Wound healing (2) /orthodontic courses by Indian dental academy

WOUND HEALINGWOUND HEALING
INDIAN DENTAL ACADEMYINDIAN DENTAL ACADEMY
LEADER IN CONTINUING EducationLEADER IN CONTINUING Education
indiandentalacademy.comindiandentalacademy.com

CONTENTSCONTENTS
INTRODUCTIONINTRODUCTION
TERMINOLOGIESTERMINOLOGIES
CLASSIFICATION OF WOUNDSCLASSIFICATION OF WOUNDS
HEALINGHEALING
REGENERATIONREGENERATION
A) proliferative potential of different cell typesA) proliferative potential of different cell types
a) labile cellsa) labile cells
b) stable cellsb) stable cells
c) permanent cellsc) permanent cells
B) Regeneration of stable cellsB) Regeneration of stable cells

C) Regeneration of permanent cellsC) Regeneration of permanent cells
REPAIRREPAIR
A) mechanism of healingA) mechanism of healing
B) Chemical mediators of healingB) Chemical mediators of healing
A) Healing by primary intentionA) Healing by primary intention
B) Healing by secondary intentionB) Healing by secondary intention
C) healing of fracturesC) healing of fractures
D) healing of mucosal surfaceD) healing of mucosal surface
E) healing of extraction socketE) healing of extraction socket
FACTORS INFLUENCING WOUND HEALINGFACTORS INFLUENCING WOUND HEALING
COMPLICATIONS OF WOUND HEALINGCOMPLICATIONS OF WOUND HEALING
BASICS OF WOUND HEALINGBASICS OF WOUND HEALINGindiandentalacademy.comindiandentalacademy.com

INTRODUCTIONINTRODUCTION
Wounds and there management are fundamentals to theWounds and there management are fundamentals to the
practice of surgery and medicine. Any elective surgicalpractice of surgery and medicine. Any elective surgical
intervention will result in a wound, in order to gainintervention will result in a wound, in order to gain
access to and deal with the underlying pathology.access to and deal with the underlying pathology.
Injury to tissue may result in cell death and tissueInjury to tissue may result in cell death and tissue
destruction. Healing on the other hand is the bodydestruction. Healing on the other hand is the body
response to injury in a attempt to restore normalresponse to injury in a attempt to restore normal
structure and function.structure and function.

TERMINOLOGIESTERMINOLOGIES
WOUNDWOUND : A wound is a breach in the normal tissue: A wound is a breach in the normal tissue
continuum, resulting in a variety of cellular and molecularcontinuum, resulting in a variety of cellular and molecular
sequelae.sequelae.
REPAIRREPAIR : Replacement of lost tissue by scar tissue: Replacement of lost tissue by scar tissue
formation, this occurs when the surrounding specializedformation, this occurs when the surrounding specialized
cells do not possess the capacity to proliferate.cells do not possess the capacity to proliferate.
REGENERATIONREGENERATION : Replacement of lost tissues by tissue: Replacement of lost tissues by tissue
similar in type. This occurs due to proliferation ofsimilar in type. This occurs due to proliferation of
surrounding undamaged specialized cells.surrounding undamaged specialized cells.
RESOLUTIONRESOLUTION : is the repair that occurs in tissues and: is the repair that occurs in tissues and
tissue spaces with exudates by digestion of the exudationtissue spaces with exudates by digestion of the exudation
and subsequent resorption.and subsequent resorption.

RECONSTITUTION : Replacement of the tissue defectsRECONSTITUTION : Replacement of the tissue defects
by undifferentiated cells.by undifferentiated cells.
ULCER : is any breach in the epithelial surface.ULCER : is any breach in the epithelial surface.
PRESSURE SORES : these are chronic wounds followingPRESSURE SORES : these are chronic wounds following
tissue necrosis from pressure.tissue necrosis from pressure.
SCAR : any mark left after the healing of a wound whereSCAR : any mark left after the healing of a wound where
the damaged tissues fail to repair themselves completelythe damaged tissues fail to repair themselves completely
and are replaced by connective tissue.and are replaced by connective tissue.
DEGENARATION : the deterioration and loss ofDEGENARATION : the deterioration and loss of
specialized function of the cells of a tissue and organ. Thespecialized function of the cells of a tissue and organ. The
changes may be caused by a defective blood supply or bychanges may be caused by a defective blood supply or by
a disease.a disease.

CLASSIFICATIONCLASSIFICATION
ACUTE WOUNDSACUTE WOUNDS ::
a)a) Closed wounds :Closed wounds :
- Bruise/contusion.- Bruise/contusion.
- Hematoma.- Hematoma.
b)b) Open wounds :Open wounds :
- Puncture wounds and Bites.- Puncture wounds and Bites.
- Abrasion and friction burns.- Abrasion and friction burns.
- Lacerations.- Lacerations.
c)c) Complex woundsComplex wounds ::
- Crush/Avulsion.- Crush/Avulsion.
- Internal organs.- Internal organs.
- War wounds and G un shot injuries.- War wounds and G un shot injuries.
- Tissue loss.- Tissue loss.indiandentalacademy.comindiandentalacademy.com

CLASSIFICATIONCLASSIFICATION
d) Injury to special tissuesd) Injury to special tissues ::
- Fat.- Fat.
- Muscle.- Muscle.
- Nerve.- Nerve.
- Artery.- Artery.
- Vein.- Vein.
CHRONIC WOUNDSCHRONIC WOUNDS ::
-- Ulcers.Ulcers.
- Pressure sores.- Pressure sores.

HEALINGHEALING
Healing is the replacement of the deadHealing is the replacement of the dead
or damaged tissue by cells derived fromor damaged tissue by cells derived from
the parenchymal cells or connectivethe parenchymal cells or connective
elements of the injured tissue.elements of the injured tissue.
The process of healing involves 2The process of healing involves 2
distinct processes :distinct processes :
I.I. Regeneration.Regeneration.
II.II. Repair.Repair.

REGENERATIONREGENERATION
when healing takes place by proliferation of thewhen healing takes place by proliferation of the
parenchymal cells and usually results inparenchymal cells and usually results in
complete reconstruction of original tissues.complete reconstruction of original tissues.
Some parenchymal cells are short lived whileSome parenchymal cells are short lived while
others have longer life span. In order toothers have longer life span. In order to
maintain proper structures of tissues, these cellsmaintain proper structures of tissues, these cells
are under constant regulatory control of theirare under constant regulatory control of their
cell cycle.cell cycle.

CELL CYCLECELL CYCLE
Cell cycle is defined as the period between twoCell cycle is defined as the period between two
successive cell divisions and is divided into 4successive cell divisions and is divided into 4
phases.phases.
GG11- pre synthetic growth phase.- pre synthetic growth phase.
S – DNA synthetic phase.S – DNA synthetic phase.
GG22 – premitotic growth phase.– premitotic growth phase.
M – mitotic phase.M – mitotic phase.
GG00 – quiescent cells are in physiologic– quiescent cells are in physiologic
state.state.

