hi everyone this is my seminar on pigmented lesions of oral cavity

1. PIGMENTED LESIONS OF
ORAL CAVITY
Rupali Bham
UG Student
Guru Nanak Dev Dental College And Research Institute
BDS final year
Roll No:- 3623

2. • In the course of disease, the oral mucosal tissues can assume a variety of
discolorations like brown, black or blue which constitute the pigmented lesions of
oral mucosa, and such color changes can be attributed to the deposition of either
endogenous or exogenous pigments.
• Oral pigmentation could be pathologic or physiologic.
• Pathologic pigmentation can be classified into exogenous and endogenous based
upon the cause.

3. • Exogenous Pigments come from outside in the body and gets implanted into the oral
mucosa. For ex. Drugs, smoking, amalgam tattoo or heavy metals
• Endogenous pigments are synthesized within the body itself. For ex. Melanin(most important
factor causing pigmentation), hemoglobin, hemosiderin and carotene.
• Hemoglobin imparts a red or blue appearance to the mucosa and represents pigmentation
associated with vascular lesions.
• Hemosiderin appears brown and is deposited as a consequence of blood extravasation,
which may occur as consequence of trauma or a defect in hemostatic mechanisms.

4. MELANIN
• Melanin is an endogenous, non- hematogenous pigment.
• It is produced by melanocytes in the basal layer of epithelium and is transferred to
adjacent keratinocytes via membrane bound organelles called melanosomes.
• It is also synthesized by nevus cells, which are neural crest derivatives and are found
in the oral mucosa and skin.
• Depending on the location and amount of melanin in the tissues, melanin induced
pigmentation can be either black, brown or grey in color.

5. ME

6. CLASSIFICATION

8. ME

9. HEMANGIOMA
• Hemangioma is a benign proliferation of the endothelial cells that line vascular
channels.
• Onset:- Infancy
• It regresses as the patient ages.

10. • Classification proposed by Watson and McCarthy:-
a) Capillary hemangioma
b) Cavernous hemangioma
c) Angioblastic or hypertrophic hemangioma
d) Racemose hemangioma
e) Diffuse systemic hemangioma
f) Metastasizing hemangioma
g) Nevus vinosus or port – wine stain
h) Hereditary hemorrhagic telangiectases

11. • Etiology:- often congenital in nature, follows benign course.
• Clinical features:- (a) Signs earliest sign is blanching of the involved skin, often
followed by fine telangiectases and then a red macule.
(b) Site  the most common site of occurrence is the lips, tongue, buccal mucosa
palate.
(c) Diascopy
(d) Hemangioma in children  rapid growth during the neonatal period occurring
beyond the growth rate of infant. Found on the skin, in the scalp, and within the
connective tissue of mucous membranes.

13. Differential diagnosis :-
• Mucocele, ranula and superficial cyst
• Varicosity
• Aneurysm or arteriovenous shunt
Management:-
• Sclerosing technique:- sclerosing agents such as sodium tetradecylsufate can be
used intralesionally.
• Cryosurgery

14. KAPOSI’S SARCOMA
• Synonym:- angioreticuloendothelioma
• It was described by Moritz Kaposi in 1872 in central Europe among elderly persons of
Mediterranean or Jewish origin as a multiple pigmented sarcoma of the skin.
• It is a multifocal angioproliferative neoplasm that primarily involves the skin in non-HIV infected
person.
• Pathogens or factors associated  human herpes virus type 6, cytomegalovirus, human
immunodeficiency virus, Mycoplasma penetrans, sex hormones and nitrate inhalants.

15. Clinical features :-
• Age distribution:- at any age, but most common In 5th, 6th, and 7th decades.
• sex distribution:- M>F, 20:1
• Appearance:- (a)tumor begins as a multicentric neoplastic process that manifest as multiple
red/ purple macules.
(b)advanced types nodules on skin or mucosal areas

16. • Progress :- lesion tends to enlarge, become darker and may form clusters of single
nodules.

17. Clinical presentation:- (a) classic type multiple bluish purple macules and plaques
are present on the skin of lower extremities.
(b) Endemic has 4 subtypes 
i. Benign nodular type
ii. An aggressive type
iii. A florid form
iv. A unique lymphadenopathic type
(c)Iatrogenic type

18. (d) AIDS related KS
Oral manifestations:-
• Location :- attached mucosa of the palate, gingiva and dorsum of tongue
• Appearance:- oral lesions occur as red to purple nodules and macule with mucosal
ulceration in mature cases
• Symptoms:- pain, dysphagia, difficulty with mastication and bleeding etc.
• Palpation:- lesion does not blanch with pressure.

