Chronic wound repair and healing in older adults: current status and future research

Abstract

Older adults are more likely to have chronic wounds than younger people, and the effect of chronic wounds on quality of life is particularly profound in this population. Wound healing slows with age, but the basic biology underlying chronic wounds and the influence of age-associated changes on wound healing are poorly understood. Most studies have used in vitro approaches and various animal models, but observed changes translate poorly to human healing conditions. The effect of age and accompanying multimorbidity on the effectiveness of existing and emerging treatment approaches for chronic wounds is also unknown, and older adults tend to be excluded from randomized clinical trials. Poorly defined outcomes and variables; lack of standardization in data collection; and variations in the definition, measurement, and treatment of wounds also hamper clinical studies. The Association of Specialty Professors, in conjunction with the National Institute on Aging and the Wound Healing Society, held a workshop, summarized in this article, to explore the current state of knowledge and research challenges, engage investigators across disciplines, and identify research questions to guide future study of age-associated changes in chronic wound healing.

Keywords: chronic wound; diabetic foot ulcer; pressure ulcer; venous leg ulcer; wound healing; wound repair.

Figure 1

Burn wound repair is delayed in aged mice. (A) Wound area was evaluated 0, 3, 7, 14, and 21 days after burn injury in 2-month-old (young) versus 2-year-old C57BL/6J mice. *P < .05 versus young mice. (B) Bone marrow–derived angiogenic cells were identified using fluorescence-activated cell sorting as CXCR4+/Sca-1+. (C) Human inducibility factor (HIF)-1a concentrations in response to burn injury are lower in aged than younger mice. (D) Bone marrow–derived angiogenic cells from young male mice (Y) administered through tail vein injection to recipient female mice with burn wounds were less able to home in older recipients (O) than in younger ones (Y). Donor cells were identified using the Sry gene as a marker. *P < .01 versus young recipients. N = normal; B = burned. Adapted from Zhang X et al.

Figure 2

Implications of age-associated inflammation for infection. In a mouse model, older mice inoculated with Staphylococcus aureus fail to clear infection, unlike younger mice. *P < .001 versus young at same time point using two-way analysis of variance. Source: Brubaker et al.