Not all cells of body divide at same pace. SomeNot all cells of body divide at same pace. Some
mature cells do not divide at all while othersmature cells do not divide at all while others
complete cell cycle in 16-24hr.complete cell cycle in 16-24hr.
The main difference between slow dividing andThe main difference between slow dividing and
rapidly dividing cells is duration of Grapidly dividing cells is duration of G11 phase.phase.
Entry and progression of cells through the cellEntry and progression of cells through the cell
cycle are controlled by changes in the levels andcycle are controlled by changes in the levels and
activities of a family of proteins called cyclins.activities of a family of proteins called cyclins.

PROLIFERATIVE POTENTIAL OFPROLIFERATIVE POTENTIAL OF
DIFFERENT CELL TYPESDIFFERENT CELL TYPES
The cells of body are divided into three groupsThe cells of body are divided into three groups
on the basis of their regenerative capacity andon the basis of their regenerative capacity and
their relation to the cell cycle.their relation to the cell cycle.
1) labile cells.1) labile cells.
2) stable cells.2) stable cells.
3) permanent cells.3) permanent cells.

LABILE CELLSLABILE CELLS
These cells continue to multiply throughout lifeThese cells continue to multiply throughout life
under normal physiologic conditions.under normal physiologic conditions.
Regeneration occurs from a population of stemRegeneration occurs from a population of stem
cells with relative unlimited capacity tocells with relative unlimited capacity to
proliferate .proliferate .
when a stem cell divides, one daughter cellwhen a stem cell divides, one daughter cell
retains the ability to divide, while othersretains the ability to divide, while others
differentiates into non-mitotic cells that carry ondifferentiates into non-mitotic cells that carry on
normal function of tissues.normal function of tissues.

These include : surface epithelial cells ofThese include : surface epithelial cells of
epidermis, alimentary tract, respiratory tract,epidermis, alimentary tract, respiratory tract,
urinary tract, vagina, cervix, uterineurinary tract, vagina, cervix, uterine
endometrium, hematopoietic cells of boneendometrium, hematopoietic cells of bone
marrow and cells of lymphnodes.marrow and cells of lymphnodes.

STABLE CELLSSTABLE CELLS
These are considered to be quiescent in theirThese are considered to be quiescent in their
normal state but are capable of undergoing rapidnormal state but are capable of undergoing rapid
division in response to injury.division in response to injury.
These include: parenchymal cells of organs likeThese include: parenchymal cells of organs like
liver, pancreas, kidneys, adrenal and thyroid;liver, pancreas, kidneys, adrenal and thyroid;
mesenchymal cells like smooth muscle cells,mesenchymal cells like smooth muscle cells,
fibroblast, vascular endothelium, bone andfibroblast, vascular endothelium, bone and
cartilage cells.cartilage cells.

Permanent cellsPermanent cells
These cells lose their ability to proliferateThese cells lose their ability to proliferate
around the time of birth.around the time of birth.
These include : neurons of nervousThese include : neurons of nervous
system, skeletal muscle and cardiacsystem, skeletal muscle and cardiac
muscle cells.muscle cells.

RELATIONSHIP OF PARENCHYMALRELATIONSHIP OF PARENCHYMAL
CELLS WITH CELL CYCLECELLS WITH CELL CYCLE

Regeneration of any type of parenchymal cellsRegeneration of any type of parenchymal cells
involves following 2 process:involves following 2 process:
1) proliferation of original cells from the1) proliferation of original cells from the
margin of injury with migration so as to covermargin of injury with migration so as to cover
the gap.the gap.
2) proliferation of migrated cells with subsequent2) proliferation of migrated cells with subsequent
differentiation and maturation so as todifferentiation and maturation so as to
reconstitue the original tissuereconstitue the original tissue

REGENERATION OF STABLEREGENERATION OF STABLE
CELLSCELLS
The liver as remarkable power of regenerationThe liver as remarkable power of regeneration
successful regeneration can occur even whensuccessful regeneration can occur even when
nearly 90% of organ is removed.nearly 90% of organ is removed.
A wide range of chemical poisons andA wide range of chemical poisons and
biochemical and metabolic disorders, viralbiochemical and metabolic disorders, viral
infections all produce liver necrosis that may beinfections all produce liver necrosis that may be
focal, zonal or diffuse in distribution.focal, zonal or diffuse in distribution.
For example; the hepatic necrosis induced byFor example; the hepatic necrosis induced by
exposure to carbon tetrachloride chiefly involvesexposure to carbon tetrachloride chiefly involves
the parenchyma around the central veins.the parenchyma around the central veins.

the necrotic cells are removed by lysis andthe necrotic cells are removed by lysis and
phagocytosis, but the supporting stromaphagocytosis, but the supporting stroma
survives.survives.
Proliferation soon occurs in the surviving liverProliferation soon occurs in the surviving liver
cells through out each lobule and new cellscells through out each lobule and new cells
migrate into the centrilobular zones, beingmigrate into the centrilobular zones, being
guided by persistent reticulin framework, whichguided by persistent reticulin framework, which
normally supports the columns of hepatocytes.normally supports the columns of hepatocytes.

Remarkably satisfactory regeneration is achievedRemarkably satisfactory regeneration is achieved
within 2 weeks, but if necrosis is again inducedwithin 2 weeks, but if necrosis is again induced
before regeneration is complete or the lesionbefore regeneration is complete or the lesion
reults in damage of supporting stroma,reults in damage of supporting stroma,
regeneration nodules of liver tissue are formedregeneration nodules of liver tissue are formed
with out restotation of normal architecture.with out restotation of normal architecture.

REGENERATION OF PERMANENTREGENERATION OF PERMANENT
CELLSCELLS
REGENERATION OF PERIPHERAL NERVESREGENERATION OF PERIPHERAL NERVES ::
The divided ends of a sectioned nerve becomeThe divided ends of a sectioned nerve become
united by proliferating schwann cells andunited by proliferating schwann cells and
fibroblast which arise from cut end, thoughfibroblast which arise from cut end, though
mainly from distal stump.mainly from distal stump.
On about 3On about 3rdrd
day, the myelin sheath and axon ofday, the myelin sheath and axon of
the remaining intact nerve degenerate back asthe remaining intact nerve degenerate back as
far as the next node of ranvir of the proximalfar as the next node of ranvir of the proximal
surviving axon.surviving axon.

From the peripheral end of viable axonFrom the peripheral end of viable axon
appear numerous new sprouts .appear numerous new sprouts .
In the peripheral stump, there isIn the peripheral stump, there is
breakdown and phagocytosis of the axonbreakdown and phagocytosis of the axon
and myelin, as well as proliferation ofand myelin, as well as proliferation of
surviving schwann cells.about 50 dayssurviving schwann cells.about 50 days
after injury, the peripheral stump consistsafter injury, the peripheral stump consists
of tubes filled with elongated schwannof tubes filled with elongated schwann
cells.cells.
Of the fibrills emerging from the proximalOf the fibrills emerging from the proximal
stump one or more enter the old neuralstump one or more enter the old neural
tube.one of the entering fibrils inturn growtube.one of the entering fibrils inturn grow
into the new functional axon.into the new functional axon.indiandentalacademy.comindiandentalacademy.com

After crushing or division and suture of aAfter crushing or division and suture of a
nerve, function is restored after an initialnerve, function is restored after an initial
lag of 20 to 40 days, the rate of advance islag of 20 to 40 days, the rate of advance is
being 2-3 mm per day.being 2-3 mm per day.
The success of regeneration depends onThe success of regeneration depends on
width of the union scar and the allignmentwidth of the union scar and the allignment
of the cut ends , the nature of interveningof the cut ends , the nature of intervening
tissue, and suturing of cut ends.tissue, and suturing of cut ends.

