Melasma – epidemiology, classification - Prof. Torello Lotti, MD


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Postinflammatory hyperpigmentation
Drug induced hyperpigmentation
Solar lentigos
Café au lait macules
Nevus of Ota

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Melasma – epidemiology, classification - Prof. Torello Lotti, MD

  1. 1. MELASMA Epidemiology, Classification, PathophysiologyThe International School of Vitiligo & Pigmentary Disorders. Barcelona, Spain - 2-5 November 2011 Prof. Lotti T, Betti S, M.D. Barcelona, November 2011
  2. 2.  Melasma Postinflammatory hyperpigmentation Drug induced hyperpigmentation Solar lentigos Café au lait macules Nevus of Ota
  3. 3. MELASMA Melasma consists of an excessiveproduction of melanin (hypermelanosis) which causes the appearance of brownspots on sun-exposed areas of the face.
  4. 4. Skin color Extensive polymerization of the Melanins:Eumelanin monomers of tyrosine oxidized. Tipical in subjects well- pigmented (blacks, brown) The polymerization is stopped prematurely, and the mixture thus Pheomelanin obtained is bound to proteins. Typical of blond e rutile subjects Hemoglobin Stratum It is yellow and very thick in asian people corneum Reflectivity of the epidermis
  5. 5. MelanocytesDendridic shape with hemispherical body from whichdepart decreasing calibrum extensions forking severaltimes.The medium density is around 1000 / mm2 of skinsurface.
  6. 6. The numerical density of melanocytes is indipendent of skin color, that depends on the activity of melanocytes and on the persistence of melanin in keratinocytes. •In people with white skin and those of yellow skin, melanin is limited to the basal layer. •In people with black skin melanin is found up to thesurface layer.
  7. 7. MelaninTyrosin DOPA DQ Tyrosinase Indole Phenolic oxidant Ez Cisteinildope containing Copper Polimeriz.ox oxidation Eumelanine Feomelanine
  8. 8. Melanin Tyrosine Melanin TyrosinaseThe mature melanosoms arealso known as melaninegranules, they migrate intodendrites and are transferredto keratinocytes for postingportions of dendrites orphagocytosis
  9. 9. Mature melanin granules Phagocytosed by keratinocytes Break free in theStay in in lysosomes cytoplasm andwhere vengono they persist for someare digested(in time (in blacksubjects with little skin subjects)pigmented skin)
  10. 10. Changes in Melanogenesis Melasma
  11. 11. MELASMA
  12. 12. EPIDEMIOLOGY Real incidence unknown 90% women, 10% men All races Hispanic, Asian, Indo- Chinese, Africans
  13. 13. ETIOLOGY Genetic influences Exposure to UV radiation Pregnancy Oral contraceptives Cosmetic Phototoxic drugs
  14. 14. GENETIC PREDISPOSITIONthe condition is most widespread among women with skin types III orIV, such as Asian-Americans and people of Mediterranean descent.EXPOSURE TO UV RADIATIONit is the most important exacerbating factor. Ultraviolet lightnormally increases melanogenic activity in melanocytes with resultinghyperpigmentation. Once melasma has developed, exposure to sunlightwill perpetuate the condition and counteract any other treatment. UseSPF or higher sunscreens that block both UVA and UVB radiation.PREGNANCY AND CONTRACEPTIVESsome researchers believe it is induced when extrogen stimulates thepigment-producing cells in the skin to secrete more pigment.Melasma it is also known as chloasma or “mask of pregnancy” and it is avery common condition usually seen in women of childbearing age.
  16. 16. CLINICAL PATTNERS: melasma of the face Centrofacial Malar Mandibular Cleft lip and chin (chin and upper lip)centrofacial type: 63% of cases (simmetrycal involvement of the cheeks and nose). malar type: 21% of cases (simmetrycal involvementof the cheeks and nose). jaw type : 8% of cases (involvement of the maxillary branch of the mast). Lip-chin type: 8% of cases (involvementof the upper lip and chin).
  17. 17. TYPE OF PIGMENTATION Guttata Confetti like Linear Large circular patches
