PIGMENTED LESIONS 1
DR.S.KARTHIGA KANNAN
PROFESSOR
SPECIFIC LEARNING OBJECTIVES
 TO KNOW ABOUT PIGMENTS AND PIGMENTED LESIONS
 TO RECOGNISE THE CLINICAL FEATURES OF PIGMENTED LESIONS
 TO KNOW THE INVESTIGATION AND MANAGEMENT OF THESE LESIONS
FORMAT
1. INTRODUCTION OF PIGMENTS
2. CLASSIFICATION OF PIGMENTS
3. FUNCTIONS OF PIGMENTS
4. CLASSIFICATION OF DISEASES PRODUCING ENDOGENOUS PIGMENTATION
5. PHSIOLOGY OF MELANIN SYNTHESIS
6. BROWN BLACK MELANIN DERIVED PIGMENTATION
PIGMENTS
Pigments are colored substance present in most
living beings
CLASSIFICATION PIGMENTS
ENDOGENOUS PIGMENTS
EXOGENOUS PIGMENTS
Melanin
Hemoglobin
Hemosiderin
Bilirubin
Amalgam tattoo
Graphite tattoo
Heavy metals poisoning
Chromogenic bacteria
Medicines
Food stuff
Carotene
Porphyrin
FUNCTIONS OF PIGMENTS
MELANIN
: To protect from UV radiation, antioxidant
CAROTENE
: Active component of Vitamin A, antioxidant
HEMOGLOBIN: Carries Oxygen & Carbon dioxide
BILIRUBIN
: Physiological by-products of hemoglobin
HEMOSIDERIN: Physiological by-products of hemoglobin
PORPHYRIN
: Physiological by-products of hemoglobin
MELANIN
Brown black non haemoglobin derived protien
Normally present in the skin, hair, choroid of the eye ,meninges
and adrenal medulla
Synthesized in the melanocytes.
Stored in the form of cytoplasmic granules in melanophores
PHYSIOLOGY OF MELANIN SYNTHESIS
Tyrosinase
Tyrosine
Melanin
In melanocytes
MELANOCYTE
BROWN BLACK MELANIN DERIVED PIGMENTATION
Increased melanin synthesis
(Basilar melanosis)
Increased melanocytes
1.Physiologic / Racial
1.Nevus
2.Malignant melanoma
2.Malanotic macule or Ephelis
3.Post inflammatory pigmentation
4.Smokers melanosis
5.Drug induced melanosis
6.Lichenplanus
7.Peutz jegher syndrome
8.Melasma/cholasma
9.Café au lait pigmentation
10.Adisson’s disease
11.HIV melanosis
PHSIOLOGIC PIGMENTATION
ETIOLOGY AND PATHOGENESIS
Melanin production and deposition is often a
physiologic process, more especially in dark
skinned individuals.
CLINICAL FEATURES
 Site - Gingiva are the most frequent site.
The pigmentation can vary from brown to
black and may be symmetrical or asymmetrical
DIAGNOSIS
Diagnosis by clinical presentation and history but
biopsy to exclude malignancy may be required if the
patient reports any change in appearance.
MANAGEMENT
No treatment is required.
Melanotic macule & Ephelis
Increased melanin pigment
synthesis without any increase in
the number of melanocyte cells is
known as Ephelis
Intra oral counterpart of ephelis
is melanotic macule.
Etiology may be actinic exposure
or trauma.
Innocent lesion & needs no
treatment. Will not vanish on its
own.
SMOKER’S MELANOSIS
ETIOLOGY AND PATHOGENESIS
Contents of tobacco smoke are believed to
stimulate melanin production by melanocyte.
CLINICAL FEATURES
It occurs as diffuse pigmentation frequently
affecting the anterior labial gingivae, palate, and
buccal mucosa.
The intensity of the pigmentation is dependent
on the dose and duration of tobacco use.
DIAGNOSIS
Diagnosis is made based on the clinical appearance
and history of tobacco use.
MANAGEMENT
There is no specific treatment for the condition,
cessation of smoking usually resolves the
pigmentation with time.
SMOKER’S MELANOSIS
CAFÉ AU LAIT PIGMENTATION
 Bronze and tan diffuse and multifocal macular
pigmentations appear on the skin in fibrous
dysplasia and neuro fibromatosis characterized by
multiple skin nodules or even pendulous tumors.
Owing to their pale brown color, they are
referred to as café au lait spots.
