wound healing.pptx

WOUND HEALING
Dr KUMAR KULDEEP
1ST YEAR POST GRADUATE TRAINEE
PUBLIC HEALTH DENTISTRY
S.C.B DENTAL COLLEGE AND HOSPITAL
2

CONTENT
 INTRODUCTION
 CLASSIFICATION OF WOUND
 HEALING PROCESSES
 TYPES OF WOUND HEALING
 PHASES OF WOUND HEALING
 HEALING IN CASE OF SPECIALISED TISSUES
 HEALING OF EXTRACTION SOCKET
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 HEALING IN PERIODONTAL SURGERY
 FACTORS AFFECTING HEALING
 COMPLICATION OF WOUND HEALING
 CONCLUSION
 REFERENCES
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INTRODUCTION
 A skin wound results from the breakdown of the epidermal layer integrity.
 Any tissue injury with anatomical integrity disruption with functional loss can be
described as a wound. Wound healing mostly means healing of the skin.
 The wound healing begins immediately after an injury to the epidermal layer and might
take years.
 This dynamic process includes the highly organized cellular, humoral, and molecular
mechanisms. Wound healing has 3 overlapping phases which are inflammation,
proliferation, and remodeling.
 Any disruption leads to abnormal wound healing.
5
Bhat SR. SRB’s manual of surgery.6th ed.New Delhi. Jaypee Brothers Medical Publishers.2019

CLASSIFICATION OF WOUNDS
A wound is a break in the integrity of the skin or tissues
often which may be associated with disruption of the
structure and function.
Rank and Wakefield classification
a) Tidy wounds
b) Untidy wounds
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Classification based on type of wound
i. Clean incised wound
ii. Lacerated wound
iii. Bruising and contusion
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iv. Haematoma
v. Puncture wound
vi. Penetrating wounds
vii. Abrasion
viii. Crush injury
ix. Injuries to bone and joint (maybe open or closed)
x. Injuries to nerve (either clean cut or crush)
xi. Injuries to arteries and veins
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Classification based on thickness of wound
a) Superficial wound
b) Partial thickness
c) Full thickness
d) Deep wounds
e) Complicated wounds
f) Penetrating wound
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Classification of surgical wounds
a) Clean wound
b) Clean contaminated wound
c) Contaminated wound
d) Dirty infected wound
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HEALING
 Healing is the body response to injury in an attempt to restore normal
structure and function.
 Healing involves 2 distinct processes
Regeneration
Repair
A) REGENERATION
when healing takes place by proliferation of parenchymal cells and usually
results in complete restoration of the original tissues
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Mohan H. Textbook of pathology. 8th ed. New Delhi. Jaypee Brothers Medical Publishers. 2018

 Some parenchymal cells are short-lived while others have a longer lifespan.
In order to maintain proper structure of tissues, these cells are under the
constant regulatory control of their cell cycle.
 Not all cells of the body divide at the same pace. Depending upon their
capacity to divide, the cells of the body can be divided into 3 groups:
a) Labile cells- continue to multiply throughout life under normal
physiologic conditions.
e.g.- surface epithelial cells of the epidermis, alimentary tract, respiratory
tract, uterine endometrium, haematopoietic cells of bone marrow and
cells of lymph nodes and spleen.
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b) Stable cells- These cells decrease or lose their ability to proliferate after
adolescence but retain the capacity to multiply in response to stimuli throughout
adult life. Cells are in resting phase(G0)
e.g.- Parenchymal cells of organs like liver, pancreas, kidneys and thyroid;
mesenchymal cells like smooth muscle cells, fibroblasts, vascular endothelium, bone
bone and cartilage cells.
c) Permanent cells- These cells lose their ability to proliferate around the time of birth.
E.g-neurons of nervous system, skeletal muscle and cardiac muscle cells.
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 Regeneration of any type of parenchymal cells involves the following 2
processes:
i) Proliferation of original cells from the margin of injury with migration
so as to cover the gap.
ii) Proliferation of migrated cells with subsequent differentiation and
maturation so as to reconstitute the original tissue.
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B) REPAIR
 Repair when healing takes place by proliferation of connective tissue elements
resulting in fibrosis and scarring.
 Two processes are involved in repair:
1. Granulation tissue formation
2. Contraction of wounds
 Repair response takes place by participation of mesenchymal cells (consisting of
connective tissue stem cells, fibrocytes and histiocytes), endothelial cells,
macrophages, platelets, and the parenchymal cells of the injured organ.
15

