6. FOCAL MELANOCYTIC PIGMENTATION
Freckle/ephelis
⢠Commonly occurring, asymptomatic, small
(1â3 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 â
suggestive of a Metastatic tumor
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. SMOKERâS MUCOSAL MELANOSIS
⢠Tobacco smoking â major cause
⢠Tobacco smoke agents â melanocytes - melanin
⢠Women â 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 nonâ
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
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 â 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
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 â 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)
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 â
⢠Autologous epithelial grafts
⢠Punch grafting and
⢠Micropigmentation
42. HYPOADRENOCORTICISM (adrenal insufficiency, addisonâs 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. CUSHINGâS SYNDROME/CUSHINGâS DISEASE
Clinical features
⢠Characteristic âmoon faciesâ
⢠Diffuse mucocutaneous pigmentation
⢠Pattern of oral pigmentation is essentially identical
(adrenal insufficiency)
45. HYPERTHYROIDISM (GRAVESâ 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 â 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 ASSOCIATEDâŚ
⢠Familial atypical multiple mole and melanoma syndrome â
atypical nevi
⢠Epitheloid blue nevus â carney complex
⢠Common nevi â turnerâs , noonan syndrome
⢠Cowden syndrome,cronkhite-Canada syndrome- GI
disease,pigmentation,cancer susceptibility
⢠Mc cune Albright syndrome
⢠LEOPARD syndrome
⢠Croweâs sign â inguinal freckling
⢠Lisch nodules â pigmented lesions of iris