CHRONIC
INFLAMMATION
Chronic Inflammation
 Chronic inflammation is inflammation of
prolonged duration (weeks to years) in which
continuing inflammation, tissue destruction, and
healing (often by fibrosis), proceed
simultaneously
Chronic Inflammation
 May follow acute inflammation
 eg. Pneumonia  chronic lung abscess
 Repeated bouts of acute inflammation
 eg. cholecystitis , pyelonephritis
 Begin insidiously as a low grade smoldering
response - Tuberculosis
Causes
 Persistent infections by microbes that are difficult to
eradicate.
 Mycobacterium tuberculosis
 Treponema pallidum
 Immune-mediated inflammatory diseases
 Autoimmune diseases rheumatoid arthritis,
inflammatory bowel disease, and psoriasis
 Allergic diseases, such as bronchial asthma
 Prolonged exposure to potentially toxic agents.
 Silicosis (silica)
General Features of Chronic
Inflammation
 Mononuclear Cell Infiltration
 Macrophages, Lymphocytes and Plasma cells
 Tissue destruction or necrosis
 Proliferative Changes
 Attempts at healing by connective tissue replacement of
damaged tissue – angiogenesis (proliferation of small
blood vessels) and by fibrosis
MACROPHAGE
Types of Chronic
Inflammation
Chronic non-specific
inflammation
Chronic granulomatous
inflammation
Eg. Chronic cholecystitis
Chronic pyelonephritis
Eg. Tuberculosis
Leprosy
Syphilis
Chronic granulomatous
inflammation
 GRANULOMA
 Form of chronic inflammation characterised by
collections of activated macrophages, T-
lymphocytes and sometimes associated with
central necrosis
 Cellular attempt to contain an offending agent
that is difficult to eliminate
Chronic granulomatous
inflammation
 Strong macrophage and lymphocyte activation – injure
normal tissues
 EPITHELIOID CELLS – Activated macrophages develop
abundant cytoplasm and resemble epithelial cells
 Some activated macrophages fuse forming multinucleate
GIANT CELLS
 Older granulomas develop an enclosing rim of
FIBROBLASTS AND CONNECTIVE TISSUE
Giant cells
 40 to 50 µ in diameter
 abundant cytoplasm
 Langhans‘ giant cell
 20 or more nuclei in periphery
( horse shoe pattern)
 Foreign body giant cell
 nuclei scattered in cytoplasm
EPITHELIOID CELLS
 Activated macrophages with epithelial – cell like
appearance
 Cells with indistinct cell boundaries
 Abundant pale staining granular cytoplasm
 Elongated/ oval, slipper shaped nuclei
CASEOUS NECROSIS
 Grossly
 This has a granular, cheesy appearance
 Microscopically
 Appears as amorphous, structureless, granular
debris, with complete loss of cellular details
Macroscopic appearance
Fibrosis - The most prominent feature of the chronic
inflammatory reaction when most of the chronic inflammatory
cell infiltrate has subsided. This is commonly seen in chronic
cholecystitis
'Hour-glass contracture' of the stomach - lead to acquired
pyloric stenosis
Strictures - as in Crohn's disease
Chronic cholecystitis
Chronic cholecystitis
Chronic pyelonephritis
Chronic peptic ulcer of the
stomach
Acute Chronic
Duration Short (days) Long (weeks to months)
Onset Acute Insidious
Inflammatory cells Neutrophils Lymphocytes, plasma cells, macrophages
Vascular changes
Active vasodilation, increased
permeability
New vessel formation (granulation tissue)
Fluid exudation and edema + –
Cardinal clinical signs
(redness, heat, swelling, pain)
+ –
Fibrosis (collagen deposition) – +
Systemic manifestations Fever, often high Low–grade fever, weight loss, anemia
Changes in peripheral blood Neutrophil leukocytosis Lymphocytosis

Chronic inflammation

  • 1.
  • 2.
    Chronic Inflammation  Chronicinflammation is inflammation of prolonged duration (weeks to years) in which continuing inflammation, tissue destruction, and healing (often by fibrosis), proceed simultaneously
  • 3.
    Chronic Inflammation  Mayfollow acute inflammation  eg. Pneumonia  chronic lung abscess  Repeated bouts of acute inflammation  eg. cholecystitis , pyelonephritis  Begin insidiously as a low grade smoldering response - Tuberculosis
  • 4.
    Causes  Persistent infectionsby microbes that are difficult to eradicate.  Mycobacterium tuberculosis  Treponema pallidum  Immune-mediated inflammatory diseases  Autoimmune diseases rheumatoid arthritis, inflammatory bowel disease, and psoriasis  Allergic diseases, such as bronchial asthma  Prolonged exposure to potentially toxic agents.  Silicosis (silica)
  • 5.
    General Features ofChronic Inflammation  Mononuclear Cell Infiltration  Macrophages, Lymphocytes and Plasma cells  Tissue destruction or necrosis  Proliferative Changes  Attempts at healing by connective tissue replacement of damaged tissue – angiogenesis (proliferation of small blood vessels) and by fibrosis
  • 6.
  • 9.
    Types of Chronic Inflammation Chronicnon-specific inflammation Chronic granulomatous inflammation Eg. Chronic cholecystitis Chronic pyelonephritis Eg. Tuberculosis Leprosy Syphilis
  • 10.
    Chronic granulomatous inflammation  GRANULOMA Form of chronic inflammation characterised by collections of activated macrophages, T- lymphocytes and sometimes associated with central necrosis  Cellular attempt to contain an offending agent that is difficult to eliminate
  • 11.
    Chronic granulomatous inflammation  Strongmacrophage and lymphocyte activation – injure normal tissues  EPITHELIOID CELLS – Activated macrophages develop abundant cytoplasm and resemble epithelial cells  Some activated macrophages fuse forming multinucleate GIANT CELLS  Older granulomas develop an enclosing rim of FIBROBLASTS AND CONNECTIVE TISSUE
  • 12.
    Giant cells  40to 50 µ in diameter  abundant cytoplasm  Langhans‘ giant cell  20 or more nuclei in periphery ( horse shoe pattern)  Foreign body giant cell  nuclei scattered in cytoplasm
  • 13.
    EPITHELIOID CELLS  Activatedmacrophages with epithelial – cell like appearance  Cells with indistinct cell boundaries  Abundant pale staining granular cytoplasm  Elongated/ oval, slipper shaped nuclei
  • 14.
    CASEOUS NECROSIS  Grossly This has a granular, cheesy appearance  Microscopically  Appears as amorphous, structureless, granular debris, with complete loss of cellular details
  • 20.
    Macroscopic appearance Fibrosis -The most prominent feature of the chronic inflammatory reaction when most of the chronic inflammatory cell infiltrate has subsided. This is commonly seen in chronic cholecystitis 'Hour-glass contracture' of the stomach - lead to acquired pyloric stenosis Strictures - as in Crohn's disease
  • 21.
  • 22.
  • 23.
  • 24.
    Chronic peptic ulcerof the stomach
  • 25.
    Acute Chronic Duration Short(days) Long (weeks to months) Onset Acute Insidious Inflammatory cells Neutrophils Lymphocytes, plasma cells, macrophages Vascular changes Active vasodilation, increased permeability New vessel formation (granulation tissue) Fluid exudation and edema + – Cardinal clinical signs (redness, heat, swelling, pain) + – Fibrosis (collagen deposition) – + Systemic manifestations Fever, often high Low–grade fever, weight loss, anemia Changes in peripheral blood Neutrophil leukocytosis Lymphocytosis