Wound healing / dental crown & bridge courses

Wound healingWound healing
INDIAN DENTAL ACADEMYINDIAN DENTAL ACADEMY
Leader in continuing DentalLeader in continuing Dental
EducationEducation
www.indiandentalacademy.comwww.indiandentalacademy.com

Wound healingWound healing
DefinitionDefinition::
““Wound healingWound healing is an intricate process in which the skin oris an intricate process in which the skin or
another organ repairs itself after injury”.another organ repairs itself after injury”.
 Interaction of complex cascade of cellular events.Interaction of complex cascade of cellular events.
 Generates resurfacing, reconstitution, and restoration ofGenerates resurfacing, reconstitution, and restoration of
tensile strength of injuredtensile strength of injured tissuetissue..
 Under the ideal circumstances, healing a systematic process,Under the ideal circumstances, healing a systematic process,
of 3 classic phases:of 3 classic phases:
 Inflammation,Inflammation,
 Proliferation, andProliferation, and
 Maturation.Maturation. www.indiandentalacademy.comwww.indiandentalacademy.com

Phases of Wound HealingPhases of Wound Healing
 TThe inflammatory phasehe inflammatory phase::
 Initial injury causes platelet adhesion and aggregation and formation ofInitial injury causes platelet adhesion and aggregation and formation of
clot in the surface of wounds.clot in the surface of wounds.
 TThe proliferative phasehe proliferative phase::
 Formation of granulation tissue, proliferation ,migration of connectiveFormation of granulation tissue, proliferation ,migration of connective
tissue cells and re- epithelialization of wound surface.tissue cells and re- epithelialization of wound surface.
 Granulation tissue forms and the wound begins to contract.Granulation tissue forms and the wound begins to contract.
 TThe maturation phasehe maturation phase::
 Involves ECM deposition ,tissue remodelling and wound contraction.Involves ECM deposition ,tissue remodelling and wound contraction.
 Increases the tensile strength of the scar.Increases the tensile strength of the scar.

PHASES IN WOUND HEALINGPHASES IN WOUND HEALING

I. Inflammatory PhaseI. Inflammatory Phase
 Immediate to 2-5 daysImmediate to 2-5 days
 B HemostasisB Hemostasis
 VasoconstrictionVasoconstriction
 Platelet aggregationPlatelet aggregation
 Thromboplastin makes clotThromboplastin makes clot
 C InflammationC Inflammation
 VasodilationVasodilation
 PhagocytosisPhagocytosis

II. Proliferative PhaseII. Proliferative Phase
 2 days to 3 weeks2 days to 3 weeks
B) GranulationB) Granulation
 Fibroblasts lay bed of collagenFibroblasts lay bed of collagen
 Fills defect and produces new capillariesFills defect and produces new capillaries
C) ContractionC) Contraction
 Wound edges pull together to reduce defectWound edges pull together to reduce defect
D) EpithelializationD) Epithelialization
 Crosses moist surfaceCrosses moist surface
 Cell travel about 3 cm from point of origin in allCell travel about 3 cm from point of origin in all
directionsdirections

III. RemodelingIII. Remodeling (maturation)(maturation) PhasePhase
 3 weeks to 2 years3 weeks to 2 years
 B) New collagen forms which increases tensileB) New collagen forms which increases tensile
strength to woundsstrength to wounds.. Scar tissue is only 80Scar tissue is only 80
percent as strong as original tissuepercent as strong as original tissue

Scar FormationScar Formation
 TThe process of wound healing is essentially similar inhe process of wound healing is essentially similar in
all tissues and is relatively independent of the modeall tissues and is relatively independent of the mode
of injury; however, slight variation in the relativeof injury; however, slight variation in the relative
contribution of the different elements to the overallcontribution of the different elements to the overall
result may occur.result may occur.
 The final product of the healing process is aThe final product of the healing process is a scar.scar.
This relatively avascular and acellular mass ofThis relatively avascular and acellular mass of
collagen serves to restore tissue continuity, strengthcollagen serves to restore tissue continuity, strength
and function.and function.
 DelaysDelays in the healing process cause the prolongedin the healing process cause the prolonged
presence of wounds, whilepresence of wounds, while
 abnormalitieabnormalities of the healing process may lead tos of the healing process may lead to
abnormal scar formationabnormal scar formation..

