The role of vasoconstriction in the wound healing processis to curtail hemorrhaging. But after about 10 to 15 minutes,that process reverses and vasodilatation and increasedvascular permeability occur. These processes are provoked by mastcells adhering to the endothelial surface that release histamine andserotonin and by the release of kinins and prostaglandins. (See previous issue)
As a consequence of increasedvascular permeability, plasma pours from the intravascular space tothe extracellular area. Diapedis of leukocytes betweenvascular endothelial cells also occur. Histamine attracts leukocytesinto the extracellular fluid space through chemotaxis (imageexpands to 48K JPEG).
The wound responds with a flourish of acute symptoms of inflammation,which we like to think of as the 4 "ors" -- rubor, tumor, calor,and dolor (sounds like an R & B group but of course theyrefer to redness, swelling, heat, and pain).
Do you know the difference between fibrin, fibrous proteins, andfibronectins? Not quite sure? Then read this:
|Fibrin is the end product of the coagulation cascade and is found very early in wound healing. So early it's part of hemostasis. Fibrin has a little, but very little permanent structural strength.|
|Fibrous proteins (collagen, elastin, and reticulin) on the other hand are the stuff to build a bridge with or at least permanently heal wounds. Fibrous proteins make their appearance several days after the wound has occurred.|
|Fibronectins are glycoproteins that assist in the attachment of fibroblasts to the fibrin lattice-work. We'll cover fibroblasts in the next section on new tissue generation but just to whet your appetite we'll tell you that you don't have collagen without fibroblasts.|
The influx of inflammatory cellsinto the extracellular space precipitates both nonspecific andspecific immune responses. Those pushy complement factors act first.They not only directly destroy microorganisms or mark them for laterdestruction, but also attract circulating phagocytes, among them thepolymorphonuclear leukocytes(PMNs). These neutrophils have alimited scavenging role, eating and digesting foreign materialthrough acid hydrolytic enzymes. (Image expands to 84K JPEG).
Monocytes, mostly lymphocytes, then push their wayin but function mainly as immunoreactants. As they enter theconnective tissue they differentiate into free and fixedmacrophages. The mighty macrophage is the key player. These whitecells have both scavenger and nonscavenger functions. With no slightintended to the other inflammatory cells, without macrophages thereis no healing or what healing occurs is poor.
Macrophages stimulate other wound healing processes, attract otherphagocytes, prompt vascular and connective tissue neogenesis, orderthe prostaglandins to sustain the inflammatory process and vasculardilatation, shore up the complement factors, require interleukin toproduce fever and attract more neutrophils, and if that weren'tenough, they release tissue-destroying enzymes to rid the wound ofdebris. Job done, they humbly flow from the wound as part of thepus.
It takes 3 to 5 days for macrophage products to cause thedifferentiation of fibroblasts from resting mesenchymal cells inconnective tissue. You guessed it -- that 3 to 5 days is called theLag Phase. Fibroblasts are responsible for synthesizingcollagen, and collagen makes up about 50% of the scartissue.
While the macrophage and team are launching their nonspecific immuneresponse, the specific immune response is also at work. Theb-lymphocytes produce antigen-specific immunoglobulins (IgG, IgA,IgM, IgE, IgD) that either destroy foreign material directly or markthem for phagocytic destruction. The T-lymphocytes produce noantibodies but their so called killer cells, destroy antigen, thehelper cells assist in the maturation and function of theb-lymphocytes, and the suppresser cells, restrain helper cells andb-lymphocytes from overreacting.
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