INTRODUCTION
In 2007, Kaya and Saurat coined the term dermatoporosis when describing chronic aging and fragile skin. This is typically represented by atrophic skin with purpura and white pseudoscars on the extremities of elderly patients1 (Figure 1). Dermatoporosis occurs as a natural byproduct of aging, but it can also be accelerated by chronic actinic damage, genetic susceptibility, and long-term use of topical and systemic corticosteroids. Similar to osteoporosis, the skin may atrophy following an alteration in collagen, elastin, and the ground substance of the extracellular matrix (ECM).1-4 The ECM provides constant support to newly developing vessels, and to the long-established vascular system keeping the histological structure of the vessel wall in shape but also withstanding the mechanical forces levied on the vessel by flow and pressure within the vessels.5 The complex network of elastic fibers and structural collagen support fibers are well adapted to carry out this function in the ECM. In addition, the ECM provides informational cues to the vascular cells regulating their proliferation and differentiation.5
Thinning or atrophy of ECM components caused by photo-aging results in loss of support to these vessels, thereby increasing their vulnerability and fragility and making them extremely sensitive to the slightest trauma (Figure 2).4,6 Although the
Thinning or atrophy of ECM components caused by photo-aging results in loss of support to these vessels, thereby increasing their vulnerability and fragility and making them extremely sensitive to the slightest trauma (Figure 2).4,6 Although the
