inflammation and wound healing

1. GOOD MORNING

2. INFLAMMATION AND
WOUND HEALING
PRESENTED BY
Dr.R.Balaji
Post graduate
Dept of oral and maxillofacial
surgery
Farooqia Dental college &
Hospital
“A SMILE CAN HEAL A THOUSAND WOUNDS”
-art smith-

3. OVERVIEW Introduction
 Definition of inflammation
 Causes and types of inflammation
 Events in acute inflammation
 Chemical mediators of acute
inflammation
 Factors determining variation of
inflammatory response
 Systemic effects of acute inflammation
 Fate of acute inflammation
 Chronic inflammation and its types
 References

4. INTRODUCTION TO INFLAMMATION
 INFLAMMATION (derived
from LATIN word
inflammare, (To set on
fire)is a localized
protective response
elicited by injury or
destruction of tissues
which serves to destroy
,dilute or wall of both the
injurious agent and
injured tissues

5. DEFINITION
Inflammation is defined as the local
response of living mammalian tissues
to injury due to any agent .It is a
body defence reaction in order to
eliminate or limit the spread of
injurious agent as well as to remove
the consequent necrosed cells and
tissues
.
Terms ending with suffix “itis”denote
inflammation

6. HISTORY OF INFLAMMATION
• Aulus celsus ,a Roman physician and
medical writer (1st century AD) named 4
cardinal signs of inflammation saying
‘”rubor et tumour cum calore et
dolore”(meaning : redness and swelling
come with heat and pain)
• virchow added 5th clinical sign “functio
laesa “ ie loss of function
Cohnheim gave first description of
diapedesis in 1873
John hunter (1973) stated “inflammation is
not a disease but a specific response that has a
salutary effect on its host“

7. CAUSES OF INFLAMMATION
1.INFECTIVE AGENTS like bacteria ,viruses,and their
toxins,fungi,parasites.
2.IMMUNOLOGICAL AGENTS like cell mediated and
antigen antibody reactions.
3.PHYSICAL AGENTS like
heat,cold,radiation,mechanical trauma
4.CHEMICAL AGENTS like organic and inorganic
poisons
5.INERT MATERIALS such as foreign bodies

8. INFLAMMATION
• Protective
response by body
INFECTION
• Invasion of harmful
microbes into the body
and their resultant ill
effects by toxins

9. CARDINAL SIGNS OF INFLAMMATION

10. SIGNS OF INFLAMMATION SEEN IN A POST EXTRACTION
PATIENT

11. TYPES OF INFLAMMATION
ACUTE INFLAMMATION CHRONIC INFLAMMATION
(Depending upon the defence capacity of the host and duration of response)
• Rapid onset
• Slow duration
• Accumulation of fluids
and plasma at the
affected site
• Polymorphonuclear
neutrophils as
inflammatory cells
• Represents early body
reactions followed by
repair
• Slower onset
• Longer duration
• Occurs after the causative
inflammation persist for a
longer time
• Lymphocytes ,plasma
cells,macrophages are
chronic inflammatory cells
• Simultaneous inflammation
and repair

12. ACUTE INFLAMMATION
CHANGES IN
ACUTE
INFLAMMATION
VASCULAR
EVENTS
CELLULAR
EVENTS
HAEMO
DYNAMIC
CHANGES
CHANGES IN
VASCULAR
PERMEABILITY
1)
2)
EXUDATION OF
LEUCOCYTES
PHAGOCYTOSI
S

13. SEQUENCE OF HAEMODYNAMIC CHANGES
TRANSIENT
VASOCONSTRICTION
PERSISTANT
PROGRESSIVE
VASODILATION
ELEVATION OF LOCAL
HYDROSTATIC
PRESSURE
STASIS OF
MICROCIRCULATION
EMIGRATION

14. STRUCTURE OF BLOOD VESSEL

15. LEWIS TRIPLE RESPONSE (OR) RED LINE RESPONSEThe features of haemodynamic
changes in inflammation are best
demonstrated by Lewis.
He induced the changes
in the skin of the inner aspect of
forearm by firm stroking with a
blunt point.The reaction elicited is
known as ”red line response” or
“triple response”

16. LEWIS TRIPLE RESPONSE
1) Red line (vasodilation of
micro vasculature)
2) Flare (bright reddish
appearance surrounding the
red line due to vasodilation of
adjacent arterioles)
3)wheal(swelling or oedema
due to transudation of fluid)

17. BODY FLUID COMPARTMENTS
INTRACELLULAR FLUID
COMPARTMENT
EXTRACELLULAR FLUID
COMPARTMENTS
INTRAVASCULAR FLUID
(plasma)
EXTRAVASCULAR FLUID
INTERSTITIAL FLUID TRANSCELLULAR FLUID

