On the basis of histological alterations chronic inflammation can be divided in to four forms. They are as follows:
1. Chronic fibrous inflammation:
This Indicates severe inflammatory condition and is characterized by exudation rich in fibrin that does not clear easily. The fibrous tissue producing fibrin in the region of inflammation differentiates in to myofibroblasts.
Contraction of these myofibroblasts like smooth muscles results in mechanical defects. Stiffened joints, stenosis (narrowing) of ducts are the best examples for mechanical defects developed by fibrous inflammation.
2. Chronic serous inflammation:
Serous inflammation is the mildest form of reaction characterized by accumulation of clear fluid (without any cells) due to minimal increase in vascular permeability. Although it occurs in very mild inflammation, it may have grave consequences.
Serous inflammation is marked by the outpouring of a thin fluid that is derived from either the plasma or the secretions of mesothelial cells lining the peritoneal, pleural, and pericardial cavities depending on the size of injury.
For example, the skin blister resulting from a burn or viral infection represents a large accumulation of serous fluid, either within or immediately beneath the epidermis of the skin. Serous pericarditis, pleuritis, peritonitis; rheumatoid arthritis (serous fluid in joints) etc. are some more examples for serous inflammation.
3. Chronic suppurative inflammation:
It is a type of acute inflammation characterized by infiltration of neutrophils at the microscopic level and formation of puss at the gross level.
Abscess is a special type of suppurative inflammation marked by collection of dead neutrophils (pus formation) in the cavity formed by the tissue inflammatory cells and decaying tissues. The encapsulation is an attempt to keep the puss from infecting neighboring structures.
Some abscesses are easily diagnosed clinically, as they are painful and may “come to a head” such that puss becomes visible, but deep and chronic abscesses may just look like a tumor clinically and require biopsy to distinguish them from neoplasm.
The infecting organisms responsible for the formation of abscesses vary. Staphylococcus bacteria are prevalent in skin abscesses, but a multitude of other organisms, including viruses, bacteria, fungi, amoebas and worms, can be involved as well, depending on the site of the abscess.
In some cases, the cause for abscess formation is unknown. If not treated properly an abscess, may progress to a life- threatening infection and death also, especially in people susceptible to infection, such as diabetics or people on steroid medication.
When an abscess enlarges it may develop in to “sinus” (abnormal passage leading from a suppurating cavity to the body surface) or fistula (an abnormal tunnel connecting two body cavities).
4. Chronic granulomatous inflammation:
With somewhat more vascular permeability, high molecular weight solutes also pass from the intravascular to the extravascular space. There are many different plasma proteins in the high molecular weight category, but the most conspicuous of these is fibrinogen.
Contact of coagulation factor XII (Hageman factor) with collagen activates the coagulation system and ultimately leads to proteolytic cleavage of soluble fibrinogen to form insoluble fibrin, which precipitates on every available surface, grossly the serosal surfaces become shaggy and rough.
The inflamed pericardium and pleurae emit friction rubs due to this. Microscopical study of inflamed pericardium suggests the presence of a shaggy coat of preciptated fibrin on the serosal surfaces.