I. Histological Changes
Epidermis is thinner in chronologically aged skin, however is often thickened in photodamaged skin and has reduced rete pegs/rete ridges
II. Keratinocytes
- slow down of cell turnover: studies indicate that the epidermal turnover rate slows from 30-50% between our thirties and eighties which correlate with the subsequent slowing of the wound healing process as well as less-than-efficient desquamation (shedding of the outermost skin layer) process.
- decreased expression of markers of cellular differentiation result in the slowing of keratinization
- decreased level of filaggrin (a filament-associated protein that binds to keratin fibers)
- keratohyalin granules (a protein structure found in granules in the stratum granulosum of the epidermis, which may be involved in keratinization) are decreased
- decreased transglutamase I: Transglutaminases form extensively cross-linked, generally insoluble protein polymers that are indispensable to create barriers and stable structures in skin)
- cell shape changes and the barrier function reduces causing the epidermis to thin and become more susceptible to pathogen
III. Melanocytes
- increased melanogenesis (process of production of melanin by melanocytes) after exposure to UVB radiation (melanin can block UVB from entering into the skin layer which can cause DNA damage), excess melanin result in age spot.
- increased number of melanocytes and melanosomal complexes in surrounding keratinocytes result in age spot (pigmentation)
- oxidation of existing melanin
- increased tyrosinase (the enzyme for the formation of melanin from precursor tyrosine) level: inflammation caused by UV rays triggers tyrosinase level. Tyrosinase inhibitors are widely used in anti-aging cream to reduce/eliminate age spots.