Re: Why do injuries result inscar tissue?

A very good question,  A multicellular organism such as an animal is not just a collection of cells but is also a web of fibrous material 
which helps to hold the cells together and gives new properties to the tissue that cells alone could not provide.  Not only that, but 
many cells that normally adhere or stick to this extracellular fibrous material - or extracellular matrix (usually abbreviated ECM) - 
require adhesion to the ECM in order to grow normally.  Cells can stick to one another directly also, but most also need to stick to an 
underlying ECM.

The surface layer of the skin is an epithelium, a cell layer type often found at the boundaries of tissues.  The skin layer itself is 
known as the epidermis or "outer skin" layer.  Underneath it is ECM and non-epithelial sub-epidermal cells.  The cells of the 
epidermis adhere to one another and also to the ECM.  Two main components of the ECM are the well-known fibrous proteins 
collagen and fibronectin (there are also others).  Normally during development, these ECM proteins are laid down in a very criss-
crossed way, forming a very strong and even mesh that's very important for giving your skin its mechanical properties and allowing it 
to form, along with direct cell-to-cell contacts - a continuous and strong sheet of cells.

When you break your skin, you affect a lot of things.  You cut the epidermis, which is under some tension as it wraps around the 
underling cells; this is due to the ECM, cell contacts, and the internal structural elements of cells called the cytoskeleton.  So the 
skin gapes open a bit, as you often see in cuts.  The continuous cell sheet of the epidermis, so important for protecting your cells 
inside from the outside world, is broken, cells are damaged, and you often start to bleed as you rupture small blood vessels.  You 
disrupt the ECM too, of course.  You damage the underlying cells, especially as the cut is deeper.  So your body is dealing with a 
crisis, and a very complex set of events involving many types of cells it set in motion to protect yourself from infection, bleeding, loss 
of mechanical continuity of the skin, etc.

The blood clots to stop bleeding.  Although the body may want to have more blood present in the area so more immune cells can 
migrate into the troubled area, your body also needs to quickly seal off the breaks in the blood vessels so that you don't lose all 
your blood.  Immune cells rush in to fight off invading cells.  These immune cells crawl in to protect your body from invaders, and 
inflammation may occur as the cells secrete substances to get more blood and the infection-fighting cellls blood carries into the 
wound site.  Epidermal cells also want to crawl in from the sides to reseal the epidermal break.  However, they need new ECM too 
since it has been disrupted.

Although this process is not completely understood yet, it appears that cells start to lay down new ECM in order to reseal the break, 
allow cells to move in and restore the integrity of the skin.  However, the ECM "patch" is not perfect, just as a patch on a bicycle 
inner tube is not perfect and leaves a mark.  Scar tissue seems to in large part come from ECM.  The new ECM deposited is less 
criss-crossed than the original ECM that was damaged.  More of the fibers of collagen and other long molecules lie parallel to one 
another.  As the ECM deposits, required to mend the skin but not the same in structure as the original ECM, scar tissue may 
develop.  Moreover, often way more ECM is deposited than needed and it gets highly crosslinked in an oxygen-dependent reaction 
to form even tougher scar tissue.  That's when you get the really ugly scars; with some of thse ugly scars, cosmetic surgery more 
often doesn't help than does at present.  We really need to understand how this ECM deposition occurs and how we might be able 
to make it more natural and "criss-crossed" early during wound healing.  There is some hope to answering these questions and 
solving the problem of scars developing by studying the difference between embryonic and adult wound healing.  Adult wounds 
tend to scar.  However, wounds (at least small wounds) in embryos tend to heal without a trace.  Some of the difference between 
the two, altough we don't at present know how these differences are really related to the difference in scarring during healing, is in 
a lack of a strong immune response in the embryo and the mobilization of a much smaller set of cells.  Another difference is in the 
pattern of ECM deposition, which seems more like the original pattern in the embryo compared to the adult.  Another difference may 
be related to the mechanisms of epidermal layer closure, but this is another can of worms.

Of course, you are right that cell proliferation occurs at the same time during adult wound healing, but movement of existing cells 
into the wound is also important.  New ECM has to be laid down to restore the skin to health but, unfortunately, the healing process 
itself results in scar tissue being formed.  This can be ugly on the skin or even dangerous, if the wound is internal and thick scar 
tissue develops in internal organs.  The body has repaired the immediate dangers that the wound has created, but it hasn't done it 
perfectly.  I think that practical answers to making wound healing more "perfect" are not too far off with more research.  There are 
already several promising approaches.