Our topic here quickly will be through what's known as your
wound healing. Wound healing at first will be primary intention.
Now what that means is the fact that here with primary intention
is the fact that the, let's say that you have taken a piece of paper
and you've gotten yourself a paper cut. If you've gotten a
paper cut you have created or introduced a wound, correct.
In your skin. Now, if you have introduced a wound the edges of
the wound might be far apart or they might be close together.
If they are far apart, you will call that secondary intention.
If there are close together it will be a primary intention.
So the primary intention, you don't have to lay down as much
granulation tissue. Think of this as being a pothole in a road.
If it's a little pothole you can get away from you can get away
with for the most part fibrosis, it bring the wound together, healing.
But if the edges of the wound are far apart and now it's a knife
wound, far apart. You need to put in alot of asphalt into the
pothole to clean it up, right. To fix it. The asphalt of a pothole
in a road is equivalent to granulation tissue. We'll talk about
granulation tissue in great detail which includes the fact
that it has collagen and it has angiogenesis with VEGF.
All this is going to help you bring wounds back together. Once
we get through the normal, we will go through some important
in which you might lay down too much collagen. That will be a keloid.
Or there might be deficiency of collagen such as Ehlers-Danlos.
Let's begin. Day 1 you have a fibrin clot, a hematoma. Also keep
in mind if you cut yourself with a knife, then not only are you
introducing a wound but you are also cutting through your blood
vessels. Two things occuring at the same time. Wound and tension,
repair also hemostasis. What's that mean to you? The platelets,
we talked about hemodynamics, are going to then form a thrombus.
On day 2, the squamous cell will seal of the wound. The
macrophages emigrate into the wound. Day 3, depending as to how much
granulation tissue is required, it then begins to form. The
initial type of collagen that you are going to deposit,
and do not get your granulation tissue confused with granuloma,
is going to be type III collagen. The type III collagen
is then going to be replaced as you shall see soon enough. But
here during day 3 for the most part almost always day 3,
the neutrophils are going to start disappearing, apoptosis.
Macrophages, monocytes will come in and then land into the tissue
and we have our macrophages. About 4-6 we have granulation tissue
which will peak and now fibronectin is a very key glycoprotein.
In the extracellular matrix, the fibronectin provides the
infrastructure for proper intention of wound healing.
The fibronectin is also something that cancer cells will take
advantage of when they metastasize. That is how important
fibronectin is. Now we are going to skip over to week two. At this
point we have approximately, a tensile strength of approximately 10%.
About a month later though we have remodelling. Which basically
means that the type III collagen is being replaced by collagen
type I. The major enzymes here would be things like collagenase
and lysyl oxidase. Oxidase, not hydroxylase but oxidase
you have to have copper. Tensile strength here may raise up to
80% in about 3 months. But we'll never get back to proper normal.
That's important. Now, the pictures are showing you excess keloid.
Who is your patient here? Think of major contact sports.
Boxing, football. Anyhow, these sports in which you patients are
getting hurt. When they get hurt, also think of ear piercings,
piercings in general. Genetically speaking these patients and this
individuals have a predisposition of during the granulation tissue
phase, about day 3. Laying down collagen. You keep laying down
collagen excessively. And when you do, you are going to form
what's known as a keloid. Look for perhaps in a
African-American male in which the earlobes might be affected.
Or as I told you earlier, you can have contact sports and during
a cut may then have keloid formation. Versus you have a patient
in which the skin is hyperextensible. That to you should be
indicative of a diagnosis called Ehlers-Danlos in which
this is the opposite of keloid. You might then be deficient of
collagen type III or type V. Do not confuse with
osteogenesis imperfecta in which you are
only deficient of collagen type I.