orofacial pigmentations

8/18/2019 Orofacial Pigmentations

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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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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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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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Diagnosis

Biopsy

Differential Diagnosis

elanoacanthoma

ongenital syndromes )arney5s, Peut1-

6eghers, ?>P$@


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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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>phelis on the vermilion border of the lower lip.


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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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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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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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Peut186eghers syndrome2 multiple pigmented spots on the buccal mucosa.


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Peut186eghers syndrome2 multiple round spots on the lower lip.


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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


#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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>xtensive superficial spreading melanoma of the palate.


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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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Bismuth deposition within the gingival papillae.

M l Pi t ti E t i i


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Pigmentation of the buccal mucosa caused by chloro0uine.

M l Pi t ti E t i i


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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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M l Pi t ti E t i i


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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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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



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Clinical Presentation

4een in all ages

4ymmetric distribution over many sites,

gingiva most commonly

4urface architecture, texture unchanged



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Diagnosis

istory


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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



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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.



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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



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+mo,er s Melanosis

Diagnosis istory of chronic, heavy smoking Biopsy

linical appearance



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+mo,er s Melanosis Diferential Diagnosis

Physiologic pigmentation

$ddison5s disease

edication-related pigmentation

alignant melanoma



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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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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.



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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+.



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Diagnosis linical appearance and history ;luorescence of teeth may be noted with ultraviolet

illumination.


orofacial pigmentations

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