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Oral Medicine > Pigmented Lesions > Flashcards

Pigmented Lesions Flashcards

1
Q

Pigmented Lesions of
Oral and Perioral Tissues
(5)

A

I. Benign Melanocytic Lesions
II. Neoplastic
III. Exogenous Pigment
IV. Systemic
V. Other…..

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2
Q

Pigmented Lesions
I. Benign Melanocytic Lesions
(6)

A

Physiologic
Smoker’s melanosis
Traumatic melanosis
Ephelis
Lentigo
Oral melanotic macule

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3
Q

Neoplastic
(3)

A

Nevi
Melanoma
Neuroectodermal Tumor of Infancy

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4
Q

Exogenous Pigment
(2)

A

Metal pigment
- Amalgam tattoo
Drug-Induced Pigment

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5
Q

Systemic
Endocrine
-ex (1)
Genetic
-ex (1)

A
  • Addison Disease
  • Peutz Jehger Syndrome
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6
Q

Pigmentation Disorders: Physiologic
Etiology

A
  • Normal melanocyte activity
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7
Q

Pigmentation Disorders: Physiologic
Clinical Presentation
(3)

A
  • Seen in all ages
  • Symmetric distribution over
    many sites, gingiva most
    commonly
  • Surface architecture, texture
    unchanged
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8
Q

Pigmentation Disorders: Physiologic
Diagnosis
(2)

A
  • History
  • Distribution
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9
Q

Pigmentation Disorders: Physiologic
Differential Diagnosis
(3)

A
  • Mucosal melanotic macule
  • Smoking-associated
    melanosis
  • Superficial malignant
    melanoma
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10
Q

Pigmentation Disorders: Physiologic
Treatment

A
  • None
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11
Q

Pigmentation Disorders: Physiologic
Prognosis

A
  • Excellent
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12
Q

Traumatic Melanosis
Etiology
(2)

A
  • A reactive and reversible alteration of
    oral mucosal melanocytes and
    keratinocytes
  • Usually associated with local trauma
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13
Q

Traumatic Melanosis
Clinical Presentation
(6)

A
  • 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
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14
Q

Traumatic Melanosis
Diagnosis
(4)

A
  • 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
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15
Q

Traumatic Melanosis
Differential Diagnosis
(6)

A
  • Melanoma
  • Drug-induced pigmentation
  • Smoker’s melanosis
  • Mucosal melanotic macule
  • Mucosal nevus
  • Amalgam tattoo
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16
Q

Traumatic Melanosis
Treatment
(2)

A
  • None after establishing the diagnosis
  • Often resolves spontaneously
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17
Q

Traumatic Melanosis
Prognosis

A
  • Excellent
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18
Q

Pigmentation Disorders: Smoker’s Melanosis
Etiology
(3)

A
  • 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
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19
Q

Pigmentation Disorders: Smoker’s Melanosis
Clinical Presentation
(3)

A
  • 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).
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20
Q

Pigmentation Disorders: Smoker’s Melanosis
Microscopic Findings
(3)

A
  • Increased melanin in basal cell layer
  • Increased melanin production by normal numbers of
    melanocytes
  • Melanin incontinence
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21
Q

Pigmentation Disorders: Smoker’s Melanosis
Diagnosis
(3)

A
  • History of chronic, heavy smoking
  • Biopsy
  • Clinical appearance
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22
Q

Pigmentation Disorders: Smoker’s Melanosis
Differential Diagnosis
(4)

A
  • Physiologic pigmentation
  • Addison’s disease
  • Medication-related pigmentation (drug-
    induced pigmentation by chloroquine,
    clofazimine, mepacrine, chlorpromazine,
    quinidine, or zidovudine)
  • Malignant melanoma
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23
Q

Pigmentation Disorders: Smoker’s Melanosis
Treatment
(2)

A
  • None
  • Reversible, if smoking is discontinued
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24
Q

Pigmentation Disorders: Smoker’s Melanosis
Prognosis
(1)

A
  • Good, with smoking cessation
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25
Q

Mucosal Melanotic Macule and Ephelides
Etiology
(2)

A
  • Most idiopathic, some postinflammatory, some
    drug-induced
  • Multiple lesions suggest syndrome association,
    as follows:
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26
Q

Mucosal Melanotic Macule and Ephelides
* Multiple lesions suggest syndrome association,
as follows:
(4)

A
  • Peutz-Jeghers syndrome
  • Laugier-Hunziker phenomenon
  • Carney’s syndrome
  • LEOPARD syndrome
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27
Q

Mucosal Melanotic Macule and Ephelides
Clinical Presentation
(6)

A
  • 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
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28
Q

Mucosal Melanotic Macule and Ephelides
Differential Diagnosis
(3)

A
  • Melanotic macule
  • Nevus
  • Melanoma
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29
Q

