1. 1

2. Topic Outcomes
At the end of this lecture, students are able to :
1.Describe orally the signs of inflammation
2.Describe and differentiate in written between
acute and chronic inflammation
3.Explain the morphological of types of
inflammation
4.Describe in written the mechanism of healing
and repairing

3. CONTENTS
2.1: Definitions & Concepts Of Inflammation
2.2: Stages Of Inflammation
2.3: Mediators Of Inflammation
2.4: Morphologic Pattern Of Acute & Chronic
Inflammation
2.5: Repair Or Healing
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4. 2.1: Definitions & Concepts Of
Inflammation
• The local response of living mammalian
tissues to injury due to any agent.
• Body defense reaction in order to eliminate or
limit the spread of injurious agent as well as to
remove the consequent necrosed cells and
tissues.
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5. • Causes of inflammation;
i. Physical agent e.g. mechanical trauma, radiation
etc.
ii. Chemical agent e.g. simple chemical poisons,
organic poisons
iii. Infective agents e.g. bacteria, viruses, parasites,
their toxins
iv. Immunological agents e.g. Ag-Ab reaction, cell
mediated
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6. • Involves 2 basic
processes (overlapping):
Inflammatory • Have protective role
response against injurious agents
• Cause considerable
harm to the body
healing eg; anaphylaxis,
atherosclerosis etc
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7. Signs of Inflammation
• The famous 4 cardinal signs of inflammation:
(i) rubor (redness)
(ii) tumor (swelling)
(iii) calor (heat)
(iv) dolor (pain)
Added latest – functio laesa (loss of function)
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8. Heat Redness Swelling Pain Loss Of Func.
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9. 2.2: Stages Of Inflammation
INFLAMMATION
ACUTE CHRONIC
INFLAMMATION INFLAMMATION
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10. • Acute inflammation
– Short duration & represents the early body
reaction and usually followed by repair
– The main features :
(a) Accumulation of fluid & plasma at the
affected site
(b) Intravascular activation of platelets
(c) Polymorphonuclear neutrophils as
inflammatory cells
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11. • Chronic Inflammation
- longer duration and occurs either :
(a) after the causative agent of acute
inflammation persists for a long
time
(b) Stimulus that induces chronic
inflammation from the beginning
- main features :
presence of chronic inflammatory cells
(lymphocytes, plasma cells and
macrophages)

12. I) ACUTE INFLAMMATION
• The changes can be conveniently described
under:
(i) Vascular events
(ii) Cellular events
Infected toenail showing the characteristic redness and
swelling associated with acute inflammation
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13. (i) VASCULAR EVENTS
• Alteration in the microvasculature
(arterioles, capillaries & venules)
• Earliest response to tissue injury
• Alterations includes:
(a) haemodynamic changes
(b) changes in vascular permeability
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14. (a) Haemodynamic Changes
• Earliest features of inflammatory response
result from changes in the vascular flow and
calibre of small blood vessels in the injured
tissue
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15. The sequence of these changes:
Transient vasoconstriction
Persistent progressive vasodilatation
Local hydrostatic pressure
Slowing or stasis
Leucocytic margination
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16. • Lewis Triple Response/ red line response;
(Eg: form stroking with a blunt point)
i. Red line : Appears a few second;
Capillary & venules dilatation
ii. Flare : Bright reddish
appearance/flush surrounding
the red line; Anteriolar dilation
iii. Wheal : Swelling or oedema of the
surrounding skin occurring due
to transudation of fluid into the
extravascular space 17