Peutz Jegher’s syndrome
ETIOLOGY AND PATHOGENESIS
It is inherited in an genetic disease and is
characterized by a large number of peri-oral
freckles and intestinal polyps.
CLINICAL FEATURES
Multiple freckles are present at the vermillion
border of the lips and on the peri-oral skin.
 Small polyps are present in the jejunum, colon,
and gastric mucosa.
Patients may complain of abdominal pain, rectal
bleeding, and diarrhea.
DIAGNOSIS
 Familial history of similar lesions/ disease.
 Clinical appearance of peri-oral and other cutaneous freckling.
 Endoscopy and biopsy may be necessary to examine the
lower
gastrointestinal tract for polyposis.
MANAGEMENT
 There is no specific treatment for the peri-oral freckles.
 Sunscreens may be helpful since the lesions often darken and
become more prominent with sun exposure.
Addison’s Disease
ETIOLOGY AND PATHOGENESIS
It is caused by adrenocortical insufficiency
due to
auto-immune disease,
infection (usually tuberculosis),
 idiopathic factors.
Reduced serum levels of cortisol induces
an
increased
production
of
adrenocorticotropic hormone (ACTH).
 ACTH
stimulate
also
stimulate
melanocytes resulting in hyper pigmentation
of the skin and mucosal surfaces.
CLINICAL FEATURES
 There is hyperpigmentation of the skin similar to a sun-tan.
Intra-orally, multiple melanotic macules develop on the gingivae, buccal
mucosa, and lips.
Symptoms of adrenocortical insufficiency include weakness, weight loss,
nausea and vomiting, and hypotension.
DIAGNOSIS
Biopsy of a pigmented area shows nonspecific features.
Diagnosis is based on demonstrating low serum cortisol levels and elevated ACTH.
Other nonspecific serum changes include low sodium, chloride, bicarbonate, and
glucose.
MANAGEMENT
The condition is managed with replacement steroids. No specific treatment is
required for the oral pigmentation.
HIV MELANOSIS
 One of the oral manifestation of HIV/AIDS
 Causes for HIV melanosis
1. Post inflammatory pigmentation following
recurrent oral candidiasis
2. Drug induced pigmentation because of intake
of antifungal, antiviral and antibiotics for bacterial
infection
3. Secondary addission disease caused by
Co-existing tuberculous infection
NEVOCELLULAR NEVUS
Occur due to benign proliferation of
Melanocytes
Nevocellular nevus arise from basal layer
of epithelium in early life (junctional nevi)
Later, these cells proliferate into the
connective tissue & proliferate to become
a dome shaped lesion (compound nevi)
After attaining puberty, they loose the
connectivity with basal layer of epithelium
(Intradermal/ intramucosal nevi)
Thus, no junctional nevi should exist in an
adult. If it exists, premalignant activity
should be suspected
CLINICAL FEATURES
 Nevi appear as brown or blue lesions, depending on the type and depth of the
melanin.
The lesions have a uniform coloration, a sharply-defined border.
 Are most often less than 0.5 cm in diameter.
Both junctional nevi and intra-mucosal nevi are flat but compound nevi are raised.
Malignant transformation :- If Nevi shows features of
A – Asymmetry (in shape)
B- Border irregularity
C- Color variation
D- Diameter greater than a pencil eraser or 0.75cm
 Along with above features indistinct borders, ulceration, increasing size, pain and bleeding
are features that should prompt the consideration of malignant melanoma
DIAGNOSIS & TREATMENT
Diagnosis is by histopathological examination ,
Treatment is excisional biopsy itself.
MALIGNANT MELANOMA
 Most common in white population that live in sun belt
region.
 Highest prevalence is seen in Japanese.
 Malar skin has high incidence in facial region
Mucosal melanomas may occur in facial gingiva and
or anterior hard palate
Clinical Types
1. Lentigo maligna melanoma
2. Superficial spreading melanoma
3. Nodular melanoma – oral counterpart is called acral lentigenous melanoma.
Growth pattern
Two phases of growth are:
 Radial growth – good prognosis
 Vertical growth – poor prognosis
Clinical features
 They usually occur in elderly males,
 Appear as brown or black or blue in color with
irregular jagged borders.
 Depth of the lesion (in mms) is inversely
proportional to prognosis (Breslow method)
 Metastasis can be lymphatic & hematogenous to
distant visceral organs.
Investigation –Frozen section biopsy
 Management: Surgery, chemotherapy .
The eye doesn’t see what
The mind doesn’t know