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(after some deliberation in the comments, I've decided to make the question more general)

An eschar or "dry scab" often forms at a site of injury over a large cut or sore.

It seems as though the healing scab portion binds more strongly to the other scab cells than to those of the surrounding healthy tissue initially, as evidenced by the ability to remove the scab en masse without disturbing the edges of the actual wound (in surgical debridement or when the area is "picked" at). Then, the eschar bonds then bonds more strongly with the edges of the wounds (so it's more difficult to remove), and then finally, the underlying newly formed skin seems to push it off completely.

Does this accurately describe the "lifecycle" of a common dry scab, or are there other well defined stages in the process? What types of cells (platelets in the beginning? epithelials at the end?) are involved with each stage of the process?

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What makes you think that it starts binding more strongly? –  Konrad Rudolph Jul 13 '12 at 12:57
    
I thought that scabs were essentially just a protective layer of dried-out and tightly bound platelets (etc) that eventually came-away when the tissue underneath had properly formed/healed, rather than forming the new tissue themselves. Not my field though! –  Luke Jul 13 '12 at 14:26
    
@KonradRudolph Empirical evidence, no, I'm kidding, but just that there seems to come a point between when the healing begins and when it "comes away" (as LukeTheDuke put it) that it adheres to the wound edges more strongly than to itself, otherwise it would just fall off right away. –  jonsca Jul 13 '12 at 15:09
    
@LukeTheDuke Yes, not mine either, so I'm struggling with digging out the terminology a bit. –  jonsca Jul 13 '12 at 15:10
    
Terminology aside, I don't think there is a distinct point where the scab starts to bind to the wound - this is likely to be an inherent process started when with the initial clotting of the blood. As the clot thickens and binds, the scab will become harder to remove. As the skin underneath heals, the scab is gradually 'excised'(?!). This is purely speculation! –  Luke Jul 13 '12 at 15:14

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Response to cutaneous tissue damage occurs is several distinct but overlapping phases. First an scab is formed as the blood is 'allowed' to clot. A matrix is formed as the platelets adhere to one another, which contracts and 'dries' (forces out the serum) to form a scab. This process clearly happens prior to tissue regeneration/formation to reduce further blood loss.

Fibrinogen

In response to damage to blood vessels a signaling cascade is initated that results in the massive production of fibrin, which is deposited at the site of wounding and subsequently forms blood clots by activating platelets and stabilising the matrix by cross-linking (see PDB's protein of the month 2006).

So this is why clots do not appear to be attached to the surrounding tissue; the fibrin causes the blood to form a matrix that is very tightly bound to itself. Only after clot formation does the tissue remodeling occur, and it is during this stage that the scab will 'bind' more stongly to the surrounding tissue.

The Cell Types and Processes of Wound Healing

This figure (from (Li, 2007)) shows the various stages that occur and cells that are involved in acute wound healing (wounds such as burns and cuts that heal "in a timely fashion");

Major cells and their effects on wound healing

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Wow, that was perfect. Another great answer. –  jonsca Jul 25 '12 at 10:14

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