inflammation adel-1
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Acute & Chronic Inflammation
Dr Adel Abdel-Azim
Professor & Chairman of Oral Pathology
Department, Faculty of Dentistry, Ain-Shams
University, Cairo, Egypt
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Acute & Chronic Inflammation
General Introduction
1. Inflammation (Preamble)
2. Acute Inflammation
3. Chronic Inflammation
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Acute & Chronic Inflammation
General Introduction
Definition
Terminology
Main Types of Inflammation
Types of Inflammatory Cells
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Acute Inflammation - Outline
Definition
Cardinal Signs of Inflammation
Causes of Acute Inflammation
Aims of Inflammation
Classification (Other Types of Inflammation)
Types of Inflammation Based on Exudate:
Types of Inflammation Based on Histological Features
Types of Inflammation Based on Causative Agent
Stages of Acute Inflammation
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Chronic Inflammation - Outline
Definition
Causes
Mechanisms
Classification
General Features
Cells of Chronic Inflammation
Mixed Acute & Chronic Inflammation
Chronic Suppurative Inflammation
Recurrent Acute Inflammation
Granulomatous Inflammation
Definition
What is a Granuloma
Causes of Granulomatous Inflammation
Mechanism of Granuloma Formation
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Inflammation
Preamble
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Definition
Inflammation is the body reaction
against injury or irritant
Is not synonym for infection
Only affects living tissue
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Terminology
Greek or English prefix + -itis
gingivitis, metritis, pulpitis, nephritis
and son on .....
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Main Types of Inflammation
Peracute: Very rapid onset and fulminating
Acute: Rapid onset and of shorter duration
Subacute: Slower onset with longer duration
than acute
Chronic: Slowest onset with protracted
duration
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Types of Inflammatory Cells
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Types of Inflammatory Cells
1. Function (phagocytosis)
• Phagocytic cells
– Monocytes (histiocytes, macrophages)
– PNL (particularly neutrophils)
• Non-phagocytic cells
– Lymphocytes
– Plasma cells
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Types of Inflammatory Cells
2. Presence of absence of cytoplasmic granules:
1. Granulocytes
Polymorph nuclear leukocytes (PNL)
– Neutrophils
– Esinophils
– Basophils
2. Agranulocytes
• Monocytes (histiocytes, macrophages)
• Lymphocytes
• Plasma cells
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Inflammatory Cells
Acute Inflammatory Cells
• PNL – Microphages
Chronic Inflammatory Cells
– Macrophages – Histiocytes – Monocytes
– Lymphocytes
– Plasma cells
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Phagocytic Cells
1. Professional Phagocytic Cells
• PNL, microphages, osteoclasts, odontoclasts,
cementoclasts, other giant cells
2. Non-Professional Phagocytic Cells
• Many as fibroblasts, osteoblasts
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Phagocytosis
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Acute Inflammation
Definition
Cardinal Signs of Inflammation
Causes of Acute Inflammation
Aims of Inflammation
Classification (Other Types of Inflammation)
Types of Inflammation Based on Exudate:
Types of Inflammation Based on Histological Features
Types of Inflammation Based on Causative Agent
Stages of Acute Inflammation
Transient Vasoconstriction
Persistent Vasodilatation and Stasis
Increased Permeability of Vessel Walls
Fluid Exudate and Formation of Edema
Cellular Exudate (Neutrophil Emigration & Accumulation)
Resolution or progression
Chemical Mediators of Inflammation
Factors Involved in the Termination of Acute Inflammation
Outcomes (Consequences) of acute inflammation
Systemic Manifestations of Inflammation
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Definition
A rapid and transient
response to injury or
irritant
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Cardinal Signs of Inflammation
• Calor - heat, resulting from vasodilation of blood vessels
• Rubor - redness, resulting from vasodilation of blood vessels
• Tumor - swelling, resulting from edema
• Dolor - pain. resulting from local release of prostaglandin and kinins
• Functio laesa - loss (or impairment) of function
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Cardinal Signs of Inflammation
1. Heat (calor)
2. Redness (rubor, erythema)
3. Edema (tumor)
4. Pain (dolor)
5. Loss of function (functio laesa)
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Causes of Acute Inflammation
• Infections (e.g., bacterial or viral infection)
• Immune reactions (e.g., reaction to a bee sting)
• Other stimuli:
– Tissue necrosis (e.g., acute myocardial
infarction)
– Trauma, radiation, burns, foreign body (e.g.,
glass, splinter)
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Aims of Inflammation
Is the inflammation beneficial ??????
