WATCH VIDEO ABSTRACT: Dermatoporosis: Strategies for Rebuilding the Extracellular Matrix of the Skin

September 2023 | Volume 22 | Issue 9 | 861 | Copyright © September 2023


Published online August 22, 2023

Alan D. Widgerow MBBCh MMed FCS FACSa,e, Orit Markowitz MDb, Jean Carruthers MD FRCSC FRC (Ophth.)c, Carolyn Jacob MDd, Tiffany Robison MS CCRCe

aDivision Chief Research, Professor Plastic Surgery, Center for Tissue Engineering, University of California, Irvine, CA
bMarkowitz Medical, Manhattan, NY
cDepartment of Ophthalmology, University of British Columbia, Vancouver, BC, Canada
dChicago Cosmetic Surgery and Dermatology, SC; Chicago Cosmetic and Dermatologic Research, PLLC; Chicago Skin Science, LLC; Associate Clinical Professor, Northwestern’s Feinberg School of Medicine, Department of Dermatology, Chicago, IL
eAlastin Skincare, Inc., a Galderma company, Carlsbad, CA

Abstract

Dermatoporosis as a disease entity is relatively newly described, the title conceived as recently as 2007. The background of chronic skin fragility, bruising, and atrophy appears to start in some patients as early as their mid-forties, but is full blown over the age of 65 years. The dehydration and fragility of the skin with recurrent bruising and breakdown were initially attributed to increased vessel fragility and permeability thought to be associated with inherent vascular tissue defects in a milieu of increased inflammation and extracellular matrix (ECM) degradation. It has subsequently been demonstrated that this ECM breakdown directly affects the structural support system of the superficial vessels, leading to stretch, increased permeability, and vulnerability to mechanical damage. Add to that the ECM atrophy and general accumulation of non-functional metabolic waste products in the form of fragmented collagen, elastin, and increased circulating glycation end products, and it becomes apparent that much of the problem resides in a structural defect, non-functioning, dehydrated, senescent cellular matrix and unsupported vascular system that presents as dermatoporotic characteristics. This paper describes a strategy of ECM replacement to counteract these foundational deficiencies.

J Drugs Dermatol. 2023;22(9): doi:10.36849/JDD.7549

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
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