological examination is mandatory to rule out the possibility of an early malignant melanoma. Oral melanotic macule can be associated with several systemic conditions, i.e., Peutz–Jeghers syndrome, Addison's disease, and Laugier–Hunziker syndrome.
\Caféaulait macules may present at birth. They are melaninpigmented uniform brown patches of skin with irregular margins. The presence of six or more large caféaulait macules (>0.5 cm diameter prepubertal, >1.5 cm diameter postpubertal) may be associated with neurofibromatosis (NF). NF1 is characterized by the presence of several neurofibromas involving the skin, oral mucosa, nerves, central nervous system, and jaw. Albright's syndrome (polyostotic fibrous dysplasia, endocrine dysfunction, precocious puberty, and caféaulait macules), Noonan syndrome, Watson syndrome, Bloom syndrome, and ring chromosome syndromes are associated with Caféaulait macules. Microscopically, caféaulait macules generally reveal excess amounts of melanin in basal keratinocytes and subjacent macrophages. No treatment is required, but proper clinical evaluation should be done to rule out the presence of any syndromes.
Pigmented Neuroectodermal Tumor of Infancy
Pigmented neuroectodermal tumor of infancy is a rare, rapidly expansile, benign neoplasm along with a high recurrence rate. The origin of the tumor is neural crest cell, and there is also evidence of high level of urinary vanillylmandelic acid (VMA). It is clinically characterized as a painless, unencapsulated partly pigmented mass. The common site of occurrence is the maxillary region. Complete surgical excision is the treatment of choice. In few cases, chemotherapy and/or radiotherapy is indicated.
Clinically, oral melanocytic nevi present as brown, blue, and grayish lesions involving hard palate, buccal mucosa, and gingiva along with a female predilection. There are several types of nevi (intramucosal, blue, compound, and junctional). The intramucosal variant is the most common type, followed by the blue, compound, and junctional nevi. Histopathologically, melanocytic nevus is characterized by junctional or intramucosal nests of nevus cells. About 80% of oral nevi are smaller than 1 cm. Surgical excision of all intraoral pigmented nevi is the treatment of choice, and proper histopathological evaluation is also important to rule out any malignant transformation or early melanoma.
Oral melanoacanthoma presents as well-demarcated, flat, or slightly raised hyperpigmented (dark brown to black), reactive lesion. It has a property to enlarge rapidly, and the frequently involved site is buccal mucosa. Females are more commonly affected along with a history of trauma., Histopathological features include acanthosis, hyperpigmentation of the basal cell layer. There are many dendritic melanocytes that are distributed in all layers of the epithelium without any atypia. It has no malignant potentiality. Spontaneous regression of many lesions is noted after incisional biopsy or removal of traumatic irritants. Histopathological evaluation is always required to differentiate from malignant lesions.
Oral malignant melanoma (<1% of all melanomas) may have a rapid or slow growth rate. It may develop as an asymptomatic lesion (black or brown) having irregular and asymmetric borders. Sometimes, it can appear as a large, ulcerated mass coupled with bleeding, pain, and bone destruction. The commonly affected sites are hard palate and maxillary gingiva. It can also represent a metastatic lesion and in that case, tongue and buccal mucosa are the commonly affected sites. It is usually noted in between 30 and 69 years of age, and males are more frequently affected than females. Superficial spreading melanoma, nodular melanoma, lentigo maligna melanoma, and acral lentiginous melanoma are four clinicopathological types of melanoma. Histopathologically, malignant melanocytes proliferate at the epithelial and connective tissue junction, and they can also invade into the connective tissue stroma. Mucosal melanomas are associated with a much worse prognosis than cutaneous melanomas. The depth of invasion (Breslow depth) determines the prognosis. The treatment of choice for oral melanoma is radical surgical excision. Chemotherapy and immunotherapy can act as an adjunct. Early detection is of utmost importance as generally only 15% of the affected people survived for 5 years.
