WOUND HEALING AND TISSUE

REPAIR

geoeneration :Dead cels are replaced by same parenchumal

cels.
Folouwingresection of alobe of liver for tunour, rest of
eg
the iver regenerates via hyperplasia. tissue.
connective
Repair :Dead cells are replaced by ibrOus
Types of cells

Stable cell Labile cell

Permanent cel

Never divide or
Divide when Continously
required. Low dividing cels.
do not enter the
replicative potential heep entering
cell cycle. Louw
replicative potential eg, parenchymal cel cydle. Eg
liver, PCT and DcT, epithelium, skin,
E.g, Neurons, |bone marrow, GIT.
endothelial cells,
Skeletal and
osteoblasts.
cardiac muscles.

brain injury,repair can happen only by neurolia,

Follouwing a
not neurons.
adapt only by hypertrophy
Skeletaland cardiac muscle can 00:06:18

Repair
During repair space
Active

Neovascularization
Fibrosis
Inftration
withchronic
inlammatory cells
like lymphocytes
6.0 2022
Pathology v4.0 " Marrow
 trssue fornation. forrnation.
lnwmkh ol'repar iraulation blood vessel
qranulaton tissue: Nlew
neovasculari2ation:VEa.
ytokine helping n

Blood vessels

Chronic inflammation 4

red because of new blood

Granulation tissue apppears are leaky.
as these vessels
vessels fornved, and edematous

healna:
Tpes o4 (uOund

wound healing

Healina by primary
Healing by secondary
intention
intention

Cleon ond unintected Lacerated infected

wOund with tissue
uJounds u.ith oppoSed
Inorgins ond no loss and irreqular
trcsue losS. e.g margins.
Surqcol wounds e.q, RTA wounds

Heolng by pruraryntenton
Heal1ing by secondary
intention
 08 Wound Healing 65
and Tissue Repair
Steps in wound healing 00:13:32

Stages of wound healing

Fibroblast

Blood vessel
Subcutoneous fat
Bleeding Hemostasis Inflammation

macrophage
Fibrobloast
(proliferating
Proliferation Remodelling

Stagesi
Stoppaqe of bleeding.
DHemostasis : inlammatory cells heutrophils)
Acute
a) inlammation : injury, This is Pollowed
by proliferation
arrive at the site of
of monocytes, lymphocytes. vía prolifertaion of
Repair occurs
Proliferative phase :
3) macrophages and Abroblasts.
formation.
Remodelling :Scar
4)
(immediate):
At ohours
Hemostasis.
of Abrin.
With the help
clot.
Within a4
hours :
marqins start comingtowards the
Neutrophils Prom of epidermis.
beqins in the basal layer
mitosis
a4-48 hOurs :
After Dense neutrophilic inftrate.
space
Active
formed.
continuous epithelial layer is
Thin
3:
on Day macropghages.
Neutrophils are reploced by
eorly gronulation tissue,
the marqins of wound,
ih ore evident at
collagen fbres

Pathology " v4.0 " Marrow 6.0 "2022

08

On Day s ?
maximum qranulotion tissue.
maxinnum nevascularization.

collagen fbres bridge the incision.

gd week:
Decreased inlammation.
Decreased edema.
Decreased neovasculari2ation.
Increased Hbroblastic proliferation.
maxium collagen.
On Day as:
Scar formation.

In secondary intention :
more inammatory cells.
bigger clot.
more aranulation tissues.
bigger scar.
wound contraction mediated by
here, not seen in primary myotbroblasts occurs
intention.
Ater Iweek i wound reaains I0% of its
Ater 3 months (approx la normal strength.
weeKs):
wound never reaains its orioinal 0-80% of its strength.
strength.
Initialcollogen Pormed is type l
Type llis replaced by Type I collagen.
colagen.
Typei collagen :
more abundant,
Strong and has the highest tensile strenqth.
At the end the ratio of Type
icollagen :Type l colaqen : 41.

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Patholbgy y4.0" Marrow 6.0
 08 Wound Healing 67
and Tissue Repair
Factorsaffecting wound healing 00:26:42

Factors aPMecting
wound healing

LOcal foctors Systemic factors

Diabetes mellitus
Type of injury
Steriods.
Site of injury
malnutrition.
Blood supply
Presence of foreiqn Vitamin Cdetciency
body Zinc deiciency
Infections.

delayed wouund healing : Infections.

most common cause of

Collagens:
Triple helical structure.
hydroxulation and crosslinkingof
VitaminC is required for
collagen.

4types: tensile strength. Seen

in
abundant, maximum
Tupe I : most
tendons.
skin, bones and cartilage.
Present in vitreous humour and
Type I : and aqranulation
tissue.
heloid, uterus
Tupe l : Present in membrane.
Basement
Type V :
defective wound healing
00:31:58
Disorders due to space
Active

Hupertrophic scar
keloid

Pathology " v4.0" Marrow 6.0 2022

eneral 08
athology
Disorders due to deective wound healinoq

Sxcessive qranulation xcess colagen or

tissue excesS SCar

AKa proud lesh. Keloid or formation of

Red in color.
Rx:Cauterization hypertrophic scar

Keloid
Hypertrophic scar
Scar crosses wound marains Scar raised just obove the
Surtace
Donot regresses spontaneously
Spontaneous regression
Thick, haphazard colagen Thin orderls arrangement of
bundles
collagen bundles
massons trichrome stain iS used
for demnonstation

Keloid induction or cosmetic

purposes:

Desmoid:Excessive proliferation of
lbroblostS.
Q.A 19 year old truck
driver is involved in a
olunt force abdominal colision. He incurs
in tissues of the trauma. in response to this
obdomen are stimulated to enter injury ces
of the cell cycle trom the o the al phase
Active
space tupes is most likely to remainphase. which of the Gollouing ce
in Go follouwing this
a. Snooth muscle. iniury
b. endothelium.
C. Skeletal muscle.
d. Fibroblost.

e. Hepotocyte.

Pathology y4.0 " Marrow 6.0" 2022

 08 Wound Healing 69
Q.A 36 year old woman has a and Tissue Repair

removal ot an ovarian cust. sShelaparotoy

recovers
performed or
no complicotions. At the time of uneventully, with
abdominal incision was made. Thesurqery,
a Io cm long midline
tensile strength in the
Surqicol scar ill increase so her normal activities can be
resumed. most of the tensile strength wl likely be achieved
in which of the Pollowing time
periods ?
a. One week.
b. One month.
c. Three months.
d. Six months.
e. One year.

stab wound to the chest. The

Q. Aaa year-old man incurs a
months later
wOund is treated in the emerqency room. Tuwo
intact overlying
there is a Arm, 3xa cm nodular moass with
wound. On examination the
epithelium in the reqion of the This mass is
but not tender, with no erythema.
scar is Hrm,
shows Abroblasts witth abundant
excised and microscopically likely
mechanisms has most
collagen. Which of the following
events ?
produced this series of
a. Keloid formation.
tbrosarcoma.
b. Development of a
from diabetes mellitus.
c. Poor wOund healing
from suturing,
d. Foreign body response infection.
wOund
e. Staphuyloccocal
formation : Chest or sternal
most common site of Keloid
region.
Treatnent of keloid :
Intralesional injections like Triamcilone.
space
Active

Hypertrophic scar regresses spontaneously

Notreotnent required.
Exuberant qranulation tissue treated bycoutery.

Pathology v4.0"Marrow