1. WELCOME

2. 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.

3. CLASSIFICATION • ENDOGENOUS PIGMENTATION • FOCAL MELANOCYTIC PIGMENTATION • Freckle / Ephelis • Oral / labial melanotic macule • Oral melanoacanthoma • Melanocytic nevus • Malignant melanoma • MULTIFOCAL / DIFFUSE PIGMENTATION • Physiologic pigmentation • Drug induced melanosis • Smoker melanosis • Post inflammatory hyper pigmentation • Melasma (chlosma)

4. MELANOSIS ASSOCIATED WITH SYSTEMIC (OR)GENETIC DISEASE • Hypo adrenocorticism (addison’s disease) • cushing’s syndrome • Hyperthyrodism (graves disease) • Primary biliary cirrhosis • Vitamin b12 deficiency • Peutzjeghers syndrome • Café au lait pigmentation • HIV / AIDS associated melanosis

5. IDIOPATHIC PIGMENTATION Laugier – hunziker pigmentation • DEPIGMENTATION Vitiligo • HAEMOGLOBIN & IRON ASSOCIATEDPIGMENTATION • Ecchymosis • Purpura / Petechiae • Hemochromatosis

6. EXOGENOUS PIGMENTATION

9. Focal melanocytic pigmentation • Freckle / ephelis : The cutaneous freckle is a commonly occuring, asymptomatic , small (1 – 3mm), well circumsribed , tan or brown colored macule that is often seen on sun exposed regions of facial & perioral skin. Polymorphisms in mc1r gene is strongly associated with development of childhood freckles.

10. 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 (<1 cm), well circumscribed , oval or irregular in outline & often uniformly pigmented.

13. 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

14. Melanocytic nevus • Effect of sun exposure reconized in development of cutaneous nevi. • Recent study shows 90% of dermal melanocytic nevi exhibit somatic activating mutations in BRAF oncogene. • Lesions are usually asymtomatic & often present as a small (<1cm) , 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.

16. 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

17. 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.

19. Treatment is ablative surgery with wide margins . • Adjuvant radiotherapy is necessary. • Recent development is antitumor vaccine adjuvant interferon alpha – 2B therapy is used to treat primary cutaneous melanomas >4mm in thickness.

21. 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.

22. Drug induced melanosis Chief drugs include • Minocycline – tetracycline derivative • Antimalarials include chloroquine , hydroxy chloroquine , quinacrine . • Phenothiazines such as chlorpromaqzine • Oral contraceptives • Cytotoxic medications such as cyclophosphamide & busulfan

24. 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.