The document discusses wound classification and the normal process of wound healing. It defines wounds and classifies them into four categories (clean, clean-contaminated, contaminated, dirty/infected) based on the CDC's adaptation of the American College of Surgeons' wound classification schema. It then describes the four phases of normal acute wound healing: hemostasis, inflammation, proliferation, and remodeling. Hemostasis involves platelet aggregation and fibrin clot formation to stop bleeding. Inflammation brings neutrophils and macrophages to remove debris. Proliferation involves new tissue formation. Remodeling shapes the new tissue.

1. dr nikil jaindr nikil jain

2. DefinitionDefinition
WoundWound --Loss of tissue integrityLoss of tissue integrity
that leads to disruption ofthat leads to disruption of
normal anatomic structure &normal anatomic structure &
function.function.
HealingHealing --It is referred asIt is referred as
replacement of destroyed livingreplacement of destroyed living
tissue. It comprises oftissue. It comprises of
inflammation & repair .inflammation & repair .

3. CLASSIFICATIONCLASSIFICATION
““Centers for disease control & prevention(CDC)Centers for disease control & prevention(CDC)
using an adaption of American college ofusing an adaption of American college of
surgeon’s wound classification schema”surgeon’s wound classification schema”
Surgical wounds are:Surgical wounds are:
I.I.Clean woundsClean wounds
II.II.Clean-contaminated woundsClean-contaminated wounds
III.III.Contaminated woundsContaminated wounds
IV.IV.Dirty or infected woundsDirty or infected wounds

4. 1.1.Clean WoundsClean Wounds:-:-
An uninfected operative wound inAn uninfected operative wound in
which no inflammation is encountered &which no inflammation is encountered &
the respiratory, alimentary, genital orthe respiratory, alimentary, genital or
uninfected urinary tracts are notuninfected urinary tracts are not
entered. Ex. Incisions made underentered. Ex. Incisions made under
aseptic conditions.aseptic conditions.
Closed by primary union & usually areClosed by primary union & usually are
not drained.not drained.
Apposition of tissue is maintained untilApposition of tissue is maintained until
wound tensile strength is sufficient sowound tensile strength is sufficient so
that sutures or other form of tissuethat sutures or other form of tissue
apposition are no longer needed.apposition are no longer needed.

5. 2.2.Clean-Contaminated WoundsClean-Contaminated Wounds:-:-
Operative wounds in which theOperative wounds in which the
respiratory, alimentary, genital, orrespiratory, alimentary, genital, or
urinary tracts are entered underurinary tracts are entered under
controlled conditions and withoutcontrolled conditions and without
unusual contamination.unusual contamination.
Appendectomies, cholecystectomies,Appendectomies, cholecystectomies,
and hysterectomies fall into thisand hysterectomies fall into this
category, as well as normallycategory, as well as normally cleanclean
wounds which becomewounds which become contaminated bycontaminated by
entry into aentry into a viscus resulting in minimalviscus resulting in minimal
spillage of contents.spillage of contents.

6. 3.3.Contaminated WoundsContaminated Wounds:-:-
Open, traumatic wounds or injuries such asOpen, traumatic wounds or injuries such as
soft tissue lacerations, opensoft tissue lacerations, open fractures, andfractures, and
penetrating wounds;penetrating wounds; operative proceduresoperative procedures
in which grossin which gross spillage from thespillage from the
gastrointestinalgastrointestinal tract occurs; genitourinarytract occurs; genitourinary
or biliary tract procedures in the presenceor biliary tract procedures in the presence
of infected urine or bile; and operations inof infected urine or bile; and operations in
which a major break in aseptic techniquewhich a major break in aseptic technique
has occurred (as in emergency open cardiachas occurred (as in emergency open cardiac
massage)massage)
MicroorganismsMicroorganisms multiply so rapidly thatmultiply so rapidly that
within 6 hours a contaminated woundwithin 6 hours a contaminated wound cancan
become infectedbecome infected..

