Pigmented Lesions of the Oral Cavity

Pigmentation is defined as the process of deposition of pigments in tissues.

  • Augmentation of melanin production.
  • Increased number of melanocytes (melanocytosis).
  • Deposition of accidentally introduced exogenous materials.
  • Melanin.
  • Carotenoids.
  • Reduced HB.
  • Oxygenated HB.
  • Distributed in the lipids of the St.corneum and St.lucidum.
  • Induce orange to yellow pigmentation.
  • Condition is known as carotenimia.
  • Occurs due to consumption of food containing large amount of carotene like carrots, sweet potatoes and egg yolks.
  • Does not involve sclera.
  • Seen in palm, soles and soft palate.
  • No specific treatment.
  • Resolution occur following decrease dietary intake.
  • Oral pigmentation may be physiologic or pathologic.
  • Pathologic pigmentation can be classified into exogenous and endogenous based upon the cause.
  • Endogenous pigmentation in oral mucosal disease:

Pigment

Color

Disease process

Hemoglobin

Blue, red, purple

Varix, hemangioma, kaposi’s sarcoma, angiosarcoma, hereditary hemorrhagic

telangiectasia

Hemosiderin

Brown

Ecchymosis, petechia, thrombosedvarix,

hemorrhagic mucocele, hemochromatosis

Melanin

Brown, black

or gray

Melanotic macule, nevus, melanoma,

basilar melanosis with incontinence

  • Exogenous pigmentation of oral mucosa:

Pigment

Color

Disease process

Silver amalgam

Gray, black

Tattoo, iatrogenic trauma

Graphite

Gray, black

Tattoo, trauma

Lead, mercury, bismuth

Gray

Ingestion of paint or medicinals.

Chromogenic bacteria

Brown,

green, black

Superficial colonization

  • Hemangioma.
  • Varix.
  • Angiosarcoma.
  • Kaposi’s Sarcoma.
  • Hereditary Hemorrhagic Telangiectasia.
  • Hemangioma is a proliferation of endothelial cells of vascular channels.
  • It may be congenital and traumatic in origin.
  • Rare in the oral cavity but may occur on tongue, lips, buccal mucosa, gingiva, palatal mucosa, salivary glands, alveolar ridge, and jaw bones.
  • Appear as a flat reddish blue macule (port-wine stain) to a nodular blue tumefaction.
  • Vascular lesions will blanch under pressure.

The facial capillary vascular malformation is also known as “port wine stain” or “nevus flammeus” and usually is seen in the territory of the trigeminal nerve.

Have deep purple colour.

  • Diascopy.
  • Radiographs.
  • Biopsy.
  • Angiogram.
  • Doppler and conventional ultrasonography.
  • Radionuclide-labeled red cell scintigraphic scanning.

Mucocele, ranula, arteriovenous malformation, pyogenic granuloma, hemangiopericytoma.

  • Congenital one undergo spontaneous regression at a early age.
  • Radiation therapy.
  • Surgery-lasers or cryosurgery.
  • Carbon di-oxide snow.
  • Sclerosing agents-sodium morrhuate/psylliate/1%sodium tetradecyl sulfate.
  • Intralesionl steroids in children.
  • Sturge-Weber Syndrome (Encephalofacial or Encephalotrigeminal Angiomatosis).
  • Kasabach –Merritt syndrome.
  • Maffucci’s syndrome (dyschondroplasia with vascular hamartomas).
  • Von-Hippel-Lindau-Disease/syndrome.
  • Blue Rubber Bleb Nevus Syndrome.
  • Klippel Trenaunay Weber Syndrome.

Sturge-Weber syndrome (SWS) is a neurocutaneous syndrome characterized by angiomas involving the face, choroid, and leptomeninges.

  • Gingiva may show vascular hyperplasia or more massive hemangiomatous proliferation.
  • Unilateral involvement of oral mucosa.
  • Asymmetric jaw growth.
  • Altered tooth eruption sequence.

Gyriform calcifications on the skull radiographs classically described as “tram-track sign.”

