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PIGMENTATIONS
INTRODUCTION
• PIGMENTATION – Deposition of pigments in the tissues
CLASSIFICATION
• Physiologic
• Pathologic
• Exogeneous
• Endogeneous
FOCAL MELANOCYTIC PIGMENTATION
• Freckle/Ephelis
• Oral/Labial Melanotic Macule
• Oral Melanoacanthoma
• Melanocytic Nevus
• Malignant Melanoma
FOCAL MELANOCYTIC PIGMENTATION
Freckle/ephelis
• Commonly occurring, asymptomatic, small
(1–3 mm), well-circumscribed, tan- or
brown-colored macule that is often seen on
the sun-exposed regions of the facial and
perioral skin
ORAL/LABIAL MELANOTIC MACULE
• Melanotic macules - most common oral lesions
• Lower lip (labial melanotic macule) and gingiva
• Congenital melanotic macules - tongue
• Small (<1 cm), well-circumscribed,
• Oval or irregular in outline
• Uniformly pigmented
ORAL MELANOACANTHOMA
• Unusual, benign, melanocytic lesion that is unique
to the mucosal tissues
• Rapidly enlarging, ill-defined, darkly pigmented macular or plaque-like
• Asymptomatic, although pain has been reported
• Buccal mucosa - most common site
• Borders - typically irregular in appearance
• Pigmentation may or may not be uniform
MELANOCYTIC NEVUS
• No distinguishing clinical characteristics
• Asymptomatic , small (<1 cm), solitary, brown or blue, well
circumscribed nodule or macule
• Hard palate - most common site, followed by the buccal and labial
mucosae and gingiva.
• Malignant transformation of an oral nevus
has not been well documented in the literature
DIAGNOSIS
• Biopsy is necessary for diagnostic confirmation
Treatment
• Conservative surgical excision
• Laser and intense pulse light therapies
• Their value in the treatment of oral nevi
is unknown.
MALIGNANT MELANOMA
• On the facial skin, malar region - common site for melanoma
since this area is subject to significant solar exposure.
• Higher among black-skinned and japanese people
• More frequent in males than females.
• Palate - single most common site
• Maxillary gingiva - second most frequent site
• Oral melanomas have no distinctive clinical appearance.
• Macular, plaque-like or mass forming, well-circumscribed
or irregular and exhibit focal or diffuse areas of brown,
blue, or black pigmentation
• Ulceration, pain, tooth mobility or spontaneous exfoliation, root
resorption, bone loss, and paresthesia /anesthesia may be
evident.
• Tumors may be completely asymptomatic
DIAGNOSIS
• Whether the lesion is a primary neoplasm or a metastasis from a
distant site
• History of a previous melanoma, sparing of the palate and gingiva,
amelanosis
Microscopic features
• Lack of junctional activity and pagetoid spread –
suggestive of a Metastatic tumor
Management
• Primary oral melanomas- ablative surgery
• Adjuvant radiation therapy
• Immunotherapy
Multifocal/diffuse pigmentation
• Physiologic Pigmentation
• Drug-Induced Melanosis
• Smoker’s Melanosis
• Postinflammatory (Inflammatory) Hyperpigmentation
• Melasma (Chloasma)
PHYSIOLOGIC PIGMENTATION
• Multifocal or diffuse oral mucosal pigmentation
• Blacks, Asians and South-Americans - patchy to generalized
hyperpigmentation of the oral mucosal tissues - restricted to
gingiva
• Often observed in childhood
TREATMENT :
• Gingivectomy , laser therapy
SMOKER’S MUCOSAL MELANOSIS
• Tobacco smoking – major cause
• Tobacco smoke agents – melanocytes - melanin
• Women – more commonly affected because of synergistic
effect between female sex hormones and smoking
• Presentation : brown, gray or black areas
• Most common site: anterior labial gingiva,
interdental papilla of mandible
• Treatment : disappears within 3 years of smoking cessation.
ALCOHOL INDUCED PIGMENTATION
• Alcohol - increased oral pigmentation
• SITE: posterior regions of the mouth, soft palate
• Higher risk of cancers of the upper aerodigestive tract
DRUG INDUCED
• Due to synthesis and accumulation of
melanin pigments
• Deposition of drug or its metabolites
• Drugs : bleomycin , clofazinine,
chloroquine
• Presentation : diffuse brownish
discolouration of the hard palate,
gingiva, mucous membrane and tongue
• Minocycline - common cause of drug-induced non–
melanin-associated oral pigmentation.
