CHRONIC INFLAMMATION FOR MBBS AND MEDICAL STUDENTS

1. CHRONIC
INFLAMMATION
DR. ABHISHEK ANAND
MD PATHOLOGY
ASST. PROF.
3rd
Class

2. CHRONIC INFLAMMATION
Chronic inflammation is inflammation of prolonged duration
(weeks or months) in which inflammation, tissue injury and
attempts at repair coexist.
Chronic inflammation is defined as prolonged process in which
tissue destruction and inflammation occur at same time.

3. CAUSES OF CHRONIC INFLAMMATION
• CHRONIC INFLAMMATION FOLLOWING ACUTE INFLAMMATION
• PERSISTANT INFECTION
• HYPERSENSITIVE DISEASES
• PROLONGED EXPOSURE TO TOXIC AGENTS
OTHERS-
• ALZHEIMER DISEASE
• METABOLIC SYNDROME
• ASSOCIATED TYPE 2 DIABETES

4. CAUSES OF CHRONIC INFLAMMATION
I. ACUTE INFLAMMATION SOMETIMES TERNS INTO PROLONGED
INFLAMMATION.
II. PERSISTENT INFECTIONS BY MICROORGANISMS (MYCOBACTERIA,
VIRUS, PARASITE).
III. HYPERSENSITIVITY DISEASES WHICH IS EXCESSIVE AND
INAPPROPRIATE ACTIVATION OF THE IMMUNE SYSTEM
(AUTOIMMUNE DISEASES)

5. IV. PROLONGED EXPOSURE TO TOXIC AGENTS.
a. Silica results in an inflammatory lung disease called
silicosis.
b. Atherosclerosis a chronic inflammatory process of the
arterial wall induced by excessive production and tissue
deposition of endogenous cholesterol and other lipids.

6. GENERAL FEATURES
MONONUCLEAR CELL INFILTRATION
TISSUE DESTRUCTION/NECROSIS
PROLIFERATIVE CHANGES
FIBROSIS ANGIOGENESIS
(FORMATION OF NEW BLOOD VESSELS)

7. MORPHOLOGIC FEATURES
• Infiltration with mononuclear cells which include
macrophages, lymphocytes and plasma cells
• Tissue destruction induced by the persistent offending
agent or by the inflammatory cells
• Attempts at healing by connective tissue replacement of
damaged tissue by fibrosis & angiogenesis (small blood
vessels)

8. MEDIATORS OF CHRONIC INFLAMMATION
• MACROPHAGES
• LYMPHOCYTES
• EOSINOPHILS
• MAST CELLS
• NEUTROPHILS

10. ROLE OF MACROPHAGES
• The dominant cells in chronic inflammatory reactions
are macrophages
• Contribute to the reaction by secreting cytokines and
growth factors That act on various cells by destroying
foreign bodies and tissues.
• Macrophages are professional phagocytes.
• Function as effector cells that eliminate microbes in
cellular

11. THERE ARE TWO MAJOR PATHWAYS OF MACROPHAGE
ACTIVATION
• CLASSICAL PATHWAY
• ALTERNATIVE PATHWAY

12. ROLE OF LYMPHOCYTES
• Microbes and other environmental antigens
activate T and B lymphocytes which amplify
chronic inflammation.
• By their ability to secrete cytokines, CD4+ T
lymphocytes
• Promote inflammation and influence the nature of
the inflammatory reaction

13. OTHER CELLS IN CHRONIC INFLAMMATION
EOSINOPHILS-
• Abundant in immune reactions mediated by IgE and
parasitic infections
• Eosinophils have granules that contain major basic
protein; that is toxic to parasites
• Also injures host epithelial cells.

14. MAST CELLS-
• Widely distributed in connective tissues
• Participate in both acute and chronic
inflammatory reactions
Neutrophils are characteristic of acute
inflammation but many forms of chronic
inflammation lasting for months.

15. TYPES OF CHRONIC INFLAMMATION
1. CHRONIC GRANULOMATOUS INFLAMMATION it is
characterized by formation of granuloma e.g.
tuberculosis, syphilis, actinomycosis
2. CHRONIC NON SPECIFIC INFLAMMATION it is
characterised by non specific cell infiltration e.g. lung
abscess , osteomyelitis

16. GRANULOMATOUS INFLAMMATION
• Distinctive pattern of chronic inflammation
characterized by formation of granulomas.
• CHARACTERIZED PRESENCE OF
◦ ACTIVATED MACROPHAGES
◦ LYMPHOCYTES
◦ OCCASIONAL PLASMA CELLS

17. • The activated macrophages develop abundant
cytoplasm and resemble epithelial cells and are
called epithelioid cells.
• Some activated macrophages may use forming
multinucleate giant cells.

21. GRANULOMA TYPES:
• THERE ARE TWO TYPES OF GRANULOMAS:
I. Foreign body granuloma: Granuloma forms due to inert
foreign bodies like suture material, silica.
II. Immune granuloma: Granuloma forms due to agents
that are capable of inducing a persistent T cell– mediated
immune response. E.g. Granuloma in Tuberculosis.

22. WHAT IS CASEOUS NECROSIS
• Caseous necrosis is found in tubercular
granuloma.
• Caseous necrosis is granular, cheesy appearance.
• Microscopically caseous necrosis is eosinophilic,
amorphous, granular.

24. EXAMPLES OF DISEASES WITH
GRANULOMATOUS INFLAMMATION
I. TUBERCULOSIS (CASEOUS NECROSIS PRESENT).
II. SARCOIDOSIS .
III. SYPHILIS.
IV. CAT SCRATCH DISEASE.
V. CROHN’S DISEASE.

25. TUBERCULOSIS
• TUBERCULOSIS IS CAUSED BY MYCOBACTERIUM TUBERCULOSIS
• PRIMARY TUBERCULOSIS
◦ USUALLY SEEN IN CHILDREN
◦ DUE TO INITIAL (FIRST) INFECTION
• SECONDARY TUBERCULOSIS
◦ SEEN IN ADULTS
◦ REACTIVATION OF PRIMARY INFECTION

26. • FOCUS OF TUBERCULOUS INFLAMMATION
◦ WHITE COLORED LESION
◦ ROUND OR IRREGULAR BORDERS
◦ CENTRAL NECROSIS (CASEATION)
◦ SOFT, GRANULAR, CHEESY MATERIAL

28. This section showing a
granuloma with central
caseation necrosis
surrounded of lymphocytes,
epithelioid cells and giant
cells

29. ALL GRANULOMATOUS INFLAMMATION IS CHRONIC
INFLAMMATION BUT ALL CHRONIC INFLAMMATION
IS NOT GRANULOMATOUS INFLAMMATION

30. GIANT CELLS
• GIANT CELLS ARE LARGE CELLS WITH MORE THAN ONE
NUCLEUS.
• PHYSIOLOGICAL GIANT CELLS: MEGAKARYOCYTES,
SYNCYTIOTROPHOBLAST.
• PATHOLOGICAL GIANT CELLS: LANGHANS GIANT CELLS
(TUBERCULOSIS), FOREIGN BODY GIANT CELLS, TUMOR
GIANT CELL (REED-STERNBERG CELL)

31. A Langshan's giant cell A foreign body giant cell

32. SYSTEMIC EFFECT OF INFLAMMATION
• FEVER
• ACUTE PHASE PROTEIN: C-REACTIVE PROTEIN (CRP), FIBRINOGEN.
• LEUKOCYTOSIS
• INCREASED PULSE
• INCREASED BLOOD PRESSURE
• DECREASED SWEATING
• RIGORS (SHIVERING)

33. THANK YOU