Yes, inflammation aims at elimination of the noxious agents and restoration of tissue integrity.
But sometimes, one has to pay for this benefit. This payment may be represented in a form of residual scarring or other forms of inflammatory complications.
Inflammation may be harmful as in hypersensitivity, rheumatoid arthritis, anaphylactic reaction and atherosclerosis.
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Classification (Other Types of Inflammation)
Based on Exudate
Based on Histological Features
Based on Causative Agent
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Types of Inflammation Based on Exudate:
1. Suppurative (purulent) inflammation: pus
Localized proliferation of pus-forming organisms,
such as Staphylococcus aureus (e.g., skin abscess).
S. aureus contains coagulase. which cleaves fibrinogen
into fibrin and traps bacteria and neutrophils
Pyogenic bacteria, eg, staphylococci, streptococci,
gram–negative bacilli, anaerobes.
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Types of Inflammation Based on Exudate:
2. Serous inflammation: effusion
Thin, watery exudate
Insufficient amount of fibrinogen to
produce fibrin
Example - blister in second-degree burns,
viral pleuritis
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Types of Inflammation Based on Exudate:
3. Catarrhal inflammation (inflammation of
mucous membranes)
Marked secretion of mucus.
Infections, eg, common cold (rhinovirus);
allergy (e.g. hay fever).
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Types of Inflammation Based on Exudate:
4. Fibrinous inflammation: fibrinogen - fibrin
Due to increased vessel permeability.
with deposition of a fibrin-rich exudate
Often occurs on the serosal lining o f the
pericardium, peritoneum, or pleura
Danger of adhesions
Example: fibrinous pericarditis
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Types of Inflammation Based on Exudate:
5. Pseudomembranous inflammation: surface necrosis
Bacterial toxins damage mucosal lining, producing a membrane composed of necrotic tissue
Example ― pseudomembranes associated with Corynebacterium diphtheriae produces a toxin causing pseudomembrane formation in the pharynx and trachea.
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Types of Inflammation Based on Exudate:
6. Necrotizing inflammation:
Marked tissue necrosis
Highly virulent organisms (bacterial, viral,
fungal), eg, plague (Yersinia pestis),
anthrax (Bacillus anthracis),
mucormycosis, maxillofacial gangrene
(noma).
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Types of Inflammation Based on Exudate:
7. Hemorrhagic inflammation:
Destruction of blood vessel walls resulting
in leakage of a large number of red blood
cells resulting in the red coloration of
inflammatory exudate.
Example ― Epidemic hemorrhagic fever,
Leptospirosis and Plague.
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Types of Inflammation Based on Exudate:
8. Ulcerative inflammation:
Necrosis on or near the surface leads to
loss of tissue and creation of a local defect
(ulcer)
Example ― Ulcerative colitis
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Types of Inflammation Based on Exudate:
9. Granulomatous inflammation:
Is a distinct type of chronic inflammation
characterized by formation of granuloma
Example ― TB, syphilis, actinomycosis
and leprosy
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Serous Exodate
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Serous Inflammation
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Fibrinous Exodate
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Purulent Exodate
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Types of Inflammation Based on Histological Features
• Nonspecific: Produce non-specific
histologic picture
• Specific: Produce a specific histologic
picture that is peculiar to that type of
infection e.g. TB.