18. CHANGES IN VASCULAR PERMEABILITY
The appearance of Inflammatory oedema due to
increased vascular permeability of microvasculature
bed is explained on the basis of “STARLINGS
HYPOTHESIS”
In normal circumstances ,the fluid balance is
maintained by two sets of forces
1)Forces that causes outward movement of fluid
from microcirculation are INTRAVASCULAR
HYDROSTATIC PRESSURE AND OSMOTIC
PRESSURE OF INTERSTITIAL FLUID
2)Forces that causes inward movement of fluid into
circulation are INTRAVASCULAR OSMOTIC
PRESSURE AND HYDROSTATIC PRESSURE OF
INTERSTITIAL FLUID

19. Left over fluid in the interstitial compartment is
drained away by lymphatics and thus no oedema
results normally
IN INFLAMED TISSUE
 Endothelial lining of microvasculature
becomes more leaky
 Consequently ,intravascular osmotic
pressure decreases and osmotic pressure of
interstitial fluid increases resulting in
excessive out flow of fluid into the interstitial
compartment which is exudative inflammatory
oedema

21. MECHANISM OF INCREASED VASCULAR
PERMEABILITY 1)ENDOTHELIAL CELL
CONTRACTION
MICROVASCULATURE ;VENULES
RESPONSE TYPE ;IMMEDIATE (15-
30min)
PATHOGENISIS ;BY MEDIATORS LIKE
HISTAMINS,BRADIKININS,OTHERS
EXAMPLE ;MILD THERMAL INJURY
2)DIRECT ENDOTHELIAL CELL
INJURY
MICROVASCULATURE;ALL,
RESPONSE TYPE ;IMMEDIATELY AFTER
INJURY AND LAST FOR SEVERAL HOURS OR
DAYS
PATHOGENISIS;CELL NECROSIS AND
DETACHMENT
EXAMPLE; MODERATE TO SEVERE
BURNS,BACTERIAL INFECTION,ETC

22. 3)LEUCOCYTE MEDIATED
ENDOTHELIAL INJURY
MICROVASCULATURE
;VENULES,CAPILARIES
RESPONSE TYPE ;DELAYED
PROLONGED
PATHOGENESIS; ACTIVATED
LEUCOCYTES
EXAMPLE; PULMANARY VENULES
AND CAPILARIES
4)ENDOTHELIAL CELL
RETRACTION
MICROVASCULATURE;VENULES
RESPONSE TYPE ;DELAYED
PROLONGED
PATHOGENESIS ;IL-1.TNF
EXAMPLE ;INVITRO ONLY

23. Transudate and exudate

24. CELLULAR
EVENTS OF
INFLAMMATION
EXUDATION OF
LEUCOCYTES
PHAGOCYTOSI
S

25. EXUDATION OF LEUCOCYTES
1)MARGINATION AND
PAVEMENTING
a) Due to slowing and stasis ,the
central stream of cells widens and
peripheral plasma zone becomes
narrower because of loss of plasma
by exudation.This phenomenon is
known as margination
b) As a result of redistribution ,the
neutrophils of the central column
come close to the vessel wall,This is
known as pavementing

26. 2)ADHESION OR ROLLING
Peripherally marginated and pavemented
neutrophils sticks briefly to the endothelial cells
lining the vessel wall or roll over it.This
phenomenon of adherence of the leucocytes to
the vascular endothelium is known as ADHESION.
This adhesion is brought about by 4 types of
distinct adhesion molecules
1)selectins
2)addressins
3)Integrins
4)Immuoglobulin super family adhesion
molecule

27. ADHESION AND EMIGRATION

28. 3)EMIGRATION
After sticking of neutrophils to
endothelium,they move along the endothelial
surface where the neutrophils throw out
cytoplasmic pseudopods.Subsequently ,the
neutrophils lodged between the endothelial cells
and basement membrane cross the basement
membrane by damaging it with secreted
collagenases and escape out into extravascular
space.This process is known as Emigration

29. DIAPEDESIS
The passive phenomenon in which
RBC’s are forced out by raised
hydrostatic pressure through
endothelial defects left after
emigration of leucocytes ,this is known
as diapedesis
Diapedesis gives haemorrhagic
appearance to the inflammatory
exudate

30. CHEMOTAXIS
The chemotactic factor mediated transmigration of
leucocytes from the vessel lumen into a damaged
area is called chemotaxis
The agents acting as chemotactic substances for
different leucocytes are called as chemokines which
are diffused from area of tissue damage .

