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OROFACIALPIGMENTATION
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introduction
Pigmented oral lesions are a large group of disorders
in which the dark or brown color is the essential
clinical characteristic. Usually, the dark color of the
lesions is due to melanin production by either
melanocytes or nevus cells. In addition, exogenousdeposits and pigment-producing bacteria can also
produce pigmented lesions. Benign disorders,
deposits, benign and malignant neoplasms, and
systemic diseases are included in the group ofpigmented lesions.
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Melanin
elanin, a nonhemoglobin derived brown pigment, is themost common of the endogenous pigments and isproduced by melanocytes present in the basal layer ofthe epithelium.
!he number of melanocytes in the mucosa correspondsnumerically to that of skin" however, in the mucosa theiractivity is reduced.
#arious stimuli can result in an increased production of
melanin at the level of mucosa including trauma,hormones, radiation, and medications.
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Addison’s Disease
Etiology $drenal cortical atrophy%&'( idiopathic )*autoimmune+
ral manifestations due to secondary melanocyte
stimulation by increased levels of adrenocorticotropichormone )$!+ or /-lipotropin
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Addison’s Disease Clinical Presentation
Brown macular pigmentation of local or diffuse 0uality
Pigmentation usually seen in association with cutaneous
bron1ing, weakness, weight loss, salt craving, nausea,vomiting, hypotension
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Addison disease
$ddison disease2 diffuse pigmentation of the buccal mucosa
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Addison’s Disease Diagnosis
onfirmation of hypoadrenocorticism by plasma $!
levels after challenge3stimulation
Biopsy of mucosa shows melanosis
$ddison disease2 pigmentation of the buccal mucosa.
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Addison disease Diferential Diagnosis
4moker5s melanosis
Physiologic3ethnic pigmentation
eavy metal deposition3argyrosis
edication-related pigmentation
Peut1-6eghers syndrome
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Addison disease
Treatment
anagement of underlying adrenal
insufficiency by corticosteroid
replacement therapy
Prognosis
7ood with replacement therapy
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Peutz–Jeghers Syndrome
Definition Peut186eghers syndrome is a rare
genetically transmitted disorder, characteri1ed
by mucocutaneous pigmentation and intestinal
polyposis. Etiology Inherited as an autosomal dominant
trait.
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Melanoacanthoma
Etiology
$ reactive and reversible alteration of oral
mucosal melanocytes and keratinocytes
Usually associated with local trauma
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Melanoacanthoma Clinical Presentation
Unilateral dark pla0ue" rarely multiple, bilateral
ost often noted among Blacks and other non-
aucasians ccurs more often in women than men by a ratio of
92:
istory of trauma and local irritation
;orms rapidly, most often on buccal3labial mucosa
$symptomatic melanotic pigmentation
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Melanoacanthoma
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MelanoacanthomaDiagnosis linical history of rapid onset
istologic evaluation
4cattered dendritic melanocytes within
spongiotic and acanthotic epithelium
Increased number of melanocytes along
basal layer as single units
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Melanoacanthoma Diferential Diagnosis elanoma
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Melanoacanthoma
Treatment
=one after establishing the diagnosis
ften resolves spontaneously
Prognosis
>xcellent
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Mucosal Melanotic Macule andEphelides
Etiology
ost idiopathic, some postinflammatory,
some drug-induced
ultiple lesions suggest syndrome
association, as follows2 Peut1-6eghers syndrome
?augier-un1iker phenomenon arney5s syndrome
?>P$@< syndrome
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Mucosal Melanotic Macule andEphelides
Clinical Presentation ost in adulthood )fourth decade and beyond+ ost are solitary and well circumscribed
?ower 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 A ' mm in diameter
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Mucosal Melanotic Macule andEphelides
Microscopic Findings =ormal melanocyte density and morphology Increased melanin in basal cells and
subacent macrophages )mucosal melanotic
macule+
Increased melanin in basal cells with
elongated rete pegs )ephelides+
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Mucosal Melanotic Macule andEphelides
Diagnosis
Biopsy
Differential Diagnosis
elanoacanthoma
ongenital syndromes )arney5s, Peut1-
6eghers, ?>P$@
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Mucosal Melanotic Macule andEphelides
Treatment bservation Biopsy for esthetics If increase in si1e or development of atypical
signs occurs, macule should be removed torule out malignant melanoma, particularly if
on palate or alveolar mucosa.Prognosis C >xcellent
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Mucosal Melanotic Macule andEphelides
>phelis on the vermilion border of the lower lip.