Kasabach-Merritt syndrome (KMS) was first described by Haig Haigoui Kasabach and Katharine Krom Merritt in 1940. The syndrome results in a consumptive coagulopathy from platelet trapping and aggregation within a specific type of hemangioma, and can have a high mortality rate.

The hemangioma is often within the skin but can be present anywhere, including retroperitoneal organs, the mediastinum, the pelvis, visceral organs, or the mesentery.

  • Maffucci syndrome (also known as dyschondrodysplasia with hemangiomas, enchondromatosis with multiple cavernous hemangiomas, Kast syndrome, hemangiomatosis chondrodystrophica, and enchondromatosis Spranger type II) was first described in 1881.
  • Maffucci syndrome is characterized by the presence of multiple enchondromas combined with multiple soft tissue hemangiomas or lymphangiomas.
  • Given by Christoferson et al in1961.
  • Von Hippel-Lindau disease (vHL, familial cerebello-retinal angiomatosis) is a rare genetic autosomal dominant disorder associated with predisposition to vascular tumors.
  • Mutations of VHL tumor suppressor gene, located on chromosome 3p25-26, are responsible for clinical manifestation of the disease. The VHL gene product encodes VHL protein, which is responsible for HIF-1 (hypoxia-inducible factor-1) dependent cell cycle regulation and cellular pathways mediated by VEGF, PDGF, TGF-α, EPO.
  • It causes retinal hemangioblastomas, hemangioblastomas of the central nervous system, endolymphatic sac tumours, renal cell carcinomas, pancreatic cysts and tumours, pheochromocytomas and epididymal cyst adenomas.
  • Given by Bean 1958.
  • Blue rubber bleb nevus syndrome (BRBNS), also known as the Bean syndrome, is a very rare disorder characterized by multiple vascular malformations of the skin, gastrointestinal (GI) tract, and, less often, other visceral organs.
  • Typically, cutaneous lesions are usually asymptomatic, easily compressive and refill slowly upon release of pressure, and bleed spontaneously very rarely but easily upon being traumatized.
  • Present at birth.
  • Follows an autosomal dominant.
  • Multiple in nature.
  • Given byKlippel and Trenaunay 1900.
  • Klippel Trenaunay Webber Syndrome (KTWS) is a rare congenital disorder characterized by asymmetric limb hypertrophy, usually of the lower limbs, as well as vascular anomalies and capillary malformations under the skin, termed the port wine stain.
  • The three main features that describe this condition are a port wine stain or naevi which is caused by capillary malformations that create a reddish-purplish discoloration of the skin, vascular anomalies and hypertrophy of the affected limb bones and soft tissues.
  • Also known as malignant hemangioendothelioma, angioblastoma, hemangiosarcoma, and intravascular endothelioma.
  • Malignant vascular neoplasms arise from blood or lymph vessel endothelial cells or from pericytic cells of the vasculature.
  • Usually occurs in elderly patients.
  • Head and neck most common site.
  • Elevated nodular or ulcerated surface.
  • Multifocal in nature.
  • Usually occur in mandible.
  • If occurs in oral cavity- appears red/blue/purple.
  • Radical surgical excision.
  • Radiation therapy.

A varix is a dilated, tortuous vein, most commonly a vein which is subjected to increased hydrostatic pressure but poorly supported by surrounding tissue.

  • Usually occur after 60 years of age.
  • Rare in children.
  • Common in older adults.
  • It is usually painless.
  • Red/purple in colour .
  • Elevated/papular bleb like lesion.
  • Firm in consistency.
  • Ventral surface/lateral border of tongue, floor of the mouth.

Mucocele,  ranula, hemangioma.