31. a)Leukotriene B4
b)Platelet factor 4 (PF4)
c)Components of complement
system (C5a,in particular)
d)Cytokines (IL-8)
e)Monocyte chemoattractant
protein(MCP-1)
f)Eotaxin(chemotactic for
eosinophils)
CHEMOKINES

32. PHAGOCYTOSIS
Phagocytosis is defined as the process of
engulfment of solid particulate material by the
cells(cell eating)
The cells performing this function are
called phagocytes

33. PHAGOCYTES
Polymorpho nuclear
neutrophils(PMNs)
or Microphages
Macrophage
TWO MAIN TYPES OF PHAGOCYTIC CELLS

34. STAGES IN PHAGOCYTOSIS
1)ATTACHMENT STAGE
• Opsonised microbes attaches to
phagocytic surface receptors
• Opsonin are naturally occurring factors
in the serum
• Two main opsonins present in the serum
are IgG opsonin and C3b opsonin and
their corresponding receptors on the
surface of phagocytes

35. • Cytoplasmic extensions surround and engulf
the bound opsonised microbe by formation
of pseudopods around the particle
,enveloping it in a phagocytic vacuole or
phagosome
• This phagosome fuses with the lysosome of
cell to form phagolysosome
2)ENGULFMENT STAGE

37. 3)SECRETION (DEGRANULATION)
STAGE
• The preformed granule-stored products of PMNs
are discharged or secreted into the phagosome
and extracellular environment
• Besides discharge of preformed granule,Phagocytes
synthesise and secrete certain substances like
• a) Enzymes ;interleukin 2 and 6,TNF
• b)Arachidonic acid
metabolites;eg;prostaglandins and leukotriens
• c)Oxygen metabolites like super
oxide,hydrogen peroxide,hypochlorous acids etc

38. DEGRANULATION

39. 4)KILLING (OR) DEGRADATION STAGE
• In this stage the microbes embedded in phagosome is
killed by antimicrobial or bactericidal substances
present in granules of phagocytes and degraded by
hydrolytic enzymes synthesised by phagocytes
• These antimicrobial agents acts by either of the
following mechanisms;
• a)Oxygen dependant bactericidal
mechanism(NADPH Oxidase)
• b)oxygen independent bacterial
mechanism(lysosomal hydrolases,defensins,cationic
proteins)
• c)Nitric oxide mechanism

40. OXYGEN DEPENDANT BACTERICIDAL MECHANISM
2O2 2O’2
(Super oxide)
NADPH oxidase
NADPH
NADPH oxidase
NADP + H+
2O’2 + 2H H2O2
( BACTERICIDAL)
from phagocytic cell membrane

41. MPO(Myeloperoxidase) - DEPENDENT KILLING
H2O2 HOCl + H2O
MPO
Cl ,Br ,I
( HOCl is more potent anti
bacterial agent than H2O2)
MPO(Myeloperoxidase)-INDEPENDENT KILLING(matured macrophages)
H2O2
OH’
OH’
O’2
Haber-weiss
reaction
Fe
++
Fenton reaction
(Hydroxyl radical)

42. CHEMICAL MEDIATORS OF INFLAMMATION

43. VASOACTIVE AMINES
HISTAMINE
Histamine is stored in the granules of mast
cells,basophils,and platelets
Histamine is released from these cells by various agents
like
a)stimuli or substances inducing acute inflammation
eg;heat ,cold,trauma,irritant chemicals etc
b) Histamine releasing factors from
neutrophils,monocytes,and platelets,
c)Neuropeptides
d) Interleukins
The main action of histamine are vasodilation,increase vascular
permeability,itching and pain

44. 5-HYDROXYTRYPTAMINE(5-HT OR
SERATONIN )
It is present in tissues like chromaffin
cells of GIT,spleen,nervous tissues,mast
cells,and platelets
 The action of Serotonin is similar
to histamine but it is a less potent
mediator of increased permeability and
vasodilation than histamine

45. ARACHIDONIC ACID METABOLITES
 Arachidonic acid is a fatty acids
 Two main sources are from diet directly
and conversion of essential fatty acid
,linoleic acid to arachidonic acid
Arachidonic acid metabolites are obtained via
two main pathways
a)Cyclo-oxygenase
pathway(prostaglandins,
thromboxaneA2,protacyclin)
b)lipo-oxygenase pathway(5-HPETE (5-
hydroperoxy eico-satetraenoic acid),Leukotriens)

47. LYSOSOMAL COMPONENTS
The inflammatory cells contains
lysosomal granules which on release elaborate
a variety of mediators of Inflammation,They
are as follows
a)Granules of neutrophils
b)Granules of monocytes and tissue
macrophages

