Pigmented Lesions Flashcards
(83 cards)
1
Q
Pigmented Lesions of
Oral and Perioral Tissues
(5)
A
I. Benign Melanocytic Lesions
II. Neoplastic
III. Exogenous Pigment
IV. Systemic
V. Other…..
2
Q
Pigmented Lesions
I. Benign Melanocytic Lesions
(6)
A
Physiologic
Smoker’s melanosis
Traumatic melanosis
Ephelis
Lentigo
Oral melanotic macule
3
Q
Neoplastic
(3)
A
Nevi
Melanoma
Neuroectodermal Tumor of Infancy
4
Q
Exogenous Pigment
(2)
A
Metal pigment
- Amalgam tattoo
Drug-Induced Pigment
5
Q
Systemic
Endocrine
-ex (1)
Genetic
-ex (1)
A
- Addison Disease
- Peutz Jehger Syndrome
6
Q
Pigmentation Disorders: Physiologic
Etiology
A
- Normal melanocyte activity
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
8
Q
Pigmentation Disorders: Physiologic
Diagnosis
(2)
A
- History
- Distribution
9
Q
Pigmentation Disorders: Physiologic
Differential Diagnosis
(3)
A
- Mucosal melanotic macule
- Smoking-associated
melanosis - Superficial malignant
melanoma
10
Q
Pigmentation Disorders: Physiologic
Treatment
A
- None
11
Q
Pigmentation Disorders: Physiologic
Prognosis
A
- Excellent
12
Q
Traumatic Melanosis
Etiology
(2)
A
- A reactive and reversible alteration of
oral mucosal melanocytes and
keratinocytes - Usually associated with local trauma
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
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
15
Q
Traumatic Melanosis
Differential Diagnosis
(6)
A
- Melanoma
- Drug-induced pigmentation
- Smoker’s melanosis
- Mucosal melanotic macule
- Mucosal nevus
- Amalgam tattoo
16
Q
Traumatic Melanosis
Treatment
(2)
A
- None after establishing the diagnosis
- Often resolves spontaneously
17
Q
Traumatic Melanosis
Prognosis
A
- Excellent
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
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).
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
21
Q
Pigmentation Disorders: Smoker’s Melanosis
Diagnosis
(3)
A
- History of chronic, heavy smoking
- Biopsy
- Clinical appearance
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
23
Q
Pigmentation Disorders: Smoker’s Melanosis
Treatment
(2)
A
- None
- Reversible, if smoking is discontinued
24
Q
Pigmentation Disorders: Smoker’s Melanosis
Prognosis
(1)
A
- Good, with smoking cessation
25
Mucosal Melanotic Macule and Ephelides
Etiology
(2)
* Most idiopathic, some postinflammatory, some
drug-induced
* Multiple lesions suggest syndrome association,
as follows:
26
Mucosal Melanotic Macule and Ephelides
* Multiple lesions suggest syndrome association,
as follows:
(4)
* Peutz-Jeghers syndrome
* Laugier-Hunziker phenomenon
* Carney’s syndrome
* LEOPARD syndrome
27
Mucosal Melanotic Macule and Ephelides
Clinical Presentation
(6)
* 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
28
Mucosal Melanotic Macule and Ephelides
Differential Diagnosis
(3)
* Melanotic macule
* Nevus
* Melanoma
29
Nevus
Etiology
* Unknown; but, are benign tumors of
melanocytes
30
Nevus
Clinical Presentation
(4)
* Usually elevated, symmetric papule
* Pigmentation usually uniformly distributed
* Common on skin; unusual intraorally
* Palate and gingiva most often involved
31
Nevus
Diagnosis
(2)
* Clinical features
* Biopsy
32
Nevus
Differential Diagnosis
(7)
* Melanoma
* Hemangioma (Varix)
* Amalgam tattoo/foreign body
* Mucosal melanotic macule
* Kaposi’s sarcoma
* Ecchymosis
* Melanoacanthoma
33
Nevus
Treatment
(2)
* Excision of all pigmented oral lesions to rule
out malignant melanoma is advised.
* Malignant transformation of oral nevi
probably does not occur.