Granulation Tissue Formation
 The term granulation tissue derives its name from slightly granular and
pink appearance of the tissue.
 Each granule corresponds histologically to proliferation of new small blood
vessels which are slightly lifted on the surface by thin covering of
fibroblasts and young collagen.
 The following 3 phases are observed in the formation of granulation
1. PHASE OF INFLAMMATION. Following trauma, blood clots at the site of
injury. There is acute inflammatory response with exudation of plasma,
neutrophils and some monocytes within 24 hours.
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2. PHASE OF CLEARANCE. Combination of proteolytic enzymes liberated
from neutrophils, autolytic enzymes from dead tissues cells, and
phagocytic activity of macrophages clear off the necrotic tissue,
debris and red blood cells
3. PHASE OF INGROWTH OF GRANULATION TISSUE.
 This phase consists of 2 main processes:
i) Angiogenesis (neovascularisation)- Formation of new blood vessels
at the site of injury takes place by proliferation of endothelial cells
from the margins of severed blood vessels.
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 Angiogenesis takes place under the influence of following factors:
a) Vascular endothelial growth factor (VEGF) elaborated by
mesenchymal cells while its receptors are present in endothelial cells
only.
b) Platelet-derived growth factor (PDGF), transforming growth factor-β
(TGF-β), basic fibroblast growth factor (bFGF) and surface integrins
are all associated with cellular proliferation.
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ii) Fibrogenesis- The newly formed blood vessels are present in an
amorphous ground substance or matrix.
 The new fibroblasts originate from fibrocytes as well as by mitotic division
of fibroblasts.
 Some of these fibroblasts have combination of morphologic and functional
characteristics of smooth muscle cells (myofibroblasts).
 Collagen fibrils begin to appear by about 6th day.
 As maturation proceeds, more and more of collagen is formed while the
number of active fibroblasts and new blood vessels decreases. This results
in formation of inactive looking scar known as cicatrisation.
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Contraction of Wounds
 The wound starts contracting after 2-3 days and the process is
completed by the 14th day.
 During this period, 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.
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WOUND HEALING
 Healing of skin wounds provides a classical example of combination of
regeneration and repair described above.
 Wound healing can be accomplished in one of the following two ways:
a) Healing by first intention (primary union)
b) Healing by second intention (secondary union)
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HEALING BY FIRST INTENTION (PRIMARY
UNION)
 This is defined as healing of a wound which has the following
characteristics:
i) clean and uninfected;
ii) surgically incised
iii) without much loss of cells and tissue
iv) edges of wound are approximated by surgical sutures.
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The sequence of events in primary union is described below:
1. Initial hemorrhage.
2. Acute inflammatory response.
3. Epithelial changes.
4. Organisation.
5. Suture tracks. Each suture track is a separate wound and incites the
same phenomena as in healing of the primary
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 The incision causes death of a limited number of epithelial cells and connective tissue
cells, disruption of epithelial basal membrane continuity
 The narrow incisional space immediately fills with clotted blood containing fibrin and
blood cells; dehydration of the surface clot forms the well known scab that covers the
wound.
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HEALING BY SECOND INTENTION
(SECONDARY UNION)
 This is defined as healing of a wound having the following
characteristics:
I) open with a large tissue defect, at times infected
II) having extensive loss of cells and tissues
III) the wound is not approximated by surgical sutures but is left open
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The sequence of events in secondary union is described below:
1. Initial hemorrhage.
2. Inflammatory phase.
3. Epithelial changes.
4. Granulation tissue- Main bulk of secondary healing is by granulations.
Granulation tissue is formed by proliferation of fibroblasts and
neovascularisation from the adjoining viable elements.
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5. Wound contraction- Contraction of wound is an important feature of secondary
healing, not seen in primary healing. Due to the action of myofibroblasts present
in granulation tissue, the wound contracts to one-third to onefourth of its original
size.
6. Presence of infection. Bacterial contamination of an open wound delays the
process of healing due to release of bacterial toxins that provoke necrosis,
suppuration and thrombosis. Surgical removal of dead and necrosed tissue,
debridement, helps in preventing the bacterial infection of open wounds
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WOUND HEALING RESPONSE
 Divided into 4 phases
1. Bleeding Phase
2. Inflammatory Phase
3. Proliferation Phase
4. Remodeling Phase
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BLEEDING PHASE
 This is a relatively short lived phase
 Normal time for bleeding to stop depends on nature of injury and
nature of tissue
 E.g. Muscles bleeds longer with escape of blood into the tissues while
others e.g. ligament bleeds less (both in volume and duration)
 Average interval from injury to end of bleeding is usually few hours
(approx. 6-8hrs)
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 However some tissues will continue to bleed for significantly longer
period although at a significantly reduced rate
 A crush type injury to a more vascular tissue e.g. muscle could still be
bleeding (minimally) 24hrs or more post trauma
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INFLAMMATORY PHASE
 The inflammatory phase has a rapid onset (few hours) and usually last
3-5days.
 There are two essential elements to the inflammatory events :
1. Vascular Events
2. Cellular Events
 They occur in parallel and are significantly interlinked.
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VASCULAR EVENTS
 Following bleeding there’s Vasoconstriction of injured vasculature
 Tissue trauma and local bleeding activate factor XII ( Hageman factor)
 This initiates various effectors of the healing cascade including the
complement, plasminogen, kinin and clotting systems.
 Circulating platelets (thrombocytes) rapidly aggregate at the injury site and
adhere to each other and vascular subendothelial collagen to form a primary
haemostatic plug.
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 Once hemostasis is secured the reactive vasoconstriction is replaced by a more
persistent period of vasodilation mediated by histamine, prostaglandins, kinins and
leukotrienes.
 There’s also increased vascular permeability allowing blood plasma and other
cellular mediators pass through vessel wall by diapedesis and populate the
extravascular space.
 Corresponding clinical manifestation includes swelling, redness, heat and pain.
33

