pigmented lesions Flashcards
Benign Melanocytic Lesions
Physiologic
Smoker’s melanosis
Traumatic melanosis
Ephelis
Lentigo
Oral melanotic macule
Neoplastic Pigmented Lesions of
Oral and Perioral Tissues
Nevi
Melanoma
Neuroectodermal Tumor of Infancy
Exogenous Pigmentations
Metal pigment
- Amalgam tattoo/ silver
Drug-Induced Pigment
Systemic Pigmented Lesions of Oral and Perioral Tissues
Endocrine- Addison Disease
Genetic- Peutz Jehger Syndrome
physiologic pigmentation
Etiology
Clinical presentation
Diagnosis
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
physiological pigmentation dif dx
- Mucosal melanotic macule
- Smoking-associated melanosis
- Superficial malignant melanoma
Likely dx? dif?
physio pigment
dif:
* Mucosal melanotic macule
* Smoking-associated melanosis
* Superficial malignant melanoma
tx physio pigmentation
none, may montior
prognosis phyiso pig
excellent
pathologic?
No, can be seen with pigment
Traumatic Melanosis etiology
- A reactive and reversible alteration of oral mucosal melanocytes and keratinocytes
- Usually associated with local trauma
Traumatic Melanosis presentation
distribution?
* Most often noted?
* women:men?
* History of ?
* onset? most often on?
* symptoms?
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
Traumatic Melanosis Diagnosis
* Clinical history of?
* Histologic evaluation?
- Clinical history of rapid onset
- Histologic evaluation: Scattered dendritic melanocytes within spongiotic and acanthotic epithelium
- Increased number of melanocytes along basal layer as single unit
Traumatic melanosis dif dx
- Melanoma
- Drug-induced pigmentation
- Smoker’s melanosis
- Mucosal melanotic macule
- Mucosal nevus
- Amalgam tattoo
Traumatic Melanosis
Treatment and Prognosis
Treatment
* None after establishing the diagnosis
* Often resolves spontaneously
Prognosis
* Excellent
Smoker’s 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
Smoker’s Melanosis 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)
Smoker’s Melanosis micro findings
Increased melanin in basal cell layer
* Increased melanin production by normal numbers of melanocytes
* Melanin incontinence
Smoker’s Melanosis
Diagnosis
- History of chronic, heavy smoking
- Biopsy
- Clinical appearanc
smoker melanosis dif dx
Physiologic pigmentation
* Addison’s disease
* Medication-related pigmentation (drug- induced pigmentation by chloroquine, clofazimine, mepacrine, chlorpromazine, quinidine, or zidovudine)
* Malignant melanoma
smoker melanosis tx/prognosis
Treatment
* None
* Reversible, if smoking is discontinued
Prognosis
* Good, with smoking cessation
pics from a smoker
lilely smokers melanosis, no surface changes
Mucosal Melanotic Macule and Ephelides Etiology
when multiple?
- 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
mucosal melanotic macule
Mucosal Melanotic Macule and Ephelides Clinical Presentation
* Most common ages?
* Many?
* most common site?
* other sites?
* app?
* size?
- 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
dif dx?
- Melanotic macule
- Nevus
- Melanoma
Nevus
Etiology
- Unknown; but, are benign tumors of
melanocytes
nevus presentation
* Usual app
* Pigmentation?
* Common where?
* common oral sites?
- Usually elevated, symmetric papule
- Pigmentation usually uniformly distributed
- Common on skin; unusual intraorally
- Palate and gingiva most often involved
likely dx?
nevus
nevus diagnosis
clinical features and biopsy
nevus dif dx
- Melanoma
- Hemangioma (Varix)
- Amalgam tattoo/foreign body
- Mucosal melanotic macule
- Kaposi’s sarcoma
- Ecchymosis
- Melanoacanthoma
nevus tx/ prognosis
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 variants
- blue nevus
- compound
- amelanotic
- junctional
Malignant Melanoma
Etiology
- Unknown (oral)
- Cutaneous malignant melanoma with relation to sun exposure or familial-dysplastic melanocytic lesions
Mucosal Malignant Melanoma etiology
Unknown and unlike the cutaneous
malignant melanoma with relation to sun exposure or familial-dysplastic melanocytic lesions
Mucosal Malignant Melanoma presentation
Rare in?
* general age?
* Usually arises where in mouth?
* growth phases?
* Progression to?
* May arise de novo as?
* Rarely may be?
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 Malignant Melanoma
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.
Mucosal Malignant Melanoma
* growth phases?
* initial presentation
* progresses to?