Inflammatory PhaseInflammatory Phase
 The body responds quickly to any disruption of theThe body responds quickly to any disruption of the
skin’s surface.skin’s surface.
 The early events of wound healing are characterizedThe early events of wound healing are characterized
by a vascular and cellular response to injury.by a vascular and cellular response to injury.
 An incision made through a full thickness of skinAn incision made through a full thickness of skin
causes a disruption of the microvasculature andcauses a disruption of the microvasculature and
immediate hemorrhage.immediate hemorrhage.
 Within seconds of the injury, blood vessels constrictWithin seconds of the injury, blood vessels constrict
to control bleeding at the site. Platelets coalesceto control bleeding at the site. Platelets coalesce
within minutes to stop the bleeding and begin clotwithin minutes to stop the bleeding and begin clot
formation.formation.

IInflammatory phasenflammatory phase
 Vasoconstriction occurs.Vasoconstriction occurs.
 Temporary blanching of the wound.Temporary blanching of the wound.
 Reduced hemorrhage which aids in plateletReduced hemorrhage which aids in platelet
aggregation.aggregation.
 Endothelial cells retract to produceEndothelial cells retract to produce
subendothelial collagen surfaces.subendothelial collagen surfaces.

 Endothelial cellsEndothelial cells retract to expose theretract to expose the
subendothelial collagen surfaces; plateletssubendothelial collagen surfaces; platelets
attach tattach to these surfaces.o these surfaces.
 Adherence to exposed collagen surfaces and toAdherence to exposed collagen surfaces and to
other plateletsother platelets occurs throughoccurs through adhesiveadhesive
glycoproteins: fibrinogen, fibronectin,glycoproteins: fibrinogen, fibronectin,
thrombospondinthrombospondin, and von Willebrand factor., and von Willebrand factor.

Inflammatory PhaseInflammatory Phase
 PlateletsPlatelets also release factors that attract otheralso release factors that attract other
important cells to the injury.important cells to the injury. NeutrophilsNeutrophils enterenter
the wound to fight infection and to attractthe wound to fight infection and to attract
macrophages.macrophages. MacrophagesMacrophages break downbreak down
necrotic debris and activate the fibroblastnecrotic debris and activate the fibroblast
response.response.
 The inflammatory phase lasts aboutThe inflammatory phase lasts about 24 hours24 hours ..

 The aggregation of platelets results in theThe aggregation of platelets results in the
formation of the primary platelet plug.formation of the primary platelet plug.
Aggregation and attachment to exposedAggregation and attachment to exposed
collagen surfaces activates the platelets.collagen surfaces activates the platelets.
Activation enables platelets to degranulate andActivation enables platelets to degranulate and
release chemotactic and growth factors, suchrelease chemotactic and growth factors, such
as platelet-derived growth factor (PDGF),as platelet-derived growth factor (PDGF),
proteases, and vasoactive agents (eg,proteases, and vasoactive agents (eg,
serotonin, histamine).serotonin, histamine).

Stages in platelet plug formation

 The coagulation cascade occurs by 2 differentThe coagulation cascade occurs by 2 different
pathways.pathways.
 The intrinsic pathway begins with the activation ofThe intrinsic pathway begins with the activation of
factor XII (Hageman factor), when blood is exposedfactor XII (Hageman factor), when blood is exposed
to extravascular surfaces.to extravascular surfaces.
 The extrinsic coagulation pathway occurs through theThe extrinsic coagulation pathway occurs through the
activation of tissue factor found in extravascular cellsactivation of tissue factor found in extravascular cells
in the presence of factors VII and VIIa.in the presence of factors VII and VIIa.

 Both pathways proceed to the activation ofBoth pathways proceed to the activation of
thrombin, which converts fibrinogen to fibrin.thrombin, which converts fibrinogen to fibrin.
 The fibrin product is essential to woundThe fibrin product is essential to wound
healing and is the primary component ofhealing and is the primary component of
the wound matrix into which inflammatorythe wound matrix into which inflammatory
cells, platelets, and plasma proteinscells, platelets, and plasma proteins
migrate. Removal of the fibrin matrixmigrate. Removal of the fibrin matrix
impedes wound healing.impedes wound healing.