CELLULAR EVENTS
 The cytokines released provide chemotactic cues that sequentially recruit the
neutrophils and monocytes to site of injury.
 Neutrophils arrive at wound site within minutes of injury and rapidly establish
themselves as predominant cells.
 Intracellular product release include free radicals, cyclooxygenase products,
lipoxygenase products, protease, antiprotease.
 Proinflammatory cytokines released by perishing neutrophils including TNF- α and
interleukins( IL-1a,IL-1b) continue to stimulate the inflammatory response for extended
periods.
 There’s deployment of monocytes to injury site as the levels of neutrophils decline.
34

 Activated monocytes now macrophages continue with the wound micro
debridement initiated by neutrophils.
 They secrete collagenases and elastases to breakdown injured tissue
and phagocytose bacteria and cell debris (Scavengers).
 They also release growth factors and cytokines (TGFα, TGF-β, PDGF,
IGF,TNF-α and IL-1).
 Regulate local tissue remodelling by proteolytic enzymes (e.g. matrix
metalloproteases and collagenases), inducing formation of extracellular
matrix , modulating angiogenesis and fibroplasia.
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PROLIFERATIVE PHASE
 Starts as early as the 3rd day - 3 weeks post injury.
 It is stimulated by cytokines and growth factors secreted earlier. There’s
initial deposition of granulation tissue which matures to form scar
tissue.
 The processes involved are fibroplasia, angiogenesis and re-
epithelialization.
 Fibroblasts and endothelial cells migrate into the wounded area from
adjacent areas and proliferate within the 1st few days after tissue
damage
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 The damaged capillaries bud and grow forming anastomoses re-establishing
blood flow, providing oxygen and nutrients while removing metabolic waste
products.
 Fibroblasts initially produce type III collagen which becomes type I collagen as
the repair matures (during remodeling).
 They also produce fibronectin and proteoglycans which are essential
components of the ground substance.
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 New epithelium form at the surface of the dermal wound to seal off the
denuded wound surface.
 There’s proliferation of epidermal cells above the basement membrane.
 Re-epithelialization is facilitated by the shrinking of the connective
tissue to draw the wound margins together.
 Myofibroblasts derived from activated fibroblasts are responsible for
wound contraction and early repair strength, therefore reduce the size
of the final scar.
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REMODELING PHASE
 This primarily involves the collagen and its associated extracellular matrix.
 A proportion of the original fine Type III collagen is reabsorbed and replaced with
Type I collagen with more cross links and greater tensile strength.
 Homeostasis of scar collagen and ECM is regulated by serine proteases and matrix
metalloproteinases (MMP’s) under the control of regulatory cytokines.
 Old fibrous tissue is removed and new scar tissue is laid down. Final remodeling may
continue for months and possibly over a year beyond obvious healing of the damage.
39

