EPHELIS

M EI L I A AQUI NA HAKI M
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DEFINITION
Benign pigmented lesion of the oral cavity, characterized by an
increase in melanin pigmentation along the basal cell layer of the
epithelium and the lamina propria
• melanosis, lentigo, freckles, solitary labial lentigo, labial melanotic macule
and oral melanotic macules

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EPIDEMIOLOGY
• Gender equal but some journals said female > male
• most commonly observed in light-skinned individuals and are quite
prevalent in red- or light blond–haired individuals.
• Site—it is attributed to actinic exposure and therefore occurs on
vermilion border of the lower lip. Sometimes it can also occur on
gingiva, palate and buccal mucosa or sometimes in arm

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ETIOLOGY
• Genetic : Autosomal dominant  MC1R gene or Val92Met.
Another?
• Racial  racial pigmentation or physiologic pigmentation
Predisposing Factor
• Sun exposure
• Hormone

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PATHOGENESIS
• small areas of the skin that contain higher amount of melanin (the pigment protein that’s
responsible for our eye, skin, and hair color)
• Melanocytes
UV A,
UV B

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NOBODY IS THEY APPEAR
BORN WITH AFTER
EPHELIS SPENDING TIME
EXACTLY IN THE SUN

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MC1R (Arg151Cys, Arg160Trp, dan Asp294 ) controls how much of which kind of melanin to
produce, and someone actually have two main type melanin
• Darker brown : eumelanin
• Reddish yellow : pheomelanin

If they have an active MC1R gene  their body produces more eumelanin  leading to darker
hair and skin that protects against the sun

If their MC1R gene is mutated they will produce more pheomelanin leading to fairer skin, blonde,
or red hair and propensity for ephelis

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NOT ALL PEOPLE NOT ALL
WITH RED HAIR EPHELIS PEOPLE
HAVE EPHELIS HAVE RED HAIR

• MC1R mutated
• Val92Met
• Another?

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 • asymptomatic DIAGNOSIS
• small (1–3 mm)
• well-circumscribed
• Shape—lesions are oval or
irregular in outline.
• tan- or brown-colored macule
FKG Unair collection.Photo by ayu fresno,2016Greenberg & Glick 2003 that is often seen on the sun-
exposed regions of the facial and
perioral skin
• Abundant or hundred
• Darker in intensity during
childhood and adolescence

Neville, 2002
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Greenberg and glick, 2003 10
SUPPORTING EXAMINATION

Melanin deposisition (Greenberg and Glick, 2003

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DIFFERENTIAL DIAGNOSIS

Amalgam tattoo Nevi, lentigines

melanoacanthoma

Melanotic macule Greenberg & Glick 2003

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TREATMENT AND PROGNOSIS

• no therapeutic intervention is • excellent

required
• Sunscreen
• Chemical peeling
• Cryosurgery
• laser

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SMOKER’S
MEL ANOSIS
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DEFINITION
Diffuse melanosis of the anterior vestibular maxillary and
mandibular gingivae, buccal mucosa, lateral tongue, palate, and
floor of the mouth is occasionally seen among cigarette smokers.
Benign lesion

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EPIDEMIOLOGY
• occurs in 25 to 31% of tobacco users  Most smokers (including
heavy smokers)
• more than 31.000 Caucasians. 21.5% of tobacco smokers exhibited
areas of melanin pigmentation
• Race distribution—most evident in whites but some darkskinned who
smoke  prominent pigmentation
• sex distribution---- female > male  estrogen
• Age—increases with age
• Location—anterior mandibular gingiva, palate, buccal and
commissural mucosa, and inferior surface of tongue and lip mucosa

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ETIOLOGY AND PREDISPOSING
FACTOR
ETIOLOGY P R E D I S P O S I N G FAC TO R

• Polycyclic amines ---- in tobacco such • Alcohol  increase

as nicotine and benzpirenes • Hormones  estrogen
• Heat of smoke • Etnic  white
• trauma

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PATHOGENESIS
Polycyclic amines in tobacco : nicotine and benziperenes ; heat of smoke