17. Triple response
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18. (b) Altered vascular permeability
• Vascular changes begin quickly after the injury
but may develop at variables rates, depending on
the nature & severity of the original injury.
• The interchange of fluid between the vascular &
extra vascular space results from balance of fluid
into the vascular space or out into the tissues;
i. Hydrostatic pressure
ii. Oncotic pressure - protein
iii. Osmotic pressure
iv. Lymph flow
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19. Fluid interchange between blood and
extracellular fluid (ECF). (HP = Hydrostatic
pressure, OP = Osmotic pressure)
NO
OEDEMA OEDEMA
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20. Edema
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21. • MECHANISMS OF INCREASED VASCULAR
PERMEABILITY
(i) Endothelial cell contraction
(ii) Endothelial cell retraction
(iii) Direct injury to endothelial cells
(iv) Endothelial injury mediated by leucocytes
(v) Neovascularisation
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22. a) Contraction of endothelial cells
• Microvasculature : venules
• Response type :
Immediate transient (15-30 min)
• Pathogenesis :
Histamine, bradykinin, other chemical
mediators
• Examples : Mild thermal injury
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23. b) Retraction of endothelial cells
• Microvasculature : venules
• Response type :
somewhat delayed (in 4 – 6 hrs)
prolonged (for 24 hrs or more)
• Pathogenesis :
Interleukin-1(IL-1)
Tumor Necrosis Factor (TNF)
• Examples : In vitro experimental work only
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24. c) Direct injury to endothelial cells
• Microvasculature : Arteriols, venules,
capillaries
• Response type :
Immediate sustained leakage (immediate after
injury prolonged (hrs to days)
Delayed sustained leakage (delayed (2-12hrs)
prolonged (hrs-days))
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25. • Pathogenesis :
cell necrosis and detachment
• Examples : Moderate to severe burns, severe
bacterial infection, radiation injury
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26. d) Endothelial injury mediated by
leucocytes
• Microvasculature : venules, capillaries
• Response type :
delayed, prolonged
• Pathogenesis :
Leucocyte activation
• Examples : pulmonary venules and capillaries
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27. e) Neovascularisation
• Microvasculature : All levels
• Response type :
Any type
• Pathogenesis :
Angiogenesis, vascular endothelial growth
factor (VEGF)
• Examples : Healing, tumors
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28. ii) CELLULAR EVENTS
• Cellular events; cells of the acute inflammatory
response are the neutrophils, monocytes &
macrophages.
Polymorphonuclear neutrophils (PMNs)
(within 24 hrs; Life long 24-48 hrs)
Monocytes
Macrophages
(24-48 hrs; Survive much longer) 30

29. • The movements of neutrophils out of the vessels
& their role in combat can be divided into 5
steps;
i. Margination = ?
ii. Adhesion = ?
iii. Emigration/ diapedesis=?
iv. Chemotaxis = ?
v. Phagocytosis & degranulation=?
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30. • Concentrates the leucocytes adjacent to endothelial
wall- Margination
• Adherence of inflammatory cell to the endothelium/
vascular basement membrane- Adhesion
• Neutrophil lodged between endothelial cell and
basement membrane and escape out into the
extravascular space- Diapedesis
• Chemotactic factor mediated transmigration of
leucocytes to reach the interstitial tissue- Chemotaxis
• The process of engulfment of solid particulate material
bt the cell (cell eating)- Phagocytosis
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31. THE INFLAMMATION PROCESS
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32. 34

33. Neutrophil Margination
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34. FATE OF ACUTE INFLAMMATION
• Acute inflammation generally has one of FOUR
(4) outcomes;
i. Resolution – complete return to normal/ tissue
changes are slight and cellular changes are
reversible eg; resolution in lobar pneumonia
ii. Healing by scarrimg– tissue destruction is
extensive, no tissue regeneration; healing by
fibrosis
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35. iii) Suppuration – the progression process of
severe necrosis cause by pyogenic bacteria;
neutrophilic infiltration; form an abcess;
abcess – organised by dense fibrous tissue
and get calcified
iv) Progression to chronic inflammation may
follow acute inflammation, although signs
of chronic inflammation may be present at
the onset of injury; healing proceed side by
side.
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36. An abscess on the skin, showing the redness and swelling characteristic of inflammation. Black rings of
necrotic tissue surround central areas of pus
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37. II) CHRONIC INFLAMMATION
• Chronic inflammation;
prolonged process in which tissue
destruction and inflammation occur
at the same time.
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38. • Caused one of the following 3 ways:
i) Chronic inflammation following acute
inflammation – the tissue destruction is
extensive, or bacteria survive & persist in
small numbers at the site of acute
inflammation
ii) Recurrent attacks of acute inflammation –
repeated bouts of acute inflammation eg;
repeated acute infection of gallbladder
chronic cholecystitis
iii) Starting de novo – infection with organisms
of low pathogenecity (chronic from the
beginning) 40