FRACTURE HEALING
 Similar to that of soft tissue healing except that it also involves
calcification of connective tissue matrix.
 Heals by regeneration instead of repair
 Indirect healing: Fractured bone restores itself spontaneously through
sequential tissue formation and differentiation
 Direct healing: The displaced bone segments are surgically manipulated
into an acceptable alignment and rigidly stabilized through the use of
internal fixation devices.
40

STAGES OF FRACTURE HEALING
 Tissue destruction and Hematoma formation
 Inflammation and cellular proliferation
 Stage of callus formation
 Stage of consolidation
 Stage of remodeling
41

TISSUE DESTRUCTION AND HEMATOMA
FORMATION
 Hemorrhage from torn vessels in harvesian canals, marrow and
periosteum
 Formation of a mass of clotted blood (hematoma) at the fracture site
 Site becomes swollen, painful and inflamed
42

INFLAMMATION AND CELLULAR
PROLIFERATION
 Within 8hrs inflammatory reaction starts
 PMN leukocytes and subsequently macrophages move to fracture site
and scavenge debris
 Proliferation and differentiation of mesenchymal stem cells which begin
to rapidly produce a soft fracture callus
 Secretion of TGF- β, PDGF and various BMP(bone morphogenetic
protein) factors
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CALLUS FORMATION
 Granulation tissue ( soft callus) forms a few days after fracture
 Inflammation triggers cell division and growth of new blood vessels
 Among the new cells, chondrocytes secrete collagen and proteoglycans
creating fibrocartilage that forms the soft callus
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STAGE OF CONSOLIDATION
 Bony callus begins 3-4 weeks after injury and continues until firm union
is formed 2-3 months later.
 New bone trabeculae appear in the fibrocartilaginous callus
 Fibrocartilaginous callus converts into bony (hard) callus
45

STAGE OF REMODELING
 Remodeling restores the original shape and internal architecture of the
fractured bone
 Carried out by juxtaposed osteoclasts and osteoblasts called Basic
Multicellular Unit (BMU).
 Osteoclast at the leading edge of the BMU excavate bone through
proteolytic digestion
 While active osteoblast move in, secreting layers of osteoid slowly
refilling the cavity.
46

 Afterwards the osteoid begin to mineralize when its about 6 μm thick.
 Over time mechanically strong ,highly organized cortical bone replaces
the weaker disorganized woven bone
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HEALING OF NERVOUS TISSUE
CENTRAL NERVOUS SYSTEM- The nerve cells of the brain, spinal cord
and ganglia once destroyed are not replaced. The damaged neuroglial
cells, however, may show proliferation of astrocytes called gliosis.
PERIPHERAL NERVOUS SYSTEM- It shows regeneration, mainly from
proliferation of Schwann cells and fibrils from distal end.
 Briefly, it consists of the following: Myelin sheath and axon of the intact
distal nerve undergo Wallerian degeneration up to the next node of
Ranvier towards the proximal end.
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 Degenerated debris are cleared away by macrophages. Regeneration in
the form of sprouting of fibrils takes place from the viable end of axon.
 These fibrils grow along the track of degenerated nerve so that in
about 6-7 weeks, the peripheral stump consists of tube filled with
elongated Schwann cells.
 One of the fibrils from the proximal stump enters the old neural tube
and develops into new functional axon.
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HEALING OF MUSCLE
 All three types of muscle fibers have limited capacity to regenerate.
SKELETAL MUSCLE. On injury, the cut ends of muscle fibers retract but are
held together by stromal connective tissue.
 The injured site is filled with fibrinous material, polymorphs and
macrophages.
 After clearance of damaged fibers by macrophages, one of the following
two types of regeneration of muscle fibers can occur.
50

