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Melasma

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Title: Melasma


1
Melasma
2
Biology of melanocyte
  • Dendritic cell at basal layer of epidermis
  • Produce melanin and send to surrounding
    keratinocyte
  • Epidermal melanin unit (melanocytekeratinocyte)
    136

3
Biology of melanin
  • Synthesis from melanosome
  • Transport to keratinocyte via dendritic process
    of melanocyte
  • 2 type
  • eumelanin
  • pheomelanin

4
Melanin synthesis
  • Binding
  • Melanocyte Melanocortin
    1
  • stimulating hormone receptor
  • adenylase
    cyclase
  • Tyrosinase cAMP

5
Melanin synthesis
  • Tyrosine
  • tyrosinase
  • Dopa
  • Dopa quinone
  • Eumelanin
    Pheomelanin

6
Melanin synthesis
  • MSH
  • MC1R mutation of MC1R
  • Eumelanin Pheomelanin

7
Melanin transfer
  • Phagocytosis
  • melanin transfer to dermis
  • phagocytose by melanophage
  • Endocytosis
  • melanin transfer to keratinocyte via
    intercellular space

8
Melasma
  • Acquired bilateral symmetrical hypermelonosis
  • Irregular light to gray brown macule and patch
  • Ill defined margin
  • Involved sun exposure area
  • Most common in women

9
  • Melasma is a common acquired pigmentary disorder
    that occurs mainly in women (more than 90 of
    cases) of all racial and ethnic groups, but
    particularly affects those with Fitzpatrick skin
    types IVVI

10
Distribution of melasma
  • Central facial pattern (63) cheek, forehead,
    nose, chin
  • Malar pattern (21) cheek, nose
  • Mandibular pattern (16) chin

11
Cause of melasma
  • Light UVA, UVB, visible light
  • Hormone pregnancy, contraceptive pill
  • Drug dilantin, anti-malarial drug,
    tetracycline, minocycline
  • Cosmetic perfume, color
  • Genetic
  • Malnutrition liver dysfunction, B12 def.

12
Type of melasma
  • Epidermal melasma
  • Dermal melasma
  • Mixed epidermal dermal melasma

13
  • The use of a Woods lamp can often be very
    beneficial in determining the location of melanin
    deposition showing enhancement of color contrast
    in lesional skin for the epidermal type, but not
    the dermal types. The mixed type has enhancement
    in some areas of lesional skin, but not in other
    areas.2

14
  • Estrogen may play a role in melasma
    induction(OCP,HRT,pregnancy)
  • Pregnancy induced melasma will recover after some
    months

15
Epidermal melasma
  • Light or dark brown color
  • Melanin deposition in basal, suprabasal layer of
    epidermis
  • Larger melanocyte with more noticeable dendritic
    process

16
Dermal melasma
  • Blue gray color
  • Perivascular melanophage at superficial and
    middermis
  • Melanin granule in dermis

17
  • Whether the melanin is deposited in the
    epidermis or dermis is important therapeutically
    because dermal hyperpigmentation is much more
    challenging to treat

18
Postinflammatory Hyperpigmentation (PIH)
  • PIH represents a pathophysiologic response to
    cutaneous inflammation, such as acne, atopic
    dermatitis, lichen planus, and psoriasis. Similar
    to melasma, it is more obvious in patients with
    brown or black skin. It has no gender or age
    predominance.

19
  • The lesions are characteristically limited to the
    site of the preceding inflammation and have
    indistinct, feathered borders.7 Melanocytes can
    either be stimulated by the inflammatory process
    to become hypertrophic, thus secreting more
    melanin, or the number of melanocytes can
    increase

20
  • . Epidermal hyperpigmentation (e.g., associated
    with acne) occurs when increased melanin is
    transferred to keratinocytes while dermal
    pigmentation (e.g., associated with lichen planus
    and cutaneous lupus erythematosus) occurs when
    the basement membrane is disrupted and melanin
    falls into the dermis and resides within
    melanophage

21
  • Therapeutic goals for hyperpigmentation include
    promoting the degradation of melanosomes,
    inhibiting the formation of melanosomes, and
    retarding the proliferation of melanocytes.

