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

1. MELASMA
Epidemiology, Classification,
Pathophysiology
The International School of Vitiligo & Pigmentary Disorders.
Barcelona, Spain - 2-5 November 2011
Prof. Lotti T, Betti S, M.D.
Barcelona, November 2011

2.  Melasma
 Postinflammatory hyperpigmentation
 Drug induced hyperpigmentation
 Solar lentigos
 Café au lait macules
 Nevus of Ota

3. MELASMA
Melasma consists of an excessive
production of melanin (hypermelanosis)
which causes the appearance of
brownspots on sun-exposed areas of
the face.

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. Melanocytes
Dendridic shape with hemispherical body from which
depart decreasing calibrum extensions forking several
times.
The medium density is around 1000 / mm2 of skin
surface.

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. Melanin
Tyrosin DOPA DQ
Tyrosinase
Indole
Phenolic oxidant Ez Cisteinildope
containing Copper
Polimeriz.ox
oxidation
Eumelanine
Feomelanine

8. Melanin
Tyrosine Melanin
Tyrosinase
The mature melanosoms are
also known as melanine
granules, they migrate into
dendrites and are transferred
to keratinocytes for posting
portions of dendrites or
phagocytosis

9. Mature melanin granules
Phagocytosed by keratinocytes
Break free in the
Stay in in lysosomes cytoplasm and
where vengono they persist for some
are digested(in time (in black
subjects with little skin subjects)
pigmented skin)

11. Changes in Melanogenesis
Melasma

12. MELASMA

13. EPIDEMIOLOGY
Real incidence unknown
90% women, 10% men
All races
Hispanic, Asian, Indo-
Chinese, Africans

14. ETIOLOGY
 Genetic influences
 Exposure to UV
radiation
 Pregnancy
 Oral contraceptives
 Cosmetic
 Phototoxic drugs

15. GENETIC PREDISPOSITION
the condition is most widespread among women with skin types III or
IV, such as Asian-Americans and people of Mediterranean descent.
EXPOSURE TO UV RADIATION
it is the most important exacerbating factor. Ultraviolet light
normally increases melanogenic activity in melanocytes with resulting
hyperpigmentation. Once melasma has developed, exposure to sunlight
will perpetuate the condition and counteract any other treatment. Use
SPF or higher sunscreens that block both UVA and UVB radiation.
PREGNANCY AND CONTRACEPTIVES
some researchers believe it is induced when extrogen stimulates the
pigment-producing cells in the skin to secrete more pigment.
Melasma it is also known as chloasma or “mask of pregnancy” and it is a
very common condition usually seen in women of childbearing age.

16. LOCALIZATION

17. 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).

18. TYPE OF PIGMENTATION
Guttata
Confetti like
Linear
Large circular patches

19. Based on Wood’s lamp examination of the
skin, melasma can be classified into four main
clinical types and patterns, with correlation in
histology , in accordance with the depth of
melanin pigment.

20.  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.

21. MELASMA SEVERITY
It 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
theclinics.com / Elsevier Saunders

22. 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 chart
3- 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

23. 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)AC
D= darkness
H= homogeneity
A= area
F= forehead
MR= right malar
ML= left malar
C= chin
0.3,0.3,0.3,0.1= are the respective percentage of total
facial area.

24. The MASI is measured before
treatment as a baseline and after each
session of treatment

25. PATHOGENESIS
 UV irradiation is known to increase the synthesis of alpha-MSH and ACTH derived from
POMC in keratinocytes. These peptides lead to proliferation of melanocytes as well as
increase 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

26. 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. The
expression of vascular endothelial growth factor (VEGF), a major
angiogenic factor of the skin, was also investigated in melasma.
METHODS:
Erythema intensity was quantified by the increase of the a* parameter
using 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 of
factor VIIIa-related antigen and VEGF in melasma.

27. RESULTS
The 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
CONCLUSIONS
These 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
theclinics.com / Elsevier Saunders

28. Thank you for your attention
Torello Lotti
Full Professor of Dermatology
Vice Chancellor, UniMarconi.it , Roma