The document provides a comprehensive overview of melasma, an acquired hyperpigmentary disorder characterized by symmetrical facial pigmentation, with a high prevalence in women, particularly during reproductive years and pregnancy. It discusses the multifactorial etiology, including hormonal influences, UV radiation, and genetic predispositions, as well as diagnostic methods and differential diagnoses. Treatment recommendations include sun protection, topical therapies like hydroquinone, and various adjunctive treatments, with an emphasis on customized approaches depending on patient history and melasma characteristics.

1. Melasma
DR.BHAWANA CHAUDHARY
JR2
DEPARTMENT OF DERMATOLOGY

2. MELASMA
• An acquired hyperpigmentary disorder .
• Presents - bilaterally symmetrical
pigmentation involving the face .
• Color - tan to brown (epidermal
melasma) or bluish (dermal melasma)
• Seen in females
• Multifactorial etiology.

3. EPIDEMIOLOGY
Persons of any race can be affected.
Melasma is more common in darker skin types
Women - nine times more than men.
Common in reproductive years.
Melasma is present in 15% to 50% of pregnant patients.
The prevalence varies between 1.5% and 33% depending on the population.
Persons with light-brown skin types + high sun exposure - prone to the development of melasma.
50% report - positive family history of the condition.
Identical twins have been reported to develop melasma

4. Melanocyte
• Melanocytes are dendritic cells.
• Involved in pigment synthesis.
• Melanoblasts(melanocyte precursors) originate in the neural crest.
• Migrate to their final destinations in the basal layer of the epidermis, hair follicle, uveal tract and cochlea
during embryonic life
• During embryonic life, they enter the epidermis between 7 and 8 weeks of gestation and are distributed among basal
cells.
• By the 10th week, these cells contain melanosomes showing early melanization
• Factors essential in the development of the melanoblast/melanocyte lineage during embryonic life:-
• Wnt/β-catenin, MAPK and Notch pathways
• (EDNRB2)
• Stem cell factor (SCF) or c-kit ligand (inhibits apoptosis and promotes melanoblast proliferation)

5. FUNCTION-

8. • Melanocytes are in contact with
keratinocytes through their processes.
• One melanocyte is in contact with 36 basal
and suprabasal keratinocytes (epidermal
melanin unit)
• The number of melanocytes per unit of the
surface area varies at different body sites-
• no difference in the density
• racial differences is due to the
distribution and size of melanosomes
within keratinocytes

9. Melanin Synthesis and Melanosomes
• Melanin is produced in membrane bound
organelles called melanosomes within the
melanocytes.
• It is regulated by- UV exposure and ACTH,
which in humans has α-MSH (Melanocyte
stimulating hormone) activity.
• 2 types of melanin: eumelanin and
pheomelanin.
• The type of melanin synthesized depends on:-
I. the activity of the enzymes
II. presence of thiols (cysteine, glutathione and
thioredoxin).
pheomelanin eumelanin
Yellow to red Brown to black
presence of thiol
groups
absence of thiol groups
more stable and is more
effective in
photoprotection

11. • The proteins in the melanosomes include structural proteins and enzymes of melanin synthesis.
These are synthesized in the rough endoplasmic reticulum and packed into membrane bound
vesicles to form melanosomes.
• The melanosomes mature by activation of enzymes of melanogenesis and accumulation of the
melanin synthesized:-
Tyrosinase levels decrease
and acid phosphatase levels
increase, helping in the
degradation of
melanosomes

12. •CAUSES OF
MELASMA

14. Ultraviolet (UV) radiation –
• induce increased production of alpha-melanocyte–stimulating hormone and
corticotropin, interleukin 1 and endothelin 1
increased melanin production by intraepidermal
melanocytes.
• Fibroblasts in the dermal layer of the skin contribute to the development of
melasma-----
overexpression of the tyrosine kinase receptor c-kit and certain stem cell
factors
Thyroid Disease
• There is a four-fold increase in thyroid disease in melasma patients.

15. Hormonal Influences
• The mask of pregnancy - obstetric patients.
• Estrogen, progesterone, and melanocyte-
stimulating hormone - increased during the
third trimester of pregnancy .and may be a
factor.
• Nulliparous - show elevated levels of
estrogen receptors within the lesions.
• oral contraceptive pills and diethylstilbestrol
treatment for prostate cancer.
• postmenopausal and given progesterone -
progesterone as playing a primary role in the
development of melasma.

