Atypical skin ulcers

is hyaluronate which stabilizes the intercellular structures of the skin by forming a viscoelastic network in which collagen and elastin fibers are embedded. With aging, the hyaluronate in the extracellular matrix is diminished, leading to easy tearing and lacerations. The term 'dermatoporosis' has been proposed to embrace the different manifestations and implications of the skin atrophy, cutaneous fragility and insufficiency syndrome that is related to aging. The clinical manifestations of dermatoporosis usually become apparent after the age 60 years; more advanced dermatoporosis is perceived at 70 to 90 years of age. The dermatoporosis syndrome comprises: skin atrophy, senile purpura, stellate pseudoscars, frequent skin laceration, delayed wound healing and subcutaneous bleeding. On skin ultrasonography, the dermatoporotic skin is characterized by diminished thickness of the epidermis and dermis. Microscopic examination of skin biopsy specimen shows thinning of the epidermis and dermis the rete ridges being lost, as well as diminished collagen fibers, elastic fibers and mucin content in the dermis [1,2]. Dermatoporosis may be primarily related to the aging process, in which genetic factors may play a significant role [1], or may be secondary to chronic corticosteroid treatment either topical or following systemic administration. The primary and iatrogenic dermatoporosis have similar appearance on physical examination [3].Skin atrophy is seen mainly in the areas exposed to sun, which are the posterior surfaces of the forearms and the pretibial zones. The atrophic skin becomes thin, transparent, with numerous wrinkles, and often purpura and pseudoscars. Senile purpura results from minimal trauma and in the absence of a coagulation disorder. Moreover, large hematomas may accrue after minimal trauma within the virtual space between the dermis and subcutaneous adipose tissue or between the subcutaneous adipose tissue and muscle fascia. Dermatoporosis may be complicated by non-healing skin ulcers. The mechanisms responsible for delayed wound healing of the dermatoporotic skin are decreased proliferative capacity of keratinocytes and fibroblasts, abundant production of matrix metalloproteinases and secretion of cytokines which inhibit the dedifferentiation of keratinocytes [4,5]. Dermatoporosis should be treated to prevent pending complications [1,2].