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INFLAMMATION AND HEALING . Inflammation is defined as the local response of living mammalian tissues to injury due to any agent. It is a body defense reaction in order to eliminate or limit the spread of injurious agent as well as to remove the consequent necrosed cell and tissues.
C) SIGNS OF INFLAMMATION
D) TYPES OF INFLAMMATION
E) ACUTE INFLAMMATION
F) REGULATION INFLAMMATION
G) CHEMICAL MEDIATORS OF INFLAMMATION
H) CHRONIC INFLAMMATION
D) WOUND HEALING
E) HEALING IN SPECIALISED TISSUE
Inflammation is defined as the local response
of living mammalian tissues to injury due to
any agent. It is a body defense reaction in
order to eliminate or limit the spread of
injurious agent as well as to remove the
consequent necrosed cell and tissues.
The agents causing inflammation may be as under:
1.Physical agents like heat, cold, radiation, mechanical
2.Chemical agents like organic and inorganic poisons.
3.Infective agents like bacteria, viruses , and their toxins.
4.Immunological agents like cell-mediated and antigen-
Thus inflammation is distinct from infection – the former is
the protective response by the body while the latter is
invasion into the body by harmful microbes and their
resultant ill effects by toxin.
Inflammation involves two processes:
a) inflammatory response
SIGNS OF INFLAMMATION
The famous 5 cardinal signs of inflammation as:
5. Loss of function
TYPES OF INFLAMMATION
Depending upon the defense capacity of the host and duration of
response inflammation can be classified into Acute and Chronic
1. Acute inflammation is a short duration and represents the
early body reaction and is usually followed by repair . The main
features of acute inflammation are:
a) accumulation of fluid and plasma at the affected site.
b) intravascular activation of the platelets
c) polymorphonuclear neutrophils as inflammatory cells.
2. Chronic inflammation is of longer duration and occurs either
after the causative agent of acute inflammation persists for a
long time or the stimulus is such that it induces chronic
inflammation from the beginning. The characteristic feature of
chronic inflammation is presence of chronic inflammatory cells
such as lymphocytes plasma cells and macrophages.
The changes is acute inflammation can be conveniently
described under the following 2 headings:
1. Vascular events
2. Cellular events
Alteration in the microvasculature is the earliest
response to tissue injury. These alterations include :
a) Haemodynamic changes
b) Changes in vascular permeability
A) Haemodynamic changes – the earliest features of inflammatory
response result from changes in the vascular flow and calibre of small
blood vessels in the injured tissues. The sequence of these changes is
1. Irrespective of the type of injury immediate vascular response is of
transient vasoconstriction of arterioles . With mild form of injury the
blood flow may be re-established in 3-5 secs while with more severe
injury vasoconstriction last for about 5 mins.
2. Next follows persistent progressive vasodilatation which involves
mainly the arterioles . Vasodilatation results in increased blood volume
in microvascular bed of the area which is responsible for redness and
warmth at the site of acute inflammation.
3. Progressive vasodilatation in turn may elevate local hydrostatic
pressure resulting in transudation of fluid into extracellular space .
This is responsible for swelling at local site.
4. Slowing or stasis of microcirculation occurs . Slowing is attributed to
increased permeability of microvasculature the results in increased
concentration of red cells.
5. Stasis or slowing is followed by leucocytic margination or peripheral
orientation of leucocytes along the vascular endothelium after this
these move and migrate through gaps between endothelial cells into
the extravascular space. This process is called as emigration .
The reaction elicited is known as triple response or red line response
consisting of following :
1.Red line appears within a few seconds following stroking and results
from local vasodilatation of capillaries and venules.
2.Flare is the bright reddish appearance or flush surrounding the red
line and results in vasodilatation of adjacent arterioles .
3.Wheal is the swelling or edema of the surrounding skin occuring due
to transudation of fluid into the extravascular space .
B) Altered vascular permeability-
PATHOGENESIS- in and around inflamed tissue compartment which
comes from blood plasma by its escape through the endothelial wall
of peripheral vascular bed. In the initial stage the escape of fluid is
due to vasodilatation and consequent elevation in hydrostatic
pressure. This is transudate in nature. The presence of edema due to
increased vascular permeability of microvascular bed .
