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Pigmented Lesions of Oral Mucosa

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Pigmented Lesions of Oral Mucosa WELCOME PIGMENTED LESIONS OF ORAL MUCOSA Oral and Perioral pigmentation may be physiologic (or) pathologic in origin. Assume variety of discolorations, including brown,blue, grey & black. These color changes often occur due to deposition,production (or) increased accumulation of various endogenous (or) exogenous pigmented substances. sygdom.info CLASSIFICATION ENDOGENOUS PIGMENTATION FOCAL MELANOCYTIC PIGMENTATION . Freckle / Ephelis . Oral / labial melanotic macule . Oral melanoacanthoma Ũ. Melanocytic nevus ũ. Malignant melanoma MULTIFOCAL / DIFFUSE PIGMENTATION . Physiologic pigmentation . Drug induced melanosis . Smoker melanosis Ũ. Post inflammatory hyper pigmentation ũ. Melasma (chlosma) sygdom.info MELANOSIS ASSOCIATED WITH SYSTEMIC (OR)GENETIC DISEASE . Hypo adrenocorticism (addison’s disease) . cushing’s syndrome . Hyperthyrodism (graves disease) Ũ. Primary biliary cirrhosis ũ. Vitamin b deficiency Ū. Peutz jeghers syndrome ū. Café au lait pigmentation Ŭ. HIV / AIDS associated melanosis sygdom.info IDIOPATHIC PIGMENTATION Laugier – hunziker pigmentation DEPIGMENTATION Vitiligo HAEMOGLOBIN & IRON ASSOCIATED PIGMENTATION a. Ecchymosis b. Purpura / Petechiae c. Hemochromatosis sygdom.info EXOGENOUS PIGMENTATION DRUG INDUCED AMALGUM PIGMENTATION TATTOOS HEAVY METAL GRAPHITE PIGMENTATION TATTOOS MEDICINAL ORNAMENTAL METAL INDUCED TATTOOS PIGMENTATION Common causes of endogenous oral and perioral discoloration Examples of associated lesion, Etiology Source condition or disease Varix, hemangioma, lynphangioma, Developmental, hamartomatous , neoplastic, angiosarcoma, kaposi’s sarcoma, Vascular autoimmune hereditary hemorrhagic talangiectasia, CREST syndrome. Extravasated hemorrhage hemosiderin Trauma, idiopathic, genetic, inflammatory, Hematoma, ecchymosis, purpura, autoimmune petechiae, vasculitas, hemochromatosis. Melanotic macule, ephelis, actinic lentigo, melanocytic nevus, malignant Melanin Physiologic, developmental, idiopathic, melanoma, physiologic pigmentation, neoplastic, reactive drugs, hormones, genetic, chloroquine-induced pigment, lichen auto immune, infectious. planus pigmentosus, laugier-hunziker pigmentation, smokers melanosis, oral- sub mucous fibrosis, peutz-jeghers disease, adrenal insufficiency, cushing’s syndrome, HIV/AIDS. Bilirubin Trauma, alcohol, infection, neoplasia, genetic, Jaundice. auto immune. Focal melanocytic pigmentation Freckle / ephelis : The cutaneous freckle is a commonly occuring, asymptomatic , small ( – mm), well circumsribed , tan or brown colored macule that is often seen on sun exposed regions of facial & perioral skin. Polymorphisms in mcr gene is strongly associated with development of childhood freckles. Oral / labial melanotic macule Etiology is trauma More commopn in females usually in lower lip &gingiva. May develop at any age but generally tend to present in adulthood. Melanotic macules tend to be small (< cm), well circumscribed , oval or irregular in outline & often uniformly pigmented. Oral melanoacanthoma Etiology is acute trauma or a history of chronic irritation Rapidly enlarging , ill defined , darkly pigmented macular or plague like lesions. Buccal mucosa most common site of occurrence Dermatosis papulosa nigra is relatively common facial condition in older black females & represents multiple pigmented seborrheic keratoses Treatment is source of irritation should be removed Melanocytic nevus Effect of sun exposure reconized in development of cutaneous nevi. Recent study shows ŭ% of dermal melanocytic nevi exhibit somatic activating mutations in BRAF oncogene. Lesions are usually asymtomatic & often present as a small (<cm) , solitary , brown or blue , well circumscribed nodule or macule. Oral nevi present in hard palate is the most common site , followed by buccal & labial mucosa & gingiva. Treatment of melanotic nevi is complete but conservative surgical excision is the treatment of choice for oral lesions. Rare recurrence Laser & intense pulse light therapies have been used successfully Malignant melanoma Etiology is episodes of acute sun exposure , especially at young age , immunosuppresion Exhibit mutation in the BRAF , HRAS & NRAS proto oncogenes. Palate represents most common site & next comes the maxillary gingiva. They are macular , plague like or mass forming , well circumscribed or irregular & exhibit focal or diffuse areas of brown , blue or black pigmentation. Treatment is ablative surgery with wide margins . Adjuvant radiotherapy is necessary. Recent development is antitumor vaccine adjuvant interferon alpha – B therapy is used to treat primary cutaneous melanomas >Ũmm in thickness. Multifocal / diffuse pigmentation Physiologic pigmentation