1. Wound healing is the body's complex biological response to tissue injury. It involves regeneration and repair processes to restore tissue integrity and function.
2. There are four main phases of wound healing: hemostasis, inflammation, proliferation, and remodeling. Various cell types and mediators are involved in each phase to clean the wound and promote new tissue growth.
3. Wounds can heal through primary intention, secondary intention, or tertiary intention depending on factors like cleanliness and tissue loss. Primary intention involves direct wound edge approximation while secondary intention involves healing from the base up without suturing.
1. 1
WOUND HEALING
DEPARTMENT OF PERIODONTOLOGY
RAMA DENTAL COLLEGE HOSPITALAND RESEARCH
CENTRE, KANPUR, UTTAR PRADESH- 208024
2. CONTENTS
Introduction
History
Regeneration and Repair
Phases of wound healing
Types of wound healing
Mediators of wound healing
Factors affecting wound healing
Wound healing in specialized tissue
Complications of wound healing
Advances in wound healing
Future strategies
Conclusion
References 2
3. INTRODUCTION
Wound is a disruption of the normal structure and
function of the skin and underlying soft tissue.
Wound healing is the body’s response to injury in an
attempt to restore normal structure and function.
Wound healing involves two distinct processes :
- Regeneration
- Repair
3
4. 4
• a. Tidy wounds
• ► Theyare wounds like surgical incisions and wounds caused
by sharpobjects.
• ► It is incised, clean, healthy wound , without any tissue loss.
• ► Usually primary suturing is done. Healing is by primary
intention.
CLASSIFICATION OF WOUNDS
I.RANK&WAKEFIELDCLASSIFICATION
5. 5
Theyare due to:
- Crushing.
- Tearing.
- Avulsion.
- Devitalised injury.
- Vascular injury.
- Multiple irregular wounds.
- Burns.
b. Untidy wounds
• Fracture of the underlying bone maybepresent.
• Wound infection, delayed healing arecommon.
• Liberal excision of devitalised tissue and allowing to heal by secondary intention
is the management.
• Secondarysuturing, skin graft or flap maybeneeded.
6. 6
CLASSIFICATION BASED ON THE THICKNESS OF WOUND
Superficial wound- involving only epidermis and dermal papillae.
Partial thickness wound- with skin loss up to deep dermis with only
deepest part of the dermis, hair follicle shafts and sweat glands are left
behind.
Full thickness wound- with loss of entire skin and subcutaneous tissue
causing spacing out of the skin edges.
Deep wound- are the one extending deeper, across deep fascia into muscles
or deeper structures.
Complicated wound- are one associated with injury to vessels or nerves.
Penetrating wound- are one which penetrates into either natural cavities
or organs.
7. 7
CLASSIFICATION BASED ON THE INVOLVEMENT OF STRUCTURES
Simple wounds- are one involving only one organ or tissue.
Combined wounds- are one involving mixed tissues.
8. 8
Acute wounds in normal, healthy individuals heal through
an orderly sequence of physiological events that include
hemostasis, inflammation, epithelization, fibroplasia, and
maturation. Acute wound is upto 8 hours of trauma.
When this process is altered, chronic wound may develop
and is more likely to occur in patients with underlying
disorders . Chronic wounds are generally associated with
physiological impairments that slow or prevent wound
healing. Chronic wound develops after 8 hours from the
trauma.
CLASSIFICATION BASED ON THE TIME ELAPSED
9. HISTORY
9
The earliest accounts of wound healing dates back to about 2000 B.C
Galen of Pergamum emphasized the importance of maintaining a moist
environment to ensure adequate healing.
Ambriose Paré found that simply dressed gunshot wounds heal faster and are
less painful than when treated with boiling oil, the previously accepted method.
Ignaz Philipp Semmelweis advocated need for washing hands before any
treatment.
Joseph Lister began soaking his instruments in phenol and spraying the
operating rooms, reducing the mortality rates close to 50%.
10. REGENERATION
10
It is the natural renewal of a structure, produced by growth
and differentiation of new cells and intercellular substances
to form new tissues or parts.
It takes place by proliferation of parenchymal cells and
usually results in complete restoration of the original tissue.
In order to maintain proper structure of tissues ,these cells
are under constant regulatory control of their cell-cycle.