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Mucosal Melanotic Macule andEphelides
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Neus Clinical Presentation
Usually elevated, symmetric papule
Pigmentation usually uniformly distributed
ommon on skin" unusual intraorally
Palate and gingiva most often involved
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NeusMicroscopic Findings
ost are intramucosal )DdermalE+
Blue nevi are deeply situated and are composed of
spindled nevus cells. ther variants are rare" unctional and compound
nevi )no dysplastic nevi occur orally+
=evus cells are oval3round and are found in
unencapsulated nests )the0ues+.
elanin production is variable.
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Neus
Diagnosis linical features Biopsy
Differential Diagnosis elanoma #arix $malgam tattoo3foreign body ucosal melanotic macule Faposi5s sarcoma >cchymosis elanoacanthoma
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Neus
Treatment
>xcision of all pigmented oral lesions to rule
out malignant melanoma is advised.
alignant transformation of oral nevi probably
does not occur.
Prognosis
C >xcellent
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Neus
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Neus o! Ota
Etiology Idiopathic3congenital
$ proliferation of dermal melanocytes over a
specific anatomic distribution
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Neus o! Ota Clinical Presentation
acular, grayish blue discoloration of skin
and mucosa over the distribution of the
ophthalmic and maxillary branches of
the trigeminal nerve
Unilateral distribution
4clera on the involved side may be affected.
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Neus o! OtaMicroscopic Findings
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Neus o! Ota
Diagnosis
linical presentation
Treatment
=one
osmetic
Prognosis
>xcellent=evus of ta, skin hyperpigmentation.
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Peut"#$e%hers s&ndrome
Definition
Peut186eghers syndrome is a rare genetically
transmitted disorder, characteri1ed by
mucocutaneous pigmentation and intestinal
polyposis.
Etiology Inherited as an autosomal dominant
trait.
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Peutz–Jeghers Syndrome
Clinical features !he oral manifestations are the most important
diagnostic findings, and consist of oval or round,brown or black macules or spots, :8:G mm indiameter.
!he perioral skin, lips, buccal mucosa, and tongueare the most common sites affected.
!he skin lesions consist of numerous, usually
perioral, dark spots. Intestinal polyps )hamartomas+ are constant
findings, usually in the eunum and ileum.
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Peutz–Jeghers Syndrome
Laboratory tests istopathological examination, radiography of
the gastrointestinal tract.
Differential diagnosis normal pigmentation $ddison disease.
Treatment 4upportive" surgical intervention in some
cases.
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Peut"#$e%hers s&ndrome
Peut186eghers syndrome2 multiple pigmented spots on the buccal mucosa.
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Peut"#$e%hers s&ndrome
Peut186eghers syndrome2 multiple round spots on the lower lip.
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Peut"#$e%hers s&ndrome
Peut1-6eghers syndrome, multiple pigmented spots on the skin.
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Amal%am Tattoo
Etiology Implantation or passive3frictional transfer of
dental silver amalgam into mucosa
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Amal%am TattooClinical Presentation 7ray to black focal macules, usually well defined, but
may be diffuse with no associated signs of inflammation
!ypically in attached gingiva, alveolar mucosa, buccal
mucosa
ccasionally may be visible radiographically
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Amal%am Tattoo
Diagnosis
@adiographs may be useful )intraoral film
placement+ Biopsy may be necessary if clinical diagnosis
is in doubt or to rule out lesions of melanocytic
origin
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Amal%am Tattoo
Differential Diagnosis
#ascular malformation
ucosal nevus
elanoma
ucosal melanotic macule
elanoacanthoma
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Amal%am Tattoo
Treatment
Biopsy or observation only
Prognosis
?ittle clinical significance if untreated
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Mucosal Mali%nant Melanoma
Etiology
Unknown
utaneous malignant melanoma with relation to
sun exposure or familial-dysplastic melanocyticlesions
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Mucosal Mali%nant Melanoma Clinical Presentation
@are in oral cavity )A :( of all melanomas+ ost cases occur in those older than 9G years of age. Usually arises on maxillary gingiva and hard palate
ay exhibit early in situ phase2 a macular, pigmentedpatch with irregular borders
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Mucosal Mali%nant Melanoma Clinical Presentation
Progression to deeply pigmented, nodular 0uality with
ulceration
ay arise de novo as a pigmented or amelanotic nodule
@arely may be metastatic to the oral cavity as a nodular,
usually pigmented mass
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Mali%nant melanoma
>arly nodular malignant melanoma of the alveolar mucosa.