NEUROGENESIS IN CNSNEUROGENESIS IN CNS
In the CNS little repair of damage to neuronsIn the CNS little repair of damage to neurons
occurs. Even when the cell body remains intact, aoccurs. Even when the cell body remains intact, a
severed axon cannot be repaired and regrown.severed axon cannot be repaired and regrown.
CNS myelin is one of the factors inhibitingCNS myelin is one of the factors inhibiting
regeneration of neurons. After axonal damage,regeneration of neurons. After axonal damage,
near by astrocytes proliferate rapidly forming anear by astrocytes proliferate rapidly forming a
type of scar tissue and consisting a physicaltype of scar tissue and consisting a physical
barrier to regeneration. Thus injure to brain orbarrier to regeneration. Thus injure to brain or
spinal cord is usually permanent.spinal cord is usually permanent.

REGENERATION OF STRIATED MUSCLEREGENERATION OF STRIATED MUSCLE
When muscle fibers are divided, the subsequentWhen muscle fibers are divided, the subsequent
retraction of cut ends seriously handicapsretraction of cut ends seriously handicaps
regeneration. But after crushing, the ends ofregeneration. But after crushing, the ends of
injured fibers are held together by connectiveinjured fibers are held together by connective
tissue stroma.tissue stroma.
The injured site is first filled with fibrinousThe injured site is first filled with fibrinous
exudate containing neutrophils andexudate containing neutrophils and
macrophages. The damaged portions of fibersmacrophages. The damaged portions of fibers
are soon removed with short lengths ofare soon removed with short lengths of
sarcolemmal tubes filled with histiocytes beingsarcolemmal tubes filled with histiocytes being
left.left.

At about 3 days, outgrowths of sarcoplasm extend fromAt about 3 days, outgrowths of sarcoplasm extend from
the fiber stumps along these tubes. These outgrowthsthe fiber stumps along these tubes. These outgrowths
contain numerous nuclei and have a characteristiccontain numerous nuclei and have a characteristic
pointed tip.pointed tip.
The regenerating strands meet, overlap, and anastomose,The regenerating strands meet, overlap, and anastomose,
though complete restoration of muscle architecture isthough complete restoration of muscle architecture is
slow and individual fibers may be disoriented for upto 3slow and individual fibers may be disoriented for upto 3
months.months.
When the sheath of the fibers is destroyed, the outgrowthWhen the sheath of the fibers is destroyed, the outgrowth
of sarcoplasm may be obstructed by connective tissueof sarcoplasm may be obstructed by connective tissue
and therefore forms a multinucleated mass.and therefore forms a multinucleated mass.

REPAIRREPAIR
Repair is the replacement of injured tissue byRepair is the replacement of injured tissue by
fibrous tissue.fibrous tissue.
Repair response takes place by participation ofRepair response takes place by participation of
mesenchymal cells, endothelial cells,mesenchymal cells, endothelial cells,
macrophages, platelets, and the parenchymalmacrophages, platelets, and the parenchymal
cells of the injured organ.cells of the injured organ.
Two processes are involved in repair:Two processes are involved in repair:
1) granulation tissue formation.1) granulation tissue formation.
2) contraction of wounds.2) contraction of wounds.

GRANULATION TISSUEGRANULATION TISSUE
FORMATIONFORMATION
The term granulation tissue derives from theThe term granulation tissue derives from the
pink, soft, granular gross appearance. Itspink, soft, granular gross appearance. Its
histologic appearance is charecterized byhistologic appearance is charecterized by
proliferation of fibroblast and new thin walledproliferation of fibroblast and new thin walled
capillaries, in a loose extracellular matrix.capillaries, in a loose extracellular matrix.
Following phases are observed in formation ofFollowing phases are observed in formation of
granulation tissue.granulation tissue.
1) phase of inflammation.1) phase of inflammation.
2) phase of in-growth of granulation2) phase of in-growth of granulation
tissue.tissue.

INFLAMMATORY PHASEINFLAMMATORY PHASE
Immediately following injury blood clot fills theImmediately following injury blood clot fills the
wound site. There is activation of complelmentwound site. There is activation of complelment
cascade, kallikrin kinin system and fibrinolyticcascade, kallikrin kinin system and fibrinolytic
clotting systemclotting system.. Plasminogen activates plasminPlasminogen activates plasmin
and clot lysis begins.and clot lysis begins.
The clot provides tensile strength and stabillityThe clot provides tensile strength and stabillity
to the wounds and serves as a source of growthto the wounds and serves as a source of growth
factors. Production of kinins and prostaglandinsfactors. Production of kinins and prostaglandins
cause vasodilatation and increasecause vasodilatation and increase
vasopermeability.vasopermeability.indiandentalacademy.comindiandentalacademy.com

Neutrophil migrates into the clot by chemotaxisNeutrophil migrates into the clot by chemotaxis
followed by macrophages and lymphocytes andfollowed by macrophages and lymphocytes and
remove dead, damaged tissue and foreign matterremove dead, damaged tissue and foreign matter
by phagocytosis.by phagocytosis.
The presence of macrophages and T-The presence of macrophages and T-
lymphocytes are critical towards healing.lymphocytes are critical towards healing.
Macrophage digest microbial and cellular debrisMacrophage digest microbial and cellular debris
and release cytokines and growth factors.and release cytokines and growth factors.
Within 24-48 hr keratinocytes migrate from theWithin 24-48 hr keratinocytes migrate from the
edges of wounded epidermis, underneath theedges of wounded epidermis, underneath the
fibrinclot and into the wound site to from a finefibrinclot and into the wound site to from a fine
covering over wounded dermis. Lose theircovering over wounded dermis. Lose their
desmosomes and become phagocytotic 1-2 daysdesmosomes and become phagocytotic 1-2 days
after injury. Epithelial cells at wound marginafter injury. Epithelial cells at wound margin
proliferate and provide cells for furtherproliferate and provide cells for further
epithelializationepithelialization indiandentalacademy.comindiandentalacademy.com

PHASE OF DEMOLITIONPHASE OF DEMOLITION
The dead tissue cells liberate their autolyticThe dead tissue cells liberate their autolytic
enzymes. Similarly disintegrating polymorphsenzymes. Similarly disintegrating polymorphs
liberate proteolytic enzymes.liberate proteolytic enzymes.
The mononuclear cells along with largeThe mononuclear cells along with large
phagocytic macrophages infiltrate and ingestphagocytic macrophages infiltrate and ingest
particulate matters. They either digest or removeparticulate matters. They either digest or remove
them.them.
Fusion of this macrophages result in formationFusion of this macrophages result in formation
of foreign body giant cells.of foreign body giant cells.indiandentalacademy.comindiandentalacademy.com

PHASE OF INGROWTH OFPHASE OF INGROWTH OF
GRANULATION TISSUEGRANULATION TISSUE
The haematoma within the wound is soon replaced byThe haematoma within the wound is soon replaced by
Granulation tissue is mainly formed by proliferation andGranulation tissue is mainly formed by proliferation and
migration of surrounding connective tissue elements.migration of surrounding connective tissue elements.
It is in fact composed of in the first instance by capillaryIt is in fact composed of in the first instance by capillary
loops and fibroblast with variable number ofloops and fibroblast with variable number of
inflammatory cells . So initially it is a vascular tissueinflammatory cells . So initially it is a vascular tissue
which gradully turns into avascular scar tissue.which gradully turns into avascular scar tissue.