11. REPAIR
11
Repair simply restores the continuity of the diseased tissue
and re-establishes normal margins. This process is also called
“Healing by Scar”.
It takes place by proliferation of connective tissue elements
resulting in fibrosis and scarring.
2 processes are involved in repair:
a) Granulation tissue formation.
b) Contraction of wounds.
12. 12
INFLAMMATORY PHASE
Objective:- Leukocytes and macrophages destroy bacteria, cleaning the
wound of cellular debris.
Duration:-
Immediately following the Hemostasis Phase from 0 to 3 days
post injury.
Cells
Involved:-
Host cells infiltrate the wound site, such as leukocytes and
marcophages. Bacteria are destroyed by leukocytes. Macrophages
cleanse the wound of cellular debris.
Signs &
Symptoms:-
Swelling, Increased fluid, profusion of blood, Redness, Release of
Epinephrine, Histamine response, Heat, Pain.
PHASES OF WOUND HEALING
14. PROLIFERATIVE PHASE
14
Proliferative phase is categorized by :
Fibroblast migration
Collagen synthesis
Angiogenesis
Granulation tissue formation
Epithelisation
What
happens:-
The major activity focuses on angiogenesis and granulation tissue
formation.
Duration:- 3 to 21 days post injury.
Cells
Involved:-
Macrophages, fibroblasts, immature collagen, blood vessels, and
ground substance make up granulation tissue, which fills the wound’s
cavity
16. 16
REMODELING AND MATURATION PHASE
What
happens:-
For the final phase of healing, the collagen fibers in the scar are
reorganized to improve tensile strength.
Duration:- 21 days post injury and upto 1 years later.
Cells
Involved:-
Fibroblasts, MMPs, growth factors are critical in this phase.
18. 18
GRANULATION TISSUE FORMATION:
Has 3 phases—
A. PHASE OF INFLAMMATION–
-Following trauma, blood clots at the site of injury. There is acute
inflammatory response within 24 hours.
B. PHASE OF CLEARANCE–
-Neutrophils and phagocytic activity of macrophages clear off the necrotic
tissues , debris and RBC.
C. PHASE OF INGROWTH OF GRANULATION TISSUE—
-Consist of 2 main process:-- I)Angiogenesis
II)Fibrogenesis
19. 19
ANGIOGENESIS–
-Formation of new blood vessels at the site of
injury takes place by proliferation of
endothelial cells.
-Newly formed blood vessels are more leaky,
accounting for the oedematous appearance of
new granulation tissue.
-Soon, these blood vessels differentiate into
muscular arterioles, thin-walled venules and
true capillaries.
20. 20
FIBROGENESIS–
-The newly formed blood vessels are present in an amorphous ground substance
or matrix.
-The new fibroblasts originate from fibrocytes or by mitotic division of
fibroblasts.
-Collagen fibrils begin to appear by about 6th day.
-As maturation proceeds, more collagen is formed while the number of active
fibroblasts and new blood vessels decreases and results in inactive looking scar
known as cicatrisation.
21. 21
CONTRACTION OF WOUNDS: -
-It starts after 2-3 days and the process is completed by the 14th day.
-The wound is reduced by approximately 80% of its original size.
-Contracted wound results in rapid healing since lesser surface area of the
injured tissue has to be replaced.
23. 23
PRIMARY INTENTION HEALING
Wound healing by primary intention is typical for non-complicated surgical
wounds.
It can be characterized by—
i. Cleaned and uninfected.
ii. Surgically incised.
iii. Without much loss of cells and tissues.
iv. Edges of wound are approximated by surgical sutures.
Events occuring in primary intention are—
1. INITIAL HAEMORRHAGE.
2. ACUTE INFLAMMATORY RESPONSE.
3. EPITHELIAL CHANGES.
4. ORGANIZATION.
5. SUTURE TRACKS.
24. 24
•Each suture track is a separate wound and have same
phenomenon as in healing of primary wound .
•On removal of suture around 7th day, much of epithelialized
suture track is avulsed and remaining epithelial tissue gets
absorbed.
•Sometimes suture tract gets infected and resulting in STITCH
ABSCESS or when epithelial cells may persists in the tract it
causes- IMPLANTATION or EPIDERMAL CYST.
Suture Tracks
27. 27
SECONDARY INTENTION HEALING
Healing takes place from the base upwards as well as from the margins inwards.