MECHANISM OF INCREASED VASCULAR PERMEABILITY-
1) CONTRACTION OF ENDOTHELIAL CELLS-This is most common mechanism
of increased leakiness that affects venules exclusively while capillaries and
arterioles remain unaffected . The endothelial cells develop temporary
gaps between them due to their contraction resulting in vascular leakiness.
It is mediated by histamine
2) RETRACTION OF ENDOTHELIAL CELLS- in this mechanism there is
structural re-organisation of the cytoskeleton of endothelial cells that
causes reversible retraction at the intercellular junctions. This change too
affects the venules and is mediated by cytokines such as interleukin -1.
3) DIRECT INJURY TO ENDOTHELIAL CELLS- Direct injury to the endothelial
causes cell necrosis and appearance of physical gaps at the sites of
detached endothelial cells . Process of thrombosis is intiated at the site of
endothelial cells .
4) ENDOTHELIAL INJURY MEDIATED BY LEUCOCYTES –Adherence of
leucocytes to the endothelium at the site of inflammation may result in
activation of leucocytes. The activated leucocytes release proteolytic
enzymes and toxic oxygen species which may cause increased vascular
leakiness and endothelial injury.
5) NEOVASCULARISATION- In addition the newly formed capillaries under the
influence of vascular endothelial growth factor during the process of repair
and in tumors are excessively leaky.
The cellular phase of inflammation consists of 2 processes:
1. Exudation of leucocytes
1.Exudation of leucocytes- the escape of leucocytes from the lumen of
microvasculature to the interstitial tissue is the most important feature of
inflammatory response .the acute inflammation includes first line of body
defense followed by monocytes and macrophages . The changes leading
to migration of leucocytes are:
a) Changes in the formed elements of blood- in the early stage of
inflammation the rate of flow of blood is increased due to vasodilatation .
But subsequently there is slowing of blood stream. 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) Rolling and adhesion- Peripherally margination and pavemented
neutrophils slowly roll over the endothelial cells lining the vessel
walls. This is followed by transient bond between the leucocytes and
endothelial cells becoming firmer. It includes 3 phases:
3)immunoglobulins superfamily adhesion molecules
c)Emigration –after sticking of neutrophils to endothelium the former
move along the endothelial cells is found 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 locally with secreted
collagenases and escape into the extravascular space this is known as
d) Chemotaxis-The chemotactic factor ( cytokines, platelet factor etc)
mediated transmigration of leucocytes after crossing several barriers
( endothelium, basement membrane , etc) to reach the interstitial
tissues is called chemotaxis
2.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. There are mainly two
types of phagocytic cells:
a) Polymorphonuclear neutrophils (PMNs) which appear early in acute
inflammatory response also called as microphages.
b) Circulating monocytes and fixed tissue mononuclear phagocytes
called macrophages .
The process of phagocytosis is similar for both polymorphs and
macrophages and involves the following 4 steps:
1.Recognition and attachment stage(opsonisation)
2. Engulfment stage
3. Secretion stage
4. Digestion or degradation stage
CHEMICAL MEDIATORS OF INFLAMMATION
Chemical factors or permeability factors are of increased
vascular permeability , these are large and increasing
number of endogenous compounds which can enhance
vascular permeability. However, currently many chemical
mediators have been identified which partake in other
processes of acute inflammation as well eg: vasodilatation ,
chemotaxis, fever, pain etc.
The substances acting as chemical mediators of inflammation
may be released from the cells , the plasma, or damaged
tissue itself. They are broadly classified into 2 groups:
1)Mediators released by cells
2)Mediators originating from plasma
1)Cell- derived mediators-
a)Vasoactive amines-these have roles in early inflammatory response
i.e. histamine and serotonin. The main action of histamine are
vasodilatation , increased vascular permeability, itching, and pain.
