d how does it form?
- How does healing occur?
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PHYSIOLOGY OF INFLAMMATION
The four cardinal signs of inflammation are readily explained by the behavior of the underlying cells and tissues. The inflammatory response consists of several physiological processes (illustration from WebPath), all of which are triggered by the release of pharmacologically active substances such as histamine and heparin. These triggers of acute inflammation are released by mast cells, sensitive cells which are scattered throughout ordinary connective tissues and which react to tissue damage or other disturbance.
Chronic inflammation is maintained by more complex interactions among several cell types; diagram from WebPath.
The basic components of the inflammatory response are:
See illustration from WebPath.
Vasodilation (increased vascular perfusion).
- Relaxation of the smooth muscle which surrounds terminal arterioles results in increased blood flow into the connective tissue capillary bed.
- Increased tissue perfusion in turn causes redness (rubor), as more red blood cells pass through the tissue, and warmth (calor), as blood carries body heat from the body's core to cooler peripheral tissues.
Increased vascular permeability.
- The endothelial lining of capillaries (endo = inside; the endothelium is the layer of thin, flat cells which line blood vessels) becomes more leaky, allowing more fluid (blood plasma) to exude into the connective tissue spaces.
- There is normally a balance between fluid leaving vascular spaces and fluid re-entering the system. Inflammation shifts this balance, causing accumulation of interstitial fluid.
- The fluid build-up which follows this permeability change is called edema and is visible as puffiness or swelling (tumor).
Note that edema can take a variety of forms. The following links will take you to gross images at WebPath.
Emigration of leukocytes.
- Vasodilation and increased vascular perfusion are designed to prepare the way for the inflammatory infiltrate to enter the inflamed tissue.
- A combination of vasodilation with thickening of the blood (due to fluid leaking out of the vessels) causes a slowing of flow rate, which encourages leukocytes (white blood cells; leuko = white, cyte = cell) to stick to the sides of the vessels. This is called "margination" or "pavementing" (the white blood cells gather along the endothelium, like bricks paving a road). (Example from WebPath.)
- From here the leukocytes crawl between the endothelial cells and enter the inflamed connective tissue. Increased metabolic activity associated with leukocyte activity also generates heat (calor), contributing to local warmth.
Pain and/or itching (dolor) is caused by direct action on nerve endings of the chemical agents released during inflammation.
INFLAMMATORY INFILTRATE (Introduction to inflammation)
The inflammatory or leukocytic infiltrate consists of white blood cells which leave the blood and enter (infiltrate) the inflamed connective tissue
- Images of inflammatory infiltrate in skin.
- Image from WebPath of inflammatory exudate in lung alveoli.
Cells of the inflammatory infiltrate include neutrophils, lymphocytes and monocytes. Immigration of these cells into peripheral tissues is one of the principal purposes for inflammation, bringing to a site of injury the immune-system cells which can combat infection and clean up damaged tissue.
Neutrophils (neutrophilic leukocytes) are the first white blood cells to enter the tissue during acute inflammation. Neutrophils are anti-bacterial cells which lyse (break down) bacterial cells by releasing lysosomal enzymes. Neutrophils recognize bacteria as foreign by the antibody molecules which have attached to the bacterial surface. Antibody molecules (molecules which bind to one specific antigen or foreign substance which the body has previously encountered) are found in blood plasma and interstitial fluid.
Neutrophils are the most numerous of the leukocytes, about 60% of the white blood cell count. They are about 12 Ám in diameter in blood smear preparations (about twice the siz