Skin Wound Repair
Location: Outside U.S.
Date: Spring 2012
I would like to know what happens to the skin cells when we have wounds on our skin. During cell division to replace the damaged skin cells, do new cells grow or multiply to enable the wound to heal. From what I know, cells do not really grow much, so how are they able to cover the wound just depending on growth of new cells? It seems to me that cell division is important in wound healing because of the multiplication of many new cells instead. Kindly let me know which is more accurate to explain the wound healing process
Coincidentally, I just answered basically the same question from 'Leow' on the MadSciNetwork! I'm guessing both questions were submitted together, so I thought I'd go ahead & send the link to my MadSciNet answer to save time & effort:
I hope this helps,
Jeff Buzby, Ph.D.
CHOC Research Institute
The cells lining the wound begin mitotic division to produce numerous new cells. At the same time vasculation is also taking place to provide the O2 and nutrients for the rapidly dividing cells. These are new cells, pinkish and tender. You can easily discriminate these new cells from the older cells adjacent to the wound. Once the wound fills, the cells grow and this causes a slightly raised area over the wound which will eventually settle and smooth out.
With careful cleaning, the edges approximated and cell layers sealed very accurately with numerous sutures(stitches) placed, called an end to end anastomosis, the wound will heal with minimal scarring quite rapidly.
In wounds where the scar takes on a different color tone from the adjacent skin indicates the wound ends were not approximately well, especially in the basale layer. The basale layer is where our color tone is expressed by melanocytes.
Hope this helps!
Peter E. Hughes, Ph.D.
This is an excellent question! Wound healing is a very active topic of scientific research. If we could learn better how the process works, we can discover how to encourage or even improve the healing of wounds. This is particularly important for patients who have trouble healing such as diabetics or people confined to wheelchairs. If we could improve the process enough, we might be able to encourage scar-free regeneration!
Healing of a skin wound happens in a few stages. First, blood clots at the site of the injury, forming a temporary seal. During the clotting process, there are small chemical signals that are released that signal the body to start the wound healing process. After the formation of the clot, there is an immediate, short term inflammatory response. This is driven by the infiltration of a special type of white blood cell called neutrophils into the site of the injury, which takes place over about 2 days following the injury. Neutrophils are a 'first responder' kind of cell, and then phagocytose (or engulf) and digest small debris or bacteria that may have gotten into the wound. At the same time, neutrophils secrete specialized proteins called proteases that can help degrade any damaged structural molecules such as collagen. This helps clear the way for future healing.
Additionally, another kind of white blood cell, macrophages, infiltrates the wound site. Macrophages also engulf and digest debris and bacteria, but they can last for a longer period at the wound site than neutrophils. Macrophages also secrete molecules called growth factors that encourage the beginning of the healing process. They stimulate a process called angiogenesis, which is the growth of new blood vessels at the injury site. This allows for the new tissue to receive oxygen and nutrients during and after the repair process. They also encourage cells on the very surface of the skin called epithelial cells to proliferate and cover the injury site. As a side answer to your other questions, epithelial cells, which line our major organs and cover our skin, continually divide throughout our lifespans to replace lost cells from normal wear and tear. While most of the cells in the adult body rarely if ever proliferate, epithelial cells in the skin are replenished from a small population of stem cells that has the ability to continually divide throughout our life.
One very important role for macrophages is the recruitment of generalized tissue repair cells called fibroblasts to the site of the injury. These fibroblasts are very good at synthesizing new extracellular matrix (or the 'structure' of collagens and other molecules that cells live in), and are essential for the repair of damaged tissue. They start to come to the wound site about 3 days after the injury and can stay for several weeks. Initially, fibroblasts proliferate to establish a large enough number of cells, and then they begin to lay down extracellular matrix to produce a specialized kind of repair tissue called granulation tissue. Over time, this provisional tissue is remodeled by fibroblasts and other infiltrating cells to produce a tissue more closely resembling the original healthy tissue.
The details of wound healing are quite complex, and not all of it is fully understood. In principle, though, it can be thought of as an immediate clot, followed by an inflammatory phase to clean up the wound site and recruit repair cells, and then a proliferative or repair phase, where cells enter the wound site, proliferate, and produce more tissue. For simple skin wounds, our body's local stem cells can normally provide the necessary cells to fully repair the wound. Larger wounds may cause scarring due to defects in the repair process or an inadequate cell supply. Wounds in other tissues, such as bones, cartilage, muscle, or vital organs, may be much more challenging to repair normally, and often require medical intervention. An active area of research today is regenerative medicine and tissue engineering, where scientists try to discover new ways to encourage our body to regenerate itself after a trauma. Often, they need a large number of cells to fully repair the injury. Scientists often look to stem cells to provide this, which is the goal of ongoing stem cell research around the world.
Shimon Unterman Ph.D.
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Update: June 2012