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Mucosal Mali%nant Melanoma
>xtensive superficial spreading melanoma of the palate.
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Mucosal Mali%nant Melanoma
ultiple nodular malignant melanomas of the alveolar mucosa of the maxilla
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Mucosal Mali%nant Melanoma Microscopic Findings >arly stage2 atypical melanocytes at epithelial8connective tissue
interface, occasionally with intraepithelial spread ?ater infiltration into lamina propria and muscle 4trict correlation to cutaneous malignant melanoma is not well
established, although, as in skin, a similar hori1ontal or in situ growth phase often precedes the vertical invasive phase. $melanotic forms may re0uire use of immunohistochemical
identification2 4-:GG protein, B-H', elan-$ expression
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Mucosal Mali%nantMelanomaDiagnosis Biopsy
igh index of suspicion
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Mucosal Mali%nantMelanoma
Differential Diagnosis >xtrinsic pigmentation
Faposi5s sarcoma
#ascular malformation $malgam tattoo
l l
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Mucosal Mali%nantMelanomaTreatment
4urgical excision arginal parameters related to depth of invasion and
presence of lateral growth ide surgical margins" resection )including maxillectomy+
for large, deeper lesions
=eck dissection in cases of deep invasion )A
:.J' mm+
l l
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Mucosal Mali%nantMelanomaPrognosis
7enerally poor for most oral malignant
melanomas
?ess than JG( survival at ' years in most
studies
M l Pi i E i i
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Mucosal Pi%mentation' E(trinsic)Dru% or Metal Induced*
Etiology ccupational exposure%metals vapors )lead, mercury+
!herapeutic%metal salt deposits )bismuth, cis-platinum, silver, gold+"
also nonmetal agents, such as chloro0uine, minocycline, 1idovudine,
chlorproma1ine, phenolphthalein, clofa1imine.
M l Pi i E i i
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Mucosal Pi%mentation' E(trinsic)Dru% or Metal Induced*
Bismuth deposition within the gingival papillae.
M l Pi t ti E t i i
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Mucosal Pi%mentation' E(trinsic)Dru% or Metal Induced*
Pigmentation of the buccal mucosa caused by chloro0uine.
M l Pi t ti E t i i
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Mucosal Pi%mentation' E(trinsic)Dru% or Metal Induced*
Clinical Presentation ;ocal 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 ost medications cause color alteration of buccal-labial
mucosa and attached gingiva.
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Mucosal Pi%mentation' E(trinsic)Dru% or Metal Induced*
M l Pi t ti E t i i
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Mucosal Pi%mentation' E(trinsic)Dru% or Metal Induced*
Diagnosis
istory of exposure to, or ingestion of, heavy
metals or drugs
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Diferential Diagnosis
hen locali1ed2 amalgam tattoo, mucosal melanotic
macule, mucosal nevus, Faposi5s sarcoma, purpura,
malignant melanoma, ecchymosis.
hen generali1ed2 ethnic pigmentation, $ddison5s
disease
If asymmetric, in situ melanoma must be ruled out by
biopsy.
M l Pi t ti E t i i
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Mucosal Pi%mentation' E(trinsic)Dru% or Metal Induced*
Treatment
Investigation of cause and elimination ifpossible
Prognosis
>xcellent
Pi t ti Di d D
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Pi%mentation Disorders' Dru%Induced
Etiology
!herapeutic drug-related tissue pigmentation
any drugs may cause change
Pi t ti Di d D
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Pi%mentation Disorders' Dru%Induced Clinical Presentation acular 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 tetracycline use
Pi%mentation Disorders Dr %
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Pi%mentation Disorders' Dru%Induced
Microscopic Findings
ost cases are due to increased melanin
production. 4ome are related to the depositionof a drug complex or a metaboli1ed drug.