• Surrounding bone - green, blue, black
• Palatal and alveolar mucosae - diffusely discolored
MELASMA (CHLOASMA)
• common, acquired symmetric melanosis that typically develops on
sun-exposed areas
• forehead, cheeks, upper lips, and chin - most commonly affected
areas
POST INFLAMMATORY (Inflammatory hyperpigmentation)
• Mucosa overlying a nonmelanocytic malignancy may become
pigmented
• Oral pigmentation with lichen planus (lichen planus
pigmentosus)
• Upon resolution of the lichenoid lesion,
the pigmentation may or may not disappear
EXOGENOUS PIGMENTATION
• Amalgam Tattoo
• Graphite Tattoos
• Ornamental Tattoos
• Medicinal Metal-Induced Pigmentation
• Heavy-Metal Pigmentation
• Drug-Induced Pigmentation
• Hairy Tongue
HEAVY METAL INDUCED
AMALGAM TATTOO:
Etiology and Pathogenesis
• Single most common source of solitary or focal pigmentation
• Iatrogenic in origin
• Consequence of the inadvertent deposition of amalgam
restorative material into the submucosal tissue.
CLINICAL FEATURES
• Small, asymptomatic, macular, and bluish gray or even black
• Gingiva, alveolar mucosa, buccal mucosa, floor of the mouth - most
common sites.
• Often found in the vicinity of teeth with
• Large amalgam restorations / crowned teeth
that probably had amalgams,
• Apical region of endodontically treated teeth with retrograde
restorations , Areas in and around healed extraction sites
MANAGEMENT
• If compromise esthetics - surgical removal
• No radiographic evidence of amalgam - biopsy is necessary.
Differential Diagnosis
• Melanotic macule,
• Nevus,
• Melanoma.
• Pigmentation associated with other dental restorative materials
• Titanium - dental implants - potential source of exogenous oral
pigmentation
GRAPHITE TATTOOS
• Unusual source of focal exogenous pigmentation
• Most common - palate
• Traumatic implantation of graphite particles from a pencil
• Solitary gray or black macule
MEDICINAL METAL-INDUCED PIGMENTATION
• Gold and colloidal silver - associated with diffuse
cutaneous pigmentation.
• Silver - generalized blue-gray discoloration (argyria)
• Gold-induced pigment - appear blue -gray or purple (chrysiasis)
• Pigmentation may be persistent, if not permanent
• Oral lichenoid eruptions have been associated with systemic
gold therapy
• Silver nitrate and zinc oxide - associated with focal
mucocutaneous pigmentation.
• Gray-black in appearance
• Generalized black pigmentation of the tongue - attributed to
the chewing of bismuth subsalicylate tablets
• Lead, mercury, bismuth, and arsenic have all been shown to be
deposited in oral tissue if ingested
• Free marginal gingiva - outlines the gingival cuff - gray to black
appearance.
• Mercury poisoning – Acrodynia /pink disease
• Affected children may show red cheeks and nose,
red lips, loss of hair, teeth, and nails, transient
rashes, hypotonia and photophobia
HAIRY TONGUE
• Common condition of unknown etiology
• Associated with chronic antibiotic therapy
• Involves dorsal tongue, particularly middle
and posterior one-third.
• Filiform papillae are elongated - appearance of fine hairs
• Hyperplastic papillae - pigmented by colonization of
chromogenic bacteria
• Foods, drinks, and confectionaries
Hemoglobin and iron-associated pigmentation
• Ecchymosis
• Purpura/Petechiae
• Hemochromatosis
ECCHYMOSIS
• Traumatic ecchymosis - common - lips and face
• Trauma - erythrocyte extravasation into the submucosa - bright
red macule or as a swelling if a hematoma forms – hemoglobin-
hemosiderin - brown coloration
PURPURA / PETECHIAE
• Appear red initially - brown in a few days
• PETECHIAE - pinpoint or slightly larger than pinpoint
• PURPURA - multiple, small 2 to 4 mm collections of extravasated blood
• Develop as a consequence of
• Trauma or viral or systemic disease
• Secondary to platelet deficiencies or aggregation disorders - Usually
not limited to the oral mucosa occur concomitantly on the skin.