16. minor factors
associated
with melasma

17. Classification
ON THE BASIS OF DISTRIBUTION:
(1) centrofacial (most common) - forehead, cheeks, nose, upper lip (sparing the philtrum and
nasolabial folds), and chin
(2) malar- cheeks , nose
(3) mandibular - along the jawline.
Less common sites - extensor aspect of the forearms and mid upper chest

18. Location of
the
pigment:

19. HISTOPATHOLOGY
Melanin deposition in the epidermis
and solar elastosis in the dermis
(arrow)
(Hematoxylin and Eosin, HEx100)
Pendulous melanocytes in the basal
layer of epidermis (arrow) and
increased dermal melanophages
(arrowhead) (HE x400).

20. Diagnosis
History and Physical
Melasma occurs in sun-exposed areas
Presenting as symmetrically distributed hyperpigmented macules which can be confluent or
punctate.
 It is worse in areas that receive excessive sun exposure
SITES- cheeks, the upper lip, the chin, and the forehead.
Evaluation
• THYROID FUNCTON TEST( specifically pregnancy- or oral contraceptive pill-associated melasma.)
• Wood lamp examination - helps to localize the pigment to the dermis or epidermis

21. Dermoscopy of the melasma
lesion
(polarizing mode, ×20)
diffuse light-to-dark brown (white
arrow)
pseudoreticular network, multiple
brown dots, granules and globules
(black arrows)
 arcuate and annular structures (blue
arrows)
 with sparing of the perifollicular
region (green arrows)
around the openings of sweat glands
(yellow arrows)

22. Differential
diagnosis
1) Drug-induced hyperpigmentation or
discoloration
• History of medication use (e.g. doxycycline,
amiodarone-Slate-gray to violaceous discoloration of
sun-exposed skin)
• Hyperpigmentation less patterned and less irregular
in outline; may involve tip of nose
• Discrete oval or round shape of fixed drug eruption
rarely confused with melasma
• Oral contraceptives(increased pigmentation of
nipples and nevi) and phenytoin may exacerbate
melasma
Fixed drug eruption with central violaceous
hue and surrounding erythematous rim

23. 2)Postinflammatory hyperpigmentation,
-due to cutaneous lupus erythematosus,
photosensitivity reactions, contact
dermatitis (e.g. irritant contact dermatitis
to hydroquinone or tretinoin)
History of inflammatory phase with
erythema, scale, and possible pruritus or
burning
• Primary lesions – may be admixed or
elsewhere on body

24. • 3) Riehl′s Melanosis
(Pigmented Contact
Dermatitis)
• pigmented contact dermatitis to
allergens present in cosmetics,
fragrances, and Kumkum
• presents as patches of diffuse gray-
brown pigmentation on forehead,
scalp, face, and neck
• rythema, scaling, or pruritus is
occasionally present
(a) Diffuse brown pigmentation, face, forehead, ear.
(b) (b) Dermal inflammation, prominent pigment incontinence (H and E,
×100),
(c) Basal cell damage, necrotic keratinocytes, Civatte bodies, melanophages,
and dermal inflammation (H and E, ×400)

25. ) Poikiloderma of Civatte
• Presence of atrophy and telangiectasias
• Favors lateral and inferior aspects of anterior neck;
sparing of submental region
Poikiloderma of Civatte (a)
Reticulated hyper- and
hypopigmented atrophic macules,
face, neck
(b) Atrophy, telengiectasia, and
dermal fibrosis (H and E, ×100

26. 5) Lichen planus pigmentosus
• begins on the temples/in the preauricular area and involves the neck
• Coexistent classic lichen planus (~20% of patients)
• Histologic features: vacuolar degeneration of basal layer;
variable lichenoid infiltrate and epidermal atrophy
Multiple coalescing brown to gray–
brown macules in the axilla

27. 6) Erythema dyschromicum perstans
• Inflammatory phase with rim of erythema occasionally seen
• Lesions slate-gray to blue–brown
• Distribution includes sun-protected areas.
7) Erythromelanosis follicularis faciei et colli
• Red–brown patches on lateral cheeks and neck
• Superimposed tiny pale follicular papules

28. • 8) acanthosis nigricans
• velvety plaques in the hollow of the cheek and preauricular
Acanthosis nigricans (a) Macular hypermelanosis over temple. (b) Papillomatosis, acanthosis
with pigmented basal epidermis (H and E, ×100)

