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Chronic Wounds: Collagen Might Be the Answer You are seeing a resident with a chronic wound. This wound has eluded your treatment plan for years. It seems to go through a cycle during which it improves but does not close and usually deteriorates. Collagen could be the answer, and here’s why. By Debashish Chakravatrhy, PhD 34 HEALTHY SKIN TREATMENT Harmful enzymes that destroy collagen prevent healing in chronic wounds. A collagen dressing can bind to several destructive enzymes like a magnet to iron filings, allowing the body’s own collagen to heal the chronic wound. Improving Quality of Care Based on CMS Guidelines 35 Let’s take a look at the normal healing process Normal wound healing involves three specific but overlapping steps or phases – inflammatory, proliferation and maturation. After hemostasis, the control of bleeding, the groundwork is set for the wound to move into the first, or inflammatory, phase of healing. This typically lasts two to three days and involves the macrophages and neutrophils cleaning the wound debris and eliminating bacteria. These cells have a short life span and are usually able to complete their mission in that time frame of two to three days. The wound then progresses into the second phase, or proliferation. This phase involves fibroblasts appearing in the wound about three days after injury. Their main function is to manufacture extracellular matrix (ECM) proteins, growth factors and angiogenic (new blood vessel) factors. This is part of the process called granulation. The ECM consists of collagen and elastin, among other vital proteins. Collagen is secreted by the fibroblasts and is the most abundant protein in I humans, accounting for nearing 70 percent of all protein. It is one of the components that largely f you are seeing a fill the wound in normal healing. Elastin, another protein, provides strength and elasticity to the chronic wound in front of you, it may skin, though making up only about 3-4 percent of the skin’s protein. As this phase of healing be possible that your continues, cells migrate (epithelialization) and finally wound contraction occurs. problem wound is stuck in the inflammatory phase, The final phase of wound healing, maturation, can take many more months and where destructive enzymes is the final strengthening phase. During maturation, collagen continues to (examples follow) that should reorganize in the skin, gradually replacing the original scar tissue have long ago disappeared are with less-scarred, normal-appearing tissue. still present. Possibly destructive enzymes could include: • Elastase, which is secreted by neutrophils and is simply not useful at this stage in a wound’s life. Elastase destroys elastin. MMPs, keeping the MMPs occupied TIMPs are described as • Matrix metalloproteases in the activity of breaking down the “anti-MMPs” and must (MMPs). The MMPs are dressing material instead of the new outnumber the MMPs (concepproteases that are associated (de novo) collagen made by the tually speaking) for the wound with metal ions, and the worst fibroblasts working hard in a chalto heal normally. In a chronic of them are specific to collagen lenging environment. The enzymes wound, the MMP to TIMP ratio or fragments of collagen, are concentrated in the dressing, is in favor of these collagenmeaning that they seek out where collagen is plentiful, instead destroying enzymes, MMPs. collagen molecules and of in the tissue, where the fibrobchemically break them down. lasts are putting out the body’s own How should you handle • Elastase destroys other enzymes this problem? collagen at low concentrations. too – those that could be Denatured collagen, available in Bring fibroblasts to the wound that useful to the wound, such as some wound care products today, will produce fresh collagen and fill tissue inhibitors of matrix is processed chemically to the the wound bed. A very effective metalloproteinases (TIMPs). extent that it has lost the sophistimethod is to plant native collagen dressings that will bind with the 36 HEALTHY SKIN cated triple helix structure of the collagen building block that is so characteristic of skin collagen. It seems that this triple helix structure of collagen is particularly attractive to fibroblasts. Fibroblasts also thrive in structures in which they can spread out threedimensionally (as they would in real-life wound environment) and be themselves. In other words, they like to do the things that they should be doing, like secreting collagen and other important materials of the extracellular matrix. So, using a collagen product with a noticeable three-dimensional structure allows the fibroblasts to act as normally as they possibly can. Why native collagen-based dressings interact with the destructive elastase enzyme to the extent that they seem to do is still under investigation. Binding of a dressing material to elastase obviously reduces the concentration of the elastase in the wound bed, which means that less of the wound bed’s elastin is destroyed. But, perhaps more importantly, elastase is known to play a role in creating the final destructive form of MMPs. Taking elastase out of play seriously reduces the potential of MMPs being freshly and efficiently created in the wound bed. Elastase is also known to destroy the beneficial TIMP enzymes that keep the MMP in check. A reduced elastase level allows the TIMP concentration to reach a level that keeps MMP activity low in the wound bed. There is a good chance that the chronic but infection-free wound that mystified you in refusing to heal, even when you tried everything else, including addressing all other associative factors, will now proceed to healing. What, then, happens to the dressing once applied to the chronic wound? It is taken apart (in a chemical sense) by the MMPs to which it was bound. The byproducts of this binding are collagen fragments, which are consumed by the fibroblasts. The fibroblasts will synthesize fresh collagen (or the body’s own de novo collagen) and secrete it out into an environment relatively free of MMPs, without whose removal the newly synthesized collagen would have been destroyed. Improving Quality of Care Based on CMS Guidelines 37