48. a)GRANULES OF NEUTROPHILS
( Lactoferrin,lysozyme,
alkaline
phosphatase,collagenase )
PRIMARY GRANULES
(myeloperoxidase)
SECONDARY GRANULES
Releases mediators like acid
proteases,collagenase,elastase,
and plasminogen
b)GRANULES OF MONOCYTES AND
TISSUE MACROPHAGES

49. PLATELET ACTIVATING FACTOR(PAF)
 It is released from IgE sensitised
basophils,or mast cells
Actions of PAF as mediators of
inflammation are
a)increased vascular permeability
b)vasodilation in low concentration
and vasoconstriction in higher concentration
c)Bronchoconstriction
d)adhesion of leukocytes to
endothelium
e)chemotaxis

50. CYTOKINES
Cytokines are lower molecular weight regulatory
proteins(or glycoproteins(polypeptide substances)
secreted by activated lymphocytes (lymphokines)
and Monocytes(monokines)
 Main cytokines acting as a mediators of
inflammation are as follows
Interleukin-1(IL-1)
Tumour necrosis factor(TNF)
interferons and chemokines

51. OXYGEN METABOLITES
1)They are released from activated
neutrophils and macrophages
2)superoxide,H2O2,,,toxic NO products are
few oxygen metabolites
3) Role of oxygen metabolites as
inflammatory mediators includes vascular
permeability by endothelial cell damage,activation
of protease,damage of other cells,

52. NITRIC OXIDE METABOLITES
 Nitric oxide was originally described as
vascular relaxation factor ,it has recently been
included as a mediators of inflammation
 Nitric oxide has been shown to have
fungicidal and anti parasitic action
 Role of Nitric oxide in the inflammation
are vasodilation,antiplatelet activating
agent,microbicidal action,etc

53. PLASMA DERIVED MEDIATORS (plasma
proteases)
These include various products
derived from activation and interaction of
4 inter linked systems as follows
a)The Kinin system
b) The Clotting system
c)The fibrinolytic system
d)The complement system
Hageman factor (factor XII)(factor of
clotting system plays a key role in
interaction of above four systems

54. FACTOR XII(Hageman factor )
FACTOR XIIa
CLOTTING
SYSTEM
KININ SYSTEM
BRADYKININ
PERMEABILITY
FACTORS
FIBRINOLYTIC
SYSTEM
PLASMIN FIBRIN
FIBRIN SPLIT
PRODUCTS
COMPLEMENT
SYSTEM

55. THE KININ SYSTEM
Kinin system is activated by tissue injury
 Kinin system on activation by factor generates
BRADYKININ
BRADYKININ is a potent chemical mediator which
acts in the early stage of inflammation,
Effects of bradykinin are smooth muscle
Contraction,vasodilation(hypotension), Increases
vascular Permeability(edema), and also involved in
mechanism of pain.

57. THE CLOTTING SYSTEM
Activated Factor XII initiates the cascade of
clotting system resulting in the formation of
fibrinogen which is acted upon by thrombin to
form fibrin and fibrinopeptides
ACTION OF FIBRINOPEPTIDES IN
INFLAMMATION ARE
a)Increased vascular permeability
b)chemotaxis for leucocytes

59. THE FIBRINOLYTIC SYSTEM
 This system is activated
by plasminogen ,the source of
which include kallikerein of
the kinin system,endothelial
cells and leucocytes
 Plasminogen activator acts
on Plaminogen present as
component of plasma proteins
to form plasmin.
Further breakdown of fibrin
by plasmin forms
fibrinopeptides or fibrin split
products

60. THE COMPLEMENT SYSTEM
 The complement system is a part of the
immune system that enhances the ability of
antibodies and phagocytic cells to clear microbes
and damaged cells
The activation of complement system can
occur by
 1)The classical pathway (through
antigen antibody complexes
2)The Alternative pathway (via non
immunologic agents such as bacterial
toxins,IgA,cobra venoms
)

61. Complement system on activation by
either of these two pathways yields
ANAPHYLATOXINS (C3a,C4a,and
C5a)and MEMBRANE ATTACK COMPLEX
(MAC)

63. ACTION OF ANAPHYLOTOXINS IN
INFLAMMATION
 Release of histamine from mast cells and
basophils
Increased vascular permeability
C3a augments for leucocytes
C5a is chemotactic for leucocytes
Action of MAC is to cause pores in the cell
membrane of the invading microbes

64. FEW MORPHOLOGIC VARIETIES OF ACUTE INFLAMMATION
1)PSEUDOMEMBRANOUS
INFLAMMATION
It is a inflammatory
response of mucous surface to
bacterial toxins or irritant gases
resulting with a necrosed
epithelium with a false
membrane covering
example;pseudomembranous
candidiasis,diptheria etc