39. • General features of Chronic inflammation:
i. Infiltration with mononuclear cells
Infiltrated by mononuclear inflammatory cells :
phagocytes & lymphoid cells
phagocytes : circulating monocytes, tissue
macrophages, epithelioid cells, multinucleated
giants cells
ii. Tissue destruction
Central feature of lesions
iii. Proliferative changes
Result of necrosis, proliferation of small vessels
and fibroblasts; healing by fibrosis and collagen
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40. Systemic effects of chronic
inflammation
Associated with following systemic features:
1. Fever – mild fever, loss of weight and
weakness
2. Anemia – varying degree of anemia
3. Leucocytosis - general
4. ESR – elevated in all cases
5. Amyloidosis – long term cases of chronic
suppurative inflammation (secondary
systemic (AA) amyloidosis 42

41. Types of chronic inflammation
NON-SPECIFIC SPECIFIC
• Formation of granulation • Injurious agent causes a
tissue and healing by characteristic histologic
fibrosis tissue response
• Eg; Chronic osteomyelitis, • Eg;
Chronic ulcer tuberculosis, leprosy, syphili
s
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42. Types of chronic inflammation (based
on histological classification)
CHRONIC NON-SPECIFIC CHRONIC GRANULOMATOUS
INFLAMMATION INFLAMMATION
• Characterised by: • Formation of granulomas
(a) non-specific • Eg;
inflammatory cell tuberculosis, leprosy, syphili
infiltration eg; chronic s, sarcoidosis
osteomyelitis, lung abcess
(b) Infiltration by
polymorphs and abcess
formation Eg; Actinomycosis
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43. Granulomatous Inflammation
• Granulomatous inflammation; mechanism whereby the
body deals with certain “indigestible” bacteria, fungi, or
foreign particles.
• Examples;
i. Bacteria e.g. Tuberculosis, Leprosy
ii. Parasitic e.g. Schistosomiasis
iii. Fungal e.g. Blastomycosis, Histoplasma capsulatum
iv. Inorganic metals or dusts e.g. Silicosis
v. Foreign body e.g. Vascular graft
vi. Unknown e.g. Sarcoidosis
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44. INJURY
(e.g; by M. tuberculosis, talc
Failure to digest agent
Weak acute inflammatory response
Persistence of injurious agent
T cell-mediated immune response Poorly digestible agent
•Activation of CD+4 T cells (release of
lymphokines IL-1, IL-2. growth factors
IFN-ˠ and IFN-ɑ)
•Monocyte chemotactic factor
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45. Accumulation of tissue macrophages
(Increased recruitment from circulation, local proliferation)
Macrophages activated by IFN-ˠ
Transformed to epithelioid cells, giant cells
GRANULOMA
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46. Granuloma tissue
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47. • Examples of disorders associated with inflammation
include;
i. Asthma
ii. Autoimmune diseases
iii. Hypersensitivities
iv. Pelvic inflammatory disease
v. Rheumatoid arthritis
vi. Transplant rejection
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48. 2.3: Mediators Of Inflammation
• What are mediators?
i. May be circulating in the plasma or may be produced
locally by cells at the site of inflammation.
ii. Induce their effects by binding to specific reactors on
target cells.
iii. May stimulate target cells to release secondary effector
molecules.
iv. May act on only one or a very few targets.
v. Function is generally tightly regulated.
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49. • 2 types of chemical mediators of Acute inflammation;
i. Plasma-derived mediators e.g. kinin system,
coagulation & fibrinolytic system, complement
system.
ii. Cell-derived mediators e.g. vasoactive amines,
cytokines, platelet activating factor, growth factor.
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50. • Chronic inflammatory cells & mediators;
i. Macrophages
ii. T & B-lymphocytes
iii. Eosinophils
iv. Mast cells
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51. • Inflammatory cells release mediators such as;
i. Cytokines-
(IL-8, interferon-neutrophil)
ii. Vasoactive amines-
(histamine, serotinin- mast cell, basophil, platelet)
iii. Prostanoids-
(arachidonic acid metabolics)
iv. Reactive oxygen intermediates-
(released from activated neutrophil)
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52. • If the mediators in the inflammatory response are
successful;
i. Invading & infectious agents will be removed.
ii. Damaged tissues will be disposed of.
iii. New tissue will be induced to form.
iv. New blood supply to the area will be established.
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53. Chronic inflammation cells
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54. Chronic Inflammation – Lung Abscess
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55. 2.4: Morphologic Patterns Of Acute & Chronic
Inflammation
• Serous inflammation; excessive clear watery
fluid with a variable protein content but no
fibrin e.g. pleural effusion associated with
tuberculosis.
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56. Serous Inflammation - effusion
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57. Serous Inflammation - effusion
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58. • Fibrinous inflammation; the formation of