7. 4.4.dirty and infeCted Woundsdirty and infeCted Wounds :-:-
Heavily contaminated orHeavily contaminated or clinicallyclinically
infected prior to theinfected prior to the operation. Theyoperation. They
include perforated viscera, abscesses, orinclude perforated viscera, abscesses, or
neglected traumatic wounds in whichneglected traumatic wounds in which
devitalized tissue or foreign materialdevitalized tissue or foreign material
have been retained. Infectionhave been retained. Infection present atpresent at
the time of surgery can increase thethe time of surgery can increase the
infection rate of any wound by aninfection rate of any wound by an
average of four times.average of four times.

8. Depending on capacity of cells to divide they canDepending on capacity of cells to divide they can
be grouped as:be grouped as:
1.1. Labile cells-Labile cells- multiply through out lifemultiply through out life
under normal physiologic conditionsunder normal physiologic conditions ..
2.2. Stable cells-Stable cells- decrease or loose theirdecrease or loose their
ability to proliferate after adolescenceability to proliferate after adolescence
but retain their capacity to multiply inbut retain their capacity to multiply in
response to stimuli through out adultresponse to stimuli through out adult
life.life.
3.3. Permanent cells-Permanent cells- loose their ability toloose their ability to
proliferate around the time of birthproliferate around the time of birth ..

9. Wound healingWound healing
Normal wound healingNormal wound healing
regeneration or repairregeneration or repair
Abnormal wound healingAbnormal wound healing
Unregulated excessive healingUnregulated excessive healing
Deficiency in healingDeficiency in healing

10. regenerationregeneration-- healing takes placehealing takes place
by parenchymal cells and usuallyby parenchymal cells and usually
results in complete restoration ofresults in complete restoration of
original tissues.original tissues.
repairrepair-- when healing takes place bywhen healing takes place by
proliferation of connective tissueproliferation of connective tissue
elements results in fibrosis &elements results in fibrosis &
scarring.scarring.

11. Wound HealingWound Healing
3 main mechanisms3 main mechanisms
I.I. Connective tissue matrixConnective tissue matrix
depositdeposit
II.II. ContractionContraction
III.III. EpithelizationEpithelization

12. Acute wounds normally heals in aAcute wounds normally heals in a
very orderly and efficientvery orderly and efficient
manner characterized by formanner characterized by for
distinct, But overlapping phasesdistinct, But overlapping phases
I.I.Hemostasis ( coagulation)Hemostasis ( coagulation)
II.II.InflammationInflammation
III.III.ProliferationProliferation
IV.IV.RemodelingRemodeling

13. HemostasisHemostasis:-:-
The normal healing responseThe normal healing response
begins the moment the tissue isbegins the moment the tissue is
injured.injured.
The blood components spill intoThe blood components spill into
the site of injury, the plateletsthe site of injury, the platelets
come into contact with exposedcome into contact with exposed
collagen and other elements ofcollagen and other elements of
extra cellular matrix.extra cellular matrix.
This contact triggers the plateletThis contact triggers the platelet
to release clotting factor as well asto release clotting factor as well as
essential growth factors andessential growth factors and

14. The healing cascade beginsThe healing cascade begins
immediately following injury whenimmediately following injury when
the platelets come into contactthe platelets come into contact
with exposed collagen.with exposed collagen.

15. Platelet aggregation proceeds,Platelet aggregation proceeds,
clotting factor are releasedclotting factor are released
resulting in deposition of a fibrinresulting in deposition of a fibrin
clot at the site of injury.clot at the site of injury.
The fibrin clot serves as aThe fibrin clot serves as a
provisional matrix and sets theprovisional matrix and sets the
stage for the subsequent events ofstage for the subsequent events of
healing.healing.

16. Platelets not only release thePlatelets not only release the
clotting factors needed to controlclotting factors needed to control
the bleeding and loss of fluid andthe bleeding and loss of fluid and
electrolytes but they also provide aelectrolytes but they also provide a
cascade of chemical signals, knowncascade of chemical signals, known
as cytokines or growth factors, thatas cytokines or growth factors, that
initiates the healing response.initiates the healing response.
The two most important signals areThe two most important signals are
PDGF and TGF-beta.PDGF and TGF-beta.
The PDGF initiates the chemotaxisThe PDGF initiates the chemotaxis
of neutrophills, macrophages,of neutrophills, macrophages,
smooth muscle cells and fibroblasts.smooth muscle cells and fibroblasts.