• Viral disease - oral - soft palate (common)
HEMOCHROMATOSIS
• Oral pigmentation - diffuse and brown to gray
• The palate and gingiva are most commonly affected.
DEPIGMENTATION
Vitiligo
• Areas of depigmentation
• Common, acquired, autoimmune disease that is associated
with hypomelanosis
• Mechanisms remain unknown - destruction of the melanocytes
CLINICAL FEATURES
• Focal areas of depigmentation
• Vitiligo universalis
• Bilateral, symmetric areas of relatively generalized hypomelanosis
• Well-circumscribed, round, oval or elongated, pale or white-colored
MANAGEMENT
• Topical corticosteroids
• Systemic photochemotherapies (psoralen and ultraviolet A
exposure)
• Cutaneous bleaching
• Labial vitiligo –
• Autologous epithelial grafts
• Punch grafting and
• Micropigmentation
MELANOSIS ASSOCIATED WITH SYSTEMIC OR
GENETIC DISEASE
Melanosis associated with systemic or genetic disease
• Hypoadrenocorticism
• Cushing’s Syndrome/Cushing’s Disease
• Hyperthyroidism (Graves’ Disease)
• Primary Biliary Cirrhosis
• Vitamin B12 (Cobalamin) Deficiency
• Peutz-Jeghers Syndrome
• HIV/AIDS-Associated Melanosis
HYPOADRENOCORTICISM (adrenal insufficiency, addison’s disease)
Clinical features
• Weakness, poorly defined fatigue, and depression
• First sign of disease may be mucocutaneous hyperpigmentation
• Diffuse but patchy melanosis of the oral mucosa are hallmarks
• Any oral surface may be affected
DIAGNOSIS
• Requires a clinicopathologic correlation
• Endocrinopathic disease should be suspected whenever
oral melanosis is accompanied by cutaneous bronzing.
CUSHING’S SYNDROME/CUSHING’S DISEASE
Clinical features
• Characteristic “moon facies”
• Diffuse mucocutaneous pigmentation
• Pattern of oral pigmentation is essentially identical
(adrenal insufficiency)
HYPERTHYROIDISM (GRAVES’ DISEASE)
• Melanosis is a common consequence of hyperthyroidism
• 40% of black patients
• Very rarely observed in caucasian patients
• Tends to resolve following treatment of the thyroid abnormality
• The mechanism – remains unclear
PRIMARY BILIARY CIRRHOSIS
• Diffuse mucocutaneous hyperpigmentation - earliest
manifestations of primary biliary cirrhosis
• unknown etiology - thought to be autoimmune
VITAMIN B12 (COBALAMIN) DEFICIENCY
• Cutaneous and oral manifestations - generalized burning sensation and
erythema and atrophy of the mucosal tissue
• Diffuse mucocutaneous hyperpigmentation - rare complication
• Mechanisms - unknown
• Pigmentation resolves following restoration of vitamin B12 levels
PEUTZ-JEGHERS SYNDROME
• Autosomal dominant disease
• Intestinal polyposis, cancer susceptibility, and multiple, small,
pigmented macules of the lips, perioral skin, hands, and feet
• Macules - <0.5 cm in diameter
• Similar-appearing lesions develop on the
anterior tongue, buccal and labial mucosae
• Lip and perioral pigmentation is highly distinctive, although not
pathognomonic
HIV/AIDS -ASSOCIATED MELANOSIS
• Hyperpigmentation of the skin, nails, and mucous membranes
• Buccal mucosa - most frequently affected site
• Gingiva, palate, and tongue may also be involved
SYNDROMES ASSOCIATED…
• Familial atypical multiple mole and melanoma syndrome –
atypical nevi
• Epitheloid blue nevus – carney complex
• Common nevi – turner’s , noonan syndrome
• Cowden syndrome,cronkhite-Canada syndrome- GI
disease,pigmentation,cancer susceptibility
• Mc cune Albright syndrome
• LEOPARD syndrome
• Crowe’s sign – inguinal freckling
• Lisch nodules – pigmented lesions of iris
THANK YOU

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Pigmentations of the oral cavity

  • 2. INTRODUCTION • PIGMENTATION – Deposition of pigments in the tissues CLASSIFICATION • Physiologic • Pathologic • Exogeneous • Endogeneous
  • 3.