Amalgam Tattoo (Focal Argyrosis)
The most common cause of intraoral pigmentation by an exogenous agent is amalgam tattoo. Clinically, it is characterized as localized flat, solitary or multiple, blue-gray lesion of variable dimension. It is usually caused by traumatic soft-tissue implantation of dental amalgam particles., The common site of occurrence includes the gingival and alveolar mucosa. Sometimes, it is also sited on the buccal mucosa, hard palate, and floor of the mouth. Radiographically, localized radiopacities can be noted. Thus, clinical and radiographic evaluations are helpful for the diagnosis of amalgam tattoo. Occasionally, histopathological examination is mandatory to rule out melanoma by the confirmation of diagnosis.
Drugs inducing oral mucosal pigmentation include antimalarial agents (hydrochloroquine, chloroquine, quinacrine, and quinidine), tranquilizer (chlorpromazine), chemotherapeutic medications (busulfan, doxorubicin, 5-fluorouracil, and cyclophosphamide), zidovudine (azidothymidine), ketoconazole, clofazimine, minocycline, and amiodarone., The drug-induced mucosal pigmentation develops possibly due to increased melanin pigmentation. It may also develop due to direct accumulation of pigmented drug particles or by-products after being absorbed by the system., Clinically, this type of mucosal discoloration presents as a diffuse, well-demarcated, bluish-gray discoloration of the gingiva, hard palate, maxillary anterior alveolar mucosa, or tongue. Drug-induced pigmentation is usually temporary, but it may be permanent also. It usually disappears within weeks to months after withdrawal of the causative drug.,
Heavy metals such as lead, arsenic, bismuth, gold, silver, mercury, and platinum are capable of producing oral pigmentation due to an increased level in blood. The pigmentation usually involves the marginal gingiva and lips as blue-black lesion., Occupational exposure to heavy metal vapors becomes a health hazard nowadays. The lead pigmentation on the gingival margin is usually characterized by “lead lines,” while gold, bismuth, and mercury cause slate-gray appearance of the gingiva. Silver product deposition may appear on the hard palate as permanent diffuse bluish-gray pigmentation. Identification of heavy-metal pigmentation is important to avoid severe systemic toxic effects.
Diagnostic Algorism for Oral Pigmented Lesions
Detailed history and proper clinical evaluation has immense diagnostic value for racial pigmentation, smoker's melanosis, amalgam tattoo, drug-induced pigmentations, and heavy-metal pigmentation. Many systemic conditions/syndromes have indicative values for the diagnosis of oral melanotic macules and Café-au-Lait macules. Laboratory findings (high level of urinary VMA) along with the age of occurrence have a pragmatic value for the diagnosis of pigmented neuroectodermal tumor of infancy. Histopathological evaluation is of utmost importance for the diagnosis of melanocytic nevus, oral melanoacanthoma, and oral malignant melanoma. Immunohistochemical analysis also has a diagnostic appraisal to differentiate oral melanotic macules (HMB-45 negative) and oral malignant melanoma (HMB-45 positive). Although the provisional diagnosis of pigmented lesions of the oral cavity is made based on the clinical findings, histopathological evaluation is essential for a decisive diagnosis to delineate the true biological nature. Thus, complete history, clinical findings, laboratory investigations, and immunohistochemical analysis coupled with histopathological evaluation should be done according to the requirement for the diagnosis of oral pigmented lesions.
Oral mucosa is infrequently affected by the pathologies related to pigmentation. It may be physiological or pathological pigmentation. Causative agents can be exogenous or endogenous. Proper diagnosis of oral pigmented lesions is important because these pigmented lesions may be traumatic, reactive, neoplastic, or associated with systemic pathogenesis and syndromes. Thus, the accurate treatment modalities depend on the nature of the pigmented lesion.