Healing is slow and results in a large, at times ugly, scar as compared to primary
intention.
Occur in wounds having the following characteristics: –
i. Open with a large tissue defect, at times infected.
ii. Having extensive loss of cells and tissues.
iii. These wounds are not approximated by surgical sutures but are left open.
Events occuring in secondary intention are—
1. INITIAL HAEMORRHAGE.
2. INFLAMMATORY PHASE.
3. EPITHELIAL CHANGES.
4. GRANULATION TISSUE.
5. WOUND CONTRACTION.
6. PRESENCE OF INFECTION.
29. 29
A.The open wound is filled with blood clot and there is inflammatory response at the
junction of viable tissue
B. Epithelial spurs from the margins of wound meet in the middle to cover the gap
and separate the underlying viable tissue from necrotic tissue at the surface forming scab
C. After contraction of the wound ,a scar smaller than the original wound isleft
A B C
30. Difference between 1˚ & 2˚ union of
wound
FEATURES PRIMARY SECONDARY
CLEANLINESS CLEAN NOT CLEAN
INFECTION NOT INFECTED INFECTED
MARGINS SURGICALLY CLEAN IRREGULAR
SUTURES USED NOT USED
HEALING SMALL GRANULATION
TISSUE
LARGE GRANULATION
TISSUE
OUT COME LINEAR SCAR IRREGULAR WOUND
COMPLICATION NOT FREQUENT FREQUENT
31. 31
TERTIARY INTENTION HEALING
Wounds that are too heavily contaminated for primary closure but start
appear clean and well vascularized after 4-5 days of open observation
can be dealt with tertiary intention healing.
When resolution has occurred, the wound edges can be brought
together (approximated) and the wound proceeds to heal.
Most commonly indicated in:-
-infected wounds with high bacterial content,
-wounds with a long time lapse since injury, or
-wounds with a severe crush component with significant tissue
devitalization.
36. 36
WOUND HEALING IN SPECIALIZED TISSUES
FRACTURE HEALING
Healing of fracture by callus formation depends upon some clinical considerations
whether the fracture is-
Traumatic or pathologic
Complete or incomplete
Simple or comminuted or compound
However, basic events in healing of any type of fracture are similar and resemble
healing of skin wound to some extent .
37. 37
Primary Union of Fractures
Occurs in a few special situations when the ends of fracture are approximated.
Bony union takes place with formation of medullary callus without periosteal callus
formation.
Patient can be made ambulatory early but there is more extensive bone necrosis
and slow healing.
Secondary union of Fractures
Is a more common process of fracture healing.
Though it is a continuous process, secondary bone union is described under the
following 3 headings:
1. Procallus formation
2. Osseous callus formation
3. Remodelling
38. A. PROCALLUS FORMATION: Steps involved are:
The osteoid undergoes calcification and is called woven bone callus.
Cells of inner layer of the periosteum lay down collagen and osteoid
matrix in the granulation tissue.
Callus composed of woven bone and cartilage starts forming within
first few days
Ingrowth of granulation tissue occurs and with it a soft tissue callus is
formed which joins the ends of fractured bone
Hematoma formation and Local inflammatory response occurs by
exudation of fibrin, polymorphs and macrophages
38
39. .
B. OSSEOUS CALLUS FORMATION:
1. Procallus act as scaffolding on which osseous callus
composed of lamellar bone is formed.
2. Woven bone is cleared away by osteoclasts and calcified
cartilage disintegrates.
3. Newly-formed blood vessels and osteoblasts invade, laying
down osteoid and lamellar bone is formed by developing
haversian system concentrically around blood vessels.
C. REMODELLING:
During the formation of lamellar bone, osteoblastic
laying and osteoclastic removal take place remodelling the
united bone ends, which become indistinguishable from normal
bone.
39
40. 40
Complications Of Fracture Wound Healing:
1. Fibrous union- when immobilization of fractured bone is not done. False
joint develop at fracture site.(pseudo-arthrosis)
2. Non-union may result if some soft tissue is interposed between fractured
ends.
3. Delayed union may occur from to delayed wound healing due to infection,
inadequate blood supply, poor nutrition, movement and old age.
