CHRONIC INFLAMMATION

Inflammation

According to prevailing one of phases of inflammation

- exudative,

- proliferative.

The proliferation is concluding phase of

inflammation, which leads to restoration

of tissue.

Cellular proliferation in different types of inflammations.

There is no significant cellular proliferation in acute bacterial infections except in typhoid fever in which there is intestinal lymphoid hyperplasia.

Viral infections have the ability to stimulate cellular proliferation, e.g. epidermal cell proliferation in herpes simplex, chickenpox arid smallpox.

In glomerulonephritis, there is proliferation of glomerular capsular epithelial cells resulting in formation of 'crescents'.

In chronic inflammation, cellular proliferation of macrophages, fibroblasts and endothelial cells occurs.

Reproduction of cells in chronic inflammation Hematogenic origin – T-lymphocytes, B-

lymphocytes, plasma cells, monocytes, macrophages, histiocytes, epithelioud cells giant cells of Langhans and foreign bodies

Histiogenic origin – endothelium, reticular cells, fibroblasts etc.

Types of proliferative inflammation:

interstitial inflammation, granulomatous

inflammation, inflammation with

formation of polyps and pointed condyloma.

Interstitial inflammation is characterized by cellular infiltration formation in stroma of organs (myocardium, liver, kidney, lung).

The inflammatory cell infiltration consists of lymphocytes, monocytes, plasmocytes, eosinophils and other cells.

Prolonged interstitial inflammation can result in sclerosis of organ.

Granulomatous inflammation is characterized by formation of granulomas.

Granuloma is a local accumulation of cells, which have ability of phagocytosis.

Granuloma is circumscribed tiny lesion, about 1 mm in diameter, composed predominantly of macrophages,

epithelioid cells, and lymphoid cells at the periphery. In some cases granulomas contein giant cells.

The giant cells are formed by fusion of adjacent epithelioid cells and can have 50-100 nuclei. These nuclei can be

arranged at the periphery like horseshoe or ring (Langhans' giant cells), or can be present centrally (foreign body giant

cells).

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Granulomas (according to etiology)

infectious (endemic typhus and epidemic typhus, tuberculosis, leprosy, siphylis, tularemia),

noninfectious (asbestosis, silicosis, medicamentous hepatitis, lipogranuloma, oilgranuloma, granuloma around foreign body),

granulomas with unknown etiology (sarcoidosis, Crohn’s disease).

Specific granuloma is characterized by definite morphological changes, which allow to make diagnosis.

Infections, which accompanied by development of specific granulomas, are tuberculosis, leprosy, siphylis, scleroma.

Morphology of tubercular granuloma:

caseous necrosis centrally, domination of epithelioid cells

and presens of Langhans' giant cells,

vessels are absent (or very small amount of capillaries),

miliary and multiple, outcome is soft sclerosis.

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Morphology of syphilitic granuloma:

colliquative necrosis centrally,

domination of lymphocytes and plasmocytes,

large amount of capillaries, solitary, outcome is gross sclerosis.

Inflammation with formation of polyps and pointed condyloma

occurs on the mucous membranes and in the borderline

with squamous epithelium.

Polyps are the end-result of prolonged chronic irritation.

Macroscopically they are gelatinous masses with smooth and shining surface.

Microscopically they are composed of loose edematous connective tissue containing some mucous glands and varying number of inflammatory cells (lymphocytes, plasmocytes, eosinophils).

Condyloma is commonly located on the coronal sulcus on the penis or

the perineal area.

Chronic inflammation

is defined as prolonged process in which tissue,

destruction and inflammation occur at the same time.

Chronic inflammation can be caused by:

1. Chronic inflammation following acute inflammation - when the tissue destruction is extensive, or the bacteria survive and persist in small numbers at the site of acute inflammation, e.g. in osteomyelitis, pneumonia terminating in lung abscess.

2. Recurrent attacks of acute inflammation - when repeated bouts of acute inflammation culminate in chronicity of the process, e.g. in recurrent urinary tract infection leading to chronic pyelonephritis, repeated acute infection of gall bladder leading to chronic cholecystitis.

3. Chronic inflammation starting de novo.

Though there may be differences in chronic inflammatory response depending upon the tissue involved and causative organisms,

there are some basic similarities amongst various types of chronic inflammation.

General features that characterize any chronic inflammation: 1. Mononuclear infiltration. Chronic inflammatory lesions are

infiltrated by mononuclear inflammatory cells like phagocytes and lymphoid cells. Phagocytes are represented by circulating monocytes, tissue macrophages, epithelioid cells and sometimes, multinucleated giant cells. The macrophages comprise the most important cells in chronic inflammation.

2. Tissue destruction and necrosis. Tissue destruction and necrosis are common in many chronic inflammatory lesions and are brought about by activated macrophages by release of a variety of biologically active substances.

3. Proliferative changes. As a result of necrosis, proliferation of small blood vessels and fibroblasts is stimulated resulting in formation of inflammatory granulation tissue. Eventually, healing by fibrosis takes place.

The outcomes depend on the type of inflammation, morphofunctional characteristics of the definite organ or tissue.

Sclerosis develops in the majority of cases.

Thank you for your attention!