  18. 18. Based on Wood’s lamp examination of theskin, melasma can be classified into four mainclinical types and patterns, with correlation inhistology , in accordance with the depth ofmelanin pigment.
  19. 19.  EPIDERMAL: light brown, with an enhancement of pigmentation under Wood’s lamp; histologically, it is characterized by a melanin increase in tha basal, suprabasal and stratum corneum layers. DERMAL: ashen or bluish-grey; no enhancement of pigmentation under Wood’s light; histologically, there is a preponderance of melanophages in the superficial and deep dermis. MIXED: dark brown; enhancement of pigmentationunder Wood’s lamp in some areas and not in others. INDETERMINATE: inapparent under Wood’s lamp.The best terapeutical results are normally achieved in epidermal melasma.
  20. 20. MELASMA SEVERITYIt is scored using the Melasma Area and Severity Index (MASI). In this system, the face is divided into four areas- forehead, right malar, left malar and chin- which correspond, respectively, to 30%, 30%, 30% and 10% of the total facial area. Torello Lotti: Pigmentary Disorders Dermatologic Clinics Vol.25, Number 3, July 2007 / Elsevier Saunders
  21. 21. The Melasma in each of there areas is graded according to three variables:1- Percentage of total area involved on a scale from o (no involvement) to 6 (90-100% full involvement)2- Darkness scoring from 0 to 4 is assessed to a color chart3- The scale of each patient is graded according to the comparison between the darkness of the melasma and the colour of the chart: scale 0: no melasma scale 1: light brown scale 2: brown scale 3: dark brown scale 4: black
  22. 22. The MASI is then calculated using the following equation:MASI= 0.3(DF+HF)AF+0.3(DMR+HMR)AMR+0.3 (DML+HML)AML+0.1(DC+HC)ACD= darknessH= homogeneityA= areaF= foreheadMR= right malarML= left malarC= chin0.3,0.3,0.3,0.1= are the respective percentage of total facial area.
  23. 23. The MASI is measured beforetreatment as a baseline and after each session of treatment
  24. 24. PATHOGENESIS UV irradiation is known to increase the synthesis of alpha-MSH and ACTH derived fromPOMC in keratinocytes. These peptides lead to proliferation of melanocytes as well asincrease in melanin synthesis via stimulation of tyrosinase activity and TRP-1.Endotelin-1:peptide produced by endothelial cells and by keratinocytes melanocytes Recent data also showed that melasma lesions have more vascularizationas compared to the perilesional normal skin. Increased expression of vascular endothelial growth factor (VEGF) in keratinocytes was suggested as the major angiogenic factor for altered vessels in melasma
  25. 25. This is confirmed by:The vascular characteristics of melasma.Kim EH, Kim YC, Lee ES, Kang HY.J Dermatol Sci 2007.OBJECTIVES:We investigated the vascular characteristics in melasma lesions. Theexpression of vascular endothelial growth factor (VEGF), a majorangiogenic factor of the skin, was also investigated in melasma.METHODS:Erythema intensity was quantified by the increase of the a* parameterusing a colorimeter. Skin samples were obtained from lesional and non-lesional facial skin of 50 Korean women with melasma.Immunohistochemistry was performed to determine the expression offactor VIIIa-related antigen and VEGF in melasma.
  26. 26. RESULTSThe values of a* was significantly higher in the melasma lesion than that of perilesional normal skin. Computer-assisted image analyses of factor VIIIa-related antigen-stained sections revealed a significant increase of both the number and the size of dermal blood vessels in the lesional skin. There was significant relationship between the number of vessels and pigmentation in CONCLUSIONSThese data suggest that increased vascularity is one of the major findings in melasma. VEGF may be a major angiogenic factor for altered vessels in melasma. Torello Lotti: Pigmentary Disorders Dermatologic Clinics Vol.25, Number 3, July 2007 / Elsevier Saunders
  27. 27. Thank you for your attention Torello Lotti Full Professor of Dermatology Vice Chancellor, , Roma