17. TGF-beta adds another importantTGF-beta adds another important
signal for the initiation of thesignal for the initiation of the
healing cascade by attractinghealing cascade by attracting
macrophages and stimulates them tomacrophages and stimulates them to
secrete additional cytokinessecrete additional cytokines
including FGF (fibroblast growthincluding FGF (fibroblast growth
factor), PDGF, TNF a (tumor necrosisfactor), PDGF, TNF a (tumor necrosis
alpha) & IL-1 (interleukin 1).alpha) & IL-1 (interleukin 1).

18. inflammatory pHaseinflammatory pHase
Neutrophills are the next predominentNeutrophills are the next predominent
cell marker in the wound within 24cell marker in the wound within 24
hours after injury.hours after injury.

19. The major function of theThe major function of the
neutrophills is to remove foreignneutrophills is to remove foreign
material, bacteria and non-material, bacteria and non-
functional host cells and damagedfunctional host cells and damaged
matrix components that may bematrix components that may be
present in the wound site.present in the wound site.
Bacteria give of chemical signalsBacteria give of chemical signals
attracting neutrophills, whichattracting neutrophills, which
injures them by the process ofinjures them by the process of
phagocytosis.phagocytosis.

20. The mast cell is another marker cellThe mast cell is another marker cell
of interest in wound healing.of interest in wound healing.
Mast cells release granules filledMast cells release granules filled
with enzymes, histamine and otherwith enzymes, histamine and other
active amines and these mediatorsactive amines and these mediators
are responsible for theare responsible for the
characteristic signs of inflammationcharacteristic signs of inflammation
around the wound site.around the wound site.
The active amines released from theThe active amines released from the
mast cell, causes surrounding vesselsmast cell, causes surrounding vessels
to become leaky and thus allow theto become leaky and thus allow the
speedy passage of the mononuclearspeedy passage of the mononuclear

21. By 48 hours after injury, fixedBy 48 hours after injury, fixed
tissue monocytes become activatedtissue monocytes become activated
to become wound macrophages.to become wound macrophages.
These specialized woundThese specialized wound
macrophages are perhaps the mostmacrophages are perhaps the most
essential inflammatory cellsessential inflammatory cells
involved in the normal healing.involved in the normal healing.
Inhibition of macrophage functionInhibition of macrophage function
will delay the healing response.will delay the healing response.

22. Once activated these woundOnce activated these wound
macrophages also release PDGF &macrophages also release PDGF &
TGF beta that further attractsTGF beta that further attracts
fibroblasts and smooth muscle cellsfibroblasts and smooth muscle cells
to the wound site.to the wound site.

23. These highly phagocyticThese highly phagocytic
macrophages are also responsiblemacrophages are also responsible
for removing non functional hostfor removing non functional host
cells, bacteria-filled neutrophills,cells, bacteria-filled neutrophills,
damaged matrix, foreign debris anddamaged matrix, foreign debris and
any remaining bacteria from woundany remaining bacteria from wound
site.site.
The presence of woundThe presence of wound
macrophages is a marker that themacrophages is a marker that the
inflammatory phase is nearing aninflammatory phase is nearing an
end and proliferative phase isend and proliferative phase is
beginning.beginning.

24. PROLIFERATIVEPROLIFERATIVE
PHASEPHASE
As this phase progresses, the TGF-As this phase progresses, the TGF-
beta released by the platelets,beta released by the platelets,
macrophages and T-lymphocytesmacrophages and T-lymphocytes
becomes a critical signal.becomes a critical signal.
TGF-beta is considered to be aTGF-beta is considered to be a
master control signal that regulatesmaster control signal that regulates
a host of fibroblasts functions.a host of fibroblasts functions.
TGF-beta has a 3 pronged effect onTGF-beta has a 3 pronged effect on
extracellular matrix depositionextracellular matrix deposition ..