  • Excised or removed by electrosurgeryand cryosurgery.
  • Intralesional 1% sodium tetradecyl sulfate injection (directly into the lumina with a tuberculin syringe depositing .05 to 0.15 mL/cm3)
  • Caviar tongue, also known as lingual varicosities and sublingual varices, is considered as a physiological change associated with advancing age, usually developing due to senile elastolytic degeneration of sublingual veins.
  • It is mostly seen at the undersurface of the tongue along the sublingual glands where the mucosal surface is thin and translucent which permits visualisation of submucosal vascular structures.
  • In a young population, such vascular lesions could be part of Fabry, or Osler syndrome.
  • Also known as Rendu-Osler-Weber disease.
  • It is a form of hemangioma, congenital hereditary disease characterized by numerous telengiectatic or angiomatous areas which are widely distributed on the skin and mucosa of the oral cavity and which tend to undergo repeated hemorrhage.
  • HHT1 is caused by mutation of the endoglin gene on chromosome-9,where as ALK-1 mutation produces HHT-2.
  • Transmitted by both sexes as a simple autosomal dominant.
  • Male:female=1:1
  • Spider like telangectasia are present at or shortly after birth.
  • Skin lesions are most common on face/neck and chest.
  • Most important sign-epistaxis as well as bleeding from oral cavity.
  • Papules are red or brown rather than purple.
  • The lesions blanch upon pressure and regain their original color upon release.
  • It is characterized by multiple, round or oval papules measuring <0.5 cm in diameter.
  • The early oral lesion is a cherry-red macule ranging from 1 to 3 mm in diameter.

Characterized by multiple round or oval purple papules measuring <0.5mm in diameter.

Site of involvement:

  • Vermillion border of lip.
  • Gingiva.
  • Buccal mucosa.             
  • Palate.
  • Floor of mouth.
  • Tongue.

Crest syndrome, scleroderma, lupus erythematosus.

Telangiectatic areas removed for cosmetic reasons, papules can be cauterized by electrocautery.

Kaposi sarcoma (KS) was first described by the Viennese dermatologist Moritz Kaposi in 1872. Kaposi’s sarcoma is an angioproliferative neoplasm.

  • It is a proliferation of endothelial cell.
  • Dermal/submucosal dendrocytes, macrophages, lymphyocyes and mast cell plays an imp role.

Other factors are:-

  • Infections.
  • Enviornmental influences.
  • Reduced immunosurveillance.
  • HHV8.

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Four epidemiological forms of kaposi’s sarcoma

  1. AIDS-Associated Kaposi’s Sarcoma Kaposi’s sarcoma (KS)– It is a multi-focal, angioproliferative neoplasm that usually appears on the skin, but can also involve the visceral organs. In these immunocompromised patients, KS behaved more aggressively, often involving mucosal tissues, and progressed to visceral involvement leading to organ dysfunction and death.
  1. The Classic Form– In 1872, Moritz Kaposi first described the ‘‘classic’’ variant of KS that is typically observed in elderly men of Mediterranean or eastern European origin.
  • It presents with lesions confined to the lower extremity.
  • Affects men more commonly.
  1. The Endemic Form– In the 1950s, an endemic form of KS was reported to be one of the most common neoplasms observed in central Africa, affecting men, women and children.
  • Multiple localized skin tumors, involving lower extremities and/or lymph nodes.
  1. The Iatrogenic Form- This form of KS was also observed among organ transplant recipients, as well as other patients on long-term immunosuppression for other diseases.
  • Occurs mainly in renal transplant recipients, and infrequently after other solid organ or bone marrow transplants.
  • The oral tumors are red, blue, and purple, and the hard palate is the favored site.
  • Skin tumors tend to localize in the dorsal aspect of the feet and great toe.
  • African form is characterized by lymph node enlargement and can progressively involve many node groups.

HIV associated KS:

  • Cutaneous lesions begin as red macules and enlarge to become blue, purple, and ultimately brown nodular tumefactions.
  • The lower extremity shows no predilection over other cutaneous sites.
  • Lesions may appear on the arms, face, scalp or trunk.
  • Oral lesions show a predilection for posterior hard palate, begin as flat red macules of variable size and irregular configuration.
  • Typical lesions are multifocal, with numerous isolated and coalescing plaques, these lesions increase in size to become nodular growths, and involve the entire palate, protruding below the plane of occlusion.
  • Facial gingiva is the second common site of involvement.