Pseudo-arthrosis of Tibia
41. 41
Periodontalwoundhealing
HEALING FOLLOWING SCALING & ROOT PLANING
• Immediately after Scalingof Teeththe epithelial attachment willbe severed,
junctional & crevicular epithelium partiallyremoved
• Numerous polymorphonuclear leucocytes canbe seenbetween residual epithelial
cells & crevicular surface inabout 2 hrs
• There is dilation of blood vessels, oedema & necrosis in the lateral wall of the
pocket
• Theremaining epithelial cells show very little pre-mitotic activity at that time. 24
hrs after scaling awidespread & intense labeling of the cells have been observed, in
all areas of the remaining epithelium & in 2 days the entire pocket isepithlialized.
42. 42
• In 4-5 daysanew epithelial attachment mayappear at bottom of sulcus.
Depending on the severity of inflammation & the depth of the gingival
crevice, complete epithelial healing occursin 1-2weeks
• Immature collagen fibers occur within 21days.Following scaling,root
planning & curettage procedure healing occurs with the formation of a
long thin junctional epithelium with no connective tissueattachment.
43. 43
• A blood clot formsbetween the root surface & the lateral wall of the
pocket,soonafter the curettage
- Largenumber of polymorphonuclear leucocytesappearin the
areashortly after the procedure
- Thisisfollowed by rapid proliferation of granulationtissue.
- Epithelial cells proliferate along thesulcus.
HEALING FOLLOWING CURETTAGE
- Epithelisation of the inner surfaceof the lateral wall is completed in 2-7
days
- Thejunctional epithelium is alsoformed in about 5 days
- Healing results in the formation of a long junctional epithelium
adherent to the root surface.
44. 44
HEALING AFTER SURGICAL GINGIVECTOMY
• Initial responseafter gingivetomy isthe formation of a
protective surfaceclot
• Underlying tissue becomesacutely inflamed withsome necrosis
• Clot is then replaced by granulationtissue
• By24 hours there is anincreasein new connective tissuecells, mainly
angioblastsjust beneath the surfacelayer of inflammation and necrosis
45. 45
• By the 3rd daynumerous young fibroblast are located In the area
• Thehighly vasculargranulation tissue grows coronally, creating a new free
gingival margin andsulcus
• Capillaries derived from the blood vesselsof the periodontal ligament migratein
to the granulation tissueand within 2 weeks they connect with gingival
vessels.
• After 12 to 24hours ,epithelial cells at the marginsof the wound start tomigrate
over the granulation tissue, seperating it fromthe contaminated surfacelayer of
theclot
• Epithelial activity at the marginsreaches peakin 24to 33 hours
• Thenew epithelial cells arise from the basaland deeper spinous layersof the
wound edgeepithelium andmigrate over the wound over afibrin layer that is
later resorbed and replaced by aconnective tissuebed
• Theepithelial cells advancesby tumbling action,with cell becoming fixed to the
substrate by heidesmosomes andanew basement lamina
46. 46
• After 5 to 14 days,surface epithelization isgenerallycompleted
• During the first 4 weeks after gingivectomy ,keratinization isless
than it wasbeforesurgery
• Complete epithelial repair takesabout onemonth
• Vasodilation and vascularity begin to decreaseafter fourth dayof healing and
appear to be almost normal by the sixteenthday
• Completerepair of the connective tissuetakesabout 7weeks
• Theflow of gingival fluid in humansisinitiallyincreased after gingivectomy and
diminishes ashealingprogresses
• Maximal flow isreachedafter 1week,coinciding with thetime of maximal
inflammation
• In patientswith physiologic gingivalmelanosisthe pigmentation isdiminished in the
healedgingiva.
47. 47
Thereappearsto be little difference in the results obtained after shallow
gingival resection withelectrosurgery and that with periodontal knives.
However,when usedfor deep resection closeto bone, electrosurgery can
produce gingival recession,bone necrosisand sequestration, lossof bone
height, furcation exposure, and tooth mobility, which do not occur with the
useofperiodontal knives.
HEALING FOLLOWING ELECTROSURGICAL GINGIVECTOMY
48. 48
HEALING FOLLWING DEPIGMENTATION OF GINGIVA
Healingafter surgicaldepigmentation:
• After surgery it wasfound necessaryto cover the exposed lamina propria with
periodontal packsfor 7 to 10 days.Thewound healed uneventfully.After 6 weeks the
attached gingiva regenerated by only adelicate scarpresent. Thenewly formed
gingiva wasclinically non-pigmented.
