WOUND HEALING IS DISCUSSED IN GENERAL WITH APPLIED ASPECTS IN PERIODONTOLOGY

1. WOUND HEALING
PRESENTED BY
DR. MOHD. AIJAZ AHMED

2. CONTENTS
• INTRODUCTION
• REGENERATION
• REPAIR
• HEALING BY PRIMARY INTENTION
• HEALING BY SECONDARY INTENTION
• COMPLICATION OF WOUND HEALING
• WOUND STRENGTH(ECM)
• FACTORS AFFECTING WOUND HEALING
• HEALING OF SPECIALIZED TISSUES
• HEALING OF ORAL WOUNDS
• HEALING AFTER PERIODONTAL PROCEDURES
• HEALING OF IMPLANTS
• LASERS IN WOUND HEALING
• CONCLUSION
• REFERENCES

3. INTRODUCTION
• Injury to a tissue may result in cell death and tissue
destruction
• A wound is a disruption of the anatomic structure and
function in any body part.
• Healing on the other hand is a cell response to injury in an
attempt to restore the normal structure and function .

4. Involves 2 distinct processes :
– Regeneration
– Repair
At times both the processes take place simultaneously

5. • Even as cells and tissues are being injured ,
events that contain that damage and prepare the
surviving cells to replicate are set into motion.
• Entry of new cells into a tissue population is
largely determined by their proliferation rates ,
while cells can leave the population either by
cell death or differentiation into another cell
type .
• Interestingly regeneration and scar formation
are directed by the similar process of cell
growth, differentiation and cell matrix
formation.

6. REGENERATION
• Is the growth and differentiation of new cells and intercellular
substances to form new tissues or parts. Regeneration takes
place by growth from the same type of tissue that has been
destroyed or from it’s precursor
• In order to maintain proper structure of the tissue the
parenchymal cells are under the constant regulatory control of
their cell cycle which is controlled by Growth factors
• Cell cycle : Is defined as the period between two successive
cell divisions

8. Cell cycle and the proliferative capacity of
different cells types :
Cells are of 3 types depending on their capacity to
divide :
Labile cells
Stable cells
Permanent cells

9.  Regeneration of any type of parenchymal cell involves
following two processes :
 Proliferation of the original cells from the margin of the injury
which migrates so as to cover the gap
 Proliferation of the migrated cells with subsequent
differentiation and maturation so as to reconstitute the original
tissue

10. Molecular events in cell growth :
 Although many chemical mediators affect cell growth
POLYPEPTIDE GROWTH FACTORS… are most imp for
growth.
 GF have a Pleiotropic role :
 Cellular proliferation and differentiation : affecting the
expression of the genes involved in growth control
pathways
Tissue remodeling

11. Major growth factors in wound healing

12. Molecular events involved in cell division
1. Polypeptide growth factors bind to and activate their receptors
, many of which posses intrinsic kinase activity
2.Subsequently they phosphorylate a number of substrates
involved in signal transduction and generate 2nd messengers
like ras
3. The resultant kinase cascade leads to the activation of nuclear
transcription factors , initiates DNA synthesis and ultimately
culminates in cell division

13. 4. Also the process of cell proliferation is directed by a family of
proteins called Cyclins which act by controlling the
phosphorylation of the proteins involved in mitosis .

14. Extra cellular matrix and cell matrix interactions
 Functions :
1. Turgor to the soft tissue
2. Rigidity to the bone
3. Supplies a substratum for the cell division
4. Regulates growth, movement, and differentiation of the
cells living within it.

15.  ECM consists of 3 components :
1. Collagen
2. Adhesive glycoproteins : fibronectin, integrins , laminin.
3. Proteoglycans.

17.  To summarize, cell growth and differentiation involves at least
two types of signals acting in concert
 One derives from the soluble molecules such as polypeptide
growth factors and growth inhibitors .
 Other involves insoluble elements of ECM interacting with
cellular integrins.

18. REPAIR
 Healing of a wound by tissue that does not fully restore the
architecture or function of the part (AAP, Glossary of
periodontal terms).
 Is the replacement of the soft tissue by fibrous tissue . Damage
to parenchymal cells leads to a situation where , repair cannot
be accomplished by parenchymal regeneration alone.
 Thus, these cells begin being replaced by proliferating
fibroblasts and vascular endothelial cells within 24 hours .

19.  By 3 to 5 days there is granulation tissue formation, indicative
of healing is well established which then progressively
accumulates connective tissue matrix resulting in fibrosis.
 Repair involves :
1. Granulation tissue formation.
2.contraction of the wound.

20.  Granulation tissue formation :it derives its name from the
slightly granular and pink appearance of the tissue .
 Each granule histologically corresponds to proliferation of new
small blood vessels which are slightly lifted on the surface by
a thin covering of fibroblasts and young collagen .

21.  Involves three phases :
 Phase of inflammation
 Phase of clearance :
1.Combination of Proteolytic enzymes liberated by neutrophils
2. Autolytic enzymes from the dead tissue cells
3. Phagocytic activity of the macrophages .
All the above processes leading to clearance of the necrotic tissue ,
debris and RBCs .