65. 2)ULCER
ulcer is a inflammatory
lesion on the skin or mucous
membrane resulting from the
gradual disintegration of
surface epithelial tissue
An ulcer may be
superficial or it may extend
into the deeper layer of the skin
or the underlying tissue
example; oral
ulcerations,ulcers of GIT

66. 4)SUPPURATION
When acute bacterial infection
is accompanied by intense
neutrophilic infiltrate in the
inflamed tissue ,it result in
tissue necrosis.
A cavity formed which is
called an abscess and contains
purulent exudate or pus and
the process of abscess
formation is known as
suppuration

67. CELLULITIS
It is a diffuse
inflammation of subcutaneous
connective tissue resulting
from spreading effects of
substances like hyaluronidase
released by some bacteria

68. SYSTEMIC EFFECTS OF
ACUTE INFLAMMATION
ARE
1)LEUCOCYTOSIS
2)LYMPHADENITIS
3)PYREXIA
4)SHOCK (in severe
cases)

69. PYREXIA(FEVER)
Temperature is regulated in the hypothalamus
A trigger of fever called pyrogens ,causes a release
of PGE2 .PGE2 then in turn acts on the hypothalamus
which generates a systemic response back to the
body,causing heat creating effects to match a new
temperature level
Hypothalamus works like a thermostat.when
temperature set point is raised ,the body increases its
temperature through both active generation of heat and
retention of heat

71. FATE OF ACUTE INFLAMMATION
FATE OF ACUTE
INFLAMMATION
RESOLUTION
HEALING BY
SCARING
SUPPURATION
CHRONIC
INFLAMMATION

72. CHRONIC INFLAMMATION
DEFINITION
Chronic inflammation is defined as
prolonged process in which tissue
destruction and inflammation occur at the
same time CAUSES OF CHRONIC INFLAMMATION
CHRONIC
INFLAMMATION
FOLLOWING
ACUTE
INFLAMMATION
PERSISTANT
INFECTION
AUTOIMMUNITY
PROLONGED EXPOSURE
TO TOXIC AGENTS

74. TYPES OF CHRONIC INFLAMMATION
CHRONIC
GRANULOMATOUS
CHRONIC NON SPECIFIC
INFLAMMATION
CHRONIC GRANULOMATOUS INFLAMMATION
It is characterised by formation of
granuloma eg;Tuberculosis,syphils,Actinomycosis
CHRONIC NON SPECIFIC INFLAMMATION
It is characterised by non specific
cell infiltration eg;lung abcess ,osteomylitis

75. GENERAL FEAUTURES OF CHRONIC
INFLAMMATION
Though there may be differences in
chronic inflammatory response depending upon the
tissue involved and causative organism,there are
general features characterise any chronic
inflammation
1)MONONUCLEAR CELL INFILTRATION
2)TISSUE DESTRUCTION
3)PROLIFERATIVE CHANGES

76. MONONUCLEAR CELL INFILTRATION;
1)The macrophages comprise the
most predominant cells in chronic
inflammation
2)Other chronic inflammatory
cells include lymphocytes,plasma cells,mast
cells,eosinophills etc,

77. TISSUE DESTRUCTION OR NECROSIS
Tissue destruction and necrosis are
common in many chronic inflammatory
lesions and are brought about by activated
macrophages by release of variety of biological
active substances
PROLIFERATIVE CHANGES
As a result of necrosis,proliferation of
small blood vessels and fibroblast is stimulated
resulting in formation of inflammatory granulation
tissues.Eventually ,healing by fibrosis and collagen
laying take place

78. MECHANISM OF ACTION OF NASID’S

79. CONCLUSION
“The purpose of
inflammation is to
eliminate the initial cause
of cell injury,clear out
necrotic cells and tissues
damaged from the
original insult and the
inflammatory process,
and to initiate tissue
repair”

80. REFERENCES
Pathology for Dental students –Harshmohan ,2nd
edition
 Robbins Basic pathology –9th edition
Internet

81. WOUND HEALING

82. WOUND
A wound is a break in the integrity of
the skin or tissue often which may be
associated with disruption of the
structure and function
A cut or break in the continuity of any
tissue, caused by injury or operation
(Bailliere’s)

83. CLASSIFICATION OF WOUNDS
RANK AND WAKEFIELD CLASSIFICATION
1)Tidy wounds
2)untidy wounds
CLASSIFICATION BASED ON THICKNESS OF WOUND
a)superficial wound
b)partial thickness wound
c)full thickness wound
d)deep wound
e)complicated wound
f)penetrating wound