Healingfollowingcryosurgical depigmentation:
• At 2nd to 3rd day: superficial necrosis becomes apparent and a whitish slough
could be separated from the underlyingtissue, leaving aclean pink surface.
• In 1-2 weeks: normal gingiva
• In 3-4 weeks: keratinization completed.
• Nopostoperative pain, hemorrhage, infection or scarring seen in patients.
50. 50
HEALING FOLLOWING FLAP SURGERY
• Immediately after suturing of the flap againsttooth surface a clot forms between the
2 tissues
• Theclot consistsof fibrin reticulum with many polymorphonuclear leukocytes,
erythrocytes & remnentsof injured clots
• At edgeof flap numerous capillaries areseen
• 1-3days after surgery spacebetween flap & tooth surface & bone appears reduced
& the epithelial cells along border of the flap start migrating
By1week after surgery
• epithelial cells havemigrated & established anattachmentto root surfaceby means
of hemidesmosomes
51. 51
• The blood clot isreplaced by granulation tissueproliferating from the gingival
connective tissue, alveolar bone and periodontal ligament
• By2ndweek collagenfibers beginsto appear.Collagenfibers getsarranged parallel to
root surfacerather than at right angles.Theattachment between soft tissue & tooth
surfaceis weak
• Byend of one month following surgerythe epithelial attachmentiswell formed &
the gingival creviceisalsowell epithealised
• Thereisbeginning functional arrangement ofsupracrestal fibres.
In caseswhereMucoperiostealFlap
• hasbeen reflected, superficial bone necrosishavebeen observed during first 3
days
• OsteoclasticResorption occursin that areawhich reachesits peakat 4-6days
• Osteoblastic Remodelling occurssubsequently
• Lossof alveolar bone height by about 1mm may be expected
after healing.
52. 52
HEALING OF PEDICLE AUTOGRAFTS
ADAPTATION SATAGE(0-4 days): Clot & thin fibrinous exudate between flap and
root surface
-PMNLs in clot and connective tissue
-Epithelium at margins of flap starts to
proliferate-may contact tooth surface
PROLIFERATION STAGE(4-21 days): Connective tissue invades the fibrin layer
- 6-10 days- fibroblasts apposed against root
surface
-Collagen within the flap- oriented parallel to
root surface
-Thin collagen fibers adjacent to root(no
fibrous union)
-Apical proliferation of epithelium-peaks at 10-
14 days.
-Osteoclastic resorption(peaks at 6th day)-
decreases by 14th day.
- Slight cemental resorption
53. 53
ATTACHMENT STAGE(21-28 days): Collagen fibers insert into new cementum
- Cementoid deposition(by 28th day- along
the entire root)
-Connective tissue attachment
- New gingival margin, sulcus and epithelial
attachment
- Osteoblastic activity
MATURATION STAGE(28-90 days): Continuous formation of collagen fibers
-Completely formed gingival sulcus and
epithelial attachment
-Bone apposition at alveolar crest
54. 54
HEALING OF FREE GINGIVAL GRAFT
INITIAL PHASE(0-3 days): Thin layer of exudate between graft and recipient bed
- Avascular plasmatic circulation(Forman 1960; Reese &
Stark 1961)
- Epithelium of free graft gets desquamated
REVASCULARISATION(2-11 days): Anastomosis between graft and recipient site
blood vessels
- Capillaries proliferate in the graft tissue
- Fibrous union between graft and connective
tissue bed
- Re- epithelization of the graft
TISSUE MATURATION(11-42 days): Decrease in the no. of blood vessel to normal
by the 14th day
- Epithelium maturation- formation of
keratin layer
-Functional integration-by 17th day
- Morphologically distinguishable for several
months
55. 55
DONOR SITE
-Granulation tissue fills the donor site.
-Initial healing is usually complete within 2-3 weeks after the removal of
a 4to 5mm thick graft.
-Patients should wear the surgical stent for about 2 weeks to protect the
healing wound.
-Palate returns to its pre surgical contour after about 3 months.
56. 56
RECIPIENT SITE
First week- Postoperative swelling
The epithelium of the graft will slough
Epithelial cells together with fibrin form a white film on the surface of
the grafts
The “white stage” passes in 4-7 days.
Epithelium will not cover the grafted tissue until a functional capillary circulation
has been re-established.
