1. PIGMENTED LESIONS 1
DR.S.KARTHIGA KANNAN
PROFESSOR

2. 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

3. FORMAT 2. CLASSIFICATION OF PIGMENTS 3. FUNCTIONS OF PIGMENTS
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

4. CLASSIFICATION PIGMENTS
Pigments are colored substance present in most living beings
CLASSIFICATION PIGMENTS
ENDOGENOUS PIGMENTS
Melanin
Hemoglobin
Hemosiderin
Bilirubin
Porphyrin
EXOGENOUS PIGMENTS
Amalgam tattoo
Graphite tattoo
Heavy metals poisoning
Chromogenic bacteria
Medicines
Food stuff
Carotene

5. 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

7. 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

8. Tyrosinase Tyrosine Melanin In melanocytes
PHYSIOLOGY OF MELANIN SYNTHESIS
Tyrosinase
Tyrosine Melanin
In melanocytes
MELANOCYTE

9. BROWN BLACK MELANIN DERIVED PIGMENTATION
Increased melanin synthesis
(Basilar melanosis)
1.Physiologic / Racial
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
Increased melanocytes
1.Nevus
2.Malignant melanoma

10. 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.

11. 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.

12. 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

13. 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.

14. 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.

15. Familial history of similar lesions/ disease.
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.

16. 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.

17. 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.

18. 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

19. 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

20. 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.

21. 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

22. 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
- full body radiography
- Ultrasonography -abdomen
Management: Surgery, chemotherapy .
Malignant Melanoma of Oral Mucosa
IJDR 15(2): 70-73, 2004; [PMID

23. The eye doesn’t see what The mind doesn’t know
THANK YOU
The eye doesn’t see what
The mind doesn’t know