 Melanocytes are pigment-producing cells that
are derived from neural crest cells
 Melanin is formed from tyrosine by the action of
tyrosinase
 Oral melanin pigmentation ranges from brown
to black to blue according to the amount of
melanin production and the depth of the
pigment.
Etiology
 Congenital or acquired
 Benign or malignant
 Endogenous or exogenous
Causes of Oral Pigmentation
 Congenital
 Racial (Melanoplakia)
 Naevi
 Peutz-Jegher’s syndrome
 Acquired
 Endocrinopathies
 Metabolic (Hemochromatosis)
 Neoplastic
 Metals
 Food/drugs (oral contraceptives, antimalarials ,
minocycline tranquilizers)
 AIDS
Benign causes of oral pigmentation
Physiologic pigmentation
Ephelides
Lentigo
Oral melanotic macule
Smoking melanosis
Intraoral nevi
Malignant causes of oral
pigmentation
Melanoma
Neuroectodermal tumor of infancy
Endogenous causes
Postinflammatoty
hyperpigmentation
Melanoacanthoma
Addison’s syndrome
Peutz- Jegher’s syndrome
Laugier-Hunziker syndrome
Exogenous
Drugs
Amalgam tattoos
Cultural or medical tattooing
Jailhouse tattoo
Heavy metals
Racial pigmentation
 Results from increased amount of melanin
pigmentation
 Usually in Blacks and Asians, but also
Mediterranean littoral
 May be present in white descendents
 Usually involves the gingivae (attached), but can
affect other oral sites
 Variable colour and extent
 Asymptomatic
Racial pigmentation
Differential diagnosis:
Addison’s disease
Albright’s Syndrome
Heavy metal pigmentation
Use of antimalarial drugs
Ephelides
 Ephelides are sun-induced freckles that
are most commonly seen in very fairskinned individuals, especially those
with red or auburn hair.
 They occur most frequently in
childhood, and tend to reduce in
number with age.
Lentigo
 Solar lentigos, in contrast to ephelides are more common
in older individuals and persist indefinitely.
 They are common on the face and may be seen in the
perioral region.
 They range in size from 2 mm to 2 cm and are usually tan
to dark brown in colour.
 Variation in colour or irregularity of outline should raise
the suspicion of lentigo maligna and is an indication
for histological evaluation.
Naevi
They are seen in mostly young
people between the ages of 20 and
39 years.
Sixty per cent are intradermal naevi
and approximately 25% are blue
naevi.
Naevi
Usually elevated
Palate is commonly affected site
Less than 1cm diameter
Not premalignant
Naevus of Ota
an acquired oculodermal
melanocytosis involving the skin of
the face, the eyes and mucous
membranes.
It is most common in Japan,
appearing usually in female
patients in early adult life.
Melanoacanthoma
 Rare
 Usually a feature of blacks
 Aetiology unclear but probably secondary to
physical trauma
 Areas of melanotic hyperpigmentation, typically
beneath a denture
 They present as slightly elevated circumscribed
solitary asymptomatic pigmented plaques.
 Melanoacanthomas have been reported to occur
on buccal, palatal and gingival mucosa.
 Requires to be differentiated from Addison’s
disease
 No premalignant potential
Endocrinopathies causing oral
pigmentation
Addison’s disease
Nelson’s syndrome
Ectopic ACTH production
Pregnancy
Addisonian pigmentation
 May arise with any cause of adrenocortical
hypofunction (autoimmune, infection,
tumour)
 Typically involves the buccal mucosa
 May be the only clinical features of
adrenocortical hypofunction
 The pigmentation is secondary to increased
ACTH production by the anterior pituitary
Addisonian pigmentation
Pigmentation is not specific to
Addison’s however if associated with
candidal infection, endocrine studies
should be performed
Brown or black color is seen in more
than 75% of Addison’s patients
Nelson’s syndrome
 Rare
 Excess ACTH production and pituitary
expansion secondary to bilateral
adrenalectomy for Cushing’s disease.
