Resolution is a possible outcome at this stage on condition that less than a critical number of cells have been destroyed. For more patients that come to our attention, this is an unlikely scenario.
Suppuration, in the presence of infective microorganisms will result in pus formation. Pus consists of dead cell debris, living, dead and dying polymorphs suspended in the inflammatory exudate. Clearly the presence of an infection will delay the healing of a wound.
Chronic inflammation does not necessarily imply inflammation of long duration, and may follow a transient or prolonged acute inflammatory stage. Essentially there are two forms of chronic inflammation: either the chronic reaction supervenes on the acute reaction or may in fact develop slowly with no initial acute phase. Chronic supervening on acute almost always involves some suppuration while chronic ab initio can have many causes including local irritants, poor circulation, some micro-organisms or immune disturbances. Chronic inflammation is usually more productive than exudative – it produces more fibrous material than inflammatory exudate. Frequently there is some tissue destruction, inflammation and attempted healing occurring simultaneously.
Healing by fibrosis will most likely be taking place in the tissue repair scenario considered here. The fibrin deposits from the inflammatory stage will be partly removed by the fibrinolytic enzymes and will be gradually replaced by granulation tissue which becomes organized to form the scar tissue. Macrophages are largely responsible for the removal of the fibrin, allowing capillary budding and fibroblastic activity to proceed (proliferation). The greater the volume of damaged tissue, the greater the extent of, and the greater the density of, the resulting scar tissue. Chronic inflammation is usually accompanied by some fibrosis even in the absence of significant tissue destruction. The effects of acute inflammation are largely beneficial. The fluid exudate dilutes the toxins and escaped blood products include antibodies (and systemic drugs). The fibrinogen forms fibrin clots providing a mechanical barrier to the spread of micro-organisms (if present) and additionally assist phagocytosis. The gel-like consistency of the inflammatory exudate also makes a positive contribution by preventing the spread of the inflammatory mediators to surrounding, intact tissues.