 If the muscle sheath is intact, sarcolemmal tubes containing histiocytes
appear along the endomysial tube which, in about 3 months time,
restores properly oriented muscle fibres, e.g. in Zenker’s degeneration
of muscle in typhoid fever.
 If the muscle sheath is damaged, it forms a disorganised multinucleate
mass and scar composed of fibrovascular tissue, e.g. in Volkmann’s
ischaemic contracture.
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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 situations where the endomysium of individual cardiac fiber is intact
(e.g. in diphtheria and coxsackie virus infections), regeneration of cardiac fibers
may occur in young patients.
52

HEALING OF MUCOSAL SURFACES
 The cells of mucosal surfaces have very good regeneration and are
normally being lost and replaced continuously e.g. mucosa of
alimentary tract, respiratory tract, urinary tract, uterine endometrium
etc.
 This occurs by proliferation from margins, migration, multilayering and
differentiation of epithelial cells in the same way as in the epidermal
cells in healing of skin wounds.
53

HEALING OF SOLID EPITHELIAL ORGANS
 Following gross tissue damage to organs like the kidney, liver and thyroid, the
replacement is by fibrous scar e.g. in chronic pyelonephritis and cirrhosis of liver.
 However, in parenchymal cell damage with intact basement membrane or intact
supporting stromal tissue, regeneration may occur.
 For example:
 In tubular necrosis of kidney with intact basement membrane, proliferation and slow
migration of tubular epithelial cells may occur to form renal tubules.
 In viral hepatitis, if part of the liver lobule is damaged with intact stromal network,
proliferation of hepatocytes may result in restoration of liver lobule
54

HEALING OF EXTRACTION SOCKET
 The first stage of healing is the formation of a clot which is loose & fills the bony and
soft tissue socket.
 Activated platelets trigger retraction of the clot, expressing fluid so that it becomes
harder and shrinks below the level of the adjacent soft tissues, pulling any mobile
soft tissue inward to reduce the area of the clot exposed.
 Clot retraction is usually complete in 4 hours, and the surface of the clot changes
from shiny to matt. After retraction, the clot continues to stabilise by fibrin cross-
linking, so avoiding rinsing is usually recommended for 24 hours.
 Lysis of the clot begins within 2 days, caused primarily by the fibrinolytic enzyme
plasmin, generated by activation of plasminogen in the clot.
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E.W. Odell. Cawson’s essentials of oral pathology and oral medicine. 9th ed. London. 2017

 As fibrinolysis started and if the clot not well anchored to the wall, the risk of dry socket
from clot lysis or loss is highest.
 At 4 days, capillaries and fibroblasts (granulation tissue) are growing into the blood clot
from the periphery so that it is now firmly fixed to the socket wall.
 Macrophages migrate into the clot and start to demolish it ready for replacement by
granulation tissue. The surface of the clot is white and porous clinically.
 Bacterial enzymes have lysed the surface fibrin, and there are bacteria in the superficial
fibrin, which gradually disintegrates.
 Epithelium at the gingival margin undergoes hyperplasia and starts to grow over the intact
clot.
 At 8 days, the socket is filled by granulation tissue and the superficial layers contain
inflammatory cells.
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 The granulation tissue is soft or gelatinous and contains little collagen. It appears red if exposed
(‘socket granulations’).
 The lamina dura of the socket remain intact but, at higher power, osteoclasts would be seen on its
surface. There is early surface resorption.
 Depending on the surface area of the socket mouth, epithelial migration is complete between 7 and 10
days.
 At 18 days, the socket is filled by granulation tissue and the fibroblasts within it have laid down a
collagen network.
 By 6 weeks the woven bone has filled the socket and is remodeling to lamellar bone. The outline of the
lamina dura persists for a very variable length of time, depending on the bone turnover rate.
 By 3 months, it is usually not detectable radiographically, but socket outlines may persist for years in
the elderly.
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PERIODONTAL WOUND HEALING
 In this case, the wound margins are not two opposing vascular gingival
margins but comprise the rigid nonvascular mineralized tooth surface,
on the one hand, and the connective tissue and epithelium of the
gingival flap, on the other.
 The periodontal wound also includes tissue resources from the alveolar
bone and the periodontal ligament.
 Clot formation at the interface between the tooth and a gingival flap is
initiated as blood elements are imposed onto the root surface during
surgery and at wound closure in a seemingly random manner.
59
Lindhe J, Lang N P(ed.). Clinical periodontology and implant dentistry. 6th ed. United Kingdom. John Wiley and Sons. 2015