- a horizontal or in situ growth phase often precedes the vertical invasive phase
- initially, a macular, pigmented patch with irregular borders
- progresses to deeply pigmented, nodular quality with ulceration
mucosal malignant melanoma
Mucosal Malignant Melanoma
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
mucosal malignant melanoma Prognosis
- Generally poor for most oral
malignant melanomas - Less than 20% survival at 5 years in
most studies
Amalgam Tattoo
Etiology
- Implantation or passive/frictional
transfer of dental silver amalgam into
mucosa
amalgam tat 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 - Intact mucosa ovelying the black spot
- Benign or malignant melanin pigmentation is usually brownish and occurs within the epithelium (on the
surface)
Amalgam Tattoo Diagnosis
- Radiographs useful for diagnosis
- Biopsy may be necessary if clinical diagnosis is in doubt or to rule out lesions of melanocytic origin
amalgam tat dif dx
- Vascular malformation
- Mucosal nevus
- Melanoma
- Mucosal melanotic macule
- Melanoacanthoma
tx/prognosis amalgam tat
Treatment
* Biopsy or observation only
little significance if untx
tooth has an amalgam filling
amalgam tat
amalgam tat
Mucosal Pigmentation: Extrinsic(Drug or Metal Induced) 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
Mucosal Pigmentation: Extrinsic (Drug or
Metal Induced) presentation
* range?
* If heavy metals are the cause, what is common?
* Palatal changes characteristic with?
* Most medications cause color alteration where?
* Darkened alveolar bone with?
- 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)
Mucosal Pigmentation: Extrinsic (Drug or Metal Induced) Diagnosis
- History of exposure to, or ingestion of, heavy metals or drugs
- Differentiation from melanocyte-related
biopsy if necessary
Mucosal Pigmentation: Extrinsic(Drug or
Metal Induced) dif dx
when localized?
when generalized?
when asymmetric?
- 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.
Mucosal Pigmentation: Extrinsic(Drug or
Metal Induced) tx and prognosis
Treatment
* Investigation of cause and elimination if possible
Prognosis
* Excellent
silver pigmentation
can result in blue/purple macules on skin/mucosa= Argyria
Argyria
- Ag salts have antibacterial and anti-neoplastic benefits
- Bluish discoloration from therapeutic ingestion or industrial accident
argyria
silver pegs used
argyria
mercury fillings?
Pigmentation Disorders: Drug Induced Etiology
- Therapeutic drug-related tissue
pigmentation - Many drugs may cause change—
Pigmentation Disorders: Drug Induced presentation
colors?
* most common site?
* Itooth discoloration?
Macular mucosal discoloration (brown, gray, black)
* Palate and gingiva are most common sites affected
* In addition to mucosal changes, teeth in adults and children may be bluish gray owing to minocycline/tetracycline use
Drugs Capable of Producing Tissue
Pigmentation
- Antimalarials: chloroquine, mepacrine, quinidine,
- Antibiotics: tetracycline group, minocycline
- Antivirals: azidothymidine
- Phenothiazine: chlorpromazine Clofazimine
- Heavy metals: gold, mercury salts, silver nitrate, bismuth, lead
- Hormones: ACTH, oral contraceptives
- Cancer/chemotherapy drugs: busulfan, cyclophosphamide, cis-platinum
- Other: methyldopa
recovering from malaria what could this be?
plaqeunil induced pigmentation
Tetracycline Staining
Etiology
- Prolonged ingestion of tetracycline or its congeners during tooth development
- Less commonly, tetracycline ingestion causes staining after tooth formation is complete: reparative (secondary) dentin cementum may be stained.
Tetracycline Staining clinical presentation
Yellowish to gray (oxidized tetracycline) color of enamel and dentin
* May be generalized or horizontally banded depending on duration of tetracycline exposure
* Alveolar bone may also be stained bluish red (particularly with minocyline use, 10% after 1 year and 20% after 4 years of therapy).
likely rx?
tetracyline/minocycline
Tetracycline Staining
Diagnosis
- Clinical appearance and history
- Fluorescence of teeth may be noted with ultraviolet
illumination.
tetracycline dif dx
DI
Tetracycline Staining tx and prognosis
Treatment
* Restorative/cosmetic dental
techniques
Prognosis
* Good
adrenal insuff
addisons dx, 3>2>1
- Secondary adrenal insufficiency therapy
➢ cause?
➢ Cortisol, ACTH, aldosterone levels?
➢ replacement therapy dose?
➢ Impaired/destructive pituitary disease
➢ ↓Cortisol and ↓ACTH; aldosterone unchanged
➢ Lower dose replacement therapy
- Tertiary adrenal insufficiency
result of? tx?
➢ Impaired function of hypothalamus
➢ Most commonly a result of chronic exogenous steroid use
➢ Lower dose replacement therapy
Undiagnosed patient with signs and symptoms of adrenal disease should be?
promptly referred to their primary physician for comprehensive work-up
what can be seen in both hyper and hypoadrenalism
Impaired wound healing may be a consequence of both hyperadrenalism and
adrenal insufficiency
Peutz Jeghers syndrome:
inheritance pattern?
Prevalence?
when do symptoms usually appear?
oral sign?
GI?
autosomal dominant genetic condition affecting around 1/50,000 and 1/200,000 individuals
symptoms usually appear during the first decade of life
dark skin freckling (melanocytic macules) around the mouth, eyes, nostrils, fingers, oral mucosa and perianal
GI polyps (hamartomatous polyposis) causing nausea, vomiting, abdominal pain, intestinal obstruction and rectal bleeding increased risk for intestinal and other GI cancers
likely?
Peutz-jehger
PJS mucocuntaneous pigmentation
% pts with this?
common oral sites? size?
appears when? regression?
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