29. 9) Acquired bilateral nevus of Ota-like
macules (Hori nevus)
• Asian women, usually during the
fourth or fifth decade of life
• Multiple brown–gray to brown–blue
macules, primarily in the malar region
• Less common sites: lateral forehead,
temples, upper eyelids, nasal root or
alae
• Lack of ocular or mucosal involvement
a) Bilaterally, asymmetrical hyperpigmentation, forehead, temporal scalp
b) (b) Pigmented dermal melanocytes and melanophages in dermis (H and E, ×100)
c) (c) Dermal melanocytes in the dermis are highlighted (S-100 stain, ×100)

30. 10) Exogenous ochronosis
• History of hydroquinone application to areas
of hyperpigmentation followed by progressive darkening
• Superimposed small pigmented papules may also be seen
• Histologic features: banana-shaped, yellow–brown deposits
in the dermis
gray-blue macules, mild erythema and
papular lesions.
Ochronosis: Banana-shaped collagen fibers covered by
ochronotic pigment (homogentisic acid) (H and E, ×100)

31. • 11) Macular amyloidosis
• Macular dark brown, symmetrical
pigmentation occurs on central,
upper back, chest, extremities, and
face.
• Characteristic lesions consist of
rippled or reticulated pigmentation
which is typically pruritic
• Women >>men
(a) Reticulate hyperpigmentation, upper back,
(b) (b) Distended dermal papillae filled with eosinophilic material (H and E, ×100),
(c) (c) Orange-pink amyloid (Congo red stain, ×100)

32. TREATMENT
Recommendations for all patients
• Avoidance of sun exposure and tanning beds
• Daily use of broad-spectrum sunscreen (ideally SPF ≥30 with physical blocker such as zinc oxide or
titanium dioxide)
• Sun-protective hats and clothing
• Camouflage makeup
• Discontinue oral contraceptives

33. Active treatment
First-line topical therapies
• Triple combination of HQ + retinoid + corticosteroid at bedtime
• 4% HQ daily, at bedtime
• Azelaic acid (15–20%) Adjunctive topical therapies
• L-ascorbic acid (10–15%)
• Kojic acid (1–4%)
Second-line therapies
• Glycolic (start at 30% and increase as tolerated) or salicylic acid peels (20–30%) every 4–6
weeks
Third-line therapies
• Fractional laser
• Intense pulsed light (IPL)

34. Long-term maintenance
• Continue daily sunscreen and sun-protective measures
• Topical retinoid
• Topical α-hydroxy acid (e.g. glycolic acid cream)
• Other topicals, e.g. L-ascorbic acid (10–15%), azelaic acid (15–20%), or kojic acid (1–4%)

35. Topical Therapies
• HQ: The mainstay of treatment in PIH (concentrations 2 to 4% but strengths up to 10% )
MECHANISMS :-
decreases melanin production by inhibiting tyrosinase
melanosome degradation and selective cytotoxicity toward melanocytes.
Monotherapy is effective but combination + topicals like glycolic acid, kojic acid,
retinoids, and corticosteroids -improve efficacy
Kligman’s formula - 5% HQ + 0.1% tretinoin +0.1% dexamethasone in cream base.
SIDE EFFECTS - irritant reactions, contact dermatitis, nail discoloration, permanent
leukoderma, and exogenous ochronosis

36. • MEQUINOL:
 derivative of HQ
tyrosinase inhibitor
mequinol 2% + 0.01% tretinoin.
BENEFITS:- less irritant
effective in treatment of solar lentigines.
RETINOIDS:
MECHANISM:- blocking tyrosinase transcription, decreasing keratinocyte melanin uptake,
and increasing cell turnover rate.
First generation retinoid- creams, gels, and microsphere gels
concentrations ranging from 0.01% to 0.1%
Adapalene (0.1–0.3%) and tazarotene (0.05 and 0.1%. )-
 synthetic third-generation retinoids - cream and gel formulation-effective and safe in
treatment of acne induced PIH

37. Non hydroquinone skin lightening agents

38. Azelaic acid:
Naturally occurring dicrboxylic acid.
Obtained from pityrosporum cultures.
An advantage of azelaic acid over HQ is lightening of only hyperpigmented skin .
Reversible tyrosinase inhibitor + selective cytotoxic and antiproliferative effects toward
abnormal melanocytes
15% gel and 20% cream formulation = 4% HQ(efficacy)
INDICATIONS:- rosacea , acne vulgaris , melasma, PIH.
S/E- transient erythema ,stnging ,pruritus ,scaling and allergic sensitization.