Stimulation of mast cells and basophils also releases products of
arachidonic acid metabolism including release of slow-reacting
substances of anaphylaxis. Serotonin is less potent mediator of
increased vascular permeability and vasodilatation than histamine.
b)Arachidonic acid metabolites-arachidonic acid is fatty acid,
eicosatraenoic acid and it has two main sources i.e. from diet
directly and conversion of essential fatty acids
c)Lysosomal components-the inflammatory cells neutrophils and
monocytes contain lysosomal granules which on release elaborate a
variety of mediators of inflammmation.
d)Platelet activating factor(PAF)- it is released from IgE- sensatised
basophils or mast cells endothelium and platelets. They increase
vascular permeability , vasodilatation in low concentration ,
2) Plasma- derived mediators-
These include the various products derived from activation and interaction of 4
interlinked systems: kinin, clotting, fibrinolytic, and complement . Each of
these systems has its inhibitors and accelerators in plasma with negative
and positive feedback mechanisms respectively.
REGULATION OF INFLAMMATION
The onset of inflammatory responses outlines above may have potentially
damaging influence on the host tissues as evident in hypersensitivity
conditions . Such self damaging effects are kept in check by the host
mechanisms so as to resolve inflammation . Mechanisms are:
a)Acute phase reactants-these are released in plasma in response to tissue
trauma and infection. These are mainly synthesised in liver and to some
extent in macrophages.
b)Corticosteroids – glucocorticoids act as anti inflammatory agents.
c)Free cytokine receptors- cytokines in serum correlates with disease activity.
d)Suppressor T cells- prohibition of suppressor t cells is seen which inhibits the
function of T and B cells.
e)Anti-inflammatory chemical mediators-it has an anti- inflammatory action.
MORPHOLOGY OF ACUTE INFLAMMATION
1. PSEUDOMEMBRANOUS INFLAMMATION-It is inflammatory
response of mucous surface to toxins of diphtheria or irritant gases.
as a result of denudation of epithelium , plasma exudes on the
surface where it coagulates and together with necrosed epithelium.
2. ULCER- ulcers are local defects von the surface of an organ
produced inflammation. Common sites for ulceration are the
stomach, intestinal ulcers in typhoid fever , ulcers of legs. in the
acute stage there is infiltration by polymorphs with vasodilatation
while long standing ulcers develop infiltration by lymphocytes and
3. SUPPURATION(ABSCESS FORMATION)-When acute bacterial
infection is accompanies by intense neutrophilic infiltrate in the
inflamed tissue, it results in tissue necrosis. A cavity is formed which
is called abscess and contains a pus and process of abscess
formation is called suppuration.
4.CELLULITIS- it is a diffuse inflammation of soft tissue resulting from
spreading effects of substances like hyaluronidase released by some
5.BACTERIAL INFECTION OF BLOOD-This includes: a) bacteraemia
b) Septicaemia means presence of rapidly multiplying highly pathogenic
bacteria in the blood
SYSTEMIC EFFECTS OF ACUTE INFLAMMATION
1.FEVER- occurs due to bacteraemia . It is thought be mediated through
release of factors like prostaglandins, interleukins and tumor necrosis factor
in response to infection.
2.LEUCOCYTOSIS- Commonly accompanies the acute inflammatory reactions .
Typhoid fever is an acute inflammation however induces leucopenia with
3.LYMPHANGITIS- It is one of the important manifestations of localised
inflammatory injury. The lyphatics and lymph nodes that drain the inflamed
tissues show reactive inflammatory changes in the form of lymphangitis .
4.SHOCK- It may occur in severe cases. Massive release of cytokine a mediator
of inflammation in response to severe tissue injury results in profuse
systemic vasodilatation , increased vascular permeability and intravascular
volume loss. The net effect of these changes is hypotension and shock.
FATE OF ACUTE INFLAMMATION
The acute inflammation process can culminate in one of the 4 outcomes:
1.RESOLUTION-It means complete return to normal tissue following acute
inflammation . This occur when tissue changes are slight and cellular
changes are reversible.
2.HEALING-This takes place when tissue destruction in acute inflammation is
extensive so that there is no tissue regeneration but there is actually
healing by fibrosis.
3.SUPPURATION-When the pyogenic bacteria causing acute inflammation
result in severe tissue necrosis the process proresses to suppuration. Intially
there is intense neutrophillic infiltration.
4.CHRONIC INFLAMMATION-The acute inflammation may progress to chronic
inflammation in which the processes of inflammation and healing proceed
side by side.
DEFINITION AND CAUSES: Chronic inflammation is defined as
prolonged process in which tissue destruction and
inflammation occur at same time.