 In addition to activation of fibrin, thrombinIn addition to activation of fibrin, thrombin
facilitates migration of inflammatory cells tofacilitates migration of inflammatory cells to
the site of injury bythe site of injury by increasing vascularincreasing vascular
permeability. By this mechanism, factors andpermeability. By this mechanism, factors and
cells necessary to healing flow from thecells necessary to healing flow from the
intravascular space and into the extravascularintravascular space and into the extravascular
space.space.

Proliferation PhaseProliferation Phase
 On the surface of the wound,On the surface of the wound, epidermal cellsepidermal cells
burst into mitotic activity within 24 to 72burst into mitotic activity within 24 to 72
hours. These cells begin their migration acrosshours. These cells begin their migration across
the surface of the wound.the surface of the wound.
 FibroblastFibroblastss proliferate in the deeper parts ofproliferate in the deeper parts of
the wound. These fibroblasts begin tothe wound. These fibroblasts begin to
synthesize small amounts of collagen whichsynthesize small amounts of collagen which
acts as a scaffold for migration and furtheracts as a scaffold for migration and further
fibroblast proliferation.fibroblast proliferation.

Proliferation PhaseProliferation Phase
 Granulation tissue, which consists of capillaryGranulation tissue, which consists of capillary
loops supported in this developing collagenloops supported in this developing collagen
matrix, also appears in the deeper layers of thematrix, also appears in the deeper layers of the
wound. The proliferation phase lastswound. The proliferation phase lasts from 24from 24
to 72 hours and leads to the fibroblastic phaseto 72 hours and leads to the fibroblastic phase
of wouof wound healing.nd healing.

ProliferationProliferation PhasePhase
 Four to five days afterFour to five days after the injury occurs,the injury occurs,
fibroblasts begin producing large amounts offibroblasts begin producing large amounts of
collagen and proteoglycans.collagen and proteoglycans.
 Collagen fibers are laidCollagen fibers are laid down randomly anddown randomly and
are cross-linked into large, closely packedare cross-linked into large, closely packed
bundles.bundles.

ProliferationProliferation PhasePhase
 Proteoglycans appear to enhance the formationProteoglycans appear to enhance the formation
of collagen fibers.of collagen fibers.
 Within two to three weeks, the wound canWithin two to three weeks, the wound can
resist normal stresses.resist normal stresses.
 Wound strength continues to build for severalWound strength continues to build for several
months.months.
 The fibroblastic phase lasts fromThe fibroblastic phase lasts from 15 to 20 days15 to 20 days
and then wound healing enters the maturationand then wound healing enters the maturation
phase.phase.

Maturation PhaseMaturation Phase
 Fibroblasts leave the wound and collagen isFibroblasts leave the wound and collagen is
remodeled into aremodeled into a more organized matrix.more organized matrix.
 Tensile strength increases for up to one yearTensile strength increases for up to one year
following the injuryfollowing the injury..
 While healed wounds never regain the fullWhile healed wounds never regain the full
strength of uninjured skin, they can regain upstrength of uninjured skin, they can regain up
to 70 to 80% of its original strength.to 70 to 80% of its original strength.

•Impaired wound healing is a major clinical problem in diabetic patients,
affecting about 15 percent of them and is the leading cause of lower limb
amputations.
•One of the cardinal features of wound healing is the formation of new small
blood vessels at the site of injury.
•One of the ways in which this happens is by bone marrow-derived progenitor
cells called Endothelial Progenitor Cells (EPCs), in a process known as
vasculogenesis.
• Poor healing of diabetic wound is characterized by impaired vasculogenesis.
•In healthy individuals the acute wound healing process is guided and
maintained through integration of multiple signals released by
keratinocytes, fibroblasts, endothelial cells, macrophages, and platelets
and other cells.

COMPARISION BETWEEN NORMAL AND DIABETIC WOUNDCOMPARISION BETWEEN NORMAL AND DIABETIC WOUND

HEALING IS ACCOMPLISHED BY:HEALING IS ACCOMPLISHED BY:
 PRIMARY INTENTION (PRIMARY UNION)PRIMARY INTENTION (PRIMARY UNION)
 SECONDARY INTENTION (SECONDARY UNION)SECONDARY INTENTION (SECONDARY UNION)
PROCESS UNDERGONE DURING HEALING:PROCESS UNDERGONE DURING HEALING:
REGENERATIONREGENERATION
REPAIRREPAIR