22
  • Because sun exposure is an important etiologic
    factor in hyperpigmentation, all patients should
    use daily, broad-spectrum, high SPF sunscreens
    and minimize sun exposure.

23
Effective therapy
  • Retard melanocyte proliferation
  • Inhibit melanosome formation
  • Promote melanosome degradation

24
Treatment
  • Avoidance
  • Sunscreen
  • Medication hydroquinone, azelaic acid, retinoic
    acid
  • Chemical peeling
  • Dermabrasion
  • Laser

25
Topical Treatments for Melasma
  • In those patients with epidermal type melasma,
    there are multiple treatments available (see
    Table 2).6 Topical agents include phenols, e.g.,
    hydroquinone (HQ) retinoids, e.g., tretinoin
    azelaic acid kojic acid (KA) and glycolic acid
    (GA).

26
hydroquinon
  • 24 has been widely used for melasma therapy.
  • inhibits the conversion of dopa to melanin by
    inhibitin theactivity of tyrosinase.
  • may interfere with DNA and RNA synthesis, degrade
    melanosomes, and destroy melanocytes.

27
  • Reports of contact dermatitis in up to 25
  • As an itchy eruption
  • it is best to be tested in a hidden part before
    use
  • Side-effects included irritant and allergic
    contact dermatitis, PIH, nail bleaching and
    rarely, ochronosis-like pigmentation.

28
retinoids
  • 0.05-0.1
  • inhibiting tyrosinase transcription,interrupting
    melanin synthesis.
  • While tretinoin may be effective in reducing
    melasma, it typically takes at least 24 weeks to
    see clinical improvement.

29
azelaic acid
  • 1)1520) a C9 dicarboxylic acid, is a
    reversible inhibitor of tyrosinase
  • 2) shown to be as effective as HQ 4 but without
    its side effects.
  • 3) The combination of azelaic acid with 0.05
    tretinoin or 1520 glycolic acid may produce
    earlier, more pronounced skin lightening. Adverse
    effects include pruritus, mild erythema, scaling,
    and burning.

30
KOJIC ACID
  • KA 2 is generally equivalent to other therapies
    but may be more irritating.

31
Glycolic acid
  • GA 510 is an alpha-hydroxy acid
  • . It decreases pigment by many mechanisms
    including thinning the stratum corneum, enhancing
    epidermolysis, dispersing melanin in the basal
    layer of the epidermis, and increasing collagen
    synthesis in the dermis.

32
  • , HQ 5, tretinoin 0.1, and dexamethasone 0.1,
    was first introduced in 1975 and termed the
    Kligman formula
  • combination of HQ 4, tretinoin 0.05, and
    fluocinolone acetonide 0.01 (Tri-Luma,
    Galderma) proved better than any combination of
    two of the above agents, with 77 of patients
    showing complete or nearly complete clearing

33
  • Clinically significant improvement was noted as
    early as 4 weeks with maximum results at 8 weeks.
  • The most common adverse effects were mild local
    irritation, erythema, and skin peeling
  • GA peels to a topical regimen of HQ 2, GA 10
    and tretinoin 0.05 cream in PIH patients

34
Laser treatment for melasma
  • Target chromophore is melanin
  • Should destroy melanocyte in hair follicle
  • Good in dermal and mix melasma

35
Laser treatment for melasma
  • Epidermal melanin removal lPL, PDL
  • Dermal melanin removal Q-switched Ruby,
    Q-switched Alexandrite, Q-switched NdYAG
  • Fraxel

36
Epidermal melanin removal
  • No recovery time
  • Repigmentation after removal

37
Dermal melanin removal
  • Minimal downtime
  • Side effect transient erythema,
    hypopigmentation
  • Repigmentation from melanin in melanophage

38
Fraxel
  • Epidermal and dermal ablation
  • MEND formation and eliminated through skin
  • Induce melanophage disruption and release melanin
    granule into dermis
  • Downtime 3-7 d
  • Long term improvement

39
Chemical peeling
  • With AHA like TCA,Salycilic acid,and
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