ANGIOGENISISANGIOGENISIS
Solid buds of endothelial cells grow out ofSolid buds of endothelial cells grow out of
existing damaged blood vessels at the surface ofexisting damaged blood vessels at the surface of
the wound. These undergo canalisation and bythe wound. These undergo canalisation and by
anastomosis with their neighbors form a seriesanastomosis with their neighbors form a series
of vascular arcades.of vascular arcades.
These newly formed capillary loops leak proteinThese newly formed capillary loops leak protein
and thus the tissue fluid which is formed is aand thus the tissue fluid which is formed is a
very suitable medium for fibroblast growth.very suitable medium for fibroblast growth.
Gradually these capillary loops differentiate, fewGradually these capillary loops differentiate, few
acquire muscle coat and become arterioles,acquire muscle coat and become arterioles,
where as others enlarge to form thin walledwhere as others enlarge to form thin walled
venules.venules.

FIBROPLASIAFIBROPLASIA
The newly formed blood vessels are present in anThe newly formed blood vessels are present in an
amorphous ground substance or matrix. Theamorphous ground substance or matrix. The
new fibroblast originate from fibrocytes as wellnew fibroblast originate from fibrocytes as well
as by mitotic division of fibroblast.as by mitotic division of fibroblast.
Collagen fibrills begin to appear by 6Collagen fibrills begin to appear by 6thth
day . Asday . As
maturation proceeds more and more of collagenmaturation proceeds more and more of collagen
is formed while the number of active fibroblastis formed while the number of active fibroblast
and new blood vessels decrease . This results inand new blood vessels decrease . This results in
formation of inactive looking scar known asformation of inactive looking scar known as
cicatrisation.cicatrisation.

WOUND CONTRACTIONWOUND CONTRACTION
The wound gets contracting after 2-3 days andThe wound gets contracting after 2-3 days and
the process is completed by the 14the process is completed by the 14thth
day. Duringday. During
this period wound is reduced by approximatelythis period wound is reduced by approximately
80% of its original size. The magnitude of80% of its original size. The magnitude of
contraction varies with the shape, size, and sitecontraction varies with the shape, size, and site
of the wound.of the wound.
The amount of contraction depends on theThe amount of contraction depends on the
amount of skin available surrounding the woundamount of skin available surrounding the wound
to be stretched over the wound.to be stretched over the wound.

MECHANISM OF WOUNDMECHANISM OF WOUND
CONTRACTIONCONTRACTION
In order to explain the mechanism of woundIn order to explain the mechanism of wound
contraction, a number of factors have beencontraction, a number of factors have been
proposed. These are as under:proposed. These are as under:
1) Dehydration.1) Dehydration.
2) Contraction of collagen.2) Contraction of collagen.
3) contraction of granulation tissue.3) contraction of granulation tissue.
4) myofibroblast.4) myofibroblast.

FACTORS INHIBITING WOUNDFACTORS INHIBITING WOUND
CONTRACTIONCONTRACTION
Corticosteroid administration.Corticosteroid administration.
Contraction does not usually occur in burns.Contraction does not usually occur in burns.
X-irradiation.X-irradiation.
Trocinate.Trocinate.
Colchicine and vinblastin.Colchicine and vinblastin.

CHEMICAL MEDIATORS IN WOUNDCHEMICAL MEDIATORS IN WOUND
HEALINGHEALING
VASOPERMIABILITY MEDIATORSVASOPERMIABILITY MEDIATORS ::
these are the vasoactive amines(histamine,5-these are the vasoactive amines(histamine,5-
hydroxytryptanine), the peptides (bradykinin,hydroxytryptanine), the peptides (bradykinin,
leukdonin), acidic lipids (prostaglandins) andleukdonin), acidic lipids (prostaglandins) and
the neurotransmiters (nor-epinehrine,the neurotransmiters (nor-epinehrine,
epinephrine, acetylcholine).epinephrine, acetylcholine).
CHEMOTACTIC MEDIATORSCHEMOTACTIC MEDIATORS::
the complement system (C5a), the immunethe complement system (C5a), the immune
system (immunoglobulins), and the phagocyticsystem (immunoglobulins), and the phagocytic
system (sulfhydryl proteases).system (sulfhydryl proteases).

EFFECTS OF SOLUBLE MEDIATORS ONEFFECTS OF SOLUBLE MEDIATORS ON
CONNECTIVE TISSUE CELLSCONNECTIVE TISSUE CELLS
SL.NOSL.NO PROCESSPROCESS POLYPEPTIDEPOLYPEPTIDE
1.1. ChemotaxisChemotaxis PDGF, TGF-B, FGF, IL-1,PDGF, TGF-B, FGF, IL-1,
Matrix production.Matrix production.
22.. AdhesionAdhesion Fibronectin, Collagen,Fibronectin, Collagen,
Laminin, Vitronectin.Laminin, Vitronectin.
3.3. ProliferationProliferation PDGF, FGF, IGF-1.PDGF, FGF, IGF-1.
4.4. DifferentiationDifferentiation Matrix (inhibits proliferationMatrix (inhibits proliferation
and promotes differentiation)and promotes differentiation)
Growth factors, Hormones.Growth factors, Hormones.
5.5. AngiogenesisAngiogenesis FGF, TGF-B, Angiogenin.FGF, TGF-B, Angiogenin.
66.. Matrix synthesisMatrix synthesis
and remodelingand remodeling
TGF-B, TNF-TGF-B, TNF- αα, IL-1., IL-1.

Wound healing is a complex but orderly phenomenonWound healing is a complex but orderly phenomenon
involving a number of processes.involving a number of processes.
1.1. Regeneration of parenchymal cells.Regeneration of parenchymal cells.
2.2. Migration and proliferation of both parenchymal andMigration and proliferation of both parenchymal and
connective tissue cells.connective tissue cells.
3.3. Synthesis of extra cellular matrix proteins.Synthesis of extra cellular matrix proteins.
4.4. Remodeling of connective tissue and components.Remodeling of connective tissue and components.
5.5. Collagenisation and acquisition of wound strength.Collagenisation and acquisition of wound strength.

