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WOUND HEALING During inflammation, vessels

Forms of wound healing: become porous and release cells and


1. First intention blood plasma into the injured area.
2. Second intention. The newly arrived inflammatory cells
First intention (primary) healing increase metabolic demand. Since the
occurs when tissue is cleanly incised local microvasculature has been
and re approximated and repair damaged, PO2 falls while CO2 and
occurs without complication. lactate accumulate. Lactate in
Second intention (secondary) healing produce more vasodilatation and
occurs in open wounds through attract more inflammatory cells.
formation of granulation tissue* and Vicious cycle is thus set with
eventual coverage of the defect by macrophages taking the role of
spontaneous migration of epithelial releasing chemo attractants as
cells. Most infected wounds and coagulation derived factors
burns heal in this manner decrease.
Granulation tissue is the red, Macrophages release more lactate
granular, moist tissue that appears even in the presence of oxygen,
during healing of open wounds. thereby maintaining the environment
Microscopically, it contains new of injury. The environment causes
collagen, new blood vessels, them to release growth promoters and
fibroblasts, and inflammatory cells, more lactate, which in turn stimulates
especially macrophages. angiogenesis and collagen deposition.
Primary healing is simpler and By 2nd -3rd day Unless the wound
requires less time and material than becomes infected, its granulocyte
secondary healing. It sometimes population, which dominated on the
happens that primary healing is first day, has diminished.
possible but there is insufficient Macrophages now cover the cut
reserve to support secondary healing. surface.
Eg. Ischemic limb may heal In 3rd-4th Immature fibroblasts, the
primarily, but if the wound opens and product of growth signals, lie just
becomes secondarily infected, it may beneath, mixed with bud of new
not heal. vessels. More mature fibroblasts are
Healing phases scattered behind
Injury profoundly disrupts the 2.FIBROPLASIA & MATRIX
chemical environment and DEPOSITION
architecture of tissues. Fibroplasia
The postinjury environment, Replication of fibroblasts is
characterized by impaired perfusion stimulated by PDGF, IGF-1, and TGF

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