 This represents the very first healing event at the tooth– gingival flap interface (i.e.
the absorption and adhesion of plasma proteins onto the root surface).
 Within minutes, a fibrin clot attached to the root surface is developed and within
hours, one may observe the early phase of inflammation as inflammatory cells,
predominantly neutrophils and monocytes, accumulate on the root surface.
 Within 3 days the late phase of inflammation dominates the healing picture as
macrophages migrate into the wound followed by the formation of granulation
tissue.
 At 7 days, a connective tissue attachment may be seen at the root surface; however,
areas of the fibrin clot in various stages of maturation may also be observed,
depending on wound volume and tissue resources.
60

 Resorptive remodeling of the dentin surface may be evident at this observation
interval.
 Within 14 days, the newly formed collagen fibers may show an arrangement
indicative of physical attachment to the dentin.
 Ramfjord et al. (1966) reported that collagen maturation of collagenous tissues and
functional orientation of the connective tissue takes 3–5 weeks.
 In addition, new bone deposition starts to occur from days 10–21. Eventually,
cementum formation may be initiated, but not until at least 3 weeks after wound
closure.
61

 The tensile strength increased from approximately 200g at 3 days post
surgery to 340g at 5–7 days post surgery, and to >1700g at 2 weeks post
surgery.
 In other words, they found that a relatively limited periodontal wound
might not reach functional integrity until 2 weeks post surgery.
 Data from studies suggest that wound integrity during the early healing
phase depends primarily on the stabilization of the gingival flaps offered by
suturing.
 Long junctional epithelium is commonly found on the root surface after
traditional periodontal surgery and provides protection against bacterial
invasion and ankylosis
62

 Several associated studies by Karring, Nyman et al., established that cells from
periodontal ligament have the capacity to regenerate the periodontal attachment,
while the alveolar bone and gingival connective tissue do not possess this ability.
 As postulated by Melcher, findings suggest that if preference is provided to cells
originating from the periodontal ligament, periodontal regeneration may
consistently occur.
 It also appears from the studies that occlusion of cells originating from the gingiva
by means of tissue barriers, also known as GTR techniques, is of paramount
importance in achieving periodontal regeneration.
63
Munksgaard B. Biology and principles of periodontal wound healing / regeneration. Periodontology 2000. 2006;41(24):30–47.

VARIABLES AFFECTING HEALING
1. LOCAL FACTORS
a. Infection is the most important factor acting locally which delays the process of
healing
b. Poor blood supply to wound slows healing
c. Foreign bodies including sutures interfere with healing and cause intense
inflammatory reaction and infection.
d. Movement delays wound healing.
e. Exposure to ionising radiation delays granulation tissue formation.
f. Exposure to ultraviolet light facilitates healing.
g. Type, size and location of injury determines whether healing takes place by
resolution or organisation.
64

2. SYSTEMIC FACTORS
a. Age. Wound healing is rapid in young and somewhat slow in aged and debilitated
people due to poor blood supply to the injured area in the latter.
b. Nutrition. Deficiency of constituents like protein, vitamin C (scurvy) and zinc
delays the wound healing.
c. Systemic infection delays wound healing.
d. Administration of glucocorticoids has anti-inflammatory effect.
e. Uncontrolled diabetics are more prone to develop infections and hence delay in
healing.
f. Haematologic abnormalities like defect of neutrophil functions (chemotaxis and
phagocytosis), and neutropenia and bleeding disorders slow the process of
wound healing.
65

VASCULAR SUPPLY
 Tissue perfusion play fundamental roles in wound healing. Impaired local circulation hinders
delivery of nutrients , oxygen and antibodies to wound.
 Areas with good vascularity e.g. scalp and face heal well whereas those with poor blood
supply e.g. pretibial skin heal poorly
 Oxygen is necessary for:
 hydroxylation of proline and lysine,
 polymerization and cross linking of procollagen strands,
 collagen transport,
 fibroblast and endothelial cell replication
 Effective leukocyte killing
 Angiogenesis and many more
66
Guo S, Dipietro LA. Factors Affecting Wound Healing. J Dent Res. 2010;89(3):219–29.

