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.