 10% develop oral pigmentation
 Oral pigmentation like Addison’s
disease
Ectopic ACTH production
 Rare
 Excess ACTH production by bronchial
adenocarcinoma
 Oral hypermelanotic pigmentation
similar to Addison’s disease, but
possible additional involvement of the
soft palatal mucosa
Chloasma
Feature of late pregnancy
Manifests as melanotic
hyperpigmentation of the midface
Involvement of the oral mucosa is
extremely rare
Albright’s (McCune-Albright)
syndrome
 Rare
 Polyostotic fibrous dysplasia, sexual
precosity, cutaneous
hyperpigmentation, occasional other
endocrinopathies
 Possible melanotic hyperpigmentation
of the oral mucosa (in addition to
unilateral or bilateral fibrous dysplasia)
Haemochromatosis
 Autosomal recessive
 Mechanism of iron overload not clear
 Iron deposition in hepatocytes
 More commom in males (female
menstruation will lessen the iron load)
 Usually does not present clinically until
the 5th decade
Haemochromatosis
Investigations:
Elevated serum iron, reduced
TIBC, elevated ferritin
Iron in hepatocytes of biopsy
Thalassemia
Patients may have a dusky-brown
complexion - reflects iron
accumulation post-transfusion
Rarely there may be melanotic
pigmentation of the oral mucosa
and gingivae
Melanoacanthoma 
Pigmentary incontinence
 Uncommon
 Usually arises in late age in association with
oral lichen planus
 Patients are often tobacco smokers
 Areas of melanotic pigmentation in site of
present or past lichen planus
 Asymptomatic
 Exclude Addison’s disease
Smoker’s Melanosis 
Drug-induced oral mucosal
pigmentation
olours can be blue, brown, black,
grey, green
C
Drug-induced oral mucosal
pigmentation
 Blue
 Amiodarone
 Antimalarials
 Bismuth (overdose)
 Mepacrine
 Minocycline
 Quinidine
 Silver
 Sulphasalazine
Drug-induced oral mucosal
pigmentation
Brown
Betal nut
Busulphan
Clofazimine
Oral contraceptives
Cyclophosphamide
Doxorubicin
Doxycycline
Fluorouracil
HRT
Heroin
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


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HRT
Ketoconazole
Menthol
Minocycline
Pholphthalein
Propanolol
Zidovudine
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Drug-induced oral mucosal
pigmentation
Black
Amiodaquine
Betal nut
Methyldopa
Drug-induced oral mucosal
pigmentation
 Green
 Copper
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Grey
Amiodiaquine
Chloroquine
Fluoxetine
Hydroxycholoquine
Lead
Silver
Tin/zinc
Local causes of oral pigmentation
 Ecchymoses
 Ephelis
 Melanoma and other malignancies
 Melanoacanthoma
 Naevus
 Melanotic macule
 Tattoos (amalgam, ink, graphite etc)
Local causes of oral pigmentation melanotic macules
Brown or black
Usually affect lips or gingivae
Arise at any age
Not premalignant
Oral Melanotic Macule 
- tattoos
 Caused by intentional or accidental implantation of
exogenous pigments into the mucosa
 Amalgam tattoo or focal argyrosis is the most common
and appears as blue-black, non-elevated discoloration
that is usually irregular in shape and variable in size.
 Deterioration of the silver compounds of the amalgam
impart the characteristic color of the lesion
 Can affect any where but the favorable site is the gingiva.
 The clinical diagnosis can be confirmed by radiography
otherwise failure of radiographic evidence necessitates
biopsy to rule out more serious lesions
tattoos
Other tattoos include graphite
pencil wounds and India ink
tattoos
Can reflect ritual (eg gingivae, lips)
May reflect lifestyle
Harmless
Amalgam Tattoo 
Local causes of oral pigmentation bacillary angiomatosis
 Rare
 Usually a feature of HIV disease
 Caused by Bartonella quintana or
Bartonella henselae
 Gives rise to pigmented nodules
 Can affect the skin, bone and liver
 Responds to erythromycin
Local causes of oral pigmentation malignant melanoma
 Oral disease is rare
 Male:female ratio=2:1
 Mostly in persons>50 years of age
 Often affects the palate, mainly maxillary alveolar ridge,
anterior gingiva and labial mucosa, but can involve other
oral sites
 Oral lesions may be primary or secondary tumours
 Localised brown or black macule, papule, or nodule,
often with ulceration and destruction. Rarely lesions
may spread superficially
malignant melanoma
 Early recognizable signs: asymmetric lesion,
border irregularity, color variation, and diameter
enlarging
 Late signs: bleeding and ulceration, firmness on
palpation and rock-hard regional lymph nodes
 Early diagnosis when tumors are less than 1.5 mm
in diameter and complete resection are critical to
long term survival.
 Poor outcome likely
Malignant Melanoma 
Ephelis (Freckle)
 Light to dark-brown macule on the lip due
to exposure to light
 Remains unchanged in size but may darken
 Has predilection to light-skinned or redheaded persons
Investigation of oral pigmentation
 History of present complaint
 Medical history - hypoadrenocorticism, pulmonary
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disease, drug history etc
Social history - tobacco or betel nut habit? ethnicity?
Extra-oral examination - evidence of cutaneous disease etc
Intra-oral examination - localised or generalised ?
Blood pressure
Serum electrolytes
24 hour urinary cortisol
Synacthen test
Biopsy
Discoloration of teeth
 Extrinisic
 Intrinsic
 Smoking
 Tetracycline
 Beverages
 Fluorosis
 Drugs(iron,
 Amelogenesis imperfecta
chlorehexidine,
minocycline)
 Poor oral hygiene
 Betel chewing
 Kernicterus
 Porphyria