Pigmented lesions Flashcards
Etiology
• Normal melanocyte activity
Clinical Presentation
• Seen in all ages
• Symmetric distribution over
many sites, gingiva most
commonly
• Surface architecture, texture
unchanged
Diagnosis
• History
• Distribution
Differential Diagnosis
• Mucosal melanotic macule
• Smoking-associated
melanosis
• Superficial malignant
melanoma
Treatment
• None
Prognosis
• Excellent
Physiologic Pigmentation
Etiology
• A reactive and reversible alteration of oral mucosal melanocytes and keratinocytes
• Usually associated with local trauma
Clinical Presentation
• Unilateral dark plaque; rarely multiple, bilateral
• Most often noted among Blacks and other non-Caucasians
• Occurs more often in women than men by a ratio of 3:1
• History of trauma and local irritation
• Forms rapidly, most often on buccal/labial mucosa
• Asymptomatic melanotic pigmentation
Diagnosis
• Clinical history of rapid onset
• Histologic evaluation
• Scattered dendritic melanocytes within spongiotic and acanthotic epithelium
• Increased number of melanocytes along basal layer as single units
Differential Diagnosis
• Melanoma
• Drug-induced pigmentation
• Smoker’s melanosis
• Mucosal melanotic macule
• Mucosal nevus
• Amalgam tattoo
Treatment
• None after establishing the diagnosis
• Often resolves spontaneously
Prognosis
• Excellent
Traumatic melanosis
Etiology
• Melanin pigmentation of oral mucosa in heavy smokers
• May occur in up to 1 of 5 smokers, especially females taking birth control pills or hormone replacement
• Melanocytes stimulated by a component in tobacco smoke
Clinical Presentation
• Brownish discoloration of alveolar and attached labial gingiva, buccal mucosa
• Pigmentation is diffuse and uniformly distributed; symmetric gingival pigmentation occurs most often.
• Degree of pigmentation is positively influenced by female hormones (birth control pills, hormone replacement therapy).
Microscopic Findings
• Increased melanin in basal cell layer
• Increased melanin production by normal numbers of melanocytes
• Melanin incontinence
Diagnosis
• History of chronic, heavy smoking
• Biopsy
• Clinical appearance
Differential Diagnosis
• Physiologic pigmentation
• Addison’s disease
• Medication-related pigmentation (drug-induced pigmentation by chloroquine, clofazimine, mepacrine, chlorpromazine, quinidine, or zidovudine)
• Malignant melanoma
Treatment
• None
• Reversible, if smoking is discontinued
Prognosis
• Good, with smoking cessation
Smoker’s melanosis
Etiology
• Most idiopathic, some postinflammatory, some drug-induced
• Multiple lesions suggest syndrome association, as follows:
• Peutz-Jeghers syndrome
• Laugier-Hunziker phenomenon
• Carney’s syndrome
• LEOPARD syndrome
Clinical Presentation
• Most in adulthood (fourth decade and beyond)
• Most are solitary and well circumscribed
• Lower lip vermilion border most common site, mostly in young women (labial melanotic macule)
• Buccal mucosa, palate, and attached gingiva also involved (mucosal melanotic macule)
• Usually brown, uniformly pigmented, round to ovoid shape with slightly irregular border
• Usually < 5 mm in diameter
Mucosal Melanotic Macule and Ephelides
What is the most common benign melanocytic lesions?
<5mm, well-defined, surface not altered
Oral melanotic macule
Etiology
• Unknown; but, are benign tumors of melanocytes
Clinical Presentation
• Usually elevated, symmetric papule
• Pigmentation usually uniformly distributed
• Common on skin; unusual intraorally
• Palate and gingiva most often involved
Diagnosis
• Clinical features
• Biopsy
Differential Diagnosis
• Melanoma
• Varix
• Amalgam tattoo/foreign body
• Mucosal melanotic macule
• Kaposi’s sarcoma
• Ecchymosis
• Melanoacanthoma
Treatment
• Excision of all pigmented oral lesions to rule out malignant melanoma is advised.
