PRACTICAL # 06

CHRONIC INFLAMMATION
 Introduction:
Chronic inflammation is inflammation of prolonged duration
(weeks to months to years) in which active inflammation, tissue
injury, and healing proceed simultaneously.
Chronic inflammation is characterized by:
• Infiltration with mononuclear cells
including macrophages, lymphocytes, and plasma cells
• Tissue destruction
• Repair
involving new vessel proliferation (angiogenesis) and fibrosis
• It can follow acute inflammation or can be chronic right from the
beginning.
CHRONIC INFLAMMATORY CELLS
AND MEDIATORS:
Chronic inflammation results from complex interactions
between the cells that are recruited to the site of inflammation

• Macrophages
• Lymphocytes
• Plasma cells
• Eosinophils
• Mast cells
Causes of Chronic Inflammation
1. Persistent infections
– Organisms usually of low toxicity that invoke delayed
hypersensitivity reaction
– M. tuberculosis and T. pallidum causes granulomatous reaction

2. Prolonged exposure to potentially toxic agents

– Exogenous agents include silica which causes silicosis
– Endogenous causes include atherosclerosis caused by toxic
plasma lipid components

3. Autoimmunity
– Auto-antigens provoke self-perpetuating immune responses
that cause chronic inflammatory diseases like Rheumatoid
Arthritis, Multiple Sclerosis
– Responses against common environmental substances cause
chronic allergic diseases, such as bronchial asthma
 FOUR FORMS OF CHRONIC
INFLAMMATION:
On the basis of histological alterations chronic inflammation can be
divided in to four forms.They are as follows:

1. Chronic fibrous inflammation

2. Chronic serous inflammation
3. Chronic Suppurative inflammation (exudate with prominent
cellular components and Liquefactive necrosis)
4. Chronic granulomatous inflammation
EXAMPLES OF CHRONIC INFLAMMATORY DISEASES

• Tuberculosis
• Sarcoidosis
• Rheumatoid arthritis and other connective tissue
diseases
• Inflammatory bowel diseases (Crohn's disease,
ulcerative colitis)
• Silicosis and other pneumoconiosis
• Peptic ulcer of the duodenum and stomach
• Liver cirrhosis
Chronic Granulomatous Inflammation

Chronic granulomatous inflammation is a distinctive pattern of

chronic inflammatory reaction in which the predominant cell type
is an activated macrophage with modified epitheloid appearance,
also called as type IV hypersensitivity reaction or cell mediated
immunity.

TUBERCULOUS LYMPHADENITIS:
Tuberculosis is the prototype of chronic granulomatous
inflammation caused by infection and should always be excluded
as the cause when granuloma is identified. As granuloma can be
due to;
• Infectious agent
• Foreign body infiltration OR
• Unknown etiology
 HISTOLOGY

 The aggregates of epitheloid macrophages.

 Epitheloid aggregates are surrounded by a collar of lymphocytes
secreting the cytokines responsible for continuing macrophage
activation.
 Older granuloma may have a rim of fibroblasts and connective
tissue.
 Frequently, but not invariably, multinucleated giant cells up to
40 to 50 µm in diameter are found in granuloma. They consist of a
large mass of cytoplasm and many nuclei at periphery and they
derive from the fusion of 20 or more macrophages.
 In granuloma associated with certain infectious organisms (most
classically the tubercle bacillus), a combination of hypoxia and
free-radical injury leads to a central zone of necrosis. Grossly,
this has a granular, cheesy appearance raised nodular surface or
evidence of scarring is therefore called Caseous Necrosis.
 Lymphocyte

Giant cell
 CHRONIC CHOLECYSTITIS:
Chronic cholecystitis is the example of typical chronic inflammation. This
represents the following features;

 There is no mucosal ulceration.

 The lamina propria is infiltrated by lymphocytes and plasma cells
 Lymphoid follicle formation is seen both within the lamina propria and the
serosal connective tissues.
 Lamina propria is focally penetrated by Rokitansky-Aschoff sinuses.
(tubular structures present within the wall in 90%, likely herniations or
diverticula due to increased intraluminal pressure)
 A chronic inflammatory cell infiltrate is also seen in the muscle coat and
muscle hypertrophy is seen.
Rokitansky-Aschoff sinuses: tubular structures present within the
wall in 90%, likely herniations or diverticula due to increased intraluminal
pressure