HEALING BY PRIMARY INTENTIONHEALING BY PRIMARY INTENTION
Wounds in primary intention are:Wounds in primary intention are:
 Clean and uninfectedClean and uninfected
 Surgically incisedSurgically incised
 Without much loss of ells and tissuesWithout much loss of ells and tissues
 Edges of wound approximated by surgical suturesEdges of wound approximated by surgical sutures
SEQUENCE OF EVENTS-PRIMARY UNIONSEQUENCE OF EVENTS-PRIMARY UNION
 Initial haemorrhageInitial haemorrhage
 Acute inflammatory responseAcute inflammatory response
 Epithelial changesEpithelial changes
 OrganisationOrganisation
 Suture tracksSuture tracks

Primary closurePrimary closure

INITIAL HAEMORRHAGEINITIAL HAEMORRHAGE
 Just after injury ,space between approximated surface ofJust after injury ,space between approximated surface of
incised wound is filled with blood.incised wound is filled with blood.
 It then clots and seals the wound against dehydration andIt then clots and seals the wound against dehydration and
infection.infection.
ACUTE INFLAMMATORY RESPONSEACUTE INFLAMMATORY RESPONSE
 Occurs within 24 hours with appearance of polymorphs fromOccurs within 24 hours with appearance of polymorphs from
margins of incision.margins of incision.
 By 3By 3rdrd
day polymorphs are replaced by macrophages.day polymorphs are replaced by macrophages.

EPITHELIAL CHANGESEPITHELIAL CHANGES
 Basal cells of epidermis start proliferating.Basal cells of epidermis start proliferating.
 Migrate towards inisional space.Migrate towards inisional space.
 Well approximated wound is covered by a layer of epitheliumWell approximated wound is covered by a layer of epithelium
in 48 hours.in 48 hours.
 Migrated epithelial cells forms scab,which later cast off.Migrated epithelial cells forms scab,which later cast off.
 Basal cells continue to divide.Basal cells continue to divide.
 By 5By 5thth
day a multilayered new epidermis is formed which isday a multilayered new epidermis is formed which is
differenciated into superficial and deeper layers.differenciated into superficial and deeper layers.

ORGANIZATIONORGANIZATION
 By 3By 3rdrd
day, fibroblasts also invade wound area.day, fibroblasts also invade wound area.
 By 5By 5thth
day new collagen fibrils start to form.day new collagen fibrils start to form.
 In 4 weeks, scar tissue with santy cellular and vascularIn 4 weeks, scar tissue with santy cellular and vascular
elements is formed.elements is formed.
 Also few inflammatory cells and epithelised surface isAlso few inflammatory cells and epithelised surface is
also formed.also formed.
SUTURE TRACKSSUTURE TRACKS
 When sutures are removed on 7When sutures are removed on 7thth
day much ofday much of
epithelialized suture track is avulsed and remainingepithelialized suture track is avulsed and remainingwww.indiandentalacademy.comwww.indiandentalacademy.com

HEALING BY SECONDARY UNIONHEALING BY SECONDARY UNION
Healing of wounds with following characteristics:Healing of wounds with following characteristics:
 Open with large tissue defect (times infected)Open with large tissue defect (times infected)
 Having extensive loss of cells and tissuesHaving extensive loss of cells and tissues
 Wound is not approximated by surgical sutures but is leftWound is not approximated by surgical sutures but is left
open.open.
 Basic events in secondary union are similar to primary unionBasic events in secondary union are similar to primary union
but differ in having a larger tissue defect which has to bebut differ in having a larger tissue defect which has to be
bridged.bridged.
 Healing by secondary union is slow and results in large,atHealing by secondary union is slow and results in large,at
times ugly scar.times ugly scar. www.indiandentalacademy.comwww.indiandentalacademy.com

Secondary closureSecondary closure

EVENTS:EVENTS:
 Initial Haemorrhage:Initial Haemorrhage: As a result of injury, wound spaceAs a result of injury, wound space
is filled with blood and fibrin clot which dries.is filled with blood and fibrin clot which dries.
 Inflammatory Phase:Inflammatory Phase: Initial inflammatory responseInitial inflammatory response
occurs followed by appearance of macrophages which clear offoccurs followed by appearance of macrophages which clear off
debris.debris.
 Epithelial Changes:Epithelial Changes:Proliferating epithelial cells do notProliferating epithelial cells do not
cover the surface fully till granulation tissue has filled thecover the surface fully till granulation tissue has filled the
space.space.
 Granulation Tissue:Granulation Tissue:Main bulk of secondary healing isMain bulk of secondary healing is
by granulation.by granulation. www.indiandentalacademy.comwww.indiandentalacademy.com