HEALING OF SKIN WOUNDSHEALING OF SKIN WOUNDS
Healing of skin wounds provide a classicalHealing of skin wounds provide a classical
example of combination of regeneration andexample of combination of regeneration and
repair.repair.
This can be accomplished by one of the twoThis can be accomplished by one of the two
ways:ways:
1)1) Healing by first intention.Healing by first intention.
2)2) Healing by second intention.Healing by second intention.

HEALING BY PRIMARY INTENTIONHEALING BY PRIMARY INTENTION
It is defined as healing of a wound which has theIt is defined as healing of a wound which has the
following characteristics:following characteristics:
1.1. Clean and uninfected.Clean and uninfected.
2.2. Surgically incised.Surgically incised.
3.3. Without much loss of cells and tissues.Without much loss of cells and tissues.
4.4. Edges of wound are approximated by surgical sutures.Edges of wound are approximated by surgical sutures.
The incision causes focal disruption of epithelialThe incision causes focal disruption of epithelial
basement membrane continuity and death of abasement membrane continuity and death of a
relatively few epithelial and connective tissue cells. Asrelatively few epithelial and connective tissue cells. As
a result epithelial regeneration predominates overa result epithelial regeneration predominates over
fibrosis.fibrosis.

HEALING OF INCISED WOUND BYHEALING OF INCISED WOUND BY
PRIMARY INTENTION :PRIMARY INTENTION :
Initial hemorrhage – immediately after injury, the spaceInitial hemorrhage – immediately after injury, the space
between the approximated surface of incised wound isbetween the approximated surface of incised wound is
filled with blood which then clots and seals the woundfilled with blood which then clots and seals the wound
against dehydration and infection.against dehydration and infection.
With in 24 hours – neutrophils are seen at the incisionWith in 24 hours – neutrophils are seen at the incision
margin migrating towards the fibrin clot. Basal cells atmargin migrating towards the fibrin clot. Basal cells at
the cut edge of the epidermis begin to exhibit increasedthe cut edge of the epidermis begin to exhibit increased
mitotic activity.mitotic activity.
Within 24-48 hours ,epithelial cells from both edges haveWithin 24-48 hours ,epithelial cells from both edges have
begun to migrate and proliferate along the dermis ,begun to migrate and proliferate along the dermis ,
depositing basement membrane components as theydepositing basement membrane components as they
progress.

By day 3 – neutrophils have been largely replaced byBy day 3 – neutrophils have been largely replaced by
macrophages, and granulation tissue progressively invadesmacrophages, and granulation tissue progressively invades
the incision space. Collagen fibers are evident at thethe incision space. Collagen fibers are evident at the
incision margins. Epithelial cell proliferation continuesincision margins. Epithelial cell proliferation continues
yielding a thickened epidermal covering layer.yielding a thickened epidermal covering layer.
By day 5- neovascularization reaches the peak asBy day 5- neovascularization reaches the peak as
granulation tissue fills the incisional space. Collagen fibersgranulation tissue fills the incisional space. Collagen fibers
become more abundant and begin to bridge the incision.become more abundant and begin to bridge the incision.
epidermis recovers normal thickness.epidermis recovers normal thickness.
During second week, there is continued collagenDuring second week, there is continued collagen
accumulation and fibroblast proliferation. The leukocyteaccumulation and fibroblast proliferation. The leukocyte
infiltrate, edema, and increased vascularity areinfiltrate, edema, and increased vascularity are
substantially diminished.substantially diminished.

The long process of blanching begins, accomplished byThe long process of blanching begins, accomplished by
increasing collagen deposition within the incisional scarincreasing collagen deposition within the incisional scar
and the regression of vascular channels.and the regression of vascular channels.
By the end of the first month, the scar comprises aBy the end of the first month, the scar comprises a
cellular connective tissue largely devoid of inflammatorycellular connective tissue largely devoid of inflammatory
cells and covered by an essentially normal epidermis.cells and covered by an essentially normal epidermis.
The dermal appendages destroyed in the line of theThe dermal appendages destroyed in the line of the
incision are permanently lost. The tensile strength of theincision are permanently lost. The tensile strength of the
wound increases with time.wound increases with time.

Healing by secondary intentionHealing by secondary intention
It is defined as healing of the wound having followingIt is defined as healing of the wound having following
characteristics :characteristics :
1) open wound with large tissue defect, at times infected.1) open wound with large tissue defect, at times infected.
2) extensive loss of tissue and cells.2) extensive loss of tissue and cells.
3) the wound is not approximated by sutures but left3) the wound is not approximated by sutures but left
open.open.
The basic events in secondary union are similar toThe basic events in secondary union are similar to
primary union but differs in having large tissueprimary union but differs in having large tissue
defect.hence healing takes place from the base - upwardsdefect.hence healing takes place from the base - upwards
as well as from the margins – inwards.as well as from the margins – inwards.
Healing by second intention is slow and results in a large,Healing by second intention is slow and results in a large,
at times ugly, scar as compared to primary union.at times ugly, scar as compared to primary union.indiandentalacademy.comindiandentalacademy.com

INITIAL HAEMORRHAGE:INITIAL HAEMORRHAGE:
as a result of injury the wound space is filled with blood andas a result of injury the wound space is filled with blood and
fibrin clot which dries.fibrin clot which dries.
INFLAMMATORY PHASE:INFLAMMATORY PHASE:
there is an initial acute inflammatory response followedthere is an initial acute inflammatory response followed
by appearance of macrophage which clears off the debrisby appearance of macrophage which clears off the debris
as in primary union.as in primary union.
EPITHELIAL CHANGESEPITHELIAL CHANGES::
as in primary healing, the epidermal cells from both theas in primary healing, the epidermal cells from both the
margins of wound proliferate and migrate into themargins of wound proliferate and migrate into the
wound in the form of epithelial spurs till they meet in thewound in the form of epithelial spurs till they meet in the
middle and re-epithelialise the gap completely.middle and re-epithelialise the gap completely.

the proliferating epithelial cells do not cover thethe proliferating epithelial cells do not cover the
surface fully until granulation tissue from basesurface fully until granulation tissue from base
has started filling the wound space. In this way,has started filling the wound space. In this way,
pre-existing viable connective tissue is separatedpre-existing viable connective tissue is separated
from necrotic material and clot on the surface,from necrotic material and clot on the surface,
forming scab which is cast off.forming scab which is cast off.
GRANULATION TISSUE:GRANULATION TISSUE:
the main bulk of secondary healing is bythe main bulk of secondary healing is by
granulations. Granulation tissue is formed bygranulations. Granulation tissue is formed by
proliferation of fibroblast and neovascularisationproliferation of fibroblast and neovascularisation
from the adjoining viable elements. The newlyfrom the adjoining viable elements. The newly
formed granulation tissue is deep red, granularformed granulation tissue is deep red, granular
and very fragile.and very fragile.

