Skin undergoes structural and physiological changes resulting from both the natural aging process and being exposed to damaging environmental elements. Over a lifetime, skin is observed to progressively degenerate. Most notable are the changes and deterioration in the structure of the skin which are due to losses and/or a disordering of collagen, the protein primarily responsible for the tensile strength of skin, and elastin fibres (Farage et al. 2009). The elderly therefore, have an increased susceptibility to skin injuries such as pressure ulcers, and a decreased healing response.
Pressure ulcers are common among individuals with SCI, and typically occur over boney prominences, such as the ischial tuberosities and malleoli. Damage to the skin and underlying tissue caused by pressure, shearing, and/or friction due to continuous sitting are the primary causes of pressure ulcers. As collagen metabolism increases as a result of SCI, these individuals may be more susceptible to pressure ulcers than non-SCI individuals (Claus-Walker & Halstead 1982a; Claus-Walker & Halstead 1982b). As a result of the combined effects of pressure, from sitting, and reduced skin integrity, due to collagen degradation, it is estimated that 85% of individuals with SCI will experience a pressure ulcer in their lifetime (Gunnewicht 1995). Given that the mean cost of healing a wound is approximately $50,000, which translates into an annual cost of 3.6 billion dollars in the United States (Beckrich & Aronovitch 1999), there is a strong need to understand age-related changes to the skin following SCI in order to help minimize the occurrence of wounds.
In this section, 2 longitudinal studies and 2 cross-sectional studies on skin and subcutaneous tissues after SCI are reviewed.