Productive inflammation

1. CHRONIC
INFLAMMATION

2. Inflammation
According to prevailing one of
phases of inflammation
- exudative,
- proliferative.

3. The proliferation is
concluding phase of
inflammation,
which leads to restoration
of tissue.

4. 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.

5. 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.

6. Types of proliferative inflammation:
 interstitial inflammation,
 granulomatous
inflammation,
 inflammation with
formation of polyps and
pointed condyloma.

7. 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.

10. 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).

13. Infl048.htm

16. 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).

17. 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.

18. 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.

19. Infl048.htm

20. Morphology
of syphilitic granuloma:
 colliquative necrosis
centrally,
 domination of lymphocytes
and plasmocytes,
 large amount of capillaries,
 solitary,
 outcome is gross sclerosis.

27. Inflammation with formation of
polyps and pointed condyloma
occurs on the mucous
membranes and in the borderline
with squamous epithelium.

28. 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).

32. Condyloma is commonly
located on the coronal
sulcus on the penis or
the perineal area.

33. Chronic inflammation
is defined as prolonged
process in which tissue,
destruction and inflammation
occur at the same time.

34. 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.

35. 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.

36. 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.

37. The outcomes depend on the
type of inflammation,
morphofunctional
characteristics of the definite
organ or tissue.
Sclerosis develops in the
majority of cases.

38. Thank you for your
attention!