Therefore- Red stage(2nd & 3rd week)
-Normal colour as epithelialization is completed
- Epithelium thickens via stratification.
The graft reverts to its original volume or remains slightly larger as the swelling
subsides.
Tissue form is usually stable after 2 months, but some shrinkage may occur
between the 2nd and 4th months after surgery.
Final restorative measures should be initiated until after 4-6 months.
57. 57
HEALING OF CONNECTIVE TISSUE GRAFTS
Healing is similar to Free Gingival Graft.
2nd day- Epithelialization commences
7-10 days- Initial epithelialization completed
4 weeks- Keratinization commences
HEALING FOLLOWING FRENECTOMY
-Initial hemorrhage
-Acute inflammatory response- within 24 hours
-Epithelial changes- completes by 48 hours
-Organization of fibroblasts- starts around 3rd day
-Wound maturation- starts after 1 week and completes around 4 weeks.
58. 58
HEALING FOLLOWING OSSEOUS RESECTION
• Osseoussurgery initiates ainflammatory response
• Elevation of Mucoperiosteal Flapresults in temporary lossof
nutrient supply to the bone
• In additition surgicalresection of bone alsocontributes to inflammatory changes.
Necrosisof the alveolar crest & osteoclastic resorption of the bonetakesplace
initially
• Theosteoclastic resorption isfollowed by bone deposition& remodeling.
59. 59
• Theinitial lossin bone height iscompensatedtosomeextent by the repair and
remodeling.
• Thusfinal lossin bone height isclinicallyinsignificant
• Osteoblastic activity isevenseenafter 1yr.post-operatively
• As mucoperiosteum issutured backon to alveolar process the osteoclastic activity
doesn’t last for long
60. 60
HEALING AFTER IMPLANT PLACEMENT
• The interface areaconsistsof bone, marrow tissue, and a hematoma mixed with
bone fragments from the drillingprocess.
• In the early phaseof healing, woven bone is formed by osteoblasts at the surfaces
of trabecular and endosteal cortical bone surrounding the implant.
• Thenewly formed bone approaching the implant surface leads to bone
condensation into both, the implant threads and towards the implant surface.
• Consequently, the amount of bone in the threads and the degree of bone-implant
contact increasewithtime.
• In the late phasesof healing, lamellar bone replaceswoven bonein
aprocessof creeping substitution.
61. 61
STAGES OF HEALING OF IMPLANTS
.WovenBoneFormation: When bone matrix isexposed to extra-cellular fluid, non-
collagenous proteins &growth factors are set free & initiaterepair.
• Wovenbone isfirst formed & bridge agap within afew days.
• Wovenbone formation dominates the first 4-6 weeks
b. Lamellar BoneFormation : From2ndmonth post-operatively the microscopic
structure of bone changestolamellar or parallel fibered bone
c. BoneRemodelling : It begins around 3rd month post- operatively.Initially rapid
remodeling occurswhichslows down & continuos for rest of the life
Thuscomplete healing probably takeslonger than 3to6months
62. 62
HEALING IN NERVOUS TISSUES
1. Central Nervous System: The nerve cells of brain, spinal cord
and ganglia once destroyed are not replaced. Damaged neuroglial cells,
however, show proliferation of astrocytes called gliosis.
2.. Peripheral Nervous System: Cells of peripheral nervous system
show regeneration, mainly by proliferation of Schwann cells and fibrils from
distal end.
63. 63
HEALING OF MUSCLE
All 3 types of muscle have limited capacity to regenerate:
SKELETAL MUSCLE : Regeneration is similar to peripheral nerves. On injury cut
ends retract but are held together by stromal connective tissue injured site is
filled with fibrinous material, polymorphs and macrophages. It is then regenerated
either:
If muscle is intact- sarcolemmal tubes containing histiocytes appear and in about
3 month time restores properly.
If muscle sheath is damaged- it forms a disorganized multinucleate mass and scar
composed of fibrovascular tissue.
SMOOTH MUSCLE : Non-striated muscle has limited regenerative capacity e.g.,
appearance of smooth muscle in the arterioles in granulation tissue. However, in
large destructive lesions, the smooth muscle is replaced by permanent scar tissue.
CARDIAC MUSCLE : Destruction of heart muscle is replaced by fibrous tissue.