• Malignant transformation of oral nevi probably does not occur.
Prognosis
• Excellent
Nevus
Etiology
• Unknown and unlike the cutaneous malignant melanoma with relation to sun exposure or familial-dysplastic melanocytic lesionsMucosal Malignant Melanoma
Clinical Presentation
• Rare in oral cavity (< 1% of all melanomas) and sinonasal tract
• generally >30 years of age.
• Usually arises on maxillary gingiva and hard palate
• May exhibit early in situ phase: a macular, pigmented patch with irregular borders
• Progression to deeply pigmented, nodular quality with ulceration
• May arise de novo as a pigmented or amelanotic nodule
• Rarely may be metastatic to the oral cavity as a nodular, usually pigmented mass
Mucosal spread
• Early stage: atypical melanocytes at epithelial–connective tissue interface, occasionally with intraepithelial spread
• Later infiltration into lamina propria and muscle
• Strict correlation to cutaneous malignant melanoma is not well established, although, as in skin, a similar horizontal or in situ growth phase often precedes the vertical invasive phase.
Treatment
• Surgical excision
• Marginal parameters related to depth of invasion and presence of lateral growth
• Wide surgical margins; resection (including maxillectomy) for large, deeper lesions
• Neck dissection in cases of deep invasion (< 1.25 mm)
Prognosis
• Generally poor for most oral malignant melanomas
• Less than 20% survival at 5 years in most studies
Malignant Melanoma
Etiology
• Implantation or passive/frictional transfer of dental silver amalgam into mucosa
Clinical Presentation
• Gray to black focal macules, usually well defined, but may be diffuse with no associated signs of inflammation
• Typically in attached gingiva, alveolar mucosa, buccal mucosa
• Occasionally may be visible radiographically
Clinical
• Intact mucosa ovelying the
black spot
• Benign or malignant melanin
pigmentation is usually
brownish and occurs within
the epithelium (on the
surface)
Diagnosis
• Radiographs useful for diagnosis
(intraoral film placement)
• Biopsy may be necessary if clinical diagnosis is in doubt or to rule out lesions of melanocytic origin
Differential Diagnosis
• Vascular malformation
• Mucosal nevus
• Melanoma
• Mucosal melanotic macule
• Melanoacanthoma
Treatment
• Biopsy or observation only
Prognosis
• Little clinical significance if untreated
Amalgam tattoo
Etiology
• Occupational exposure—metals vapors (lead, mercury)
• Therapeutic—metal salt deposits (bismuth, cis platinum, silver, gold); also nonmetal agents, such as chloroquine, minocycline, zidovudine, chlorpromazine, phenolphthalein, clofazimine, and others
Clinical Presentation
• Focal to diffuse areas of pigmentary change
• If heavy metals are the cause, a typical gray to black color is seen along the gingival margin or areas of inflammation.
• Palatal changes characteristic with antimalarial drugs and minocycline
• Most medications cause color alteration of buccal-labial mucosa and attached gingiva.
• Darkened alveolar bone with minocycline therapy (10% at 1 year, 20% at 4 years of therapy)
Diagnosis
• History of exposure to, or ingestion of, heavy metals or drugs
• Differentiation from melanocyte-related pigmentation by
biopsy if necessary
Differential Diagnosis
• When localized: amalgam tattoo, mucosal melanotic macule,
melanoacanthoma, mucosal nevus, ephelides, Kaposi’s sarcoma,
purpura, malignant melanoma, ecchymosis
• When generalized: ethnic pigmentation,Addison’s disease
• If asymmetric, in situ melanoma must be ruled out by biopsy.
Treatment
• Investigation of cause and elimination if possible
Prognosis
• Excellent
Extrinsic mucosal pigmentation
• Ag salts have antibacterial and anti-
neoplastic benefits
• Bluish discoloration from
therapeutic ingestion or industrial
accident
Argryia
