Cellular Events
The cellular components of the inflammatory response include the early
emigration (within minutes) of the neutrophils (polymorohonucleocytes or PMN’s)
from the vessels. This is followed by several other species leaving the main
flow, including monocytes, lymphocytes, eosinophils, basophils and smaller
numbers of red cells (though these leave the vessel passively rather than the
active emigration of the while cells). Monocytes, once in the tissue spaces
become macrophages. The main groups of chemical mediators responsible for
chemotaxis are some components of the complement cascade, lymphokines, factors
released from the mast cells in the damaged tissue.
The
PMN escapees act as early debriders of the wound. Numerous chemical mediators
have been identified as having a chemotactic role, for example, PDGF (platelet
derived growth factor) released from damaged platelets in the area. Components
of the complement cascade (C3a and C5a), leukotreines (released from a variety
of white cells, macrophages and mast cells) and lymphokines (released from
polymorphs) have been identified.
These
cells exhibit a strong phagocytic activity and are responsible for the
essential tissue debridement role. Dead and dying cells, fibrin mesh and clot
reside all need to be removed. As a “bonus”, one of the chemicals released as
an end product of phagocytosis is lactic acid which is one of the stimulants of
proliferation – the next sequence of events in the repair process.
The inflammatory response
therefore results in a vascular response, a cellular and fluid exudate, with
resulting oedema and phagocytic activation. The complex interaction of the
chemical mediators not only stimulates carious components of the inflammatoryphase, but also stimulates the proliferative phase. The course of the
inflammatory response will depend upon the number of cells destroyed, the
original causation of the process and the tissue condition at the time of
insult.
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