INTRODUCTION
Defined by Kaya and Saurat in 2007, dermatoporosis is a chronic syndrome of excessive skin insufficiency/fragility.1 This loss of the skin's mechanical strength is due to modifications of the extracellular matrix (ECM) and decreased viscoelasticity of the skin, primarily through the degradation of dermal collagen and elastic fibers and reduction of the glycosaminoglycan hyaluronate (HA) that stabilizes these fibers.1 The most commonly diagnosed form is primary dermatoporosis, a result of chronological aging and chronic UV radiation exposure; secondary dermatoporosis is due to chronic topical or oral corticosteroid use. A limited number of studies from Europe have assessed the prevalence of dermatoporosis, with an estimated prevalence of 30.7-37.5% in patients 60 years and older, yet the prevalence is likely to increase as the aging population grows globally.2,3
Clinical Features of Dermatoporosis
Morphological features of dermatoporosis are skin atrophy, solar purpura, stellate pseudoscars, and superficial excoriations, particularly on sun-exposed sites (Figure 1).4 The clinical staging of dermatoporosis considers clinical signs of skin fragility and skin thickness measured by ultrasonography (Table 1). Complications of dermatoporosis range from skin lacerations and delayed wound healing to deep dissecting hematomas that require surgical evacuation. Not simply a cosmetic concern, dermatoporosis truly impacts the morbidity and mortality of patients.1
Pathophysiologic Mechanisms
HA and its cell surface receptor, CD44, are intricately linked to the pathogenesis of dermatoporosis, shown by the interaction of HA and CD44 to stimulate keratinocytes and the association of low levels of CD44 in dermatoporotic skin compared to young controls.5,6 Moreover, levels of HA and expression of CD44 are known to decrease with age and following UVA and UVB exposure.1,7 Histologically, dermatoporosis shows significant epidermal atrophy and a significantly increased number of cells in the epidermis positive for p16Ink4a, a known biomarker of senescence.8 Additional epidermal cellular markers of dermatoporosis include the preservation of Lrig1+ progenitor cells which inhibit the epidermal growth factor receptor, the decrease of Wnt signaling through loss of CD44 regulation, and the decreased expression of the calcium channel Orai-1 involved in keratinocyte proliferation.8,9
Treatment
Various topical and systemic therapies have been studied to treat dermatoporosis, including targeting the mechanistic pathways
