Pigmentations of the oral cavity

2,004 views 51 slides Jun 02, 2021
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About This Presentation

orofacial pigmentations ppt


Slide Content

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 N o 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. M alignant 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. T umors 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, A sians 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 H igher 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 . S urrounding bone - green , blue, black P alatal 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 I atrogenic 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 N o radiographic evidence of amalgam - biopsy is necessary . Differential D iagnosis Melanotic macule, Nevus, M elanoma. 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 ) P igmentation 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 – A crodynia /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 Smoking of tobacco or crack cocaine

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 O ral 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 C utaneous 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

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