Causes: 1.Chronic inflammation following acute inflammation
–when the tissue destruction is extensive or the bacteria
survive and persist in small numbers at the site of acute
2. Recurrent attacks of acute inflammation- when repeated
bouts of acute inflammation culminate in chronicity of the
process e.g. recurrent urinary tract infection .
3. Chronic inflammation starting de novo- when the infection
with organism of low pathogenicity is chronic from the
beginning. E.g. infection with Myobacterium tuberculosis
GENERAL FEATURES OF CHRONIC INFLAMMATION
1.MONONUCLEAR CELL INFILTRATION-chronic inflammatory
lesions are infiltrated by mononuclear inflammatory cells like
phagocytes and lymphoid cells. The blood monocytes on reaching the
extravascular space transform into tissue macrophages .besides the
role of macrophages in phagocytosis they may get activated in
response to stimuli such as cytokines.
2. TISSUE DESTRUCTION OR NECROSIS-Tissue destruction and
necrosis are central feature of most forms of chronic inflammatory
lesions. This is brought by activated macrophages which release a
variety of biologically active substances. E.g. protease, lipase .etc.
3. PROLIFERATIVE CHANGES –As a result of necrosis proliferation
of small blood vessels and fibroblast is stimulated resulting in
formation of inflammatory granulation tissue. Eventually healing by
fibrosis and collagen laying takes place.
2. TISSUE DESTRUCTION OR NECROSIS-Tissue
destruction and necrosis are central feature of most forms
of chronic inflammatory lesions. This is brought by
activated macrophages which release a variety of
biologically active substances. E.g. protease, lipase .etc.
3. PROLIFERATIVE CHANGES –As a result of necrosis
proliferation of small blood vessels and fibroblast is
stimulated resulting in formation of inflammatory
granulation tissue. Eventually healing by fibrosis and
collagen laying takes place.
1.FEVER-Invariably there is mild fever often with loss of weight and
2.ANAEMIA-Chronic inflammation is accompanied by anaemia of
4.ESR- It is elevated
5.AMYLOIDOSIS-Longer term cases of chronic suppurative
inflammation may develop secondary systemic amyloidosis.
TYPES OF CHRONIC INFLAMMATION
1.NON-SPECIFIC-When the irritant substance produces a non-specific
chronic inflammatory reaction with formation of granulation tissue
and healing by fibrosis , like chronic ulcer.
2.SPECIFIC-When injurious agent causes a characteristic histologic tissue
response like, tuberculosis.
Injury to tissue may result in cell death and tissue destruction.
Healing on the other hand is the body response to injury in
an attempt to restore normal structure and function. The
process of healing involves 2 processes:
1. Regeneration-when healing takes place by proliferation of
parenchymal cells and usually results in complete
restoration of the original tissue .
2. Repair – when the healing takes place by proliferation of
connective tissue elements resulting in fibrosis and
Some parenchymal cells are short lived while others have long lifespan.
In order to maintain proper structure of tissues these cells are under
the constant regulatory control of their cell cycle. These include
growth factor such as :epidermal growth factor , fibroblast growth
factor, platelet growth factor. All the cells divide at different pace ,
depending upon their capacity to divide so they are divided into 3
1. Labile cells :the cells continue to multiply throughout life under
normal physiological condition.
2. Stable cell: these cells decrease or lose their ability to proliferate
after adolescence but retain the capacity to multiply in response to
stimuli throughout the adult life.
3. Permanent cells : these cells lose their ability to proliferate around
the time of birth.
So regeneration of any type of parenchymal cells involve the following 2
1. Proliferation of original cells from the margin of injury with
migration so as to cover the gap.
2. Proliferation of migrated cells with subsequent differentiation and
maturation so as to reconstitute the original tissue.
Repair is the replacement of injured tissue by fibrous tissue. Two
processes are involved in repair:
1. Granulation tissue formation ; and
2. Contraction of wounds
Repair response takes place by participation of mesenchymal cells ,
endothelial cells , macrophages , platelets , and the parenchymal
cells of the injured organ.
Granulation tissue formation- The term granulation tissue
derives its name from slightly granular and pink appearance of the
tissue . Each granule corresponds histologically to proliferation of
new blood vessels which are slightly lifted on surface by thin
covering of fibroblast and young collagen . The 3 following phases :
1. Phase of inflammation : following trauma , blood clots at the
site of injury . There is acute inflammatory response with exudation
of plasma , neutrophils and some monocytes within 24 hours.
