A Review of Collagen and Collagen-based Wound Dressings

David Brett, BS, BS, MS

Disclosures

Wounds. 2008;20(12) 

In This Article

The Role of MMPs in Wound Chronicity

Wound bed preparation (WBP) can be described as the management of the wound to accelerate endogenous healing or to facilitate the effectiveness of other therapeutic measures.[13,14] The 4 basic aspects of WBP can be represented by the acronym: TIME. T = tissue (nonviable or deficient); I = infection or inflammation; M = moisture control; E = epidermal margin.[15] Focusing on the "E" in TIME, collagen dressings possess properties, which lend themselves to creating a wound environment favorable to the migration of cells from the epidermal margin across granulation tissue, encouraging wound closure. Due to a number of potential stimuli (local tissue ischemia, bioburden, necrotic tissue, repeated trauma, etc.), the wound has stalled in the inflammatory phase contributing to the chronicity of the wound. As a result of the aforementioned pro-inflammatory stimuli, the wound is overstimulated and inflammatory cells, such as macrophages, are present in higher numbers and are more active than they typically would be in an acute wound. In addition, the cells, such as fibroblasts and endothelial cells, are senescent and unable to function properly as they would in an acute wound. With the overabundance of macrophages, there is an overabundance of key pro-inflammatory cytokines, such as TNF-b and IL-1b, secreted by the macrophages. These pro-inflammatory cytokines signal the fibroblasts to secrete MMPs, but due to the overabundance of pro-inflammatory cytokines the fibroblasts secrete elevated levels of MMPs. At this level, MMPs not only degrade nonviable collagen, but also viable collagen laid down by the fibroblasts themselves. Additionally, the fibroblasts are unable to secrete tissue inhibitors of MMPs (TIMPs) at an adequate level to control the activity of the MMPs. These events prevent the formation of the scaffold needed for cell migration and ultimately prevent the formation of the ECM. In addition, cells in a chronic wound tend to be senescent, thus unable to communicate with other cells and unable to function properly. One result of this is a lack of endothelial cell activity slowing the formation of blood vessels. Without an adequate blood supply, tissue can die and as a result, there is an increase in wound size. All of the aforementioned phenomena impede the formation of viable granulation tissue and thus inhibit re-epithelialization (ie, wound closure).[12] One of the key contributors to wound chronicity is an overabundance (and/or activity) of MMPs in the wound; the ability to inhibit or deactivate a number of excess MMPs may help create an environment more conducive to the formation of granulation tissue, and eventual wound closure.

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