INFECTION
 Failure to follow aseptic technique is a frequent reason for introducing
virulent microorganisms into wound.
 Transformation of contaminated wounds into infected wounds is also
aided through excessive tissue trauma, remnant necrotic tissue, foreign
bodies (e.g. hair) or compromised host defences.
 It also results in larger and more prolonged inflammatory reaction
predisposing also to excess scar tissue formation.
 Most important factor in minimizing the risk of infection is meticulous
surgical technique including
67

 Thorough debridement
 Adequate hemostasis
 Elimination of dead space
 Post operative emphasis on keeping wound site clean and protecting it
from trauma
68

WOUND TENSION
 Tensions across a healing wound serves to separate the wound edges,
impairs the blood supply to the area and predisposes to wound healing
complications.
 Care should thus be taken when planning incisions, where there are
large gaps between wound edges and primary apposition might not be
appropriate or possible.
 Such defects may be bridged using skin grafts or tissue flaps.
 Better cosmetic results are obtained when incisions follow natural skin
creases on face, transversely at joints and longitudinally on long parts
of the limbs.
69

PREVIOUS IRRADIATION
 Therapeutic radiation produces collateral damage in adjacent tissue
and reduces its capacity for regeneration and repair.
 Clinical and histologic features may not be apparent for weeks, months
or even years.
 Cellular and molecular responses are immediate.
 Areas that have undergone radiotherapy suffer from patchy vasculitis,
impairing their blood supply and their healing potential.
 Damage to skin stem cells results in poor re-epithelization.
70

POOR TECHNIQUE
 Care should be taken when making incision to create a clean precise cut.
 Gentle handling of tissues is important.
 Rough handling and damaging tissues can result in tissue edge necrosis,
predisposing to poor healing and infection.
 Careful hemostasis allows good visualization and reduces tissue bruising and
hematoma formation.
 Choice of appropriate suture material and suture removal at correct time is
important and helps prevent scarring associated with the sutures themselves
71

NUTRITIONAL DEFICIENCIES
 Vitamin A is involved in epithelialisation and collagen production
 Vitamin C is important in the production and modification of collagen
 Zinc acts as an enzyme cofactor and has a role in cell proliferation deficiency
may be seen in patients on long term parenteral nutrition
 Protein is the main building block in wound healing
 Protein amino acids are essential for collagen production.
 A malnourished, hypoproteinemic patient has impaired inflammatory and
immune responses
72

SYSTEMIC DISEASES
 Several diseases are known to impair wound healing e.g. diabetes, uremia and jaundice
 Diabetes: tissue hyperglycaemia affects wound healing by affecting the immune system
including neutrophil and lymphocyte function, chemotaxis and phagocytosis.
 Uncontrolled blood glucose also hinders red blood cell permeability and impairs blood
flow through blood vessels at wound surface.
 Impaired hemoglobin release of oxygen results in oxygen and nutrient deficiency at wound
site,
 Wound ishaemia and impaired recruitment of cells renders the wound vulnerable to
infection.
73

 Uremia: can interfere with wound healing by slowing granulation tissue
formation and inducing the synthesis of poor quality collagen.
74

THERAPEUTIC AGENTS
 Systemic glucocorticoids (GC): which are frequently used as anti-
inflammatory agents, are well-known to inhibit wound repair via global
anti-inflammatory effects and suppression of cellular wound responses,
including fibroblast proliferation and collagen synthesis.
 Systemic steroids cause wounds to heal with incomplete granulation
tissue and reduced wound contraction.
 Topical low-dosage corticosteroid treatment of chronic wounds has
been found to accelerate wound healing, reduce pain and exudate, and
suppress hypergranulation tissue formation in 79% of cases
75

 Anti-neoplastic agents: Chemotherapeutic drugs delay cell migration
into the wound, decrease early wound matrix formation, lower collagen
production, impair proliferation of fibroblasts, and inhibit contraction of
wounds.
 weaken the immune functions of the patients, and thereby impede the
inflammatory phase of healing and increase the risk of wound infection.
 Chemotherapy induces neutropenia, anemia, and thrombocytopenia,
thus leaving wounds vulnerable to infection, causing less oxygen
delivery to the wound, and also making patients vulnerable to excessive
bleeding at the wound site.
76

