Melanin SynthesisMost of melasma patients are photo skin type III to V. These skin type's response to sunlight by increasing of melanin synthesis. Melasma relates to strong sun light exposure and high estrogens. Melanins are synthesized in epidermal melanocytes and transfer to epidermal keratinocytes. One melanocyte supplies thirty six keratinocytes and is called "epidermal melanin unit". Majority of melanin granules are distributed in the keratinocytes. Melanin granules in melanocytes are mainly early stage (stages I-II) which contains less melanin. UV exposure stimulates keratinocytes to release cytokines (especially endothelins) which bind to endothelin receptors on melanocyte cell membrane. The binding of keratinocytes and melanocytes is through binding of Stem Cell Factor (SCF) on keratinocytes and C-kit protein on melanocytes. Endothelins together with Melanocyte Stimulating Hormone (MSH) stimulate tyrosinase enzymes synthesis. These enzymes are essential for melanin synthesis. Any conditions producing basement membrane injuries will lead to melanin dropping down into upper dermis .They will be engulfed by macrophages transforming to what we call "melanophages". These melanophages will persist in dermis for many years. Recently, there were many published articles on finding of increase of vascular dilatation and vascular growth factor in melasma.In normal skin most of the mature melanins (stage V) will be in keratinocytes Epidermal or follicular melanocytes contain unmelanized melanin (stage I-II). This unmelanized melanin will not absorb enough laser energy to produce "Selective Photothermolysis" or photomechanical destruction of melanin and also of melanocytes. The surviving memalnocytes are the major source of recurrence of lesions after selective pigmented laser treatment (e.g. 532 nm frequencydoubled Q-switched Nd: YAG laser). For hyperpigmented lesions, mature melanin present in all these locations; keratinocytes, epidermal melanocytes and melanophages. In order to reduce hyperpigmentation, the treatment should be able to reduce melanin all three locations. In hyperpigmented lesions melanin granules also aggregate into clumps. This produces dark color, while small fragmented and dispersed melanin produce lighter colour [1][2][3][4][5][6].In summation, the following mechanisms had been used with mild to moderate result for treatment of melasma:
1.Superficial peelings e.g. chemical peels, microdermabrasion, laser resurfacing.
2.Stimulation of keratinocytes turnover. Example: vitamin A acid, glycolic acid, salicylic acid.
3.Suppression of melanin synthesis. Example: hydroquinone, arbutin, kojic acid, licorice PT40, tranxemic acid etc.
4.Reduction of pigment transfer from melanocytes to keratinocytes. Example: Niacinamide, Clove extracts
5.Destruction of melanin's containing cells (melanocytes and Keratinocytes) e.g. Q-switched laser, Fractional laser
PathogenesisMelasma is a complex disease. The pathogenesis involves: 1) Hyperfunction of clones of epidermal and follicular melanocytes in certain sun-expo...