25. First, it increases transcription ofFirst, it increases transcription of
the genes for collagen,the genes for collagen,
proteoglycans and fibronectin thusproteoglycans and fibronectin thus
increasing the over all productionincreasing the over all production
of matrix proteins.of matrix proteins.
At the same time TGF-betaAt the same time TGF-beta
decreases the secretion of proteasesdecreases the secretion of proteases
responsible for the breakdown ofresponsible for the breakdown of
matrix and it also stimulates thematrix and it also stimulates the
protease inhibitor, tissue inhibitorprotease inhibitor, tissue inhibitor
of metallo-protease.of metallo-protease.
Other cytokines considered to beOther cytokines considered to be
important are interleukinsimportant are interleukins

26. As healing progresses, severalAs healing progresses, several
responses are activated.responses are activated.
The process of epithelization isThe process of epithelization is
stimulated by presence of EGFstimulated by presence of EGF
(epithelial growth factor) and TGF-(epithelial growth factor) and TGF-
alpha that are produced byalpha that are produced by
activated wound macrophages,activated wound macrophages,
platelets and keratinocytes.platelets and keratinocytes.
Once the epithelial bridge isOnce the epithelial bridge is
complete enzymes are released tocomplete enzymes are released to
dissolve the attachment at the basedissolve the attachment at the base
of scab resulting in removal.of scab resulting in removal.

27. Due to high metabolic activity at theDue to high metabolic activity at the
wound site there is more demand forwound site there is more demand for
oxygen & nutrients.oxygen & nutrients.
Local factors in the wound microLocal factors in the wound micro
environment such as low pH, reducedenvironment such as low pH, reduced
oxygen tension and increased lactateoxygen tension and increased lactate
actually initiate the release of factorsactually initiate the release of factors
needed to bring in a new blood supply,needed to bring in a new blood supply,
this process is called angiogenesis orthis process is called angiogenesis or
neovascularizationneovascularization
It is stimulated by vascular endothelialIt is stimulated by vascular endothelial
cell growth factor, basic fibroblastcell growth factor, basic fibroblast
growth factor and TGF-beta.growth factor and TGF-beta.

28. As this phase progresses theAs this phase progresses the
predominant cell in the wound sitepredominant cell in the wound site
is fibroblast.is fibroblast.
This cell of mesenchymal origin isThis cell of mesenchymal origin is
responsible for producing the newresponsible for producing the new
matrix needed to restore structurematrix needed to restore structure
and function.and function.
Fibroblast attach to the cables ofFibroblast attach to the cables of
the provisional fibrin matrix andthe provisional fibrin matrix and
begin to produced collagen.begin to produced collagen.
Finally collagen will mature by theFinally collagen will mature by the
process of hydroxylation,process of hydroxylation,
glycosylation & cross linking.glycosylation & cross linking.

29. REMODELING PHASEREMODELING PHASE
Final maturation of collagen occursFinal maturation of collagen occurs
during the final remodeling phase.during the final remodeling phase.
This phase is characterized by continuedThis phase is characterized by continued
synthesis and degradation of the extrasynthesis and degradation of the extra
cellular matrix components trying tocellular matrix components trying to
establish a new equilibrium.establish a new equilibrium.

30. In summary the healing cascadeIn summary the healing cascade
begins with an orderly process ofbegins with an orderly process of
hemostasis & fibrin depositionhemostasis & fibrin deposition
which leads to an inflammatory cellwhich leads to an inflammatory cell
cascade, characterized bycascade, characterized by
neutrophills, macrophages &neutrophills, macrophages &
lymphocytes with in the tissue.lymphocytes with in the tissue.
This is followed by attraction &This is followed by attraction &
proliferation of fibroblasts &proliferation of fibroblasts &
collagen deposition & finallycollagen deposition & finally
remodeling by collagen crossremodeling by collagen cross
linking & maturation.linking & maturation.

35. TyPES OF wOund HEALIngTyPES OF wOund HEALIng
• Healing by Primary intentionHealing by Primary intention
• Healing by Secondary intention.Healing by Secondary intention.

36. PRImARy wOund cLOSuREPRImARy wOund cLOSuRE
Def.Def.--
approximateapproximate
the acutelythe acutely
disrupteddisrupted
tissue withtissue with
sutures, etc.sutures, etc.
IndicationIndication--cleanclean
surgicalsurgical
wound, cleanwound, clean
contaminatedcontaminated

37. Primary wound closurePrimary wound closure

38. Healing by firstHealing by first
intentionintention
1. Initial hemorrhage1. Initial hemorrhage::
wound is filled withwound is filled with
blood which then clotsblood which then clots
and seals the woundand seals the wound
against dehydrationagainst dehydration
and infectionand infection
2. Inflammatory phase2. Inflammatory phase::