Hemangioma, erythroplakia,melanoma, pyogenic granuloma,giant cell granuloma.

Immunohistochemistry

  • Kaposi sarcoma lesional cells stain positively with the endothelial markers factor VIII–related antigen, CD31 (PECAM-1), and CD34. CD34 tends to show stronger expression than CD31 in advanced-stage lesions of KS.
  • Kaposi sarcoma spindle cells also express several lymphatic specific markers such as D2-40 (which binds to the podoplanin antigen), LYVE-1 (a homologue of the CD44 glycoprotein receptor for hyaluronan), VEGFR-3 (the receptor for vascular endothelial growth factor C), and Prox-1.
  • Identification and localization of HHV8 within KS lesional cells by using LNA-1 immunohistochemistry.
  • Electrocautery.
  • Intralesional injection of 1% sodium tetradecyl sulphate.
  • Intralesional 1%vinblastin sulphate, biweekly injections.
  • Cutaneous freckle or ephelis represents an increase in melanin pigment synthesis by basal-layer melanocytes, without an increase in the number of melanocytes.
  • Ephelides are common, uniform, small, light brown macules localized on sun-exposed areas of skin, including the perioral skin and lips.
  • Site of involvement is vermilion border of the lips mainly lower lip(due to increased solar exposure).
  • Macular lesion and ranges from quite small to over a centimeter in size.
  • Lip ephelides are asymptomatic and occur equally in men and women.
  • Melanin is produced by melano­cytes in the basal layer of the epithelium and is transferred to adjacent keratinocytes via membrane-bound organelles called melanosomes.
  • Also synthesized by nevus cells, derived from the neural crest and are found in the skin and mucosa.
  • Eumelanin
  • Pheomelanin
  • Mixed type melanin
  • Neuromelanin
  • Oxymelanin.
  • It is intraoral counterpart to the ephelis is the oral melanotic macule.
  • Also known as focal melanosis.
  • It is a benign, solitary, well-demarcated, dark brown macule, most commonly located on the vermilion border of the lower lip followed by the palate, gingival and buccal mucosa.
  • Female to male ratio is almost 2:1.
  • Mean age of onset is 30 years.

Nevus, early superficial spreading melanoma, amalgam tattoo, focal ecchymosis.

  • Melanoacanthoma is a rare, benign, solitary, well-demarcated, flat or slightly raised hyper pigmented lesion.
  • Lesions typically develop after trauma.
  • Found on the buccal mucosa.
  • More frequently unilateral.
  • Occur in young black females.
  • Also known as Oral melanocytic nevus, mole, nevocellular nevus mucosal melanocytic nevi.
  • Nevi are due to benign proliferations of melanocytes.
  • Categorized as hamartomas, developmental malformations, the nevi are benign proliferations of nevus cells in either epithelium or connective tissue.
  • Congenital.
  • Acquired.

On the basis of the histologic location:

  • Junctional nevus – When nevus cells are limited to the basal cell layer of the epithelium.
  • Compound nevus – Nevus cells are in the epidermis and Dermis
  • Intradermal nevus (common mole) – Nests of nevus cells are entirely in the dermis.

Oral nevi follow the same classification where the term intradermal is replaced by intramucosal.

  • Occur in 1–2.5% of neonates.
  • In later stages it may change from flat, pale tan macules to elevated, verrucous, hairy lesions.
  • 15% occur on the skin of the head and neck.
  • Intraoral occurrence is extremely rare.

Congenital nevi of skin classified as:

  • Small nevi: Greater than 1 cm in diameter and usually 3–5 cm.
  • Garment nevi: Greater than 10 cm in diameter and cover large areas of the skin.
  • Extremely common.
  • Appear in eighth month of life and increase in number with age.
  • Peak numerically in the late third decade of life.
  • Numbers of nevi begin to decrease as one ages.
  • It is blue on the skin because melanocytic cells reside deep in connective tissue and because the overlying vessels dampen the brown coloration of melanin, yielding a blue tint.
  • Rarely undergoes malignant transformation.
  • Occurs chiefly on the buttocks, dorsum of the feet and hands and face.
  • Present at birth or appear in early childhood and persist unchanged throughout life.
  • The lesion is smooth, exhibits hairs growing from its surface.
  • Color varies from brown to blue or bluish black.
  • Appear as brown macular or nodular lesion.
  • Seen at any age.
  • Found on the palate, gingival, buccal mucosa, lips.
  • Once they reach a given size, their growth ceases, and the lesions remain static.