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|1||Sreeja C, Ramakrishnan K, Vijayalakshmi D, Devi M, Aesha I, Vijayabanu B. Oral pigmentation: A review. J Pharm Bio All Sci 2015;7:3-8.|
|2||Kauzman A, Pavone M, Blanas N, Bradley G. Pigmented lesions of the oral cavity: Review, differential diagnosis, and case presentations. J Can Dent Assoc 2004;70:682-3.|
|3||Eisen D. Disorders of pigmentation in the oral cavity. Clin Dermatol 2000;18:579-87.|
|4||Ferreira L, Jham B, Assi R, Readinger A, Kessler HP. Oral melanocytic nevi: A clinicopathologic study of 100 cases. Oral Surg Oral Med Oral Pathol Oral Radiol 2015;120:358-67.|
|5||Maria NG, Luca V, Cinzia C. Oral mucosa pigmented lesions: An overview of the recent literature and 3 case reports. Dentist Case Rep 2018;2:40.|
|6||Lenane P, Powell FC. Oral pigmentation. J Eur Acad Dermatol Venereol 2000;14:448-65.|
|7||Joseph AR, James JS, Jordan Richard CK. Pigmented lesions. In: Oral Pathology Clinical Pathologic Correlations. 6th ed. Missouri: Elsevier Saunders; 2012. p. 134-47.|
|8||Amir E, Gorsky M, Buchner A, Sarnat H, Gat H. Physiologic pigmentation of the oral mucosa in Israeli children. Oral Surg Oral Med Oral Pathol 1991;71:396-8.|
|9||Gondak RO, da Silva-Jorge R, Jorge J, Lopes MA, Vargas PA. Oral pigmented lesions: Clinicopathologic features and review of the literature. Med Oral Patol Oral Cir Bucal 2012;17:e919-24.|
|10||Hedin CA. Smokers' melanosis. Occurrence and localization in the attached gingiva. Arch Dermatol 1977;113:1533-8.|
|11||Çerman AA, Altuna IK. Oral pigmentation. J Pigmentary Disord 2016;3:1-4.|
|12||Agarwal P, Saxena S, Kumar S, Gupta R. Melanotic neuroectodermal tumor of infancy: Presentation of a case affecting the maxilla. J Oral Maxillofac Pathol 2010;14:29-32.|
|13||Müller S. Melanin-associated pigmented lesions of the oral mucosa: Presentation, differential diagnosis, and treatment. Dermatol Ther 2010;23:220-9.|
|14||Chandler K, Chaudhry Z, Kumar N, Barrett AW, Porter SR. Melanocanthoma: A rare cause of oral hyperpigmentation. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1997;84:492-4.|
|15||Mirowski GW, Waibel JS. Pigmented lesions of the oral cavity. Dermatol Ther 2002;15:218-28.|
|16||Barker BF, Carpenter WM, Daniels TE, Kahn MA, Leider AS, Lozada-Nur F, et al. Oral mucosal melanomas: The WESTOP Banff workshop proceedings. Western Society of Teachers of Oral Pathology. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 1997;83:672-9.|
|17||Neville BW, Dam DD, Allen CM, Bouquot JE. Epithelial Pathology. Oral and Maxillofacial Pathology. 2nd ed. Philadelphia: W.B. Saunders; 2007. p. 376-80.|
|18||Pérusse R, Blackburn E. Differential diagnosis of pigmented lesions of the oral cavity. J Can Dent Assoc 1984;50:783-7.|
|19||Buchner A, Hansen LS. Amalgam pigmentation (amalgam tattoo) of the oral mucosa. A clinicopathologic study of 268 cases. Oral Surg Oral Med Oral Pathol 1980;49:139-47.|
|20||Meleti M, Vescovi P, Mooi WJ, van der Waal I. Pigmented lesions of the oral mucosa and perioral tissues: A flow-chart for the diagnosis and some recommendations for the management. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2008;105:606-16.|
|21||Fernandes D, Ferrisse TM, Navarro CM, Massucato EM, Onofre MA, Bufalino A. Pigmented lesions on the mucosa: A wide range of diagnoses. Oral Surg Oral Med Oral Pathol Oral Radiol 2015;119:374-8.|
|22||Granstein RD, Sober AJ. Drug- and heavy metal–induced hyperpigmentation. J Am Acad Dermatol 1981;5:1-8.|