84. HEALING
Healing is the body’s response to injury in an attempt to restore normal structure
and function
HEALING
PROCESSE
S
REGENERATIO
N
REPAIR

85. CLASSIFICATION BASED ON TYPE OF WOUND
1)Clean incised wound
2)lacerated wound
3)Brusing and contusion
4)Haematoma
5)puncture wound
6)abrasion
7)crush injury
8)penetrating wounds
CLASSIFICATION OF SURGICAL WOUNDS
1)Clean wound
2)clean contaminated wound
3)contaminated wound
4)dirty infected wound

86. REGENERATION
 When healing takes place by proliferation of
parenchymal cells and usually results in complete
restoration of the original tissues
 The goal of all surgical procedure should be
regeneration which returns the tissues to their normal
microstructure and function
Depending upon their capacity to divide,the cells can be divided intO
LABILE CELLS
STABLE CELLS
PERMANENT CELLS
CELLS

87. REPAIR
 It is a healing outcome in which tissues do not
return to their normal architecture and function
Repair typically results in the formation of scar
tissues
REPAIR PROCESS
GRANULATION TISSUE
FORMATION
CONTRACTION OF WOUNDS

88. GRANULATION TISSUE
 The term granulation tissues derives its name from slightly
granular and pink appearance of the tissue
 Each granule corresponds histologically to proliferation of new
small blood vessels which are slightly lifted on the surface by thin
covering of fibroblast and young collagen

89. FORMATION OF GRANULATION TISSUE
PHASE OF
INFLAMMATION
 (acute inflammatory
response within 24
hours)
PHASE OF CLEARANCE
 proteolytic enzymes from
neutrophils,autolytic
enzymes from dead tissue
cells,phagocytic activity
of macrophages clear off
the necrotic tissues,debris
and rbc
PHASE OF IN GROWTH
OF GRANULATION
ANGI0GENESIS
FORMATION
OF FIBROUS
TISSUE

90. ANGIOGENESIS OR NEO VASCULARISATION
 Proliferation of endothelial cells from the margins of served
blood vessels
 The proliferated cells are solid buds but within a few hours
develop a lumen and start carrying blood
 The newly formed blood vessels are more leaky ,accounting
for the oedematous appearance

91. FIBROUS TISSUE FORMATION
FIBROCYTES (Connective tissue)
FIBROBLAST
NUMBER OF ACTIVE FIBROBLAST
AND NEW BLOOD VESSELS
DECREASES
COLLAGEN FIBRILS(appears by about 6th day)
COLLAGEN
INACTIVE SCAR FORMATION (CICATRISATION)
Maturation

92. CONTRACTION OF WOUND
 The wound starts contracting after 2-3 days and
the process is completed by the 14th day
 During this period wound is reduced by approximately
80 of its original size
 Contracted wound results in rapid healing since lesser
surface area of the injured tissue has to be replaced
CONTRACTION
OF COLLAGEN
DEHYDRATION
MYOFIBROBLAST
MECHANISM
OF WOUND
CONTRACTION

93. WOUND HEALING
 Healing of wound provides a classical example of
combination of regeneration and repair
 Healing of wound can be accomplished in one of the
following two ways
WOUND HEALING
PRIMARY UNION
(Healing by first intension )
SECONDARY UNION
(Healing by second intension )

94.  CHARECTERISTICS OF WOUND HEALING
 PRIMARY UNION SECONDARY UNION
Wound is clean and
uninfected
Without much loss of cells
and tissues
Edges of wound are
approximated by surgical
sutures
 Wound is open with large tissue
defect,at times infected
 Having extensive loss of tissues
 The wound is not approximated
by surgical sutures but is left
open

95. HEALING BY FIRST INTENSION (PRIMARY UNION)
1)INITIAL HAEMORRHAGE
 Immediately after injury,the space
between the approximated surfaces of
incised wound is filled with blood
 The filled blood clots seals the wound
against dehydration and infection
2)ACUTE INFLAMMATORY RESPONSE
 This occurs within 24 hrs with
appearance of PMN from the margins of
incised wound
 By 3rd day ,polymorphs are replaced by
macrophages

96.  3)EPITHELIAL CHANGES
 The basal cells of epidermis from
both the cut margins start
proliferating and migrating
towards incisional space in the
form of epithelial spurs
 These migrated epithelial cells
separate the under lying viable
dermis from the overlying
necrotic material and clot
forming a SCAB
 By 5th day ,a multilayered new
epidermis is formed which is
differentiated into superficial and
deep layers
 A well approximated wound is
covered by a layer of epithelium
in 48hours