Pi%mentation Disorders Dru%
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Pi%mentation Disorders' Dru%InducedDiagnosis istory linical appearance
Differential Diagnosis Physiologic changes 4moker5s melanosis
Treatment
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Drugs Capable o ProducingTissue Pigmentation $ntimalarials2 chloro0uine, mepacrine, 0uinidine, old-time
antimalarials $ntibiotics2 tetracycline group, minocycline $ntivirals2 a1idothymidine Phenothia1ine2 chlorproma1ine lofa1imine eavy metals2 gold, mercury salts, silver nitrate, bismuth, lead ormones2 $!, oral contraceptives ancer3chemotherapy drugs2 busulfan, cyclophosphamide,cis-
platinum ther2 methyldopa
Pi%mentation Disorders
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Pi%mentation Disorders'Ph&siolo%ic
Etiology
=ormal melanocyte activity
Pi%mentation Disorders
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Pi%mentation Disorders'Ph&siolo%ic
Clinical Presentation
4een in all ages
4ymmetric distribution over many sites,
gingiva most commonly
4urface architecture, texture unchanged
Pi%mentation Disorders
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Pi%mentation Disorders'Ph&siolo%ic
Pi%mentation Disorders
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Pi%mentation Disorders'Ph&siolo%ic
Diagnosis
istory
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Pi%mentation Disorders'Ph&siolo%ic
Differential Diagnosis
4moking-associated melanosis
4uperficial malignant melanoma
Treatment
=one
Prognosis
>xcellent
+mo,er’s Melanosis
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+mo,er s Melanosis
Etiology
elanin pigmentation of oral mucosa in heavy
smokers
ay occur in up to : of ' smokers, especiallyfemales taking birth control pills or hormone
replacement
elanocytes stimulated by a component intobacco smoke
+mo,er’s Melanosis
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+mo,er s MelanosisClinical Presentation Brownish discoloration of alveolar and attached labial
gingiva, buccal mucosa Pigmentation is diffuse and uniformly distributed"
symmetric gingival pigmentation occurs most often.
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+mo,er s melanosis
4moker5s melanosis of the gingiva.
+mo,er’s Melanosis
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+mo,er s Melanosis Microscopic Findings
Increased melanin in basal cell layer
Increased melanin production by normal
numbers of melanocytes
elanin incontinence
+mo,er’s Melanosis
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+mo,er s Melanosis
Diagnosis istory of chronic, heavy smoking Biopsy
linical appearance
+mo,er’s Melanosis
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+mo,er s Melanosis Diferential Diagnosis
Physiologic pigmentation
$ddison5s disease
edication-related pigmentation
alignant melanoma
+mo,er’s Melanosis
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+mo,er s Melanosis
Treatment
=one
@eversible, if smoking is discontinued
Prognosis
7ood, with smoking cessation
Tetrac&cline +tainin%
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Tetrac&cline +tainin%
Etiology Prolonged ingestion of tetracycline or its congeners during
tooth development
?ess commonly, tetracycline ingestion causes staining
after tooth formation is complete2 reparative )secondary+
dentin cementum may be stained.
Tetrac&cline +tainin%
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Tetrac&cline +tainin%Clinical Presentation
Kellowish to gray )oxidi1ed tetracycline+ color of enamel
and dentin
ay be generali1ed or hori1ontally banded depending on
duration of tetracycline exposure $lveolar bone may also be stained bluish red
)particularly with minocyline use, :G( after : year and
JG( after H years of therapy+.
Tetrac&cline +tainin%
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Tetrac&cline +tainin%
Tetrac&cline +tainin%
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Tetrac&cline +tainin%
Tetrac&cline +tainin%
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Tetrac&cline +tainin%
Diagnosis linical appearance and history ;luorescence of teeth may be noted with ultraviolet
illumination.
Differential Diagnosis