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Types of Inflammation Based on Causative Agent
• Aseptic (sterile) - chemical substances,
radiation
• Septic (caused by living organisms)
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Stages of Inflammation
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Stages of Acute Inflammation
1. Transient Vasoconstriction
2. Persistent Vasodilatation and Stasis
3. Increased Permeability of Vessel Walls
4. Fluid Exudate and Formation of Edema
5. Cellular Exudate (Neutrophil Emigration &
Accumulation)
6. Resolution or progression
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Stages of Inflammation
1. Transient vasoconstriction
2. Persistent vasodilatation
3. Increased Permeability
4. Fluid exudate (edema)
5. Cellular exudate (Neutrophil emigration & accumulation)
6. Resolution or progression
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Mechanism of Inflammation
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Acute Inflammation – Continue ....
Chemical Mediators of Inflammation
Factors Involved in the Termination of Acute
Inflammation
Outcomes (Consequences) of acute
inflammation
Systemic Manifestations of Inflammation
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Chemical Mediators of Inflammation
Derived from plasma, leukocytes, local tissue,
bacterial products.
Example — arachidonic acid mediators are
released from membrane phospholipids in
macrophages, endothelial cells, and platelets).
They have short half-lives (e.g., seconds to
minutes).
They may have local and systemic effects.
Example — histamine may produce local signs of
itching or systemic signs of anaphylaxis.
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Functions of Chemical Mediators of Inflammation
• Vasodilation; Examples ― histamine, nitric oxide.
• Vasoconstriction; Example ― thromboxane.
• Increase vessel permeability; Example ― histamine, bradykinin.
• Produce pain; Example ― bradykinin
• Produce fever; Examples ― IL-1, T N F
• Chemotactic; Examples ― IL8
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Factors Involved in the Termination of Acute Inflammation
• Short half-life of inflammatory mediators
• Lipoxins
– Anti-inflammatory mediators
– Derive from arachidonic acid metabolites
– Inhibit transmigration and chemotaxis
• Resolvins
– Synthesized from omega-3 fatty acids
– Inhibit production and recruitment of inflammatory cells to the site of inflammation
• Clearance of neutrophils by apoptosis
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Outcomes (Consequences) of acute inflammation
Resolution
Healing by repair or regeneration
Progression into chronic inflammation.
Spread
Direct-e.g. cellulitis
Lymphatic
Blood vessels: Pyaemia - Septicaemia
Death
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Systemic Manifestations of Inflammation
• Pyrexia (fever)
• Negative nitrogen balance
• Increased erythrocyte sedimentation rate
• Anemia
• Leucocytosis
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Chronic Inflammation - Outline
Definition
Causes
Mechanisms
Classification
General Features
Cells of Chronic Inflammation
Lymphocytes and plasma cells
Macrophages
Eosinophils
Basophils
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Chronic Inflammation - Definition
Is the persistence of inflammation with
attempts of repair resulting from
persistence of the injurious agent.
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Chronic Inflammation - Causes
Persisting infection or prolonged exposure to
irritants (intracellular surviving of agents - TB)
Repeated acute inflammations (otitis, rhinitis)
Primary chronic inflammation - low virulence,
sterile inflammations (silicosis)
Autoimmune reactions (rheumatoid arthritis,
glomerulonephritis, multiple sclerosis)
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Chronic Inflammation - Mechanisms -1
• Defective acute inflammatory response
– Poor blood supply
– Poor general nutrition
– Abnormal neutrophil function
– Anti-inflammatory drugs, especially
corticosteroids
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Chronic Inflammation - Mechanisms - 2
• Agent is resistant to phagocytosis and/or
intracellular destruction
– Intracellular infectious agents, e.g. tuberculosis,
salmonellosis, brucellosis, viral infections
– Foreign-body reactions.