With time, the scar on maturation becomes paleWith time, the scar on maturation becomes pale
and white due to increase in collagen andand white due to increase in collagen and
decrease in vascularity. hair follicles and sweatdecrease in vascularity. hair follicles and sweat
glands are not replaced unless their viableglands are not replaced unless their viable
residues remain which may regenerate.residues remain which may regenerate.
WOUND CONTRACTION:WOUND CONTRACTION:
contraction of wound is an important feature ofcontraction of wound is an important feature of
secondary healing, not seen in primary healing .secondary healing, not seen in primary healing .
Due to the action of myofibroblasts present inDue to the action of myofibroblasts present in
granulation tissue, the wound contracts to one-granulation tissue, the wound contracts to one-
third to one-fourth of its original size. Woundthird to one-fourth of its original size. Wound
contraction occurs at a time when activecontraction occurs at a time when active
granulation tissue is being formed.granulation tissue is being formed.

WOUND STRENGTHWOUND STRENGTH
Carefully sutured wounds have approximatelyCarefully sutured wounds have approximately
70% to 80% of the strength of unwounded skin.70% to 80% of the strength of unwounded skin.
When sutures are removed, usually at 1 week,When sutures are removed, usually at 1 week,
wound strength is approximately 10% of that ofwound strength is approximately 10% of that of
unwounded skin, but this increases rapidly overunwounded skin, but this increases rapidly over
the next 4 weeks.the next 4 weeks.
The recovery of tensile strength results fromThe recovery of tensile strength results from
collagen synthesis exceeding degradation duringcollagen synthesis exceeding degradation during
first 2 months and from structural modificationfirst 2 months and from structural modification
of collagen when synthesis declines at later time.of collagen when synthesis declines at later time.

HEALING OF FRACTURESHEALING OF FRACTURES
Bone fractures heal by regeneration as this tissueBone fractures heal by regeneration as this tissue
contains undifferentiated stem cells. Healingcontains undifferentiated stem cells. Healing
depends on whether the fracture is-depends on whether the fracture is-
1) TRAUMATIC OR PATHOLOGICAL.1) TRAUMATIC OR PATHOLOGICAL.
2) COMPLETE OR INCOMPLETE.2) COMPLETE OR INCOMPLETE.
3) SIMPLE, COMMINUTED AND COMPOUND3) SIMPLE, COMMINUTED AND COMPOUND
How ever basic events in healing of any type ofHow ever basic events in healing of any type of
fracture are similar and resemble healing of skinfracture are similar and resemble healing of skin
wound to same extent.wound to same extent.

PRIMARY UNION OF FRACTURES:PRIMARY UNION OF FRACTURES:
This occurs occasionally in a few situationsThis occurs occasionally in a few situations
when the ends of fracture are approximated likewhen the ends of fracture are approximated like
by application of compression plates/clamps. Inby application of compression plates/clamps. In
this case bony union takes place with formationthis case bony union takes place with formation
of medullary callus without periosteal callusof medullary callus without periosteal callus
formation. There is extensive bone necrosis andformation. There is extensive bone necrosis and
slow healing.slow healing.
SECONDARY UNION:SECONDARY UNION:
Is the more common process and occurs in theIs the more common process and occurs in the
following stages – 1) procallus formationfollowing stages – 1) procallus formation
2) osseous callus formation2) osseous callus formation
3) remodelling.3) remodelling.

PROCALLUS FORMATIONPROCALLUS FORMATION
Steps involved in the formation of procallusSteps involved in the formation of procallus
formation are as follows –formation are as follows –
a) FORMATION OF FRACTURE HAEMATOMA-a) FORMATION OF FRACTURE HAEMATOMA-
forms due to bleeding from torn blood vessels,forms due to bleeding from torn blood vessels,
filling the area surrounding the fracture. Loosefilling the area surrounding the fracture. Loose
mesh work is formed by blood and fibrin clotmesh work is formed by blood and fibrin clot
which acts as framework for subsequentwhich acts as framework for subsequent

b) LOCAL INFLAMMATORY RESPONSE:b) LOCAL INFLAMMATORY RESPONSE:
this occurs at the site of injury with exudation ofthis occurs at the site of injury with exudation of
fibrin, polymorphs and macrophages. Thefibrin, polymorphs and macrophages. The
macrophages clear away the fibrin, red blood cellmacrophages clear away the fibrin, red blood cell
inflammatory exudate and debris. Fragment ofinflammatory exudate and debris. Fragment of
necrosed bone are scavenged by macrophagesnecrosed bone are scavenged by macrophages
and osteoclasts.and osteoclasts.
c) INGROWTH OF GRANULATION TISSUE:c) INGROWTH OF GRANULATION TISSUE:
Begins with neovasculrisation and proliferationBegins with neovasculrisation and proliferation
of mesenchymal cells from periosteum andof mesenchymal cells from periosteum and
endosteum. A soft tissue callus is thus formedendosteum. A soft tissue callus is thus formed
which joins the ends of fractured bone withoutwhich joins the ends of fractured bone without
much strength.much strength. indiandentalacademy.comindiandentalacademy.com

d) CALLUS COMPOSED OF WOVEN BONE ANDd) CALLUS COMPOSED OF WOVEN BONE AND
CARTILAGE:CARTILAGE:
This process starts within the first few days. TheThis process starts within the first few days. The
cells of inner layer of the periosteum havecells of inner layer of the periosteum have
osteogenic potential and lay down the collagenosteogenic potential and lay down the collagen
as well as osteoid matrix in the granulationas well as osteoid matrix in the granulation
tissue. The osteoid undergoes calcification and istissue. The osteoid undergoes calcification and is
called woven bone callus.called woven bone callus.

OSSEOUS CALLUS FORMATIONOSSEOUS CALLUS FORMATION
The procallus acts as scaffolding on whichThe procallus acts as scaffolding on which
osseous callus composed of lamellar bone isosseous callus composed of lamellar bone is
formed. The woven bone is cleared away byformed. The woven bone is cleared away by
osteoclasts and the calcified cartilageosteoclasts and the calcified cartilage
desentigrates.desentigrates.
In their place newly formed blood vessels andIn their place newly formed blood vessels and
osteblasts invade, laying down osteoid which isosteblasts invade, laying down osteoid which is
calcified and lamellar bone is formed bycalcified and lamellar bone is formed by
developing haversian system concentricallydeveloping haversian system concentrically
around the blood vessels.around the blood vessels.

REMODELLINGREMODELLING
During the formation of lamellar bone,During the formation of lamellar bone,
osteoblastic laying and osteoclastic removal areosteoblastic laying and osteoclastic removal are
taking place remodelling the united bone ends,taking place remodelling the united bone ends,
which after some time, is indistinguishable fromwhich after some time, is indistinguishable from
normal bone.normal bone.
The external callus is cleared away, compactThe external callus is cleared away, compact
bone is formd in place of intermediate callus andbone is formd in place of intermediate callus and
the bone marrow cavity develops in internalthe bone marrow cavity develops in internal
callus.callus.