However, in cases where endomysium of individual cardiac fiber is intact
regeneration of cardiac fibers may occur in young patients
64. 64
HEALING OF MUCOSAL SURFACES
The cells of mucosal surfaces have very good regeneration and are normally
being lost and replaced continuously.
This occurs by proliferation from margins, migration, multilayering and
differentiation of epithelial cells in the same way as in epidermal cells in
healing of skin wounds.
65. 65
COMPLICATIONS OF WOUND HEALING
1. Wound infection
Wound infection result from gross bacterial contamination of susceptible wounds, where
the bacterial burden of replicating microorganisms actually impair healing.
Continual presence of a bacterial infection stimulates the host immune defenses leading
to production of inflammatory mediators, such as prostaglandins and thromboxane.
These cause wound hypoxia , leading to enhanced bacterial proliferation and continued
tissue damage.
Neutrophil proteases and endotoxins released by the breakdown of bacteria by the host
defense mechanism cause further destruction of newly formed cells and their collagen
matrix, resulting in impaired wound healing.
Clinical manifestation of wound infection include : erythema, warmth, swelling, pain,
odor, and pus.
66. 66
2. Deficient scar formation–
This may occur due to inadequate formation of granulation tissue .
3. Wound dehiscence-
Dehiscence result from tissue failure rather than improper suturing techniques.
The dehisced wound may be closed again or left to heal by secondary intention,
depending upon the extent of the disruption and the surgeon’s assessment of
the clinical situation.
4. Implantation (epidermal) cyst-
formation may occur due to persistence of epithelial cells
in the wound after healing.
67. 67
5. Proliferative scarring-
The two common forms of hyperproliferative healing are hypertrophied scars
and keloids.
These are characterized by hypervascularity and hypercellularity.
It results from altered apoptotic behaviour, which leads to scarring , persistent
inflammation, and an overproduction of extracellular matrix components,
including glycosaminoglycans and collagen type I.
Keloid
68. 68
6. Pigmentation- Healed wounds may at times have rust like colour
due to staining with haemosiderin .
7. Excessive contraction– An exaggeration of wound contraction may
result in formation of contractures or cicatrisation.
69. 69
ADVANCES IN WOUND HEALING
Advances in wound care include :
1. Growth factors :
• Currently, PDGF-BB is used for the treatment of cutaneous ulcers, specifically
diabetic foot ulcers.
• Recombinant KGF-2 enhance the formation of granulation tissues in rabbits and
wound closure in human meshed skin grafts.
• rhBMP-2 and rhBMP-7 induce undifferentiated mesenchymal cells to
differentiate into osteoblasts
• Platelet-rich fibrin (PRF) is a second-generation PRP where
autologous platelets and leucocytes are present in a complex fibrin matrix to
accelerate the healing of soft and hard tissue and is used as a tissue-engineering
scaffold for filling the intrabony defects and furcation defects.
70. 70
2. Dermal and Mucosal substitutes :
• Immediate coverage protects the wound from water loss, drying and
mechanical injury and so accelerates wound healing .
• Autologous grafts remains standard for replacing dermal mucosal surfaces , a
no. of bioengineered substitutes can be used in surgical practice.
Engineered skin contains all the components necessary to modulate healing and
allow healing that replicates native tissue and limits scar formation .
71. 71
Bioengineered Skin
• Living bioengineered skin equivalents provide a
living supply of growth factors and cytokine and a
collagen matrix to build upon.
• The mechanism of action is not fully understood
on how these skin equivalents initiates wound healing,
but it has been studied extensively with the Apligraf product.
• The cells contained in the Apligraf grow and proliferate,
producing growth factors, collagens, and extracellular matrix
proteins, which stimulate re-epithelization, formation of
granulation tissue, angiogenesis, and neutrophil and
monocyte chemotaxis.
• Apligraf acts as a potent cellular remedy that can provide a
different and adaptable response in acute and chronic
wounds.
72. 72
3. Hydrotherapy
• Hydrotherapy supports wound healing by debriding the wound, warming the
injured extremity, and providing gentle limb resistance for physical therapy.
• New forms used are pulsed lavage and the VersaJet.
• Pulsed lavage delivers an irrigating solution under pressure (4 to 15 psi) and
the rate of granulation tissue formation was greater in patients receiving
pulse lavage compared with those receiving conventional Hydrotherapy.