is more common Mostly occur in gingiva Treatment is gingivectomy & laser therapy have been used to remove pigmenteds oral mucosa. Effects of treatment is temporary & may eventually recur. Drug induced melanosis Chief drugs include a) Minocycline – tetracycline derivative b) Antimalarials include chloroquine , hydroxy chloroquine , quinacrine . c) Phenothiazines such as chlorpromaqzine d) Oral contraceptives e) Cytotoxic medications such as cyclophosphamide & busulfan Clinically the pigment can be diffuse yet localised to one mucosal surface , often hard palate Lesions are flat & without any evidence of nodularity or swelling. Diagnosis & treatment is discolaration tends to fade within a few months after the drug is discontinued. Smokers melanosis Diffuse melanosis of anterior facial maxillary & mandibular gingivae , buccal mucosa , lateral tongue , palate & floor of mouth occasionally seen among cigarette smokers. Pigmented areas are brown , flat & irregular. Melanin synthesis is stimuylated by tobbaco smoke products. Heat of smoke may stimulate pigmentation. Post inflammatory pigmentation Focal or diffuse pigmentation in areas that were subjected to previous injury or inflammation. The mucosa overlying a non melanocytic malignancy may become pigmented. Melasma / chloasma Acquired symmetric melanosis that typically develops on sun exposed areas of skin & frequently on face. Forehead , cheeks , upperlips & chin are most commonly affected areas. Melasma has been used to describe any form of generalised facial hyperpigmentation including those related to post inflammatory changes & medication use. Melanosis associated with systemic or genetic disease Hypoadrenocortism: As steroid levels decrease , there is a compensatory activity by ACTH secretion , but if persists , the serum levels of alpha melanocyte stimulating hormone also increase. Mucocutaneous hyperpigmentation Generalised bronzing of skin &diffuse but patchy melanosis of oral mucosa. Treatment is exogenous steroid replacement therapy. Cushings syndrome Prolonged exposure of endogenous or exogenous corticosteroids. Due to activating , germline mutations in ACTH receptor. Weight gain & characterstic “moon facies”. Diffuse mucocutaneous pigmentation. Treatment is surgical , radiation or medicinal therapy. Hyperthyroidism Ũ% of black patients with thyrotoxicosis may present mucocutaneous pigmentation. Pigmentation tends to resolve following treatment of thyroid abnormality. Primary biliary cirrhosis Autoimmune Develops in middle aged women. Disease results from damage to small intra hepatic bile ducts. Oral mucosal tissues are not affected Vitamin B deficiency Generalised burning sensation & erythema & atrophy of the mucosal tissue. Pigmentation resolves followimg vitamin B levels. Peutz – jeghers syndrome Autosomal dominant disease associated with mutations in STK/LKB tumor suppresor gene. Intestinal polyposis , cancer susceptibility & multiple , small , pigmented macules of lip , perioral skin , hand & feet. Resemble ephelides usually <.ũmm in diameter. Lesion may develop on anterior tongue , buccal & labial mucosa. Lip & perioral pigmentation is higly distinctive Café –au – lait pigmentation Identified in number of different genetic disorders include a) Neuro fibromatous type b) Mccune – albright syndrome c) Noonans syndrome Present as tan or brown colored , irregularly shaped macules of variable size. Occur anywhere on skin , oral macular pigmentation have been reported. HIV / AIDS Pigmentation may be related to intake of various medications , anti fungal & anti retoviral drugs. May also occur due to adreno cortical destruction by virulent infectious organisms. Significant correlation between mucocutaneous pigment & CDŨ counts / micro litre lessthan or equal to . Buccal mucosa is most affected site ,gingiva , palate &tongue involved. Idiopathic pigmentation Laugier – hunziker pigmentation: Hyperpigmentation of oral mucosal tissues involve lips & buccal mucosa. Pigmentation of esophageal , genital & conjunctival mucosae & acral surfaces. Nail involvement in form of longitudinal melanotic streaks & without evidence of dystrophic change. Multiple , discrete , irregularly shaped brown oral macules & not more than ũmm in diameter. Treatment of mucocutaneous melanosis Laser therapy has proven effective but recurrence occur in % of treated patients. Various types of lasers. a. Super pulsed CO b. Q – switched Nd – YAG c. Switched alexandrite lasers Cryotherapy Phototherapy include intense pulsed light & fractional photothermolysis. First- line therapy involves application of tropical medicaments , that is bleaching cream. Simple agents such as azelaic acid or hydroquinone. Triple combination therapy a. Ũ% hydroquinone b. .ũ% retinoic acid c. .% fluocinolone acetonide has
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