COMPLICATIONS OF FRACTURECOMPLICATIONS OF FRACTURE
HEALINGHEALING
FIBROUS UNION- may result instead ofFIBROUS UNION- may result instead of
osseous union if the immobilisation of fracturedosseous union if the immobilisation of fractured
bone is not done.bone is not done.
PSUEDOARTHROSIS- is a false joint of fibrousPSUEDOARTHROSIS- is a false joint of fibrous
tissue that forms due to persistent abnormaltissue that forms due to persistent abnormal
movement at fracture site.movement at fracture site.
NON-UNION- may result if some soft tissues isNON-UNION- may result if some soft tissues is
interposed between the fractured ends.interposed between the fractured ends.
DELAYED UNION- may occur from causes ofDELAYED UNION- may occur from causes of
delayed wound healing in general such asdelayed wound healing in general such as
infection, inadequate blood supply, poorinfection, inadequate blood supply, poor
nutrition and old age.nutrition and old age.

HEALING OF MUCOSALHEALING OF MUCOSAL
SURFACESURFACE
The cells of mucosal surfaces have veryThe cells of mucosal surfaces have very
good regeneration and are normally beinggood regeneration and are normally being
lost and replaced continuously .lost and replaced continuously .
eg; mucosa of alimentary tract, respiratoryeg; mucosa of alimentary tract, respiratory
tract,urinary tract.tract,urinary tract.
This occurs by proliferation andThis occurs by proliferation and
differentiation of epithelial cells in thedifferentiation of epithelial cells in the
same way as in the epidermal cells insame way as in the epidermal cells in
healing of skin wounds.healing of skin wounds.

HEALING OF TOOTH SOCKETHEALING OF TOOTH SOCKET
Initially the socket fills with blood clot (fibrin)Initially the socket fills with blood clot (fibrin)
within a few minutes, forming a plug beneathwithin a few minutes, forming a plug beneath
this after several days there is a proliferation ofthis after several days there is a proliferation of
granulation tissue composed of endothelial cells,granulation tissue composed of endothelial cells,
fibroblast and cells halfway between fibroblastfibroblast and cells halfway between fibroblast
and smooth muscle cells (myofibroblast).and smooth muscle cells (myofibroblast).
The bone of the socket is remodelled byThe bone of the socket is remodelled by
osteoclast and osteoblast. The surface squamousosteoclast and osteoblast. The surface squamous
epithelium grows over the fibrin and granulationepithelium grows over the fibrin and granulation
tissue plug and completely covers the wound intissue plug and completely covers the wound in
one to two weeks.one to two weeks.

FACTORS INFLUENCING WOUND HEALINGFACTORS INFLUENCING WOUND HEALING
many systemic and local host factors influence themany systemic and local host factors influence the
adequacy of the inflammatory reparative response.adequacy of the inflammatory reparative response.
GENERAL/SYSTEMIC FACTORSGENERAL/SYSTEMIC FACTORS ::
1)1) AGE : wound healing is fast in young age, but normal inAGE : wound healing is fast in young age, but normal in
old age unless associated with debilitating disease.old age unless associated with debilitating disease.
2)2) NUTRITIONNUTRITION : As a profound effect on wound healing.: As a profound effect on wound healing.
a)a) Protein deficiencyProtein deficiency : Protein depletion causes: Protein depletion causes
impairment of granulation tissue and collagenimpairment of granulation tissue and collagen
formation. A high protein diet hastens the rate of tensileformation. A high protein diet hastens the rate of tensile
strength gain.strength gain.
it is always not due t0 inadequate intake butit is always not due t0 inadequate intake but
may be due to excessive loss .may be due to excessive loss .

b) Vitamin A :b) Vitamin A :
is required for proper epithelisation which may beis required for proper epithelisation which may be
hampered due to its deficiency.hampered due to its deficiency.
c) Vitamin C :c) Vitamin C :
deficiency which results in scurvy due to production ofdeficiency which results in scurvy due to production of
abnormal collagen.abnormal collagen.
d) Zinc, Calcium, Copper and Manganese deficiency :d) Zinc, Calcium, Copper and Manganese deficiency :
Zinc is an essential component of many enzymes likeZinc is an essential component of many enzymes like
metaloenzymes, DNA and RNA polymerase. Others aremetaloenzymes, DNA and RNA polymerase. Others are
essential minerals which are required for proper woundessential minerals which are required for proper wound
healing. These may be depleted in intestinal fistulas andhealing. These may be depleted in intestinal fistulas and
burns.burns.

3)3) CIRCULATORY STATUSCIRCULATORY STATUS ::
can regulate wound healing. Inadequate blood supplycan regulate wound healing. Inadequate blood supply
usually caused by arteriosclerosis and venoususually caused by arteriosclerosis and venous
abnormalities that retard venous drainage and impairabnormalities that retard venous drainage and impair
healing. Haematologic abnormalities like defect ofhealing. Haematologic abnormalities like defect of
neutrophil function (chemotaxis and phagocytosis),neutrophil function (chemotaxis and phagocytosis),
neutropenia and bleeding disorders slow the process ofneutropenia and bleeding disorders slow the process of
wound healing.wound healing.
4)4) METABOLIC DISORDERSMETABOLIC DISORDERS::
diabetic patients in which the disease has been present fordiabetic patients in which the disease has been present for
many years show poor wound healing. The pathology ofmany years show poor wound healing. The pathology of
diabetes is characterised by microvascular disease, withdiabetes is characterised by microvascular disease, with
thickened but more permeable basement membranes. Thethickened but more permeable basement membranes. The
delayed wound healing is primarily ischemic in origin anddelayed wound healing is primarily ischemic in origin and
this patients are more prone for infection.this patients are more prone for infection.

Chronic stress adversely affects wound healing.Chronic stress adversely affects wound healing.
HORMONESHORMONES::
1) CORTICOSTEROIDS: the effects of this hormones on1) CORTICOSTEROIDS: the effects of this hormones on
granulation tissue formation and wound contraction asgranulation tissue formation and wound contraction as
profound effect as they inhibit cytokine production,profound effect as they inhibit cytokine production,
chemotaxis, bacterial killing by macrophages andchemotaxis, bacterial killing by macrophages and
neutrophils and reduce collagen production.neutrophils and reduce collagen production.
2) Desoxycorticosterone acetate and anabolic steroids2) Desoxycorticosterone acetate and anabolic steroids
like testosterone are also concerned with increase in thelike testosterone are also concerned with increase in the
speed of healing.speed of healing.

LOCAL FACTORS AFFECTINGLOCAL FACTORS AFFECTING
Position of skin wound.Position of skin wound.
Blood supply.Blood supply.
Tension.Tension.
Infection.Infection.
Movement.Movement.
Exposure to ionizing radiation.Exposure to ionizing radiation.
Foreign bodiesForeign bodies

Adhesion to bony surface.Adhesion to bony surface.
NecrosisNecrosis
Lymph drainage.Lymph drainage.
Faulty technique of wound closure.Faulty technique of wound closure.
Heat.Heat.
Cold.Cold.
Smoking.Smoking.

