INTRODUCTION
Facial aging is a complex process affecting different areas and structures of the face in various ways. This article focuses on the most common problems our patients complain about and present in the doctor’s consultation, and out- lines a science-based, indication-specific, therapeutic concept focusing on alternatives to standard injectables and devices for rejuvenation in aesthetic dermatology.
Skin Aging and Beyond
Skin aging is a continuous ongoing process typically dividable into two mechanisms, extrinsic and intrinsic aging. Photoaging is the major trigger for skin changes from extrinsic factors. The predominant pathomechanism is the formation of free radicals causing oxidative damage and induction of an inflammatory milieu taking place in the epidermis and dermis but mainly in the dermis. The results are a decrease in collagen type I and degeneration of extracellular fibers.1 Clinically speaking, the skin atrophies in all layers, gets thinner and less elastic, and presents wrinkles and folds (solar elastosis) as well as irregular pigmentation, broken vessels, and possibly skin cancer and its precursors. Intrinsic skin aging is a process based on chronobiologic, genetically determined aging, and can be influenced by hormones as the skin is a typical target organ for those molecules: estrogens are responsible for elasticity, water retention, and circulation; androgens increase sebum production; gestagens inhibit the enzymatic depletion of connective tissue. The drop in hormones in menopause result in typical skin changes: the thickness of the epidermis decreases through the reduced proliferation activity of keratinocytes and restricted capacity for differentiation. Throughout the dermis, a depletion of up to 30% of the collagen bers occurs in the first five years of menopause. Further to this, skin matrix proteins get reduced. Additionally, the skin’s function wanes in terms of sebum and sweat production, and overall, the skin gets thin (like cigarette paper), rough, wrinkly, more sensitive, and easily vulnerable. Benign lesions such as seborrheic keratosis can occur. So, looking at the overall structural and functional changes of the epidermis and dermis throughout the aging process, one can see again alterations in dermal collagen, elastin, and glycosaminoglycans,1 a loss in the content of hyaluronic acid with an overall thinning and loss of elasticity, impaired response to ultraviolet light, etc.2 Even though facial aging starts at the surface by showing signs of aging on the skin, the aging process goes far beyond and nally involves all facial structures such as the muscles, retaining ligaments, fat pads, and bone structures. But, over time, the facial fat pads get redistributed, atrophying and separating. Further to this, a remarkable bony resorption takes place and doesn’t give the needed structural support. All this results in de ation and sagging of the midface in a three-dimensional