39. 3.Epithelial changes3.Epithelial changes::
Epidermal cells from bothEpidermal cells from both
the margins proliferate &the margins proliferate &
migrate in the form ofmigrate in the form of
epithelial spurs.epithelial spurs.
A well approximated woundA well approximated wound
is covered by a layer ofis covered by a layer of
epithelium in 48 hrs.epithelium in 48 hrs.
The migrated epidermalThe migrated epidermal
cells separate thecells separate the
underlying viable dermisunderlying viable dermis
from overlying necroticfrom overlying necrotic
material & clot, forming amaterial & clot, forming a
scab which is cast off.scab which is cast off.

40. 4. Organization4. Organization::
By 3By 3rdrd
day fibroblastsday fibroblasts
also invade thealso invade the
wound area.wound area.
By 5By 5thth
day newday new
collagen fibrils startcollagen fibrils start
forming.forming.
In 4 weeks, the scarIn 4 weeks, the scar
tissue with scantytissue with scanty
cellular & vascularcellular & vascular
elements, a fewelements, a few
inflammatory tissueinflammatory tissue
is formed.is formed.::

41. Healing by secondHealing by second
intentionintention
1.1. Inflammatory phase:Inflammatory phase:
2.2. Initial hemorrhage:Initial hemorrhage:

42. Wound contraction and epithelializationWound contraction and epithelialization

43. 3.Epithelial changes:3.Epithelial changes:
epidermal cellsepidermal cells
migrate in the formmigrate in the form
of epithelial spursof epithelial spurs
but do not coverbut do not cover
the surface fullythe surface fully
until granulationuntil granulation
tissue from base hastissue from base has
started filling thestarted filling the
wound spacewound space..

44. 4. Granulation4. Granulation
tissuetissue::
The main bulk ofThe main bulk of
secondary healing issecondary healing is
by granulation tissue.by granulation tissue.
5.Wound contraction5.Wound contraction::
Important feature ofImportant feature of
secondary healing.secondary healing.
Wound contracts toWound contracts to
one-third to one fourthone-third to one fourth
of its original sizeof its original size

46. factors influencing woundfactors influencing wound
HealingHealing
A)A)General factorsGeneral factors
1. Age1. Age
2. Temperature2. Temperature
3. Nutrition: deficiency of3. Nutrition: deficiency of
a. Proteina. Protein -- interfere with formation ofinterfere with formation of
granulation tissue & collagen.granulation tissue & collagen.
- wound lacks tensile strength- wound lacks tensile strength
- Synthesis of pro collagen is- Synthesis of pro collagen is
hamperedhampered

47. Vitamin C deficiency:Vitamin C deficiency:
• Results in capillary fragilityResults in capillary fragility
• Formation of unstable collagen which isFormation of unstable collagen which is
quicklyquickly
degraded by collagenolysis.degraded by collagenolysis.
Vitamin E:Vitamin E:
• Serves as membrane stabilizer & plays anServes as membrane stabilizer & plays an
important role in lysosome functionimportant role in lysosome function
Vitamin A deficiencyVitamin A deficiency::
• Decrease collagen synthesis and stabilityDecrease collagen synthesis and stability

48. Zinc DeficiencyZinc Deficiency::
-DNA & RNA polymerase, are zinc-DNA & RNA polymerase, are zinc
dependent.dependent.
-Zinc excess also inhibit healing-Zinc excess also inhibit healing
4. Corticosteroids:4. Corticosteroids:
- suppression of immune system.- suppression of immune system.
5. Medicaments:5. Medicaments:
warferrin & heparin decrease formationwarferrin & heparin decrease formation
of fibrinof fibrin
matrix.matrix.
6. Diabetes :6. Diabetes :
a.a. Increased susceptibility to infectionsIncreased susceptibility to infections
due todue to

49. b. Hyperglycemia results in decreasedb. Hyperglycemia results in decreased
activity of phagocytes & production ofactivity of phagocytes & production of
abnormal collagen.abnormal collagen.
c. Insulin is required for earliest stages ofc. Insulin is required for earliest stages of
collagen formation.collagen formation.
7.Depressed general resistance; infection7.Depressed general resistance; infection
8.Shock:8.Shock:
9.Malignancy:9.Malignancy:

50. 10. Genetic defects10. Genetic defects
11. Coagulation disorders:11. Coagulation disorders:
Formation of poor fibrin network &Formation of poor fibrin network &
abnormalabnormal
platelet adhesionplatelet adhesion
12. Smoking:12. Smoking:
CO2 binds preferentially to hemoglobinCO2 binds preferentially to hemoglobin
nicotine is potent vasoconstrictornicotine is potent vasoconstrictor
,associated,associated
with hypercoaguability & predisposeswith hypercoaguability & predisposes

51. local factorslocal factors
1.1. InfectionInfection
2.2. MovementMovement
3.3. Poor blood supplyPoor blood supply
4.4. Presence of foreign bodiesPresence of foreign bodies
5.5. HaematomaHaematoma
6.6. oedemaoedema
7.7. Surgical causesSurgical causes

52. Healing of FracturesHealing of Fractures
 Healing of fractures can beHealing of fractures can be
considered in many stages, in fact itconsidered in many stages, in fact it
is continuous and different stagesis continuous and different stages
overlap in different areas.overlap in different areas.
 Integrity of periosteumIntegrity of periosteum alone canalone can
ensure adequate blood supply.ensure adequate blood supply.
1.1. Haematoma formationHaematoma formation::
 Due to torn blood vessels. TheDue to torn blood vessels. The
broken fragments may furtherbroken fragments may further
damage soft tissues. Haematomadamage soft tissues. Haematoma
holds the fragments together looselyholds the fragments together loosely

53. 2.Inflamatory reaction2.Inflamatory reaction::
Hyperemia of the reaction causesHyperemia of the reaction causes
decalcification of bone adjacent to thedecalcification of bone adjacent to the
fracture. Macrophages phagocytose redfracture. Macrophages phagocytose red
cells and debris of soft tissues.cells and debris of soft tissues.
Resorption of necrosed bone is a slowResorption of necrosed bone is a slow
process, it is executed throughprocess, it is executed through
osteoclasts and is helped by acid pHosteoclasts and is helped by acid pH
which develops in the area.which develops in the area.
3. Organization of granulation tissue3. Organization of granulation tissue
Granulation tissue originates from softGranulation tissue originates from soft
tissues of bone (marrow, endosteum andtissues of bone (marrow, endosteum and

54. 4. Formation of provisional callus4. Formation of provisional callus: (Latin –: (Latin –
hard).hard).
Is hard calcified granulation tissueIs hard calcified granulation tissue
uniting the fractured ends. Theuniting the fractured ends. The
formation begins between 6th andformation begins between 6th and
10th day.10th day.
The main contribution comes fromThe main contribution comes from
the undamaged cells of thethe undamaged cells of the
periosteum& endosteum.periosteum& endosteum.

55. Formation of nonlamellar bone:Formation of nonlamellar bone:
 Follows intra-membranous ossification.Follows intra-membranous ossification.
 Osteoid laid by osteoblastsOsteoid laid by osteoblasts
subsequently get calcified.subsequently get calcified.
 Calcification is helped by alkalinity ofCalcification is helped by alkalinity of
tissues, alkaline phosphatase secretedtissues, alkaline phosphatase secreted
by osteoblasts ,local super saturation ofby osteoblasts ,local super saturation of
calcium derived by resorption of bonycalcium derived by resorption of bony
spicules.spicules.
 Bony callus predominates wheneverBony callus predominates whenever
fracture segments are properlyfracture segments are properly
immobilizedimmobilized..

56. Formation of cartilage:Formation of cartilage:
 The process is same as endochondralThe process is same as endochondral
ossification.ossification.
 Cartilage formation occurs prominentlyCartilage formation occurs prominently
in superficial part of callus.in superficial part of callus.
 Greater the movement of fracturedGreater the movement of fractured
fragments or their separation, larger thefragments or their separation, larger the
amount of cartilage formed.amount of cartilage formed.
 Provisional callus is completely formedProvisional callus is completely formed
in 2 to 3 weeks.in 2 to 3 weeks.