Complications of wound healingComplications of wound healing
Infection of wound due to entry of bacteriaInfection of wound due to entry of bacteria
delays the healing.delays the healing.
Implantation cyst formation may occur due toImplantation cyst formation may occur due to
persistance of epithelial cells in the wound afterpersistance of epithelial cells in the wound after
healing.healing.
Pigmentation: healed wounds may at times havePigmentation: healed wounds may at times have
rust like colour due to staining withrust like colour due to staining with
haemosiderin.haemosiderin.
Contractures: an exaggeration of woundContractures: an exaggeration of wound
contraction may result in formation ofcontraction may result in formation of
contractures.contractures. indiandentalacademy.comindiandentalacademy.com

Deficient scar formationDeficient scar formation: this may occur due: this may occur due
to inadequate formation of granulation tissue.to inadequate formation of granulation tissue.
This can lead to two types of complications:This can lead to two types of complications:
1)1) wound dehiscencewound dehiscence or rupture of wound this isor rupture of wound this is
most common after abdominal surgery and ismost common after abdominal surgery and is
due to increased abdominal pressure and can bedue to increased abdominal pressure and can be
generated by vomiting and coughing also calledgenerated by vomiting and coughing also called
as incisional hernia.as incisional hernia.
2) wound ulceration due to inadequate2) wound ulceration due to inadequate
vascularization.vascularization.

Excessive formation of repair componentsExcessive formation of repair components
results in:results in:
a)a) keloid or hypertropic scarkeloid or hypertropic scar: accumilation of: accumilation of
excessive amounts of collagen may give rise toexcessive amounts of collagen may give rise to
tumorous scar.tumorous scar.
b) exuberant granulation tissue formation: hereb) exuberant granulation tissue formation: here
excessive amounts of granulation tissueexcessive amounts of granulation tissue
protrudes above the level of surrounding skinprotrudes above the level of surrounding skin
and blocks re-epithelizationand blocks re-epithelization

DermoidsDermoids and aggressive fibromatosis:and aggressive fibromatosis:
exuberant proliferation of fibroblast andexuberant proliferation of fibroblast and
other connective tissue elements thatother connective tissue elements that
recur after excision. These lie in therecur after excision. These lie in the
interface between benign proliferationsinterface between benign proliferations
and malignant low grade tumor.and malignant low grade tumor.
NeoplasiaNeoplasia: rarely scar may be the site for: rarely scar may be the site for
development of carcinoma later.development of carcinoma later.
e.g; squamous cell carcinoma in scar.e.g; squamous cell carcinoma in scar.

WOUND INFECTIONWOUND INFECTION
TYPES OF WOUND INFECTIONTYPES OF WOUND INFECTION::
1)1) WOUND ABSCESSWOUND ABSCESS: Is surrounded by an: Is surrounded by an
acute inflammatory response and a pyogenicacute inflammatory response and a pyogenic
membrane composed of fibrinous exudates,membrane composed of fibrinous exudates,
oedema and cells of acute inflammation.oedema and cells of acute inflammation.
2)2) CELLULITIS AND LYMPHATICSCELLULITIS AND LYMPHATICS: This is: This is
non suppurative invasive infection of tissues.non suppurative invasive infection of tissues.
Spreading infection is typical of organismsSpreading infection is typical of organisms
such as B. haemolytic streptococci,such as B. haemolytic streptococci,
staphylococci, c.perfringens.staphylococci, c.perfringens.

3)3) Bacteraemia and septicemia-Bacteraemia and septicemia-
unusal in superficial wounds but common afterunusal in superficial wounds but common after
anastomotic infection and when proceduresanastomotic infection and when procedures
taken through infected tissue.taken through infected tissue.
4)4) Specific wound infectionsSpecific wound infections: gas gangrene and: gas gangrene and
tetanus.tetanus.
a)a) Gas gangreneGas gangrene: Is caused by c. perfringes.: Is caused by c. perfringes.
The gram+ive spore bearing bacilli are widelyThe gram+ive spore bearing bacilli are widely
found in nature particularly soil and faeces andfound in nature particularly soil and faeces and
is relevant to military and traumatic surgery.is relevant to military and traumatic surgery.
Patient who are immunocompromised,Patient who are immunocompromised,
malignant and diabetic are at high risk.malignant and diabetic are at high risk.

wound infections are associated with severe localwound infections are associated with severe local
wound pain and crepitus in the tissues. Oedemawound pain and crepitus in the tissues. Oedema
and spreading gangrene follow the release ofand spreading gangrene follow the release of
collagenase, hyalouronidase.collagenase, hyalouronidase.
b)b) TetanusTetanus: Is caused by clostridium tetani,: Is caused by clostridium tetani,
produces exotoxin which inhibits cholinestaraseproduces exotoxin which inhibits cholinestarase
and causes hyperexcitability of motor neurons.and causes hyperexcitability of motor neurons.
symptoms and signs- dyspepsia, jaw stiffnesssymptoms and signs- dyspepsia, jaw stiffness
and severe pains in the neck, back and abdomenand severe pains in the neck, back and abdomen
precede the tonic muscle spasm . Respirationprecede the tonic muscle spasm . Respiration
and swallowing becomes difficult, reflexand swallowing becomes difficult, reflex
convulsions occur affecting all musclesconvulsions occur affecting all muscles

BASICS OF WOUND HEALINGBASICS OF WOUND HEALING
1)1) Minimal tissue damage.Minimal tissue damage.
2)2) Debridement and cleansing of wound-Debridement and cleansing of wound-
debridement is the removal of dead tissue anddebridement is the removal of dead tissue and
cleansing is removal of foreign bodies.cleansing is removal of foreign bodies.
debridement can be autolytic, enzymatic,debridement can be autolytic, enzymatic,
mechanical and surgical. Cleansing ismechanical and surgical. Cleansing is
accomplished by irrigation with sterile saline.accomplished by irrigation with sterile saline.
3)3) Maximal tissue perfusion and oxygenation.Maximal tissue perfusion and oxygenation.
4)4) Prevent further injury and keeping wound wellPrevent further injury and keeping wound well
nourished this implies decreasing andnourished this implies decreasing and
eliminating edema and pressure, tetanuseliminating edema and pressure, tetanus
prophylaxis.prophylaxis.

5) Providing materials for healing such as proteins5) Providing materials for healing such as proteins
for angiogenesis, fibroblast proliferation,for angiogenesis, fibroblast proliferation,
collagen synthesis and scar remodelling, proteincollagen synthesis and scar remodelling, protein
also support immune system to preventalso support immune system to prevent
infection. Carbohydrate and fats supply extrainfection. Carbohydrate and fats supply extra
energy.energy.
6)Maintaining a moist environmentfor6)Maintaining a moist environmentfor
preservation of the wound exudate, that containspreservation of the wound exudate, that contains
WBC, lysosomal enzymes, lymphokines, andWBC, lysosomal enzymes, lymphokines, and
growth factors. Wounds kept in moistgrowth factors. Wounds kept in moist
environment have lower infection rates.environment have lower infection rates.

BIBLIOGRAPHYBIBLIOGRAPHY
1) Basic pathology ; Robbins 71) Basic pathology ; Robbins 7thth
edition.edition.
2) Essential pathology for dental students;2) Essential pathology for dental students;
Harsh mohan 2Harsh mohan 2ndnd
edition.edition.
3) Andersons pathology; 93) Andersons pathology; 9thth
edition.edition.
4) Concise textbook of surgery; Das 34) Concise textbook of surgery; Das 3rdrd
edition.edition.

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