Melanotic macules,amalgam tattoos, physiologic ethnic pigmentation, smoker’s melanosis.

In the case of blue nevus, the melanin particles are deep to the surface, so that the light reflected back has to pass through the overlying tissue. Colors with long wavelengths tend to be more absorbed by the tissues; the shorter wavelength blue light is more likely to be reflected back to the observer’s eyes.

  • Common cause of oral pigmentation.
  • Symmetrically distributed, especially on the gingiva in dark-skinned individuals.
  • Seen anywhere in the oral cavity, including the buccal mucosa, hard palate, lips and tongue.
  • Pigmentation arises from increased melanocyte activity rather than increased melanocyte number.
  • Increases with age, smoking, hormones, and medications.
  • Diagnosis can be made clinically.
  • No treatment is required.

It is a malignancy of pigment producing cells (melanocytes), which are located primarily in the skin, but also found in the ears, gastrointestinal tract, eyes, oral and genital mucosa and leptomeninges.

  • Etiology is unknown.
  • Most likely due to a multistep process of genetic mutations that alter the cell cycle and render the melanocytes more susceptible to the carcinogenic effects of UVR.
  • Superficial spreading melanoma (SSMM).
  • Lentigo maligna melanoma.
  • Nodular melanoma.
  • Acral lentiginous melanoma (characterized by the site of origin; palm, sole or subungual).
  • Malignant melanoma in-situ and lentigo maligna are considered premalignant lesions.

Commonly displays the ABCDE warning signs:

A: Asymmetry.

B: Border irregularity.

C:  Colour variation.

D: Diameter > 6mm.

E:  Evolving (changing).

It tends to present as a flat or slightly elevated brown lesion with variegated pigmentation (i.e. black, blue, pink or white discoloration) with an irregular shape often > 6mm.

  • Slow growing or changing patch of discoloured skin with variegated shape and colour.
  • Often shows slow progressive changes from in situ lentigo maligna (LM) to invasive LMM.
  • May be detected using the ABCDE rule.
  • May arise on any site, but common on exposed areas of the head and neck.
  • Usually presents as a rapidly enlarging lump (weeks to months).
  • One third of nodular melanomas are amelanotic i.e. non-pigmented and may be ulcerated.
  • Start as a slowly enlarging flat patch of discoloured skin.
  • Tends to follow the ABCDE rule.
  • Although initially smooth at first, it later becomes thicker with an irregular surface.
  • Mucosal melanomas are extremely rare.
  • Higher among Japanese people than among other populations.
  • Oral Melanomas occur on: Anterior labial gingival, anterior aspect of hard palate.
  • In early stages, oral melanomas are macular brown and black plaques with an irregular outline.

Seborrhoeic keratosis, benign melanocytic naevi, blue naevi and vascular lesions.

  • Lesions usually appear as slightly raised, skin coloured or brown spots, which gradually thicken and develop a rough warty surface.
  • Later they may darken to become dark brown to black.
  • Having ‘stuck on’ appearance.

Unusual appearance with at least 3 of the following features:

  • Blurred or ill-defined borders.
  • Irregular shape.
  • Variegated colour
  • Flat and raised components or size 6mm or more.
  • Also known as Campbell de Morgan spots.
  • Lesions usually develop on the trunk and can appear red or blue/black in colour.
  • Increase in number in middle-aged individuals.
  • These are benign slow growing dermal nodules, often occurring on the limbs.
  • They may have a pigmented halo.
  • They are symmetrical, helping distinguish them from melanoma.