20. Differential diagnosis:-
• Hemangioma
• Purpura
• Nevi
• Melanoma
Management :-
• Radiation therapy
• Surgical eradication
• Systemic chemotherapy  vinblastine and vincristine

21. • Intralesional injection:- the intralesional use of vinblastine (dose- 0.01to0.04mg) for
small KS lesion of mouth.
• Combination therapy for AIDS related Kaposi’s sarcoma:-
Single agents, combined chemotherapy, or Zidovudine with interferon- alpha and
radiotherapy

22. ,L,MM

23. MELANOTIC MACULE
• 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.
• Most common pigmentation to occur in oral cavity of light skinned individuals.
Etiology :-
• Genetic
• Racial
• Environmental factors

24. Clinical features:-
• Age :- middle aged adults, F>M
• Site :- vermillion border of lower lip, also occur on gingiva, palate and buccal
mucosa.
• Color and appearance:- well circumscribed flat area of pigmentation that may be
brown, black, blue or gray in color.
• Size :- less than 1 cm in diameter.
• Shape :- lesions are oval or irregular in outline

26. Differential diagnosis:-
• Amalgam tattoo
• Ecchymosis patch
• Focal melanosis
• Melanoplakia
Managemment:-
• Surgical excision

27. MELANOMA
Also called as melanocarcinoma.
Malignant neoplasm.
Third most common cancer of skin.
It is neoplasm of epidermal melanocytes.
Growth phase:-
(a) Radial growth phase:-
• initial phase of growth of tumor.
• Neoplastic process is confined to the epidermis.

28. (b)Vertical growh phase :- begins when neoplastic cells populate the underlying dermis.
TYPES:-
A. Based on clinical features:
1. Pigmented nodular type
2. Non-pigmented nodular type
3. Pigmented macular type
4. Pigmented mixed type
5. Non- pigmented mixed type

29. B. Clinicopathologic Types
1. Superficial spreading melanoma
2. Nodular Melanoma
3. Lentigo-maligna melanoma
4. Acral lentiginious melanoma
CLINICAL FEATURES:
• Age and sex : 40-70 years, average being 55 years. More common in men.
• Site: Most frequent- palate and maxillary gingiva

30. • Superficial spreading melanoma:
i. Sharply outlined, slightly elevated pigmented patch.
ii. Lesion presents as a tan, brown, black or admixed lesion on sun exposed skin.
iii. Common sites of origin are intercapsular area of males and the back of legs of
females.
• Nodular Melanoma:
i. Clinically it appears as darkly pigmented elevations on skin or mucous membrane
ii. Invasive in nature from the start and metastasizes early
iii. Poor prognosis

31. • Lentigo-maligna melanoma:- Appears as a flat, irregularly pigmented patch with an
ill defines margin.
• Acral Lentiginous melanoma:- begins as a darkly pigmented, irregularly marginated
macule which later develops a nodular invasive growth phase.
ORAL MANIFESTATIONS:-
• Site:- Palate and maxillary gingiva
• Color and appearance:- Brown to black macule with irregular borders
• Signs:- Ulceration may develop early but many lesions are dark, lobulated, exophytic
masses without ulceration at the time of diagnosis.

32. Symptoms:- Pain is not a common feature except in ulcerated lesions.
R/F:-
• Only soft tissues are affected
• Moth eaten appearance
DIFFERENTIAL DIAGNOSIS:-
• Oral melanotic macule
• Pigmented fibroma

33. Fig:- oral melanoma

34. MANAGEMENT:-
• Surgical excision
• Radiotherapy
• Pre-operative Chemotherapy: The first line chemotherapeutic agent is
dimethyltriazeno, imidazole carboxamide solely or in combination with vincristine.
• Intralesional injection

35. ADDISON’S DISEASE
• Also called as ‘Chronic adrenal insufficiency’
• Hormonal disorder resulting from a severe or total deficiency of the hormones
made in the adrenal cortex.
• Characterized by bronzing of the skin and pigmentation of the mucous membrane
ETIOLOGY:-
• Tuberculosis
• Autoimmune disorders
• Adrenocortical destruction

36. • Others:- bilateral tumor metastasis, leukemic infiltration, and amyloidosis of adrenal
cortex.
CLINICAL FEATURES :-
• Signs and symptoms:- fatigue, weakness,weight loss, nausea, abdominal pain,
diarrhea, vomiting and mood disturbances.
• Skin signs:- generalized darkening of skin(hyperpigmentation)
• Pigmentation :- deep tanning of the skin and the mucous membrane with heavier
deposits of melanin over the pressure points.
• Color :-bluish black to pale brown or deep chocolate.

