8.10 Aged Skin

Ethnicity-specific ageing characteristics.

Caucasians: greater skin wrinkle formation and sagging with an earlier onset. More prone to skin desquamation.

Afro-American and Caucasian women: higher prevalence of age-related dryness.

Asian women: Later wrinkling in the facial area, more sensitive to mechanical stimuli and exogenous chemicals, pigment spot intensity as cardinal skin ageing sign.

Intrinsically (genetically/hormonally) aged skin: macroscopically thin and atrophic, exhibits fine wrinkles, subcutaneous fat loss, prominent dryness and reduced elasticity in areas which are not light (sun)-exposed inner side of the upper arm and the gluteal region.

Extrinsically (photo-) aged skin: deeper wrinkles, thickening of the epidermis, dullness, roughness and mottled discoloration in constantly UV-exposed skin regions, facial skin, hand skin. Telangiectasias and pigmentary discoloration might also be observed in advanced and severe degrees of photoaging.

Light-protected skin: Epidermal thinning (10-50%), atrophy of the stratum spinosum, increased heterogeneity in size of basal cells, decreased mitotic activity, flattening of the dermoepidermal junction decrease and heterogeneity of melanocytes, decrease of Langerhans cells, reduction of dermal thickness, atrophy of the extracellular matrix, reduction and disintegration of collagen and elastic fibers, reduction of cutaneous microvasculature, decrease of skin appendages, thinning of subcutaneous fat.

Light-exposed skin: Epidermal thickening, impaired proliferation, and differentiation of keratinocytes, sparse distribution of collagen fibers, stellate phenotype of fibroblasts increases in mast cells and neutrophils, flattening of the dermoepidermal junction, thickening of the vascular walls of arterial and venous capillaries, marked regression and disorganization of small blood vessels.

Gradual development in healthy individuals. In women, rapid progression in approx. 10 years after menopause. Quick development in progeria syndromes.

Aged skin risks the development of common skin lesions (e.g., dry skin, pruritus, telangiectasias, senile purpura, freckling, lentigines, guttate hypomelanosis, stellate pseudoscars, solar comedones, colloid milia, lichen sclerosus et atrophicus).

It is also prone to

• Benign tumors (e.g. seborrheic keratoses, cherry angiomas).

• Premalignant tumors (e.g. actinic keratosis, Morbus Bowen, lentigo maligna).

• Malignant tumors (e.g., basal cell carcinoma, squamous cell carcinoma, malignant melanoma, cutaneous lymphomas, angiosarcoma, Merkel cell carcinoma, Kaposi sarcoma, atypical fibroxanthoma, sebaceous carcinoma, cutaneous metastases).

• Infectious diseases (e.g. dermatophytosis, cellulitis, zoster).

• Bullous dermatoses (e.g. bullous pemphigoid, pemphigus vulgaris).

• Autoimmune diseases (e.g., contact dermatitis, atopic dermatitis, vitiligo, psoriasis, lupus erythematosus).

• Lichen simplex chronicus.

• Pressure ulcers, lower extremity ulcers.

• Vulvodynia, glossodynia, atrophic balanitis.

Clinical signs, photographic severity scales and other imagine methods assess the severity of skin ageing features. Fluorescent detection of Advanced Glycosylated Elements (AGEs) at the frontal forearm area.

Consequent avoidance of overexposure to extrinsic factors, diagnosis and treatment of underlying internal diseases (the skin is mirror of the body), regular topical care and systemic and nutritional uptake of antioxidants (vitamins D, C, E, carotenoids).

Moderate to severe skin ageing: skin anti-aging cosmetics, camouflage (make-up), chemical peelings, dermabrasion, ultrasound energy devices, LASER resurfacing.

Deeper, severe aging: injection of botulinum toxin or fillers, collagen or hyaluronic acid injections, own fat, Gore-Tex implants.