 Granulation tissue is formed by proliferation of fibroblasts andGranulation tissue is formed by proliferation of fibroblasts and
neovascularization from adjoining viable elementsneovascularization from adjoining viable elements
 Newly formed granulation tissue is deep red ,granular andNewly formed granulation tissue is deep red ,granular and
very fragile.very fragile.
Wound Contraction:Wound Contraction:Imp. feature of secondary healing.Imp. feature of secondary healing.
 Not seen in primary healing.Not seen in primary healing.
 Due to action of myofibroblasts present in granulationDue to action of myofibroblasts present in granulation
tissue,wound contracts to 1/3tissue,wound contracts to 1/3rdrd
to 1/4to 1/4thth
of original size.of original size.
Presence of Infection:Presence of Infection: Bacterial contamination of anBacterial contamination of an
open wound delays process of healing.open wound delays process of healing.
 Necrosis is provoked,along with suppuration and thrombosis.Necrosis is provoked,along with suppuration and thrombosis.
 Surgical removal of dead and necrosedSurgical removal of dead and necrosed
tissue,debridement,help in preventing bacterial infection oftissue,debridement,help in preventing bacterial infection of
open wounds.open wounds.

Delayed primary closureDelayed primary closure

Partial thickness wound healingPartial thickness wound healing

TISSUE RESPONSES TO INJURYTISSUE RESPONSES TO INJURY
 Vasular eventsVasular events
 Cellular eventsCellular events
 Chemical mediatorsChemical mediators
Vascular EventsVascular Events
 Immediate transient vasoconstrictionImmediate transient vasoconstriction
 Active vasodilationActive vasodilation
 Permeability changePermeability change

Cellular EventsCellular Events
• Platelets
• Neutrophils
• macrophages
• lymphocytes
• fibroblasts
• endothelial cells
Role of platelet
Hemostasis
Release of platelet granules
•alpha granules dense granules and lysosymes

NeutrophilsNeutrophils
 Protection against infectionProtection against infection
 Intacellular products releaseIntacellular products release
free radicalsfree radicals
cyclooxygenase productscyclooxygenase products
lipooxygenase productslipooxygenase products
Protease and antiproteaseProtease and antiprotease
band 2 proteinband 2 protein

MacrophagesMacrophages
Phagocytosis
Initiation of fibroblasts
Release of cellular products:
neutral proteases, complement
factors, reactive oxygen metabolites,
growth factors, fibronectin, enzyme inhibitors

Chemical mediatorsChemical mediators
 Vasoactive agentsVasoactive agents
histaminehistamine
serotoninserotonin
Arachidonic acidArachidonic acid
 Chemotatic fatorsChemotatic fators
 CytokinesCytokines

Cytokines in wound healingCytokines in wound healing
 TGF-betaTGF-beta
 PDGFPDGF
 FGFFGF
 EGFEGF
 IGF-1IGF-1
 InterleukinsInterleukins
 TNF

What are cytokines?What are cytokines?
 Cytokines are proteins produced by many cell types,Cytokines are proteins produced by many cell types,
principally activated lymphocytes and macrophages.principally activated lymphocytes and macrophages.
 Play important role in acute and chronic inflammation.Play important role in acute and chronic inflammation.
 Messenger molecules of immune system.Messenger molecules of immune system.
 Called as interleukins, because they mediate communicationCalled as interleukins, because they mediate communication
between leucocytes.between leucocytes.

HEALING OF EXTRACTION WOUNDSHEALING OF EXTRACTION WOUNDS
Immediate reaction following an extraction:Immediate reaction following an extraction:
 Blood fills the soket.Blood fills the soket.
 RBC get entrapped in fibrin meshwork.RBC get entrapped in fibrin meshwork.
 Ends of blood vessels in Pdl are sealed off.Ends of blood vessels in Pdl are sealed off.
 Vasodilation occurs in 24-48 hours.Vasodilation occurs in 24-48 hours.
 Blood vessels gets engorged in remnants of Pdl.Blood vessels gets engorged in remnants of Pdl.
 Leuocytes mobilize to immdiate area around clot.Leuocytes mobilize to immdiate area around clot.
 Surface of blood clot is covered by a layer of fibrin.Surface of blood clot is covered by a layer of fibrin.www.indiandentalacademy.comwww.indiandentalacademy.com