  • 4.
  • 5. FOCAL MELANOCYTIC PIGMENTATION • Freckle/Ephelis • Oral/Labial Melanotic Macule • Oral Melanoacanthoma • Melanocytic Nevus • Malignant Melanoma
  • 6. FOCAL MELANOCYTIC PIGMENTATION Freckle/ephelis • Commonly occurring, asymptomatic, small (1–3 mm), well-circumscribed, tan- or brown-colored macule that is often seen on the sun-exposed regions of the facial and perioral skin
  • 7. ORAL/LABIAL MELANOTIC MACULE • Melanotic macules - most common oral lesions • Lower lip (labial melanotic macule) and gingiva • Congenital melanotic macules - tongue • Small (<1 cm), well-circumscribed, • Oval or irregular in outline • Uniformly pigmented
  • 8. ORAL MELANOACANTHOMA • Unusual, benign, melanocytic lesion that is unique to the mucosal tissues • Rapidly enlarging, ill-defined, darkly pigmented macular or plaque-like • Asymptomatic, although pain has been reported • Buccal mucosa - most common site • Borders - typically irregular in appearance • Pigmentation may or may not be uniform
  • 9. MELANOCYTIC NEVUS • No distinguishing clinical characteristics • Asymptomatic , small (<1 cm), solitary, brown or blue, well circumscribed nodule or macule • Hard palate - most common site, followed by the buccal and labial mucosae and gingiva. • Malignant transformation of an oral nevus has not been well documented in the literature
  • 10. DIAGNOSIS • Biopsy is necessary for diagnostic confirmation Treatment • Conservative surgical excision • Laser and intense pulse light therapies • Their value in the treatment of oral nevi is unknown.
  • 11. MALIGNANT MELANOMA • On the facial skin, malar region - common site for melanoma since this area is subject to significant solar exposure. • Higher among black-skinned and japanese people • More frequent in males than females.
  • 12. • Palate - single most common site • Maxillary gingiva - second most frequent site • Oral melanomas have no distinctive clinical appearance. • Macular, plaque-like or mass forming, well-circumscribed or irregular and exhibit focal or diffuse areas of brown, blue, or black pigmentation
  • 13. • Ulceration, pain, tooth mobility or spontaneous exfoliation, root resorption, bone loss, and paresthesia /anesthesia may be evident. • Tumors may be completely asymptomatic
  • 14. DIAGNOSIS • Whether the lesion is a primary neoplasm or a metastasis from a distant site • History of a previous melanoma, sparing of the palate and gingiva, amelanosis Microscopic features • Lack of junctional activity and pagetoid spread – suggestive of a Metastatic tumor
  • 15. Management • Primary oral melanomas- ablative surgery • Adjuvant radiation therapy • Immunotherapy
  • 16. Multifocal/diffuse pigmentation • Physiologic Pigmentation • Drug-Induced Melanosis • Smoker’s Melanosis • Postinflammatory (Inflammatory) Hyperpigmentation • Melasma (Chloasma)
  • 17. PHYSIOLOGIC PIGMENTATION • Multifocal or diffuse oral mucosal pigmentation • Blacks, Asians and South-Americans - patchy to generalized hyperpigmentation of the oral mucosal tissues - restricted to gingiva • Often observed in childhood TREATMENT : • Gingivectomy , laser therapy
  • 18. SMOKER’S MUCOSAL MELANOSIS • Tobacco smoking – major cause • Tobacco smoke agents – melanocytes - melanin • Women – more commonly affected because of synergistic effect between female sex hormones and smoking • Presentation : brown, gray or black areas • Most common site: anterior labial gingiva, interdental papilla of mandible • Treatment : disappears within 3 years of smoking cessation.