Oral mucosal pigmentation caused by certain drug is known asdrug-induced pigmentation.

  • Antimalarials: quinacrine, chloroquine, hydroxychloroquine.
  • Quinidine.
  • Zidovudine (AZT).
  • Tetracycline.
  • Minocycline.
  • Chlorpromazine.
  • Oral contraceptives.
  • Clofazimine.
  • Ketoconazole.
  • Amiodarone.
  • Busulfan.
  • Doxorubicin.
  • Bleomycin.
  • Cyclophosphamide.
  • Deposition of the drug per se or a metabolite thereof.
  • Stimulation of melanin production.
  • Bacterial metabolism of the drug, alone or in combination. 
  • Drug‑induced post‑inflammatory changes to the mucosa (oral lichenoid reaction)
  • Pigmentations can be large yet localized, usually to the hard palate.
  • Multifocal lesions found throughout the mouth.
  • In either case, lesions are flat and without any evidence of nodularity or swelling.
  • Teeth in adults and children may be bluish gray owing to minocycline/tetracycline.

Hyperpigmentation of the facial skin, particularly in the periorbital and perioral regions associated with oral contraceptives (melasma) and third trimester of pregnancy (chloasma).

The colour ranges from:

  • Brown (with oral contraceptives).
  • Blue–black (associated with hydroxychloroquine treatment).

• Café au lait spots (CALS) are cutaneous hyperpigmented flat macules or patches (>1 cm) that usually appear in childhood and tend to increase in number and size until puberty.
• As the term implies, these lesions have the color of coffee with cream and vary from small ephelis-like macules to broad diffuse lesions.
• Seen in McCune-Albright syndrome, LEOPARD syndrome, ataxia telangiectasia syndrome, neurofibromatosis.

Pigmentation caused by endocrinal disorders like:

  • Addison’s disease.
  • Pituitary-based Cushing’s syndrome.
  • Bronzing of the skin and patchy melanosis of the oral mucosa.
  • Deposition of melanin in the skin and mucous membrane.
  • Lesion consists of multiple focal dark spots or generalized diffuse streaks of hyperpigmentation that may be macular, flat, brown, and variable in shape.
  • Pale brown to deep chocolate pigmentation spreading over the buccal mucosa from the angles of the mouth and/or developing on the gingiva, tongue and lips.
  • Serum steroid and ACTH determinations helps in diagnosis.
  • Pigment will disappear once appropriate therapy for the endocrine problem is initiated.
  • Progressive hyperpigmentation of the skin, nails, and mucous membranes.
  • Diffuse multifocal macular brown pigmentations of the buccal mucosa.
  • Show no features of adrenocortical disease.

In HIV, immune system gets dysregulated, which leads to increase in inflammatory mediators like interleukin (IL)‑1, (IL)‑6, tumor necrotic factor (TNF)α which in turn cause a febrile response, as a result of which α melanocytes stimulating hormone (MSH) is released from the anterior pituitary.

The syndrome consists of mucocutaneous macules, intestinal polyposis and increase the risk of carcinomas of the pancreas, gastro‑intestinal tract, thyroid, and breast.

  • Multiple focal melanotic brown macules.
  • The macules appear as freckles or ephelides, usually measuring < 0.5 cm in diameter.
  • Lesions may occur on the anterior tongue, buccal mucosa, and mucosal surface of the lips.
  • Ephelides present on the fingers and hands.
  • Lesions on the perioral areas are pathognomonic.
  • Ecchymosis.
  • Petechia.
  • Hemochromatosis.
  • Due to erythrocyte extravasation into the submucosa will appear as a bright red macule or as a swelling if a hematoma forms.
  • Lesion becomes brown coloration in few days (hemoglobin degraded to hemosiderin).
  • Common site is lip and face.
  • Oral mucosa usually uncommon.
  • May be present in oral mucosa due to trauma.

These are Capillary hemorrhages that appear red initially and turn brown in few days (hemoglobin degraded to hemosiderin).