97. ORGANISATION
 By 3rd day ,fibroblast
also invade the wound area.
 By 5th day ,new collagen
fibrils start forming which
dominate till healing is
completed
 By 4th week,the scar tissue
with scanty cellular , vascular
elements with few
inflammatory cells and
epithelialised surface is
formed

98. HEALING BY SECONDARY INTENTION(SECONDARY UNION)
1)INITIAL HAEMORRHAGE
 As a result of injury ,the wound
space is filled with blood and fibrin
clot which dries
2)INFLAMMATORY PHASE
 There is an initial acute
inflammatory response followed by
appearence of macrophages which
clear of the debris as in primary union

99.  EPITHELIAL CHANGES
 As in the primary healing, the epidermal cells from both the margins of the
wound proliferate and migrate into the form of epithelial spurs till they meet
in the middle and reepithelialise the gap completely
 These proliferated epithelial cells do not cover the surface fully until
granulation tissue from the base has started filling the wound space
 After these epithelial cells meet in the middle they separate the underlying
viable tissues from necrotic tissue at the surface forming scab

100.  GRANULATION TISSUE FORMATION
 The main bulk of secondary healing
is by granulation
 Granulation tissue is formed by
proliferation of fibroblasts and
neovascularisation from the adjoining
viable elements
 The newly formed granulation tissue is
deep red,granular and very fragile .
 The specialised structure of skin like
hair follicle and sweat glands are not
replaced unless their viable residues
remain which may regenerate

101.  WOUND CONTRACTION
 Contraction of wound is an important feature of
secondary healing ,and not seen in primary healing
 Wound contraction occurs at a time when active
granulation tissues is being formed(approximately 4 to 5
days after wounding )
 Due to the action of myofibroblasts present in granulation
tissue,the wound contracts to one third of its original size
 Maximal contraction occurs for 12 to 15 days although it
will continue if wound remain opens

102. COMPLICATION OF WOUND HEALING
 1)INFECTION
 Due to entry of bacteria
 Delays wound healing
 2)PIGMENTATION
 Healed wounds
may at times have rusted like
colour due to staining with
haemosiderin
 Some coloured particulate
material left in the wound may
persist and impart colour to the
healed wound

103. 3)DEFICIENT SCAR FORMATION
 This may occur due to
inadequate formation of granulation
tissue
 Inadequate scar formation may
result in dehiscence and Ulceration
4)INCISIONAL HERNIA
 Incisional hernia is a type of
hernia caused by an incompletely
healed surgical wound ,
 Hernia that occurs through a
previously made incision,ie the scar
left from a previous surgical
operation
 Commonest sites are abdomen and
inguinal region

104. 5) HYPERTROPHIED SCAR AND KELOID FORMATION
 Hypertrophied scars are excessively formed scars which are
painful and ugly in appearance
 Excessive formation of collagen in healing may result in
keloid(claw like) formation
 Hypertrophied scars differ from keloid by confining to the borders
of initial wound while keloids have tumour like projections of
connective tissue

105. 6) EPIDERMAL CYST FORMATION
 Due to persistence of
epithelial cells in the wound
after healing
7) EXCESSIVE CONTACTION OF WOUND
 An exaggeration of
wound contraction may
result in formation of
contractures or
cicatrisation
eg;Dupuytren’s(palmar)
contracture

106. MARJOLINS ULCER
 Aggressive ulcerating squamous cell carcinoma
presenting in an area of previously traumatized
,chronically inflammed, or scarred skin
 They are commonly present in context of chronic
wounds including burns ,injuries ,venous ulcers
,ulcers from osteomyelitis .and post radiotherapy scars

107. EXTRACELLULAR MATRIX (WOUND STRENGTH
1) The wound is
strengthened by
proliferation of fibroblast
and myofibroblast which
gets structural support from
the extracellular matrix
(ECM)
2) In addition to
providing structural
support ,ECM can direct
cell
migration,attachment,
differentiation,and
organisation

108. 5 MAIN
COMPONENTS
OF ECM
COLLAGEN ADHESIVE
GLYCOPROTEIN
BASEMENT
MEMBRANE
PROTEOGLYCONS
ELASTIC FIBRES

109. FACTORS INFLUENCING WOUND HEALING
LOCAL FACTORS SYSTEMIC FACTORS
 Infection
Delays wound healing
 Poor blood supply
slows healing process
 Foreign bodies
causes intense inflammatory reaction
and infection
 Exposure of ionising radiation
Delays granulation tissue formation
 Type,size&,location of injury
Determines whether healing takes
place by resolution or organisation
 Age
wound healing is rapid in young
age,and somewhat slow in aged people
 Nutrition
Deficiency of constituents like
protein,vitamin C ,zinc delays wound
healing
 Other factors
smoking,obesity,alcohol,stress,etc
 Systemic diseases
Uncontrolled diabetis , Immuno
suppressive diseases like HIV, Auto
immune diseases like SLE,Haematologic
diseases like anemia,neutropenia,bleeding
disorders slows healing process