39. Kojic acid:
A fungal metabolite derieved from aspergillus ,acetobacter ,and penicillium.
 mechanism:- inhibits tyrosinase by chelating copper at the active site of the enzyme.
Used in 1–4% concentration
KA + glycolic acid / HQ for an increased efficacy.
INDICATIONS:- melasm ,PIH.

40. Arbutin:
 naturally occurin D-glucopyranoside derivative of HQ
extracted from dried leaves of blueberry, cranberry, pear, or bearberry plants.
MECHANISM- It inhibits melanosome maturation in addition to blocking tyrosinase enzyme.
synthetic derivatives :- Alpha arbutin and deoxyarbutin
exhibit greater tyrosinase inhibiting ability .
effectively used in treatment of solar lentigines.

41. Niacinamide:
o a highly stable, physiologically active form of vitamin B3 .
o Inhibits melanosome transfer to keratinocytes ------ reducing pigmentation.
o It also decreases the proinflammatory markers that are important in the development of PIH.
o concentrations of 2–5% - improve melasma and UV-induced hyperpigmentation.

42. Licorice root extract:
• Roots of glycyrrhiza glabra.
o its active ingredients- glabridin ------ inhibits tyrosinase
liquiritin --- brings about melanin dispersion and removal.
o Has anti-inflammatory activity (inhibiting superoxide anion and cyclo oxygenase activity.) antiviral,
antimicrobial, and anticarcinogenic properties.
o 20% cream X BD for 4 weeks.
o It has been found safe and effective in melasma

43. Ascorbic acid:
o A natural antioxidant found in fruits, vitamin C .
o Skin lightening, antiinflammatory, and photoprotective properties.
o MECHANISM:- It deactivates tyrosinase via a copper ion interaction and reduces
dopaquinone, a substrate needed in melanin synthesis. It
o Effective in UV-induced hyperpigmentation, solar lentigines, and melasma

44. • Soy: (Soy proteins like soybean)
• trypsin inhibitor (STI) and Bowman-Birk inhibitor (BBI)
• inhibit the activation of protease-activated receptor-2 (PAR-2) cell receptors on
keratinocytes
• -thereby blocking phagocytosis of melanosomes
• -uptake of melanin by keratinocytes.
• Used alone or in combination with retinol, salicylic acid, or sunscreens
• Used to reduce signs of photodamage and PIH in all skin types

45. New products
N-acetyl glucosamine (NAG):
 An amino sugar
MECHANISM:- inhibits tyrosinase by blocking its glycosylation.
effectively lighten solar-induced hyperpigmentation (either alone or in combination with
niacinamide.)

46. • Aloesin
 LMW glycoprotein (aloe vera)
 Hydophilic nature
 Competitively inhibits tyrosinase,tyrosine
hydroxylase and 3,4-
dihydrophenylalanineoxidase.
 Used in combination with arbutin or
deoxyarbutin for synergistic effects.
Proanthocyanidin
 Extracted from grape seed
 Antioxidant property
 Orally administered

47. • Orchid extract
Antioxidant property
Similar to vit C
Coffeeberry extract
 Antioxidant property
 Reduces hyperpigmentation and
photodamage.
• Mulberry extract
 Morus alba L
 Tyrosinase inhibitor + superoxide
scavenging activity

48. Pycnogenol
• Derieved from bark of maritime pine pinus pinaster.
• Main constituents – procyanidins ,polyphenolic monomers ,phenolic or cinnamic acids.
• Antioxidant ,anti –inflammatory propreties .
• Oral- reduce melasma severity.
• Dose-50mg twice daily*90days

49. Chemical Peels
Glycolic acid (GA) Salicylic acid (SA)
alpha-hydroxy acid beta-hydroxy acid
concentrations of 20–70%, concentrations ranging from 20–30%
neutralized with water or sodium bicarbonate does not require neutralization
disperses basal layer melanin, induces epidermolysis,
and stimulates dermal collagen synthesis
disrupting intercellular lipid linkages and inducing
keratolysis
epidermal melasma and PIH reducing PIH