May be due to:

  • Can occur in skin and oral mucosa with soft palate.
  • Can be red or brown in color.
  • Platelet deficiencies or aggregation disorders.
  • Autoimmune or idiopathic thrombocytopenic purpura (ITP).
  • HIV-related ITP.
  • Aspirin toxicity.
  • Myelophthistic lesions.
  • Myelosuppressive chemotherapy.
  • It is an inherited recessive disorder.
  • In this excess iron deposited in the body results in eventual scelorsis and dysfunction of the involved tissue organs. Occur secondary to:
  1. Chronic anemia.
  2. Porphyria.
  3. Cirrhosis.
  4. Post-caval shunt for portal hypertension.
  5. Excess intake of iron
  • Brown to gray in color.
  • Diffuse macule.
  • May occur in palate and gingival.
  • Diagnosis can be confirmed by biopsy with prussian blue stain.
  • Medical management is required.
  • Amalgam Tattoo.
  • Graphite Tattoo.
  • Hairy Tongue.
  • One of the most common causes of intraoral pigmentation.
  • Twice as common as melanotic macules and 10 times as common as oral nevi.
  • Gingiva and alveolar mucosa are most commonly involved.
  • It presents as localized, blue‑gray lesion.
  • Biopsy should be performed to demonstrate the presence of amalgam particles in the connective tissue.
  • Previous areas of mucosal abrasion contaminated by amalgam dust.
  • Broken amalgam pieces can fall into extraction sites
  • If dental floss becomes contaminated with amalgam particles of a recently placed restoration.
  • Amalgam from the endodontic retrofill procedures can be left within the soft tissue.
  • Incorporation of graphite into the oral mucosa through accidental injury with a graphite pencil.
  • Commonly occurs in children.
  • Appears as an irregular gray to black macule in the anterior palate region.
  • Common condition of unknown etiology.
  • Lesion involves the dorsum, particularly the middle and posterior one-third.
  • Children affected rarely.
  • The papillae are elongated, having appearance of hairs.
  • The hyperplastic papillae then become pigmented by the colonization of chromogenic bacteria that imparts green to brown to black colour.
  • Coffee and tea, also contribute to the diffuse coloration.
  • Treatment consists of brushing the tongue and avoidance of tea and coffee for a few weeks.
  • Exposure to heavy metals may be massive, resulting in acute reactions or it may be minimal over a longer period producing a chronic changes.
  • Oral alterations can be produced by ingestion of following metals:
  1. Lead.
  2. Mercury.
  3. Silver.
  4. Bisthmuth.
  5. Arsenic.
  6. Gold.

Occurs chiefly as an occupational hazard due to:

  • Inhalation of lead vapor or dust
  • Chewing on wood painted with lead containing paint[in child]
  • Increasing environmental levels of lead.
  • Serious GIT disturbances.
  • Nausea/vomiting.
  • Constipation/colic pain.
  • Peripheral neuritis[characterized by wrist drop or foot drop].
  • Hypochromic anemia.
  • Skeletal changes.
  • Characterictic “lead line” is formed.
  • Gray or bluish-black line occurs in gingival.
  • More diffuse in nature.
  • Ulcerative stomatitis may also be seen.
  • Metallic taste may be present.
  • Treatment of oral lesion can be done secondary to systemic treatment.
  • Also known as mercurialism.
  • Due to occupational contact, self medication with mercurial compound, suicide attempts.
  • May be acute or chronic.
  • Gastric disturbance.
  • Diarrhea.
  • Excitability.
  • Insomnia.
  • Headache.
  • Mental depression.
  • Fine tremors of fingers and limbs as well as of lips and tongue.
  • Desquamative dermatitis.
  • Increased flow of ropy, viscid saliva.
  • “Hot mouth” itching and metallic taste.
  • Dry, cracked lips.
  • Faint diffused gray pigmentation of gingiva.
  • Enlarged painful and ulcerated tongue.
  • Swelling of gingiva may be seen.
  • Gray to black color of mucosa may be seen.
  • Loosening of teeth.

