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Chronic inflammation and wound healing1Cellular components WWAMI lecture Nicole Meissner-Pearson Outcome of acute inflammation Complete resolution due to elimination of the offending agent and regeneration of injured tissue with normal function Healing by connective tissue replacement (fibrosis/scar formation) Occurs after large tissue destruction, fibrinous exudation into serous cavities tissue without regeneration capabilities Progression to chronic inflammation Resulting in granuloma formation to wall off injurious agent and tissue fibrosis (scar formation) Definition of chronic inflammation an inflammatory response of prolonged duration (weeks – months - years) provoked by the persistence of the causative stimulussimultaneous presence of acute inflammation, tissue destruction and repair Causes of chronic inflammation Infectious organisms that resist clearance and form a persistent infection in tissue or undrained abscess cavities e.g mycobacterium tuberculosis, actinomycetes, treponema palidum and Staph aureus (in bone and pleural cavities) Exposure to irritant non-living foreign material that can not be removed implanted materials into wounds (wood splinters), inhaled materials (silica, asbestos), deliberately introduced material (surgical suture material or prosthesis) Potentially normal tissue components as seen in auto-immune diseases Beta islet cell in diabetes mellitus type I, Acetyl cholin receptor in Myastenia gravis Characteristics of chronic inflammation Infiltration of mononuclear cells Tissue destruction Healing with scar formation and fibrosis The dominant cellular player in chronic inflammation is the tissue macrophage In chronic inflammation macrophage accumulation persists by different mechanisms Continued recruitment of monocytes from the circulation Local proliferation Prolonged survival and immobilization Outcome of chronic inflammation Ulcers Fistulas Granulomatous diseases Fibrotic diseases (Scaring) and combi
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