• The VersaJet Hydrosurgery System is a water jet–powered surgical tool
designed to efficiently debride a wound by removing damaged tissues and
contaminants precisely, without the collateral trauma associated with
traditional surgical modalities .
73. 73
4. Hyperbaric Oxygen:
-Dividing cells in a wound require an oxygen tension of at least 30
mmHg.
-Tissues in wounds that are not healing have partial pressure of
oxygen values of 5 to 20 mmHg
- Many reports in the literature have demonstrated benefit from
hyperbaric oxygen treatment for a variety of conditions, including
amputations, osteoradionecrosis, surgical flaps, and skin grafts.
In addition to simply providing more oxygen to the wound site,
hyperbaric oxygen therapy also increases expression of nitric oxide,
which is crucial for wound healing.
74. 74
5. Lasers
• Lasers for open wound management are low-energy lasers capable of raising
tissue temperature 0.1°C to 0.5°C. This is called as bio-stimulation.
• It is caused by the stimulation of ascorbic acid uptake by cells, stimulation of
photoreceptors in the mitochondria respiratory chain, changes in cellular ATP
and cell membrane stabilization.
• It increase healing (especially when combined with hyperbaric oxygen
treatments) of ischemic, hypoxic, and infected wounds.
The 2 most common lasers used clinically are helium-neon lasers and gallium-
arsenide lasers.
75. 75
6. Electrostimulation
In 1982, Barker described the “skin battery.” He found that the skin surface was
always negatively charged (compared with the deeper skin layers), and he
measured transcutaneous voltages up to 40mV.
Electrostimulation is believed to restart or accelerate the wound-healing process
by imitating the natural electrical current that occurs in skin when it is injured.
Electrical current applied to wounded tissue increases the migration of cells vital
to the wound-healing process (i.e., neutrophils, macrophages, and fibroblasts).
Electrostimulation may also play a role in wound healing through improved blood
flow.
76. 76
7. Negative Pressure Therapy
• Negative pressure therapy (or vacuum-assisted closure), uses a sub-atmospheric
pressure dressing to convert an open wound into a controlled closed wound.
The negative pressure removes interstitial fluid and edema to improve tissue
oxygenation. It also removes inflammatory mediators that suppress the normal
progression of wound healing.
Granulation tissue forms more rapidly and 5 days of therapy decreases the wound
bacterial count.
77. 77
FUTURE STRATEGIES
Gene Therapy :
Gene therapy is the future for wound-healing strategies. Current research is
aimed at inserting growth factor genomes into the wound.
Inserting the desired genome can be accomplished through several
different vehicles:
biologic (viral) techniques,
chemical methods via cationic liposomes, and
physical insertion:
hypodermic needle,
microseeding,
particle-mediated transfer (using a gene gun), and
electroporation
78. 78
CONCLUSION
The variety of wounds present challenges to the physician to select the most
appropriate management to facilitate healing.
A complete wound history along with knowledge of the healing potential of the
wound, as it relates to the specific medical and environmental considerations for
each patient, provides the basis of decision making for wound management.
It is essential to consider each wound individually in order to create the optimal
conditions for wound healing.
Understanding of wound healing is as important as knowing the pathogenesis
of disease, because satisfactory wound healing is the ultimate goal of treatment.
If we are able to understand the mechanism of wound healing, we can design
treatment approaches that maximize favorable conditions for wound healing to
occur.
79. 79
REFERENCES
Pathology By Harsh Mohan - 4th edition.
Peterson's Principles of Oral and Maxillofacial Surgery, Third Edition 3rd Edition
by Michael Miloro , GE Ghali , Peter Larsen , Peter Waite .
Carranza’s Clinical Periodontology- By Newman, Takei, Klokkevold, Carranza 10th
Edition.
Wound Healing: An Overview. George Broughton.Plast. Reconstr. Surg. 117: 1e-S,
2006
Biology of wound healing. Ikramuddin Aukhil. Perio 2000, vol. 22. 2000 -44-50.
Polypeptide growth factors and attachment proteins in periodontal wound healing
and regeneration. Raul G. Caffesse & Carlos R. Quinones.
-Perio 2000, vol.1 1993- 69-79
-Perio 2000, vol 24:connective tissue of periodontium (cell biology of woundhealing)
• Journel of dental rsearch2010 march,89(3),219-229
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