110. FRACTURE HEALING
BONE FRACTURE
 Bone fracture is a medical
condition in which there is a break
in the structural continuity of bone
or periosteum
Bone fracture can be the result of
high force impact or stress , trauma
or due to certain medical conditions
that weakens the bone
Word fracture derived from latin
word “fractura” means ‘to break’

111. FRACTURE TYPES
 SIMPLE FRACTURE
 COMPOUND FRACTURE
 COMMINUTED FRACTURE
 COMPLICATED FRACTURE
 GREEN STICK FRACTURE
 IMPACTED FRACTURE
 HAIR LINE FRACTURE
 COMPRESSION FRACTURE
 PATHOLOGICAL FRACTURE

112. FRACTURE HEALING
 Fracture healing depends upon the type of fracture
FRACTURE HEALING MECHANISM
PRIMARY UNION SECONDARY UNION
PROCALLUS
FORMATION
OSSEOUS CALLUS
FORMATION
REMODELLING

113. INTERNAL STRUCTURE OF A BONE

114.  Mechanism of bone healing seen when
there is no motion at the fracture site(ie;
Rigid internal fixation )
 Bony union takes place with formation of
medullary callus without periosteal callus
formation
 Slow healing process with extensive bone
necrosis
PRIMARY UNION OF FRACTURE
PRIMARY
FRACTURE UNION
CONTACT HEALING
 Haversian remodelling directly across the
fracture site if no gap exists
GAP HEALING
 Deposition of lamellar bone if small gaps
exists

115. SECONDARY UNION
1)PROCALLUS FORMATION
STEPS INVOLVED IN PROCALLUS
FORMATION
a) HAEMATOMA
 Forms due to bleeding of torn blood
vessels,filling the area surrounding
the fracture
 Loose meshwork is formed by blood
and fibrin clot which acts as frame
work for subsequent granulation
tissue formation

116.  b)INFLAMMATORY RESONSE
 Local inflammatory response
occurs at the site of injury with
exudation of fibrin
,polymorphs,and macrophages
 The macrophages clear away the
fibrin,red blood
cells,inflammatory exudate and
debris
 Fragments of necrosed bone are
scavenged by macrophages and
osteoclasts

117. PROVISIONAL OR PROCALLUS FORMATION
 The cells of the inner layer of the
periosteum have osteogenic potential and
lay down osteoid matrix in the granulation
tissue
 These osteoid undergo calcification to form
woven bone callus
 Woven bone callus consist of woven
bone,and cartilage ,which temporarily
immobilizes the fractured ends
 These woven bone covers the cortex on
either ends of fractured bone and bridges
the gap between the two ends giving spindle
shaped appearance to the union .The
procallus formed is divides into
external,intermediate,and internal procallus

118.  c)FORMATION OF SOFT TISSUE CALLUS
 Ingrowth of granulation tissue
begins with neo vascularisation
and proliferation of mesenchymal
cells from periosteum and
endosteum
 A soft tissue callus is thus
formed which joins the end of
fractured bone without much
strength

119. OSSEOUS CALLUS FORMATION
 The woven bone is cleared away
by incoming osteoclasts and the
calcified cartilage disintegrate
 In their place ,newly formed
blood vessels and osteoblasts
invade
 These osteoblasts lay down
calcified osteiods and as a
result,lamellar bone is formed by
developing haversian system
concentrically around the blood
vessels

120.  3)BONE REMODELLING
 The remodelling process substitutes
the lamellar bone(trabecular bone) with
compact bone
 The Trabecular bone is first resorbed
by osteoclasts,creating a shallow
resorption pit known as “HOWSHIPS
LACUNA”
 Then osteoblast deposit compact bone
within the resorption pit
 As when the compact bone is formed in
place of intermediate callus ,Eventually
the external callus is cleared away,and
the bone marrow cavity develops in
internal callus

121. COMPLICATION OF FRACTURE HEALING
1)FIBROUS UNION
 Occurs if the immobilisation of fractured bone is not done
,occasionally a false joint may develop which is called as pseudo
arthrosis
2) NON UNION
 Results if some soft tissue interposed between the fractured ends
3)DELAYED UNION
 can occur as a result of infection,poor nutrition ,inadequate
blood supply,old age,etc

122. THANK YOU