Inflammation
And
Healing
Dr S Porter
University of Cambridge
What is inflammation?
The bodys response to injury
A protective response
Connected to the repair process
resolution
cycle
chronic
acute
Inflammatio
n
sub-acute
bleeding
inflammation
proliferation
remodelling
time
Bacteria
Radiation
Toxin
Virus
Causes
of
inflammation
Chemical
Protozoa
Fungi
Tumour
Immunological
Cardinal signs
Sign
1. Rubor (red)
2. Calor (hot)
3. Tumor (swelling)
4. Dolor (pain)
5. Functio laesa
(loss of function)
Reason
Increased blood flow due to
vascular dilatation gives
redness and heat.
Increased vascular permeability
gives oedema causing swelling.
chemical mediators and
mechanical pressure stimulate
sensory nerve endings giving
pain.
Pain and swelling result in loss
of function.
Fluid escapes from vessels because of
endothelial cell Retraction, opening up
gap-junctions.
Margination-White blood cells move to
the margins of the capillaries Exudation of
protein-rich oedema Emigration- of
polymorphs through vessel wall
Chemotaxis movement towards chemical
mediators
Opsonisation by immunoglobulins on
bacteria provides a fibrin scaffold.
the site of injury
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leukocytes margination rolling adhesion
emigration of:
neutrophils (1-2 days)
monocytes (2-3 days)
chemotaxis
Although migration of cells was detected from the early days of the
development of microscopy (Leeuwenhoek), description of chemotaxis
was first made by T W. Engelmann (1881) and W.F. Pfeffer (1884)
phagocytosis - lysosomal enzymes,
passive emigration of Red blood cells
Histamine
Histamine
Nitric oxide
Cytokines
Cytokines IL-1,
IL-1,
TNF.
TNF.
Serotonin
Chemical
mediators
Substance P
Plasma
Plasma
proteases
proteases and
and
the
the complement
complement
system
Prostaglandins
Arachidonic
Arachidonic
acid
acid metabolites
metabolites
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PHAGOCYTOSIS
Recognition and attachment
Foreign objects coated with
opsonins which attach to
receptors on polymorph surface.
Engulfment
Cell membrane fuses around
an object.
Lysosomes empty into the
vacuole, often before vacuole
has time to seal - this gives
rise to 'regurgitation during
feeding' and enzymatic damage
to surrounding tissue.
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Outcomes of acute inflammation
1.
Resolution - restoration to normal, limited injury
chemical substances neutralized
normalization of vascular permeability
apoptosis of inflammatory cells
lymphatic drainage
2. Scar
tissue destruction
fibrinous inflammtion
purulent inflammation abscess formation (pus)
3. Progress to chronic inflammation
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Chronic inflammation
Causes
persisting infection
prolonged exposure to irritants
repeated acute inflammations (PID, tennis elbow)
sterile inflammation (silicosis)
autoimmune reactions (RA MS)
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When do specific cells appear following trauma?
trauma
capillaries
fibroblast
lymphocyte
Neutrophyl
macrophage
thrombocytes
10
11
12
Days post injury
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The factors affecting healing
Systemic factors
Age
Stress
Ischemia
Diabetes
Obesity
Medication ( NSAIDS)
Alcoholism and smoking
Immunocompromised conditions
Nutrition
15
Local factors
infection
Foreign
body
Delayed
healing
oedema
ischaemia
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Bone healing
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Examples of inflammation:
1
Match the inflammation:
A -Tonsilitis,
D - Bursitis,
B - Appendicitis,
E - Pneumonia,
C - Blister,
F- Rheumatoid Arthritis
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The End