2. Phase of clearance : combination of proteolytic enzymes
liberated from neutrophils , autolytic enzymes from dead tissue
cells and phagocytic activity of macrophages clear off the necrotic
tissue , debris and red blood cells.
3. Phase of ingrowth of granulation tissue : the phase consists
of 2 main processes : a) Angiogenesis : formation of new blood
vessels at the site of injury takes place by proliferation of
endothelial cells from the margins of severed blood vessels. Initially,
the proliferated endothelial cells are solid buds but within few
hours develop lumen and start carrying blood . Soon these blood
vessels differentiate into muscular arterioles thin walled . The
process of angiogenesis is stimulated by proteolytic destruction of
basement membrane .
b) fibrogenesis : the newly formed blood vessels are present in
amorphous ground substance . The new fibroblast originate from
fibrocytes as well as by mitotic division of fibroblasts. Some of these
fibroblasts have combination of morphologic and functional
characteristics of smooth muscle cells. Collagen fibrils begin to
appear by about 6th day. More and more collagen fibres are formed
and new blood vessels decrease. This results in formation of inactive
looking scar known as cicatrisation.
Contraction Of Wound – the wound starts contracting after 2-3
days and the process by the 14th day. During this period the wound is
reduced by approximately 80% of its original size. Contracted wound
results in rapid healing since lesser surface of injured tissue has to be
replaced. In order to explain the mechanism of wound contraction a
number of factors have been proposed :
1. Dehydration as result of removal of fluid by drying of wound.
2. Contraction of collagen
3. Discovery of myofibroblasts appearing in active granulation tissue .
These cells have features intermediate between fibroblasts and
smooth muscle cells. Their migration into wound area and active
contraction decrease their size.
Healing of skin wounds provides a classical example of combination of
regeneration and repair. This can be accompanied by one of the two
following ways :
1. Healing by first intention (primary union)
2. Healing by second intention ( secondary union)
Healing by first intention
This is defined as healing of wound which has following features :
a) Clean and uninfected
b) Surgically incised
c) Without much loss of cells and tissue
d) Edges of wound and approximated by surgical sutures.
The events in primary union are :
- Initial haemorrhage – immediately after injury the space between the
approximated surface of incised wound filled with blood which then
clots and seals the wound against dehydration and infection.
- Acute inflammatory response - this occurs within 24 hrs of
appearance of polymorphs from the margins of incision . By 3rd day ,
polymorphs are replaced by macrophages.
- Epithelial changes – the basal cells of epidermis form both the cut
margins start proliferating and migrating towards incisional space in
the form of epithelial spurs. The migrated epithelial cells separate the
underlying viable dermis from the overlying necrotic material and
clot forming scab which casts off . By 5th day multilayered new
epidermis in formed which is differentiated into superficial and
- Organisation - by the 3rd day fibroblast also invade the wound area.
By the 5th day new collagen fibrils start forming which dominate till
healing is completed . In 4 weeks the scar tissue with scanty cellular
and vascular elements a few inflammatory cells and epithelialised
surface is formed .
- Surface tracks – each suture track is a separate wound and incites the
same phenomena as in healing of primary wound i.e. filling the space
with haemorrhage some inflammatory reactions .when sutures are
removed around 7th day much of epithelialised suture track is avulsed
Healing by second intention
This is defined as healing of wound having the following characteristics :
1. Open with large tissue defect at times infected
2. Having extensive loss of cells and tissues
3. The wound is not approximated by surgical sutures but is left open.
The basic events in secondary union but differ in having larger tissue defect
which has to be bridged . Hence healing takes place from the base
upwards as well as from the margins inwards. This healing is slow , ugly,
scar as compared rapid healing and neat scar of primary union.
- Initial haemorrhage – as a result of injury the wound space is filled with
blood and fibrin clot which dries.
- Inflammatory phase – there is initial acute inflammatory response
followed by appearance of macrophages which clear off the debris as in
- Epithelial changes – epidermal cells from both margins of wounds
proliferate and migrate into wound in form of epithelial spurrs till they
meet in centre and re-epithelialise the gap completely. However epithelial
cells do not cover completely .