38. DIFFERENTIAL DIAGNOSIS:-
• Hyperpituitarism
• Peutz-Jegher’s syndrome
MANAGEMENT:-
• Corticosteroid maintenance therapy provided by aaverage dose of 25 to 40 mg
cortisone.

39. PEUTZ-JEGHER’S SYNDROME
• Also called as hereditary intestinal polyposis syndrome.
• Rare familial disease.
• First described by Peutz in 1921and Jegher in 1949.
• Autosomal dominant disorder featuring gastrointestinal polyp and the pigmented
macule on the lip and skin.
ETIOLOGY:- Mutations in the STK11 gene (also known as LKB1) cause most cases
of Peutz-Jeghers syndrome. The STK11 gene is a tumor suppressor gene, which
means that it normally prevents cells from growing and dividing too rapidly or in an
uncontrolled way

40. CLINICAL FEATURES:-
• Age :- childhood onset with no sex predilection
• Intestinal polyps
• Symptoms :- polyp becomes symptomatic b/w the ages of 10 and 30, and may
cause ulceration with bleeding, obstruction, diarrhoea and intussusceptions.
• Tuberous sclerosis
• Pigmentation:- multifocal macular melanin pigmentation
• Sites:- lower lip and buccal mucosa
• Color of pigmentation:- bluish black on skin , orally as brownish macules
MANAGEMENT:- no Rx for oral lesions.

42. ALBRIGHT’S SYNDROME
• Type of fibrous dysplasia involving all the bones in the skeleton accompanied by
the lesions of the skin and endocrine disturbances of varying types.
• Skin lesions:- café-au-lait spots(irregularly pigmented melanotic spots)
• Color:- light brown
• More common on lips.
DIFFERENTIAL DIAGNOSIS:-
• Addisons disease
• Peutz-Jegher’s syndrome

45. AMALGAM TATTOO
• Also called as localized argyrosis.
• Common intraoral pigmented lesions.
• Charac. By the deposit of restorative debris composed of mixture of silver, mercury,
tin , zinc and copper in subepithelial connective tissue.
ETIOLOGY:-
• Restorative work
• Removal of old filling
• Drug extraction
• Retrograde amalgam filling

46. • Site:- common sites are gingiva and alveolar mucosa, mandibular region affected
more commonly than maxillary region.
• Age and sex distribution:-  occur at any age, rarely seen below 12 years
F>M, 1.8:1
• Appearance:- flat macule, or slightly raised lesion with well defined or diffused
margins.
• color:- blue black
• R/F:- presence of metal

48. Differential diagnosis:-
• Superficial hemangioma
• Nevus and melanoma
Management:-
• Surgical excision

50. ACRODYNIA
• Also called as pink disease or swifts disease, dermato-polyneuritis, mercurialism.
• Uncommon disease caused due to a mercurial toxicity reaction.
Etiology :-
1. Medicinal use
2. Mercury in amalgam
3. Mercury in paint
4. Night cream
5. Mercurial diuretics

51. Clinical features :-
• Age :- frequently in young adults.
• Dysphagia, nausea, abdominal pain,intestinal colic and diarrhea.
• Headache, tremors of fingers and tongue, insomnia and mental depression.
• Renal symptoms:- severe intoxication and can be the cause of death.
• Color:- hands, feet, nose and cheeks assume pink color.
• Raw beef appearance

52. Oral manifestations:-
• Symptoms:- (a) increase in inflow of ropy viscid saliva. That cause dribbling
(b) itching sensation and metallic taste in oral cavity.
• Gingiva :- extremely sensitive or painful and may exhibit ulceration.
• Ulcerative stomatitis.
• Swollen salivary glands and lymph nodes.
• Tongue is enlarged, painful and ulcerated. Tremors may be present.
• Lips are dry, cracked and swollen.
• Bruxism.
• Loss of teeth.
• Necrosis of bone.

54. Management:-
• Supportive measure:- bed rest.
• Control of salivary flow:- Atropine or belladonna
• Chelating agents:- BAL- British anti lewisite(2,3-dimercaptopropanol), DMSA(2,3-
dimercaptosuccinic acid) and DMPS (2,3-dimercaptopropane-1-sulfonate).