Alcohol, Melanocyte
etnic,
trauma
Melanin

Melanin binding with

toxic agent

Protect oral mucosa

from tobacco smoke

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 OBJECTIVE

DIAGNOSIS • Color—black-brown
• 0,5-1 sentimeter
SUBJECTIVE
• Correlating the smoking history with the • diffuse
clinical presentation and medical history • Flat
• correlated with the number of cigarettes • Irregular
consumed per day. 1-3 cigarettes/day 9%, • Most anterior labial gingiva
more than 15 cigarettes/day 31%
• Significantly increase during the first year
• associated with pipe smoking of smoking
• Other causes of melanin pigmentation, • Brown coated tongue
such as trauma, Peutz- Ieghers syndrome,
drug-related pigmentation, endocrine
disturbances and racial pigmentation
should be ruled out.

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Johnson & Bain 2000 FKG Unair. Photo by Hasrul,2016
 SUPPORTING EXAMINATION
• Biopsy  fontan masson
• increased melanin pigmentation of the
basal cell layer of the surface epithelium.
Similar to a melanotic macule
• Mild infiltrate lymphocyte http://img.medscapestatic.com/pi/meds/ckb/49/28249tn.jpg

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http://www.doctorc.net/Labs/Lab2/IMAGES/MELANIN%20FONTANA%20MASSON.JPG
DIFFERENTIAL DIAGNOSIS

(Kauzman et al. 2004) 21

TREATMENT AND PROGNOSIS
T R E AT M E N T P RO G N O S I S

• With cessation of smoking, • good

improvement is expected over the
course of 3 years.

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DRUG-INDUCED
PIGMENTATION
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• Pigmentation induced by some of DEFINITION
drugs

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• Location—usually on hard palate. EPIDEMIOLOGY
• Age: No predilection
• Sex: Females

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• Several antimalarial drugs:
quinacrine, chloroquine, and
hydroxychloroquine ETIOLOGY
AND
• manage autoimmune diseases, and
PREDISPO
oral: Quinoline, hydroxyquinoline,
SING
and amodiaquine  10%
FACTOR
• treatment of acne vulgaris:
minocycline

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• Birth control pills: Malasma,
Chloasma  brown pigmentation
• Tranquilizers: chlorpromazine
• phenolphthalein, and estrogens
• chemotherapeutic agents:
doxorubicin , busulfan ,
cyclophosphamide, or 5-fluorouracil
• medication of AIDS : zidovudine
(AZT) , clofazimine, or ketoconazole

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• Melanin accumulation : drug
stimulating melanocytes ; drug bind
melanin  stable complex PATHOGE
• Accumulation medication itself NESIS
without any association to melanin
• Synthesis special pigments: lipofuscin
 drug induced
• Deposition of iron : drug damage
dermal vessel  leakage RBC and
lysis

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D I AG N O S I S

• Minocycline pigmentation—brown
melanin deposits on the hard palate,
gingiva, mucous membranes, and the
tongue Brusch et al, 2010
• Birth control pill pigmentation—brown
pigmentation of facial skin and
perioral region. Brusch et al, 2010
• Phenolphthalein—circumscribed area
of hyperpigmentation on skin and
oral mucosa.
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https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3311937/figure/Fig1/
• chlorpromazin—diffuse grayish of
the hard palate Neville, 2002

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• some have, and the typical finding
is basilar melanosis with melanin SUPPORTING
incontinence characterized by free EXAMINATION
melanin in the connective tissue.

Prussian blue, Brusch et al, 2010

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 Addison disease Superficial melanoma

DIFFERENTIAL
D I AG N O S I S

http://www.contempclindent.org/articles/2012/3/4/images/Cont
empClinDent_2012_3_4_484_107450_f2.jpg
https://encrypted-
tbn1.gstatic.com/images?q=tbn:ANd9GcSfPkY5VVMcmm
9wCKk2r1M2SAYhgLa5ek54ysYpdn8lSRO5EkA0

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• Cessation of the medication is
recommended  1 year

TREATMENT AND
PROGNOSIS
• Good

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THANK YOU

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