57. 5. Formation of definitive callus5. Formation of definitive callus::
External callus is removed, intermediate callusExternal callus is removed, intermediate callus
converted into compact cortical bone and theconverted into compact cortical bone and the
internal callus is turned into cancellous boneinternal callus is turned into cancellous bone
&hollowed out to form the marrow cavity.&hollowed out to form the marrow cavity.
Fat & marrow cells reappear in cavity. old & newFat & marrow cells reappear in cavity. old & new
bone are firmly cemented.bone are firmly cemented.
It is a complex process and regulated by hormonesIt is a complex process and regulated by hormones
& growth factors.& growth factors.

59. Healing of extractionHealing of extraction
SocketSocket
Socket heal by second intention.Socket heal by second intention.
Events in 1Events in 1stst
weekweek
When a tooth is removed ,socket fillsWhen a tooth is removed ,socket fills
with blood which coagulates to seal itwith blood which coagulates to seal it
from oral environment.from oral environment.
Inflammation & clearance of debrisInflammation & clearance of debris
such as bone fragments.such as bone fragments.

60. Fibroplasia also begins during first week.Fibroplasia also begins during first week.
Epithelium migrates until it meetsEpithelium migrates until it meets
epithelium from other side or it finds aepithelium from other side or it finds a
bed of granulation tissue.bed of granulation tissue.
Osteoclasts accumulate along theOsteoclasts accumulate along the
crestal bone.crestal bone.
22ndnd
weekweek
Osteoid deposition along alveolar boneOsteoid deposition along alveolar bone
lining.lining.
Epithelium may be fully intact.Epithelium may be fully intact.

61. 33rdrd
& 4& 4thth
weekweek
Epithelization of most socket beingEpithelization of most socket being
complete .complete .
Resorption of cortical bone from crestResorption of cortical bone from crest
and wall of socket.and wall of socket.
4-6 months4-6 months
Complete resorption of cortical boneComplete resorption of cortical bone
lining.lining.
Epithelium moves toward the crest asEpithelium moves toward the crest as
bone fills socket. eventually becomingbone fills socket. eventually becoming
level with adjacent crestal gingiva.level with adjacent crestal gingiva.

62. Hyperbaric oxygenHyperbaric oxygen
• Beneficial effects:Beneficial effects:
1. Decreased local tissue edema1. Decreased local tissue edema
2. Improved cellular metabolism2. Improved cellular metabolism
3. Improved local tissue oxygen.3. Improved local tissue oxygen.
4. Improved leukocyte-killing ability.4. Improved leukocyte-killing ability.
5. Increased effectiveness of antibiotics5. Increased effectiveness of antibiotics

63. 6. Enhanced uptake of platelet derived6. Enhanced uptake of platelet derived
growth factor.growth factor.
7. Promotion of collagen deposition.7. Promotion of collagen deposition.
8. Promotion of neoangiogenesis.8. Promotion of neoangiogenesis.
9. Enhanced epithelial migration.9. Enhanced epithelial migration.
..

64. abnormality in Woundabnormality in Wound
HealingHealing
i.i. Excessive wound healingExcessive wound healing
ii.ii. Inadequate wound healingInadequate wound healing

65. exceSSive WoundexceSSive Wound
HealingHealing
5-15% of wounds5-15% of wounds
Excessive wound healing canExcessive wound healing can
result in Hypertrophic scar orresult in Hypertrophic scar or
Keloid formation.Keloid formation.

66. Hypertrophic scarHypertrophic scar::
remain withinremain within
the borders ofthe borders of
the originalthe original
scarscar

67. KeloidKeloid -- extendextend
beyond thebeyond the
original scaroriginal scar
marginsmargins

68. Excessive Wound HealingExcessive Wound Healing
Differ clinically and biologicallyDiffer clinically and biologically ::
Hypertrophic scarHypertrophic scar - develop in- develop in
weeks after injury, regress overweeks after injury, regress over
period of time.period of time.
KeloidKeloid -- can develop up to 1 year,can develop up to 1 year,
usually do not regress, usuallyusually do not regress, usually
recur after excision.recur after excision.

69. inadequate Woundinadequate Wound
HealingHealing
• Disrupted normal sequenced ofDisrupted normal sequenced of
wound healingwound healing
• Chronic wound - pressure ulcer,Chronic wound - pressure ulcer,
diabetic ulcer, venous static ulcer,diabetic ulcer, venous static ulcer,
etc.etc.