Sunday, April 25, 2010

WOUND HEALING 1

1. WOUND HEALING Process

All living tissue responds to any injury with inflammation. This process is a part of the healing of the wound caused by physical injury and must be differentiated from infection caused by bacterial injury because the treatment differs.

Inflammation has similar characteristics in all modes of injury, which may be caused by:
• Physical trauma (including surgical trauma).
• Thermal: heat and cold
• Radiation, chemicals and
• Infection

The three overlapping time segments of the repair process are inflammation, proliferation, and remodeling. During the inflammatory phase homeostasis occurs and an acute inflammatory infiltrates are produced.
The proliferative phase has fibroplasia, granulation, contraction, and epithelizlization.
The final phase is remodeling which involves scar maturation.

Inflammation
Inflammation precedes the process of wound healing.
After tissue injury, the injured vessel immediately constrict and thromboplastic tissue products many from the sub endothelium, are released.
Platelets aggregates form the initial homeostatic(blood stopping) plug. The coagulation and complement cascades are initiated.
The intrinsic and extrinsic coagulation pathways lead to activation of prothrombin to thrombin, that converts fibrinogen to fibrin, this is subsequently polymerized into a stable clot.

As thrombus is formed, homeostasis in the wound is complete.
The aggregated platelets degranulate releasing powerful chemo attractants for inflammatory cells, activation factors for local fibroblasts and endothelial cells, and vasoconstrictors.
Platelet adhesiveness is achieved through integrin receptors such as GPIIIa


1.1
- The inflammatory response begins with local vaso-constriction

Platelets release granules providing
• Growth factor
• Adhesive glycoproteins
• Vasoactive serotonin
• Hydrolases

Fig 1.1
- The arterioles in the area of injury subsequently show dilation and increased blood flow.
- There is, in addition, opening of new capillaries resulting in congestion with excess blood and slowing of blood flow in the venous channels.
- The R.B.C. separate out and form a central core in the lumen of the capillaries.
- The W.B.Cs are displaced towards the walls (margination) of the capillaries and there is increased permeability due to serotenin with exudation of fluid into the surrounding tissue,
The chemical factors that initiate these events are histamine, serotonin, bradykinin, complement factors and prostaglandin’s.

- The W.B.C. (Neutrophils+ Monocytes) exit from the vessels by chemotaxisis and aggregate at the site of injury.
- The monocytes differentiate into macrophages and show phagocytosis.

*The repair process is initiated within minutes after on injury.
After the transient vasoconstriction induced by platelet factors local small vessels dilate caused by the effects of the coagulation and complement cascades.
Bradykinin is a potent vaso dilutor and a vascular permeability factor that is generated by activation of Hageman factor in the coagulation cascade.
The complement cascade generates the C3 and C5 anaphylatoxins, which directly increase blood vessel permeability and attract ncutrophils and monocytes to the wound area..
These complement components also stimulate the release of histamine and leukotrienes C4 and D4 form mast cells. The local endothelial cells then break cell to cell contact, which enhances the migration of inflammatory cells into the wound site.

White blood cells (first neutrophils, later monocytes) and plasma proteins leak form the blood vessel and enter the wound site. The early neutrophil infiltrate remove cellular debris, foreign bodies and bacteria. Activated complement fragments aid in bacterial killing through opsonization.
The primary role of the neutrophil is to sterilize the wound. The initial neutrophil infiltrate is decreased in clean surgical wounds when compared to contaminated or infected wounds.

The environment in the wound space is hypoxic, hypoglycemic and acidotic.*

The objective of all these events is protective. The final outcome is removal of the causative agents and the effects produced by these agents (necrotic tissue and cells) leading finally to repair.
The information in between astrix* is basic sciences data that will help those with a an interest postgraduate courses.
Send all questions to drmmkapur@gmail.com

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