 NSAIDS: , systemic use of ibuprofen has demonstrated an anti-
proliferative effect on wound healing, resulting in decreased numbers
of fibroblasts, weakened breaking strength, reduced wound contraction,
delayed epithelialization and impaired angiogenesis.
77

AGE
 Wound healing is faster in young and protracted in elderly.
 Decline in healing results from gradual reduction of tissue metabolism
as one ages which is also due to decreased circulatory efficiency.
 This results in delayed onset of healing, protraction of phases, and an
inability to reach same level of healing.
 There’s also decreased tensile strength and wound closure rate
78

SMOKING
 It has negative impact on wound healing due to the effects of nicotine, carbon
monoxide, and hydrogen cyanide from smoke.
 Smoking causes decreased tissue oxygenation due peripheral
vasoconstriction.(nicotine- sympathetic stimulation-release epinephrine.
 It also increases carboxyhaemoglobin( CO, 200 times affinity to Hb than oxygen),
platelet aggregation and blood viscosity(nicotine- reduced fibrinolytic activity).
 It also decreases collagen deposition, hindered epithelial regeneration.
79

COMPLICATIONS OF WOUND HEALING
 Infection
 Dehiscence
 Incisional hernia
 Hypertrophic scarring
 Keloid scarring
 Contractures
80
Kumar V, Abbas A.K, Aster J.C. Robbins basic pathology. 10th ed. Pennsylvania: Elsevier. 2018

DEHISCENCE
 Partial or Total breakdown of the layers of a surgically repaired wound.
 Most instances result from tissue failure rather than improper suturing
techniques.
 Dehisced wound may be closed again or left to heal by secondary
intention depending on the extent of disruption and surgeons clinical
assessment
81

INCISIONAL HERNIA
 Dehiscence of deeper layers of a wound in which the skin layer remains
intact.
 There’s protrusion of underlying structures through the deeper defect.
 Particularly important for abdominal wounds where viscera such as
small intestine can herniate with risks of irreducibility, obstruction and
strangulation
82

PROLIFERATIVE SCARING
 Two common forms
I. Keloids
II. Hypertrophic scars
 Keloids
 Keloids are overgrowth of dense fibrous tissue that usually develops
after healing of skin injury.
 The tissue extends beyond the borders of the original wound that does
not usually regress spontaneously and tends to recur after excision.
83

 This is in contrast with hypertrophic scars which typically do not expand beyond the
boundaries of the initial injury.
 May undergo partial spontaneous resolution.
 Standard treatment
 Corticosteroid injections
 Occlusive dressings
 Compression dressings
 Excisional Surgery
 Radiation
 Freezing (Cryosurgery)
 Laser therapy
 Interferon therapy
85

CONTRACTURES
 Can occur in any wound but more frequently in wounds that experience
delay healing, burns and those which incision crosses langer’s lines.
 Contraction of a scar across a joint can result in marked limitation of
movement.
 It is thus important to avoid vertical incisions across a joint.
 Surgical treatment of scar contracture can include skin grafting, local
flap or wound z-plasty.
86

CONCLUSION
 Tissue healing is a complex and dynamic system which enables effective repair of
damaged tissue.
 Appropriate surgical technique with sterile environment thereby controlling
infection and better knowledge of factors affecting the healing influence the process
in a positive way.
88

REFERENCES
Bhat SR. SRB’s manual of surgery.6th ed. New Delhi: Jaypee Brothers Medical
Publishers.2019
Mohan H. Textbook of pathology. 8th ed. New Delhi: Jaypee Brothers Medical
Publishers. 2018
Kumar V, Abbas A.K, Aster J.C. Robbins basic pathology. 10th ed. Pennsylvania:
Elsevier. 2018
E.W. Odell. Cawson’s essentials of oral pathology and oral medicine. 9th ed.
London: Elsevier. 2017
89

Lindhe J, Lang N P(ed.). Clinical periodontology and implant dentistry. 6th ed.
United Kingdom. John Wiley and Sons. 2015
Guo S, Dipietro LA. Factors Affecting Wound Healing. J Dent Res. 2010;89(3):219–
29.
Munksgaard B. Biology and principles of periodontal wound healing /
regeneration. Periodontology 2000. 2006;41(24):30–47.
90

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