Chronic mercury exposure to infants and children due to:

  • Teething powder.
  • Ammoniated mercury ointment.
  • Calomel lotion.
  • Bichloride of mercury disinfectant.
  • In young infants.
  • Skin of hands/feet/nose/ears become red or pink and have cold clammy feeling.
  • Extreme irritability.
  • Photophobia.
  • Muscular weakness.
  • Tachycardia.
  • Hypertension.
  • Insomnia.
  • GIT upset
  • Stomatitis
  • Profuse salivation.
  • Gingiva becomes sensitive and painful.
  • Premature shedding of teeth.
  • Analysis of saliva and urine for presence of metal.
  • Discontinuation of possible exposure.
  • Administration of dimercaprol (BAL).

Characterized by permanent discolouration of skin and mucous membrane due to systemic absorption of silver compound like:

  • Silver containing nasal drops.
  • Silver- arsphenamine injection used for syphilis.
  • Chewing photographic films.
  • Deeply discolored nail beds.
  • Slate gray, violet or cyanotic skin.
  • Pigmentation of gingival and mucosal tissue.
  • Localized argyria developed due to use of topical silver containing preparations.

Based on objective findings.

Source of contact should be eliminated.

  • It is toxic reaction following gold therapy.
  • Occur in 10 to 40% of patient receiving gold therapy.
  • Vesiculation and ulcerations of oral mucosal and gingival tissue.
  • Diagnosis is based on the basis of therapeutic administration of gold compound.
  • Discontinuation of auric therapy is the line of treatment.
  • Mostly used for treating dermatologic disorders.
  • Usually occurs in buccal mucosa and gingiva.
  • Characteristic “bismuth line” is seen, thin blue-black along with marginal gingival.
  • May be seen on lips, ventral surface of tongue.
  • No specific treatment.
  • If the source is discontinued lines disappear.

Arsenism develop from industrial exposure or accidental or intentional poisoning.

  • Arsenic was used to treat many conditions.
  • Chronic exposure due to drinking of contaminated water.
  • Diffuse macular hyperpigmentation.
  • Palmer and planter hyperkeratosis.
  • Dermatitis, pigmentation and ulceration(chronic cases).
  • Oral tissues are extremely painful and deep red in colour.
  • Painful areas of necrotizing ulcerative stomatitis.
  • Dryness of mouth.
  • Surface anesthetic ointment like lidocaine or dyclonine HCL used for symptomatic relief.

It is classical symptom of phosphorus poisioning i.e periostitis and osteomyelitis of jaws usually mandible.

  • Necrosis at site of injury.
  • Retained tooth.
  • Decayed tooth.
  • Periodontal pocket.
  • Garlic like odor.
  • Rapid disintegration of teeth.
  • Osteomyelitis resistant to treatment.
  • Surgical procedure should be done under prophylactic antibiotics.
  • It was first described in 1970 by Laugier and Hunziker
  • Acquired benign macular hyperpigmentation disorder with unknown (or definite) etiopathogenesis.
  • Characterized by a varying number of asymptomatic, lenticular (lens-shaped), or linear, brown to black mucocutaneous macules, usually less than 5 mm in diameter.
  • Located on the lips, buccal mucosa, and hard palate.
  • Oral pigmentation usually persists, whereas the cutaneous lesions often fade after puberty.
  • Nails are affected and usually presents as single or double stripes or as homogeneous pigmentation on one-half of the nail or complete nail (melanonychia).
  • Pigmentation may spread from the proximal nail fold into the surrounding skin, which is known as Hutchinson’s sign or pseudo-Hutchinson’s sign.
  • LHS, it is also seen in Peutz–Jeghers syndrome (PJS), subungual hematoma, racial pigmentation, and AIDS, in association with the use of certain drugs such as minocycline and zidovudine, and in Bowen’s disease.
  • Drug-induced pigmentation, HIV associated pigmentation, smoker’s melanosis.
  • History .
  • Dermoscopy.
  • Binocular stereo microscope.
  • Pigmentations (color, size and shape or by chemical testing).

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