34
Nevus
Prognosis
* Excellent
35
Nevus - variants
(4)
* blue nevus
* compound
* amelanotic
* junctional
36
Malignant Melanoma
Etiology
(2)
* Unknown
* Cutaneous malignant melanoma with relation to sun exposure or familial-dysplastic
melanocytic lesions
37
Mucosal Malignant Melanoma
Etiology
* Unknown and unlike the cutaneous
malignant melanoma with relation to sun
exposure or familial-dysplastic melanocytic
lesions
38
Mucosal Malignant Melanoma
Clinical Presentation
(7)
* 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
Mucosal Malignant Melanoma
Mucosal spread
(3)
* 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
Mucosal Malignant Melanoma
* a horizontal or in situ growth phase often precedes the ---
* initially, a ---
* progresses to ---
vertical
invasive phase
macular, pigmented patch with irregular borders
deeply pigmented, nodular quality with ulceration
41
Mucosal Malignant Melanoma
Amelanotic forms may require use of immunohistochemical
identification:
S-100 protein, HMB-45, Melan-A expression
42
Mucosal Malignant Melanoma
Treatment
(4)
* 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
Mucosal Malignant Melanoma
Prognosis
(2)
* Generally poor for most oral
malignant melanomas
* Less than 20% survival at 5 years in
most studies
44
Amalgam Tattoo
Etiology
(1)
* Implantation or passive/frictional
transfer of dental silver amalgam into
mucosa
45
Amalgam Tattoo
Clinical Presentation
(3)
* 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
Amalgam Tattoo
Clinical
(2)
* Intact mucosa ovelying the
black spot
* Benign or malignant melanin
pigmentation is usually
brownish and occurs within
the epithelium (on the
surface)
47
Amalgam Tattoo
Diagnosis
(2)
* 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
Amalgam Tattoo
Differential Diagnosis
(5)
* Vascular malformation
* Mucosal nevus
* Melanoma
* Mucosal melanotic macule
* Melanoacanthoma
49
Amalgam Tattoo
Treatment
(1)
* Biopsy or observation only
50
Amalgam Tattoo
Prognosis
* Little clinical significance if untreated
51
#27 Lesion: Amalgam Tattoo
Prevalence (# Lesions/1,000) =
0.6 for Males, 1.0 for Females, 0.8 Total
52
Mucosal Pigmentation: Extrinsic(Drug or
Metal Induced)
Etiology
(2)
* 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
Mucosal Pigmentation: Extrinsic(Drug or
Metal Induced)
Clinical Presentation
(5)
* 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
Mucosal Pigmentation: Extrinsic(Drug or
Metal Induced)
Diagnosis
(2)
* History of exposure to, or ingestion of, heavy
metals or drugs
* Differentiation from melanocyte-related
pigmentation by
biopsy if necessary
55
Mucosal Pigmentation: Extrinsic(Drug or
Metal Induced)
Differential Diagnosis
(3)
* 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
Mucosal Pigmentation: Extrinsic(Drug or
Metal Induced)
Treatment
* Investigation of cause and elimination if possible
57
Mucosal Pigmentation: Extrinsic(Drug or
Metal Induced)
Prognosis
* Excellent
58
Argyria
(2)
* Ag salts have antibacterial and anti-
neoplastic benefits
* Bluish discoloration from
therapeutic ingestion or industrial
accident
59
IAMT
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
Pigmentation Disorders: Drug Induced
Etiology
(2)
* Therapeutic drug-related tissue
pigmentation
* Many drugs may cause change—
(see list on next slide)
61
Pigmentation Disorders: Drug Induced
Clinical Presentation
(3)
* 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
Pigmentation Disorders: Drug Induced
Drugs Capable of Producing Tissue
Pigmentation
(8)
* 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
Tetracycline Staining
Etiology
(2)
* 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
Tetracycline Staining
Clinical Presentation
(3)
* 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
Tetracycline Staining
Diagnosis
(2)
* Clinical appearance and
history
* Fluorescence of teeth may
be noted with ultraviolet
illumination.
66
Tetracycline Staining
Differential Diagnosis
* Dentinogenesis imperfecta
67
Tetracycline Staining
Treatment
* Restorative/cosmetic dental
techniques
68
Tetracycline Staining
Prognosis
* Good
69
Primary adrenal insufficiency
* Addison Disease
➢ Destruction of adrenal cortex
o ↓Cortisol and ↑ACTH
70
Addisons disease
➢ Etiology
(3)
o Most commonly autoimmune
❑ What does this mean?
o Chronic infectious disease and sepsis
❑ HIV, CMV, fungal infection
o Drugs
71
Addisons disease
➢ Cannot tolerate stress (emotional or physical)
o Adrenal crisis
72
Addisons disease
➢ Requires cortisol replacement
(2)
o Surgery and stress may require supplemental
corticosteroids
o Pain control is important
73
Adrenal insufficiency
* Secondary adrenal insufficiency
(3)
➢ Impaired/destructive pituitary disease
➢ ↓Cortisol and ↓ACTH; aldosterone
unchanged
➢ Lower dose replacement therapy
74
Tertiary adrenal insufficiency
(3)
➢ Impaired function of hypothalamus
➢ Most commonly a result of chronic
exogenous steroid use
➢ Lower dose replacement therapy
75
Hyperpigmentation and adrenal crisis do not usually occur/less likely with
---- adrenal insufficiency
secondary and tertiary
76
Undiagnosed patient with signs and symptoms of adrenal disease should be
promptly referred to their primary physician for
comprehensive work-up
77
Determine type and severity of adrenal disease
* Hyperadrenalism
(3)
➢ 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
Impaired wound healing may be a consequence of both (2)
hyperadrenalism and
adrenal insufficiency
79
Adrenal insufficiency
➢ Necessity for supplemental corticosteroids? Discuss dosage w/physician
o Depends on?
(3)
✓ Type
✓ Severity/ stability/ medical status
✓ Dental procedure being performed (long: >1hr or invasive) /type
of stress/dental infection
80
Signs of adrenal crisis
(5)
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
Pain control
(2)
o Adequate anesthesia, long-acting agent at end of procedure
o Good post-up pain control
82
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 ....
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
Genetic - Peutz Jeghers Syndrome
mucocutaneous pigmentation
(3)
-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