50. Priming combinations

53. COSMETIC CAMOUFLAGE FOR MELASMA
• It is a make-up used to conceal the skin discoloration and normalize the appearance of
skin helping in improving self –esteem and quality of life.
• Different from foundations and have 25% more pigment .
GOALS :-
1. Match all skin tones and blend into the surrounding area.
2. Conceal adequately
3. Water and sweat resistant
4. Stay for sufficient time
5. Be easy to apply

54. • TYPES:-
1. Full concealment
2. Pigment blending
3. Subtle coverage

56. Laser and Light-Based Therapy
• used as an adjunct to topical treatment or in cases of treatment failure.
• Good results have been reported with :--
1. Quality-switched (QS) Nd:YAG laser (1064 nm) - PIH.
2. QS ruby laser (694 nm) - improvement in postsclerotherapy hyperpigmentation in patients.
3. Erbium fiber fractional photothermolysis (1550 nm)- treatment of PIH with .
4. Fractional thulium fiber laser (1927 nm) - PIH.
5. Intense pulse light - PIH needs evaluation.

57. • Melanin has a broad absorption spectrum (630–1100 nm)
• Melanosomes have a short thermal relaxation time (50–500 nanoseconds).
• Longer wavelengths (>600nm) penetrate deeper to target the dermal pigment, but
melanin absorption is better with shorter wavelengths.
• PREOPERATIVE PREPARATION:
o Informed consent
o Patients counseling according to expected reasonable results
o H/O allergy to topical anesthetics
o H/O – herpes labialis ( if +nt – oral acyclovir/valciclovir –start 1day before to procedure
and continue 5days after)
o Presence of keloid /hypertrophic scar
o H/O topical retinoids oral retinoid use

58. o Pretreatment photographs
o Pre and post treatment application of topical depigmenting agents ,photoprotection ,use
of sunscreen.
o Test spots (Q-switched lasers)
o Eye protection ,eyes shields,universal precaution.
Q-Switched Nd:YAG
o works by targeting specific pigment in the skin, which targets the damaged
skin cells in the treatment area.
o Longer wavelength (1064) ,penetrates deep into dermis ,selectively absorbed
by melanin chromophore.
o Low dose laser-cause sublethal injury of melanosomes by causing
fragmenetationand expulsion of melanin granules into cytoplasm.

59. • Dermal vascular- cause subcellular damage to upper dermal vascular plexus.
• PARAMETERS USED:-
 Fluence - <5J/cm²
 Spot size-6mm
 Frequency- 10Hz
 Session- 5 -10at 1 week intervals
SIDE EFFECTS-hypopigmentation
Depgmentation- due to phototoxicity and cellular destruction of melanocytes caused by use
of high fluence.

60. • Q-switched ruby laser (QSRL)
• wavelength of 694 nm
• pulse duration of around 40 nsec - effective modality for the removal of
tattoos and cutaneous pigmented lesions.
• Based on the principle of selective photothermolysis, selective damage to
cutaneous pigment or pigmented cells ,allowing the scar-free elimination of
endogenous or exogenous pigment in the skin.
• Indications- tattoos (amateur, professional, accidental, or cosmetic)
• lentigines
• used for lightening or even removing other pigmented lesions (nevus spilus
or café au lait macules.)
• pigmented lesions of mucous membranes
• s/e - postinflammatory hyperpigmentation, myoplasma, and Becker' nevus .

61. Erbium- Yttrium Aluminium Garnet (Er:YAG) Laser (2940)
• a solid-state laser containing an Er-YAG crystal which emits a wavelength of 2940
nanometers. It is mainly used in bone surgery.
• Causes skin ablatio with minimal thermal damage .
• Minimal risk of postinflammatory hyperpigmentation.
• Fluence – 5.1 – 7.6J/cm²

62. Pulsed dye laser
• Laser which uses an organic dye mixed in a solvent as the lasing medium
• Pulse duration of laser energy is shorter than the target structure’s thermal relaxation time
(which is the time taken for the target to cool by 50% of its peak temperature after
irradiation.)
• Target the melanin and cut. Vasculature.
• Fluence – 7-10J/cm²
• Pulse duration- 1.5ms

63. • Intense Pulsed Light Therapy
absorption of light energy by melanin in keratinocytes and melanocytes
leading to epidermal coagulation due to photothermolysis followed by
microcrust formation.
Wavelength-500- 1200nm
Pulse 5-10ms
Pulse delay 10-20ms
Low fluence 6-14J/cm²
Sessions 3-5
Interval 4-8weeks

64. THANK YOU