Nevus
Etiology

A
  • Unknown; but, are benign tumors of
    melanocytes
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30
Q

Nevus
Clinical Presentation
(4)

A
  • Usually elevated, symmetric papule
  • Pigmentation usually uniformly distributed
  • Common on skin; unusual intraorally
  • Palate and gingiva most often involved
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31
Q

Nevus
Diagnosis
(2)

A
  • Clinical features
  • Biopsy
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32
Q

Nevus
Differential Diagnosis
(7)

A
  • Melanoma
  • Hemangioma (Varix)
  • Amalgam tattoo/foreign body
  • Mucosal melanotic macule
  • Kaposi’s sarcoma
  • Ecchymosis
  • Melanoacanthoma
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33
Q

Nevus
Treatment
(2)

A
  • Excision of all pigmented oral lesions to rule
    out malignant melanoma is advised.
  • Malignant transformation of oral nevi
    probably does not occur.
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34
Q

Nevus
Prognosis

A
  • Excellent
35
Q

Nevus - variants
(4)

A
  • blue nevus
  • compound
  • amelanotic
  • junctional
36
Q

Malignant Melanoma
Etiology
(2)

A
  • Unknown
  • Cutaneous malignant melanoma with relation to sun exposure or familial-dysplastic
    melanocytic lesions
37
Q

Mucosal Malignant Melanoma
Etiology

A
  • Unknown and unlike the cutaneous
    malignant melanoma with relation to sun
    exposure or familial-dysplastic melanocytic
    lesions
38
Q

Mucosal Malignant Melanoma
Clinical Presentation
(7)

A
  • 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
    Etiology
  • Unknown and unlike the cutaneous
    malignant melanoma with relation to sun
    exposure or familial-dysplastic melanocytic
    lesions
39
Q

Mucosal Malignant Melanoma
Mucosal spread
(3)

A
  • 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.
40
Q

Mucosal Malignant Melanoma
* a horizontal or in situ growth phase often precedes the —
* initially, a —
* progresses to —

A

vertical
invasive phase
macular, pigmented patch with irregular borders
deeply pigmented, nodular quality with ulceration

41
Q

Mucosal Malignant Melanoma
Amelanotic forms may require use of immunohistochemical
identification:

A

S-100 protein, HMB-45, Melan-A expression

42
Q

Mucosal Malignant Melanoma
Treatment
(4)

A
  • 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)
43
Q

Mucosal Malignant Melanoma
Prognosis
(2)

A
  • Generally poor for most oral
    malignant melanomas
  • Less than 20% survival at 5 years in
    most studies
44
Q

Amalgam Tattoo
Etiology
(1)

A
  • Implantation or passive/frictional
    transfer of dental silver amalgam into
    mucosa
45
Q

Amalgam Tattoo
Clinical Presentation
(3)

A
  • 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
46
Q

Amalgam Tattoo
Clinical
(2)

A
  • Intact mucosa ovelying the
    black spot
  • Benign or malignant melanin
    pigmentation is usually
    brownish and occurs within
    the epithelium (on the
    surface)
47
Q

Amalgam Tattoo
Diagnosis
(2)

A
  • 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
48
Q

Amalgam Tattoo
Differential Diagnosis
(5)

A
  • Vascular malformation
  • Mucosal nevus
  • Melanoma
  • Mucosal melanotic macule
  • Melanoacanthoma
49
Q

Amalgam Tattoo
Treatment
(1)

A
  • Biopsy or observation only
50
Q

Amalgam Tattoo
Prognosis

A
  • Little clinical significance if untreated
51
Q

27 Lesion: Amalgam Tattoo

Prevalence (# Lesions/1,000) =

A

0.6 for Males, 1.0 for Females, 0.8 Total

52
Q

Mucosal Pigmentation: Extrinsic(Drug or
Metal Induced)
Etiology
(2)

A
  • 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
53
Q

Mucosal Pigmentation: Extrinsic(Drug or
Metal Induced)
Clinical Presentation
(5)

A
  • 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)
54
Q

Mucosal Pigmentation: Extrinsic(Drug or
Metal Induced)
Diagnosis
(2)

A
  • History of exposure to, or ingestion of, heavy
    metals or drugs
  • Differentiation from melanocyte-related
    pigmentation by
    biopsy if necessary
55
Q

Mucosal Pigmentation: Extrinsic(Drug or
Metal Induced)
Differential Diagnosis
(3)

A
  • 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.
56
Q

Mucosal Pigmentation: Extrinsic(Drug or
Metal Induced)
Treatment

A
  • Investigation of cause and elimination if possible
57
Q

Mucosal Pigmentation: Extrinsic(Drug or
Metal Induced)
Prognosis

A
  • Excellent
58
Q

Argyria
(2)

A
  • Ag salts have antibacterial and anti-
    neoplastic benefits
  • Bluish discoloration from
    therapeutic ingestion or industrial
    accident
59
Q