  • 19. ALCOHOL INDUCED PIGMENTATION • Alcohol - increased oral pigmentation • SITE: posterior regions of the mouth, soft palate • Higher risk of cancers of the upper aerodigestive tract
  • 20. DRUG INDUCED • Due to synthesis and accumulation of melanin pigments • Deposition of drug or its metabolites • Drugs : bleomycin , clofazinine, chloroquine • Presentation : diffuse brownish discolouration of the hard palate, gingiva, mucous membrane and tongue
  • 21. • Minocycline - common cause of drug-induced non– melanin-associated oral pigmentation. • Surrounding bone - green, blue, black • Palatal and alveolar mucosae - diffusely discolored
  • 22. MELASMA (CHLOASMA) • common, acquired symmetric melanosis that typically develops on sun-exposed areas • forehead, cheeks, upper lips, and chin - most commonly affected areas
  • 23. POST INFLAMMATORY (Inflammatory hyperpigmentation) • Mucosa overlying a nonmelanocytic malignancy may become pigmented • Oral pigmentation with lichen planus (lichen planus pigmentosus) • Upon resolution of the lichenoid lesion, the pigmentation may or may not disappear
  • 24. EXOGENOUS PIGMENTATION • Amalgam Tattoo • Graphite Tattoos • Ornamental Tattoos • Medicinal Metal-Induced Pigmentation • Heavy-Metal Pigmentation • Drug-Induced Pigmentation • Hairy Tongue
  • 25. HEAVY METAL INDUCED AMALGAM TATTOO: Etiology and Pathogenesis • Single most common source of solitary or focal pigmentation • Iatrogenic in origin • Consequence of the inadvertent deposition of amalgam restorative material into the submucosal tissue.
  • 26. CLINICAL FEATURES • Small, asymptomatic, macular, and bluish gray or even black • Gingiva, alveolar mucosa, buccal mucosa, floor of the mouth - most common sites. • Often found in the vicinity of teeth with • Large amalgam restorations / crowned teeth that probably had amalgams, • Apical region of endodontically treated teeth with retrograde restorations , Areas in and around healed extraction sites
  • 27. MANAGEMENT • If compromise esthetics - surgical removal • No radiographic evidence of amalgam - biopsy is necessary. Differential Diagnosis • Melanotic macule, • Nevus, • Melanoma. • Pigmentation associated with other dental restorative materials • Titanium - dental implants - potential source of exogenous oral pigmentation
  • 28. GRAPHITE TATTOOS • Unusual source of focal exogenous pigmentation • Most common - palate • Traumatic implantation of graphite particles from a pencil • Solitary gray or black macule
  • 29. MEDICINAL METAL-INDUCED PIGMENTATION • Gold and colloidal silver - associated with diffuse cutaneous pigmentation. • Silver - generalized blue-gray discoloration (argyria) • Gold-induced pigment - appear blue -gray or purple (chrysiasis) • Pigmentation may be persistent, if not permanent • Oral lichenoid eruptions have been associated with systemic gold therapy
  • 30. • Silver nitrate and zinc oxide - associated with focal mucocutaneous pigmentation. • Gray-black in appearance • Generalized black pigmentation of the tongue - attributed to the chewing of bismuth subsalicylate tablets
  • 31. • Lead, mercury, bismuth, and arsenic have all been shown to be deposited in oral tissue if ingested • Free marginal gingiva - outlines the gingival cuff - gray to black appearance. • Mercury poisoning – Acrodynia /pink disease • Affected children may show red cheeks and nose, red lips, loss of hair, teeth, and nails, transient rashes, hypotonia and photophobia
  • 32. HAIRY TONGUE • Common condition of unknown etiology • Associated with chronic antibiotic therapy • Involves dorsal tongue, particularly middle and posterior one-third. • Filiform papillae are elongated - appearance of fine hairs • Hyperplastic papillae - pigmented by colonization of chromogenic bacteria • Foods, drinks, and confectionaries
  • 33. Hemoglobin and iron-associated pigmentation • Ecchymosis • Purpura/Petechiae • Hemochromatosis
  • 34. ECCHYMOSIS • Traumatic ecchymosis - common - lips and face • Trauma - erythrocyte extravasation into the submucosa - bright red macule or as a swelling if a hematoma forms – hemoglobin- hemosiderin - brown coloration
  • 35. PURPURA / PETECHIAE • Appear red initially - brown in a few days • PETECHIAE - pinpoint or slightly larger than pinpoint • PURPURA - multiple, small 2 to 4 mm collections of extravasated blood • Develop as a consequence of • Trauma or viral or systemic disease • Secondary to platelet deficiencies or aggregation disorders - Usually not limited to the oral mucosa occur concomitantly on the skin. • Viral disease - oral - soft palate (common)
  • 36. HEMOCHROMATOSIS • Oral pigmentation - diffuse and brown to gray • The palate and gingiva are most commonly affected.