FIRST WEEK WOUNDFIRST WEEK WOUND
 Fibroblasts begin to proliferate from connective tissue intoFibroblasts begin to proliferate from connective tissue into
remnants of Pdl and these fibrobasts begin to grow into clotremnants of Pdl and these fibrobasts begin to grow into clot
around the periphery.around the periphery.
 Clot is gradually replaced by granulation tissue.Clot is gradually replaced by granulation tissue.
 Epithelium at periphery of wounds exihibit proliferation.Epithelium at periphery of wounds exihibit proliferation.
 Crest of bone exihibit osteoclastic activity .Crest of bone exihibit osteoclastic activity .
 Endothelial proliferation signals the beginning of capillaryEndothelial proliferation signals the beginning of capillary
growth.growth.
 Thick layers of leucocytes gather over the surface of clot andThick layers of leucocytes gather over the surface of clot and
edges of wound continue to exihibit proliferation.edges of wound continue to exihibit proliferation.www.indiandentalacademy.comwww.indiandentalacademy.com

SECOND WEEK WOUNDSECOND WEEK WOUND
 Blood clot becomes organised by fibroblast growing into clotBlood clot becomes organised by fibroblast growing into clot
and forming fibrin meshwork.and forming fibrin meshwork.
 New delicate capillaries have penetrated to the center of clot.New delicate capillaries have penetrated to the center of clot.
 Remnants of Pdl have been undergoing degeneration.Remnants of Pdl have been undergoing degeneration.
 Epithelial proliferation over the surface of the wound isEpithelial proliferation over the surface of the wound is
extensive.extensive.

THIRD WEEK WOUNDTHIRD WEEK WOUND
 Clot appears almost completely organised by maturation ofClot appears almost completely organised by maturation of
granulation tissue.granulation tissue.
 Very young trabaculae of osteoid or uncalcified bone areVery young trabaculae of osteoid or uncalcified bone are
forming around the entire periphery of wound from socket wall.forming around the entire periphery of wound from socket wall.
 Early bone is formed by osteoblasts derived from pleuripotentEarly bone is formed by osteoblasts derived from pleuripotent
ells of original Pdl.ells of original Pdl.
 Cortical bone of alveolar socket undergoes remodelling so thatCortical bone of alveolar socket undergoes remodelling so that
it no longer consists of such dense layer.it no longer consists of such dense layer.
 Crest of alveolar bone have been rounded off by osteoclasticCrest of alveolar bone have been rounded off by osteoclastic
ativity and surface of wound becomes completelyativity and surface of wound becomes completely
epithelialized.epithelialized. www.indiandentalacademy.comwww.indiandentalacademy.com

FOURTH WEEK WOUNDFOURTH WEEK WOUND
 There is continious deposition ,remodelling and resorbtion ofThere is continious deposition ,remodelling and resorbtion of
bone filling in the alveolar bone.bone filling in the alveolar bone.
 Due to this,crest of alveolar bone undergoes considerableDue to this,crest of alveolar bone undergoes considerable
amount of osteoclastic reabsorbtion during healing process.amount of osteoclastic reabsorbtion during healing process.
 Due to this bone filling socket does not extend beyondDue to this bone filling socket does not extend beyond
alveolar bone crest.alveolar bone crest.

RADIOGRAPHIC CHANGES IN HEALINGRADIOGRAPHIC CHANGES IN HEALING
SOCKETSOCKET
 Loss of lamina dura and at same time bone develops at baseLoss of lamina dura and at same time bone develops at base
and at sites of socket.and at sites of socket.
 After socket being filled with bone,all traces of lamina dura isAfter socket being filled with bone,all traces of lamina dura is
gone.gone.
 Cortical bone formation occurs at the surface of alveolarCortical bone formation occurs at the surface of alveolar
bone.bone.
 Alveolar margins undergo some resorbtion ,surface usuallyAlveolar margins undergo some resorbtion ,surface usually
becomes flat or slightly curved but smooth.becomes flat or slightly curved but smooth.