- Granulation tissue – the main bulk of secondary healing is by
granulation. Granulation tissue is formed by proliferation of
fibroblasts and neovascularisations from adjoining viable element .
The newly formed granulation tissue is deep red , granular and very
fragile . With time the scar maturation becomes pale andwhite due to
increase in collagen and decrease in vascularity.
- Wound contraction – contraction of wound is an important feature of
secondary healing not seen in primary healing . Due to action in
myofibroblasts present in granulation tissue the wound contracts to
one-third to one-fourth of its original size.
- Presence of infection – bacterial contamination of an open wound
delays the process of healing due to release of bacterial toxins that
provoke necrosis , suppuration and thrombosis.
Complications of wound healing
During the course of healing, following complications may occur :
1. Infection of wound due to entry of bacteria delays the healing.
2. Implantation cyst formation may occur due to persistance of
epithelial cells in wound after healing .
3. Pigmentation – healed wound may at times have rust like colour
due to staining with haemosiderin. Some coloured particulate
material left in the wound may persist .
4. Deficient scar formation – this may occur due to inadequate
formation of granulation tissue.
5. Incisional hernia – a weal scar, especially after laparotomy may be
site of bursting open of wound or an incisional wound.
6. Hypertrophied scars and keloid formation – at time the scar formed
is excessive , ugly and painful. Excessive formation of collagen in
healing may result in formation of keloids.
7. Excessive contraction
Factors Influencing Healing
Two types of factors influence the wound healing :
A. Local factors : 1. infection – most important factor which delays
2. Poor blood supply to wound slows healing
3. Foreign bodies including sutures interfere healing and cause intense
4. Movement delays wound healing
5. Exposure to ionising radiation delays granulation tissue formation .
6. Exposure to ultraviolet light facilitates healing
7. Type , size, location of injury determines whether healing takes place
by resolution or organisation.
B. Systemic factors : 1. age – wound healing is rapid in young and
somewhat slowed in aged
2. Nutrition – deficiency of constituents like proteins, vit. C. and zinc
delays wound healing
3. Systemic infection delays wound healing .
4. Administration of glucocorticoids has anti-inflammatory effect.
5. Uncontrolled diabetics are more prone to develop infection
6. Haematologic abnormalities like defect of neutrophils, and bleeding
disorders slow the process of wound healing.
HEALING IN SPECIALISED TISSUES
In some specialised tissues either repair or regeneration may
predominate . Some of the examples are :
1. Fracture healing
Healing of fracture by callus formation depends on some clinical
considerations whether fracture is
- Traumatic or pathological
- Complete or incomplete
- simple or compound
However basic events in healing of any type of fracture are similar and
resemble healing of skin wound
1. Primary union of fracture occurs in few special situations when the
ends of fracture are approximated as is done by application of
compression clamps. In this case the bony union takes place with
formation of medullary callus without periosteal callus formation.
2. Secondary union is more common process of fracture healing .
Though it is continous process secondary bone union is under 3
a) procallus formation
b) osseous callus formation
Complications of fracture healing : fibrous union may result instead of
osseous union if immobilisation of fractured bone is done.
Non-union : may result if some soft tissue is interposed between
Delayed union : may occur from causes of delayed wound healing in
general such as infection etc.
2. Healing of nervous tissue
Central nervous system : the nerve cells of brain , spinal cord , ganglia
once destroyed are not replaced . Axons of CNS also does not show
any regeneration. The damaged neuroglial cells may show
proliferation of astrocytes called gliosis.
Peripheral nervous system : the peripheral nerves shows regeneration
mainly from proliferation of schwann cells and fibrils from distal end.
3. Healing of muscle
Skeletal muscle :the regeneration of striated muscle is similar to
peripheral nerves. On injury the cut end of muscle fibres retract but
are held together by stromal connective tissue. the injured site is
filled with fibrous material, polymorphs and macrophages.
Smooth muscle : non-striated muscles has limited regenerative capacity
e.g. appearance of smooth muscle in arteriole in granulation tissue.
The smooth lesions are replaced by permanent scar tissue.
Cardiac muscle : destruction of heart muscle is replaced by fibrous
tissue . However the situation where endomysium of indivisual
cardiac fibre is intact, regeneration of cardiac fibre may occur in