  • 37. DEPIGMENTATION Vitiligo • Areas of depigmentation • Common, acquired, autoimmune disease that is associated with hypomelanosis • Mechanisms remain unknown - destruction of the melanocytes
  • 38. CLINICAL FEATURES • Focal areas of depigmentation • Vitiligo universalis • Bilateral, symmetric areas of relatively generalized hypomelanosis • Well-circumscribed, round, oval or elongated, pale or white-colored
  • 39. MANAGEMENT • Topical corticosteroids • Systemic photochemotherapies (psoralen and ultraviolet A exposure) • Cutaneous bleaching • Labial vitiligo – • Autologous epithelial grafts • Punch grafting and • Micropigmentation
  • 40. MELANOSIS ASSOCIATED WITH SYSTEMIC OR GENETIC DISEASE
  • 41. Melanosis associated with systemic or genetic disease • Hypoadrenocorticism • Cushing’s Syndrome/Cushing’s Disease • Hyperthyroidism (Graves’ Disease) • Primary Biliary Cirrhosis • Vitamin B12 (Cobalamin) Deficiency • Peutz-Jeghers Syndrome • HIV/AIDS-Associated Melanosis
  • 42. HYPOADRENOCORTICISM (adrenal insufficiency, addison’s disease) Clinical features • Weakness, poorly defined fatigue, and depression • First sign of disease may be mucocutaneous hyperpigmentation • Diffuse but patchy melanosis of the oral mucosa are hallmarks • Any oral surface may be affected
  • 43. DIAGNOSIS • Requires a clinicopathologic correlation • Endocrinopathic disease should be suspected whenever oral melanosis is accompanied by cutaneous bronzing.
  • 44. CUSHING’S SYNDROME/CUSHING’S DISEASE Clinical features • Characteristic “moon facies” • Diffuse mucocutaneous pigmentation • Pattern of oral pigmentation is essentially identical (adrenal insufficiency)
  • 45. HYPERTHYROIDISM (GRAVES’ DISEASE) • Melanosis is a common consequence of hyperthyroidism • 40% of black patients • Very rarely observed in caucasian patients • Tends to resolve following treatment of the thyroid abnormality • The mechanism – remains unclear
  • 46. PRIMARY BILIARY CIRRHOSIS • Diffuse mucocutaneous hyperpigmentation - earliest manifestations of primary biliary cirrhosis • unknown etiology - thought to be autoimmune
  • 47. VITAMIN B12 (COBALAMIN) DEFICIENCY • Cutaneous and oral manifestations - generalized burning sensation and erythema and atrophy of the mucosal tissue • Diffuse mucocutaneous hyperpigmentation - rare complication • Mechanisms - unknown • Pigmentation resolves following restoration of vitamin B12 levels
  • 48. PEUTZ-JEGHERS SYNDROME • Autosomal dominant disease • Intestinal polyposis, cancer susceptibility, and multiple, small, pigmented macules of the lips, perioral skin, hands, and feet • Macules - <0.5 cm in diameter • Similar-appearing lesions develop on the anterior tongue, buccal and labial mucosae • Lip and perioral pigmentation is highly distinctive, although not pathognomonic
  • 49. HIV/AIDS -ASSOCIATED MELANOSIS • Hyperpigmentation of the skin, nails, and mucous membranes • Buccal mucosa - most frequently affected site • Gingiva, palate, and tongue may also be involved
  • 50. SYNDROMES ASSOCIATED… • Familial atypical multiple mole and melanoma syndrome – atypical nevi • Epitheloid blue nevus – carney complex • Common nevi – turner’s , noonan syndrome • Cowden syndrome,cronkhite-Canada syndrome- GI disease,pigmentation,cancer susceptibility • Mc cune Albright syndrome • LEOPARD syndrome • Crowe’s sign – inguinal freckling • Lisch nodules – pigmented lesions of iris