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Chronic Inflammation - Mechanisms - 3
• The provoking agent is a body constituent as in:
– Auto-immune diseases, e.g. diffuse lymphocytic
thyroiditis (Hashimoto’s disease), auto-immune
atrophic gastritis, adrenal atrophy, etc.
– Reactions to altered self-antigens, e.g. contact
dermatitis to rubber, nickel, etc.
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Chronic Inflammation - Classification
1. Clinical
– Following acute inflammation, e.g. chronic osteomyelitis
– Arising de novo, e.g. brucellosis, tuberculosis
2. Histological
– Specific - having a reproducible histological pattern, e.g. tuberculosis, syphilis, leprosy
– Non-specific - showing only the general features of inflammation, e.g. chronic pulpitis
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General Features
1. Continuing some features of acute inflammation
– Polymorph infiltration
– Fibrinous exudation
– Increased vascularity
2. Features of healing-repair and/or regeneration
3. Infiltration by chronic inflammatory cells
– Lymphocytes
– Plasma cells
– Macrophages
– Eosinophils
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Cells of Chronic Inflammation
1. Lymphocytes
2. plasma cells
3. Macrophages
4. Eosinophils
5. Basophils
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Mixed Acute & Chronic Inflammation
Features of both types of inflammation may
coexist in certain circumstances, as in
chronic suppurative inflammation and
recurring acute inflammation.
Two Types:
1. Chronic Suppurative Inflammation
2. Recurrent Acute Inflammation
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Chronic Suppurative Inflammation
Example: Chronic suppurative osteomyelitis
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Recurrent Acute Inflammation
Repeated attacks of acute inflammation may occur
if there is a predisposing cause, eg, in the
gallbladder when there are gallstones.
Each attack of acute inflammation is followed by
incomplete resolution.
Depending on the time of examination, the picture
may be mainly that of chronic inflammation or of
acute superimposed on chronic inflammation.
The terms subacute inflammation and acute-on-
chronic inflammation are also used to denote this
pattern.
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Granulomatous Inflammation - Outline
Definition
What is a Granuloma
Causes of Granulomatous Inflammation
Mechanism of Granuloma Formation
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Granulomatous Inflammation - Definition
A distinct pattern of chronic inflammation
characterized by formation of granulation
tissue.
It is a protective response to chronic infection
or foreign material, preventing dissemination
and restricting inflammation.
Some autoimmune diseases such as
rheumatoid arthritis and Crohn’s disease are
also associated with granulomas.
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What is a Granuloma
A granuloma is a localized mass of
granulation tissue with aggregations of
chronic inflammatory cells.
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Granuloma
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Causes of Granulomatous Inflammation
Bacteria: Tuberculosis, Leprosy, Syphilis,
Actinomycosis
Parasites: Schistosomiasis
Fungi: Histoplasmosis, Blastomycosis
Foreign body Granulomas
Endogenous ( keratin, necrotic bone or adipose
tissue uric acid crystals)
Exogenous (wood, silica, asbestos, silicone)
Unknown cause such as sarcoidosis
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Mechanism of Granuloma Formation
The classic example for the immune granuloma is that caused by the TB. In this disease, the granuloma is referred to as a tubercle and is characterized by the presence of central caseous necrosis. Caseating necrosis is rare in other granulomatous diseases.
There are many atypical presentations that it is always necessary to identify the specific etiologic agent by: special stains for organisms (acid-fast stains for tubercle bacilli), culture methods (tuberculosis, fungal disease), and serologic studies (syphilis). In sarcoidosis, the etiologic agent is unknown.
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Mechanism of Granuloma Formation
1. Bacilli are inhaled by droplets
2. Then phagocytosed by alveolar macrophages.
Macrophages fail to digest the phagocytosed
bacteria and accumulate at the site of injury.
3. A localized inflammatory response recruits more
mononuclear cells
4. The granuloma consists of a kernel of infected
macrophages surrounded by foamy macrophages
and a ring of lymphocytes and a fibrous cuff.
5. The granuloma may caseates, ruptures and spills
into the airway