IAMT

A

all mercury dental fillings leak substantial amounts of mercury, therefore, it is the conclusion of the International Academy of Oral Medicine and Toxicology that implanting time-release mercury silver dental fillings in children or adults is neither fare not necessary since numerous suitable alternative already exist

60
Q

Pigmentation Disorders: Drug Induced
Etiology
(2)

A
  • Therapeutic drug-related tissue
    pigmentation
  • Many drugs may cause change—
    (see list on next slide)
61
Q

Pigmentation Disorders: Drug Induced
Clinical Presentation
(3)

A
  • 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
62
Q

Pigmentation Disorders: Drug Induced
Drugs Capable of Producing Tissue
Pigmentation
(8)

A
  • Antimalarials: chloroquine,
    mepacrine, quinidine, old-time
    antimalarials
  • 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
63
Q

Tetracycline Staining
Etiology
(2)

A
  • 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.
64
Q

Tetracycline Staining
Clinical Presentation
(3)

A
  • 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).
65
Q

Tetracycline Staining
Diagnosis
(2)

A
  • Clinical appearance and
    history
  • Fluorescence of teeth may
    be noted with ultraviolet
    illumination.
66
Q

Tetracycline Staining
Differential Diagnosis

A
  • Dentinogenesis imperfecta
67
Q

Tetracycline Staining
Treatment

A
  • Restorative/cosmetic dental
    techniques
68
Q

Tetracycline Staining
Prognosis

A
  • Good
69
Q

Primary adrenal insufficiency
* Addison Disease

A

➢ Destruction of adrenal cortex
o ↓Cortisol and ↑ACTH

70
Q

Addisons disease
➢ Etiology
(3)

A

o Most commonly autoimmune
❑ What does this mean?
o Chronic infectious disease and sepsis
❑ HIV, CMV, fungal infection
o Drugs

71
Q

Addisons disease
➢ Cannot tolerate stress (emotional or physical)

A

o Adrenal crisis

72
Q

Addisons disease
➢ Requires cortisol replacement
(2)

A

o Surgery and stress may require supplemental
corticosteroids
o Pain control is important

73
Q

Adrenal insufficiency
* Secondary adrenal insufficiency
(3)

A

➢ Impaired/destructive pituitary disease
➢ ↓Cortisol and ↓ACTH; aldosterone
unchanged
➢ Lower dose replacement therapy

74
Q

Tertiary adrenal insufficiency
(3)

A

➢ Impaired function of hypothalamus
➢ Most commonly a result of chronic
exogenous steroid use
➢ Lower dose replacement therapy

75
Q

Hyperpigmentation and adrenal crisis do not usually occur/less likely with
—- adrenal insufficiency

A

secondary and tertiary

76
Q

Undiagnosed patient with signs and symptoms of adrenal disease should be
promptly referred to their primary physician for

A

comprehensive work-up

77
Q

Determine type and severity of adrenal disease
* Hyperadrenalism
(3)

A

➢ BP and glucose levels
➢ Avoid NSAIDs and aspirin → peptic ulcers, GI bleed
➢ If osteoporosis and osteopenia
o More prone to periodontal bone loss –
o May have history of bisphosphonate use

78
Q

Impaired wound healing may be a consequence of both (2)

A

hyperadrenalism and
adrenal insufficiency

79
Q

Adrenal insufficiency
➢ Necessity for supplemental corticosteroids? Discuss dosage w/physician
o Depends on?
(3)

A

✓ Type
✓ Severity/ stability/ medical status
✓ Dental procedure being performed (long: >1hr or invasive) /type
of stress/dental infection

80
Q

Signs of adrenal crisis
(5)

A

o Hypotension - Monitor BP – vasopressors, patient position, fluid
replacement
o Abdominal pain
o Myalgia
o Fever
o Supplement with 100 mg of hydrocortisone and send to ED

81
Q

Pain control
(2)

A

o Adequate anesthesia, long-acting agent at end of procedure
o Good post-up pain control

82
Q

Genetic - Peutz Jeghers Syndrome
Peutz Jeghers syndrome (PJS) is an autosomal
dominant genetic condition affecting around
1/50,000 and 1/200,000 individuals
symptoms usually appear during the…
dark skin freckling (melanocytic macules) around
the …. causing
….
increased risk for ….

A

first decade of life
mouth, eyes, nostrils, fingers, oral mucosa
and perianal
GI polyps (hamartomatous polyposis)
nausea, vomiting, abdominal pain, intestinal
obstruction and rectal bleeding
intestinal and other GI cancers

83
Q

Genetic - Peutz Jeghers Syndrome
mucocutaneous pigmentation
(3)

A

-seen in 95% patients
-1 mm to 5 mm in size
-appears by 1 or 2 years of age. fades after puberty except buccal mucosa

Oral Medicine (13 decks)

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