INTRODUCTION
Dermatoporosis is a cutaneous syndrome characterized by a progressive loss of skin strength and structural integrity.1-4 Its clinical features include atrophy, purpura, lacerations, delayed healing, and, in advanced cases, dissecting hematomas.1-4 Skin fragility may range from thinning, wrinkling, and laxity in midlife to marked atrophy with purpuric lesions in older individuals.2,5,6 This spectrum reflects the varying contributions of intrinsic aging, photoaging, environmental exposure, and other factors that drive tissue decline.5,6
Visible bruising is a clinically relevant feature of dermatoporosis because it is readily apparent to subjects, can be distressing, and may indicate reduced tissue support.7,8 In mature skin, dermal thinning, extracellular matrix deterioration, vascular fragility, and reduced subcutaneous support can lower the threshold for vessel rupture and ecchymosis.7,8 Morphologic studies using reflectance confocal microscopy and ultrasonography have demonstrated structural changes in dermatoporosis, supporting the value of objective assessment of skin structure in this condition.9
The biology of bruise-prone mature skin is multifactorial. Intrinsic aging and chronic ultraviolet exposure alter epidermal function, collagen and elastin organization, dermal thickness, vascular support, and skin biomechanics.10-13 Type I collagen loss contributes to dermal thinning and reduced tensile strength, while altered hyaluronan-CD44 signaling has been implicated in dermatoporosis-associated atrophy and purpura.14-17 Cellular senescence provides another mechanistic framework for age-related skin fragility, as senescent fibroblasts and keratinocytes
Visible bruising is a clinically relevant feature of dermatoporosis because it is readily apparent to subjects, can be distressing, and may indicate reduced tissue support.7,8 In mature skin, dermal thinning, extracellular matrix deterioration, vascular fragility, and reduced subcutaneous support can lower the threshold for vessel rupture and ecchymosis.7,8 Morphologic studies using reflectance confocal microscopy and ultrasonography have demonstrated structural changes in dermatoporosis, supporting the value of objective assessment of skin structure in this condition.9
The biology of bruise-prone mature skin is multifactorial. Intrinsic aging and chronic ultraviolet exposure alter epidermal function, collagen and elastin organization, dermal thickness, vascular support, and skin biomechanics.10-13 Type I collagen loss contributes to dermal thinning and reduced tensile strength, while altered hyaluronan-CD44 signaling has been implicated in dermatoporosis-associated atrophy and purpura.14-17 Cellular senescence provides another mechanistic framework for age-related skin fragility, as senescent fibroblasts and keratinocytes