HEALING OF FRACTUREHEALING OF FRACTURE
 After fracture haversian vessels of bone are torn at fractureAfter fracture haversian vessels of bone are torn at fracture
sites.sites.
 Due to disruption of blood vessels, there is extravasation ofDue to disruption of blood vessels, there is extravasation of
blood in that area.blood in that area.
 At the same time there is lack of circulation and lack of localAt the same time there is lack of circulation and lack of local
blood supply.blood supply.
 Osteocytes die due to tearing of vessels at fracture site andOsteocytes die due to tearing of vessels at fracture site and
death of bone marrow ocurs adjacent to fracture line.death of bone marrow ocurs adjacent to fracture line.
 Blood clot which forms play major role in healing of fractureBlood clot which forms play major role in healing of fracture
through replacement by granulation tissue and thenthrough replacement by granulation tissue and then
replacement of bone.replacement of bone.www.indiandentalacademy.comwww.indiandentalacademy.com

Callus FormationCallus Formation
 It is a structure which unites the fractured ends of bone and isIt is a structure which unites the fractured ends of bone and is
composed of varying amount of fibrous tissue,cartilage andcomposed of varying amount of fibrous tissue,cartilage and
bone.bone.
 TYPES OF CALLUS:TYPES OF CALLUS:
 External Callus: Consists of new tissues which formsExternal Callus: Consists of new tissues which forms
around the outside of the two fragment of bone.around the outside of the two fragment of bone.
 Internal Callus: Consists of new tissue arising from theInternal Callus: Consists of new tissue arising from the
marrow cavity.marrow cavity.

FACTORS AFFECTING HEALINGFACTORS AFFECTING HEALING
 GeneralGeneral
 LocalLocal
GENERAL FACTORSGENERAL FACTORS
 Nutrition: Malnutrition delays healing.Nutrition: Malnutrition delays healing.
 Vitamin A, C,Copper,Mg and zincVitamin A, C,Copper,Mg and zinc
 Protein deficieny leads to delayed formation of granulation tissue andProtein deficieny leads to delayed formation of granulation tissue and
collagen.collagen.
 Anaemia,jaundice,diabetes and malignany.Anaemia,jaundice,diabetes and malignany.
 Pus formation.Pus formation.
LOCAL FACTORSLOCAL FACTORS
 Poor blood supply.Poor blood supply.
 Local infection(organism eat suture material &destroy granulat.Local infection(organism eat suture material &destroy granulat.

 Nerosis delays healing(due to adhesion to bony surface)Nerosis delays healing(due to adhesion to bony surface)
 Position of wounds:Skin wounds parallel to line of longer healPosition of wounds:Skin wounds parallel to line of longer heal
faster as collgen bundles are present in dermis.faster as collgen bundles are present in dermis.
 Those at right angles heal slower.Those at right angles heal slower.
 LOCATION OF WOUNDS:Wounds in area with good vascularLOCATION OF WOUNDS:Wounds in area with good vascular
supply heal faster relatively as compared to avascular areas.supply heal faster relatively as compared to avascular areas.
 IMMOBILIZATION:In areas of constant movement formationIMMOBILIZATION:In areas of constant movement formation
of new connective tissue is continiously disrupted.(in corner ofof new connective tissue is continiously disrupted.(in corner of
mouth)mouth)
OTHER FACTORSOTHER FACTORS
Physical factors: Mild traumatic injury may actually favour healingPhysical factors: Mild traumatic injury may actually favour healing
Local Temp: Affets local circulation and cell multiplication.Local Temp: Affets local circulation and cell multiplication.
In hyperthermia,healing is accelerated &delayed in hypothermia.In hyperthermia,healing is accelerated &delayed in hypothermia.

 Corticosteroids in early stage delays healing,but once healingCorticosteroids in early stage delays healing,but once healing
is established it does not interfere.is established it does not interfere.
 Deoxycortisterone increases healing.Deoxycortisterone increases healing.
HORMONES: ACTH and cortisones interfere healing.HORMONES: ACTH and cortisones interfere healing.
UV Rays increases healing while x-rays delays healing.UV Rays increases healing while x-rays delays healing.
Wound healing is delayed in pregnancy and diabetes.Wound healing is delayed in pregnancy and diabetes.

REFERENCESREFERENCES
 Harsh Mohan-Textbook of Pathology for Dental Students.2Harsh Mohan-Textbook of Pathology for Dental Students.2ndnd
Edition.Moshby publicationEdition.Moshby publication
 Oral Pathology-ShafersOral Pathology-Shafers
 Robins-General Pathology of Diseases.Robins-General Pathology of Diseases.

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