Abstract
Chronic wounds, such as venous ulcers, are characterized by physiological impairments manifested by delays in healing, resulting in severe morbidity. Surgical debridement is routinely performed on chronic wounds because it stimulates healing. However, procedures are repeated many times on the same patient because, in contrast to tumor excision, there are no objective biological/molecular markers to guide the extent of debridement. To develop bioassays that can potentially guide surgical debridement, we assessed the pathogenesis of the patients' wound tissue before and after wound debridement. We obtained biopsies from three patients at two locations, the nonhealing edge (prior to debridement) and the adjacent, nonulcerated skin of the venous ulcers (post debridement), and evaluated their histology, biological response to wounding (migration) and gene expression profile. We found that biopsies from the nonhealing edges exhibit distinct pathogenic morphology (hyperproliferative/hyperkeratotic epidermis; dermal fibrosis; increased procollagen synthesis). Fibroblasts deriving from this location exhibit impaired migration in comparison to the cells from adjacent nonulcerated biopsies, which exhibit normalization of morphology and normal migration capacity. The nonhealing edges have a specific, identifiable, and reproducible gene expression profile. The adjacent nonulcerated biopsies have their own distinctive reproducible gene expression profile, signifying that particular wound areas can be identified by gene expression profiling. We conclude that chronic ulcers contain distinct subpopulations of cells with different capacity to heal and that gene expression profiling can be utilized to identify them. In the future, molecular markers will be developed to identify the nonimpaired tissue, thereby making surgical debridement more accurate and more efficacious.
Highlights
Chronic wounds, such as venous ulcers, are reaching epidemic proportions, affecting mostly elderly or disabled persons [1]
Chronic wounds are rapidly increasing among an elderly population with dysfunctional valves in their lower extremity deep veins, as well as among an increasing number of people with diabetes, neuropathic foot ulcers, and pressure ulcers [1]
In this report, we have identified a method utilizing gene expression profiling that distinguish the area of surgical debridement in a chronic wound
Summary
Chronic wounds, such as venous ulcers, are reaching epidemic proportions, affecting mostly elderly or disabled persons [1]. The most common etiology of these ulcers is secondary to deep vein thrombosis or a dysfunctional valve [2]. These ulcers significantly impair an eminence of life and increase healthcare expenditures for millions of people around the world. Surgical debridement is the mainstay of treatments of chronic wounds [4,5] and is done in part to stimulate healing. Chronic wounds are rapidly increasing among an elderly population with dysfunctional valves in their lower extremity deep veins, as well as among an increasing number of people with diabetes, neuropathic foot ulcers, and pressure ulcers [1]. We encounter limitations in early treatment, deriving from the lack of knowledge of wound-healing mechanisms at the molecular level
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