fibrin is striking e.g. in acute pleurisy.
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59. Fibrinous Inflammation
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60. • Purulent (Suppurative) inflammation;
production of pus is the main characteristic
e.g. abscess & acute apendicitis.
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61. Purulent Inflammation - PUS
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62. Purulent Inflammation - PUS
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63. • Ulceration; complication of many disease
process
• Divided into 2 groups;
i. Simple ulcer
ii. Malignant (cancerous) ulcer
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64. A skin ulcer resulting from infection with Corynebacterium
diphtheriae
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65. Mouth Apthus Ulcer
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66. Gastric Ulcer
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67. 2.5: Repair Or Healing
• The processes that take place during & after
the injury are;
i. Removal of dead & foreign material.
ii. Regeneration of injured tissue from cells
of the same type.
iii. Replacement of damage tissue by new
connective tissue.
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68. • Cells can be divided into 3 major groups;
i. Labile (continuous dividing) e.g. epithelial &
blood cells.
ii. Stable (low level of replication; decrease or lose
their ability to proliferate after adolescence) e.g.
fibroblast, smooth muscle cells, bone & cartilage
cells
iii. Permanent (never divide) e.g. nerve cells, cardiac
myocytes.
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69. HEALING
• 2 processes:
(i) Granulation tissue formation
(ii) Contraction of wounds
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70. (i) Granulation tissue formation
• 3 phases :
(a) PHASE OF INFLAMMATION
trauma, blood clots (site of injury)
acute response :exudation of plasma,
neutrophils, monocytes (24 hours)
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71. (b) PHASE OF CLEARANCE
- proteolytic enzymes from neutrophils
- Autolytic enzymes from dead tissue
cells
- Phagocytic activity : macrophages
(function : clear of the necrotic tissue,
debris & RBCs)
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72. (c) PHASE OF INGROWTH OF GRANULATION
2 main processes:
i. Angiogenesis (neovascularisation)
formation of new blood vessels
ii. Fibrogenesis
formation of fibrocytes and mitotic
division by fibroblasts; myofibroblasts
In 6th days, more collagen is formed
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73. ii) Contraction of wounds
• Start after 2 -3 days; completed: 14th day
• Wound reduced 80% of its original size
• Contraction occur: rapid healing process
• Factors under mechanism of wound
contraction:
(a) dehydration
(b) contraction of collagen
(c) myofibroblasts
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74. WOUND HEALING
1. Healing by first intention (Primary union)
characteristics:
- clean & uninfected
- surgical incised
- without much loss of cells & tissue
- edges of wound – surgical sutures
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75. 2. Healing by second intention (Secondary
union)
Characteristics:
- Large tissue defect
- extensive loss of cells & tissues
- not approximated by surgical sutures but
left open
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76. • 5 stages of healing (primary Union);
i. Initial Haemorrhage
ii. Acute Inflammation response
iii. Epithelial changes
iv. Organization
v. Suture tracks
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77. • 6 stages of healing (secondary Union);
i. Initial Hemorrhage
ii. Inflammation phase
iii. Epithelial changes
iv. Granulation tissue
v. Wound contraction
vi. Presence of infection
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78. • Repair; regeneration of injured tissue by
parenchymal cells of the same type.
• Replacement by connective tissue occur when
repair by parenchymal regeneration alone cannot
be accomplished.
• Involves production of Granulation tissue.
• Replacement of parenchymal cells with
proliferating fibroblasts & vascular endothelial
cells.
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79. Scars present on the skin, evidence of fibrosis &
healing of a wound
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80. Granulation tissue
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81. Healing Skin wound
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82. Healing - Skin scar
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83. • Factors affecting healing;
i. Systemic e.g. age, nutrition, immune
status.
ii. Local e.g. infection, blood supply,
mobility, foreign body.
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84. "Each time you are honest and conduct
yourself with honesty, a success force will
drive you toward greater success. Each
time you lie, even with a little white
lie, there are strong forces pushing you
toward failure."
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85. THANK YOU
FOR YOUR ATTENTION
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