22.  Phase of ingrowth of granulation tissue :
Consists of two main processes
 Angiogenesis (neovascularization)
 Formation of fibrous tissue(fibrogenesis)

23. Angiogenesis
Is necessary to sustain newly formed
granulation tissue .
Takes place by proliferation of
endothelial cells from the margins of the
severed vessels .
Relies on the extra cellular matrix in the
wound bed

24. Initially the endothelial cells are solid buds , but
within few hours develop a lumen and starts
carrying blood .
Newly formed blood vessels are leaky accounting
for edematous appearance of the new granulation
tissue .
Soon these blood vessels differentiate into
muscular arterioles , thin walled venules and true
capillaries

26. Fibrous tissue formation
Newly formed blood vessels are present in an
amorphous ground substance or matrix. The new
fibroblast originate from fibrocytes as well as the
mitotic division of the fibroblasts .
As the maturation proceeds : there is an increase
in the collagen , and a decrease in the fibroblasts
and blood vessels .
This leads to the formation of scar know as
CICATRISATION

27.  THUS FIBROSIS OCCURS IN TWO STEPS :
 Emigration and proliferation of the fibroblasts at the site of
injury
 Deposition of these cells which in turn increases collagen
synthesis
 Above process is directed by growth factors and growth
inhibiting factors, sources of which are the macrophages and
activated endothelial cells.

28. Wound contraction and ECM organization
 Is a superbly orchestrated interaction of cells, ecm,
cytokines
 Characterized by the appearance of
MYOFIBROBLASTS which is said to correspond to
the contraction of the wound
 This contraction requires the stimulation by the TGF
B1&B2 AND PDGF ,and attachment of fibroblasts to
collagen matrix through integrin receptors.
 Also metalloproteinases secreted by macrophages
play an imp. role in degradation of the collagen
which is required for wound contraction.

30. Healing by first intention
Is defined as a wound which has the following
characters
• Clean and uninfected
• Surgically incised
• Without much loss of cells and tissues
• Edges of the wound are approximated by the surgical
sutures

31. • Primary union involves the following sequence of
events:
 INITIAL HAEMORRHAGE
 ACUTE INFLAMMATORY RESPONSE
 EPITHELIAL CHANGES
 ORGANIZATION
 RESPONSE TO SUTURES

32.  INITIAL HAEMORRHAGE
• Immediately after injury, the space bw the opposing surfaces
of the skin becomes filled with blood , due to hemorrhage of
the severed vessels .
• Clot forms, which seals the incision against dehydration and
infection .

33.  ACUTE INFLAMMATORY RESPONSE :
o Ensues within 24 hours .
o Margins are infiltrated by neutrophils, monocytes
and swollen by fluid exudate.
o Autolytic enzymes liberated by dead tissue cells .
o Proteolytic enzymes by the neutrophils

34. o Phagocytic activity by monocytes and tissue
macrophages which appear by 3rd day clear away
necrotic tissue debris and RBCs .
o Ingested Hb gets converted into hemosiderin and
hematoidin .

35.  EPITHELIAL CHANGES :
o Basal cells of the epidermis from both the cut margins
start proliferating and migrating towards incisional space
in the form of epithelial spurs
o Well approx. wound is covered by a layer of epithelium in
48 hours.
o Migrated epidermal cells separate the underlying viable
dermis…. Scab which is cast off
o By 5th day multilayer epidermis is formed which
differentiates in to superficial and deeper layers.

36. Organization :
o Proceeds in the incisional deficit of the dermis,
protected by the overlying new epidermis.
o By the 3rd day : capillary buds
fibroblasts

37. • New collagen by the 5th day-dominates till healing is
complete.
• 4th week Scar tissue with scanty cellular and vascular
elements , few inflammatory cells and epithelialised
surface is formed.

38.  RESPONSE TO SUTURES :
o Each suture track is a separate wound
o Incites the same phenomena as in healing of primary
wound
o When the sutures are removed around the 7th day
much of the epi. suture track is avulsed and remaining
epi. tissue in track is absorbed .

39. PRIMARY UNION OF SKIN WOUNDS
A.The incised wound as well as suture track on either side are filled with blood clot and
there is inflammatory response from the margins
B.spurs of epidermal cells migrate along the incised margin on either side as well as round
the suture track.formation of granulation tissue also begins from below.
C.removal of sutures at around 7 th day result in scar tissue at the sites of incision and
suture track

40. Healing by secondary intention
 Is defined as-
 Wound open with a large tissue defect, at times
infected
 Extensive loss of cells and tissues
 Not approximated by sutures, but is left open

41. Secondary union consists of the following events :
 Initial hemorrhage
 Inflammatory process
 Epithelial changes
 Granulation tissue formation
 Wound contraction
 Presence of infection

42. Granulation tissue formation :
 Proliferating fibroblasts and neovascularization
 Newly formed connective tissue:deep red, granular
and very fragile.
 With time scar matures :increased collagen
decreased vascularity

43. Wound contraction
 Not seen in primary healing
 Myofibroblasts are the cells responsible for the
contraction of the wound
 13rd to 14h its original size

44. Presence of infection
 Bacterial contamination delays healing due to release
of bacterial contaminants and provoke necrosis ,
suppuration , thrombosis.
 Surgical removal of the dead tissue ‘debridement’
helps in preventing bacterial infection of the open
wounds.

45. secondary union of wound
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
seperate 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 is left

47. COMPLICATIONS OF WOUND HEALING
• Infection of wound due to entry of bacteria delays the healing
• Stich abscess –infection of suture track
• Implantation (epidermal) cyst formation may occur due to persistence of
epithelial cells in the wound after healing
• Pigmentation of healed wounds may at times may have rust like colour
due to staining wih haemosiderin
• Deficient scar formation due to inadequate formation of granulation tissue
• Incisional hernia/wound dehisence a weak scar,especially after laprotomy
may be the site of bursting open of a wound

48. • exuberant granulation/proud flesh Another deviation in
wound healing is the formation of excessive amounts of
granulation tissue, which protrudes above the level of the
surrounding skin and in fact blocks re-epithelialization
• Hypertrophied scars and keloid formation at times scar
formed is excessive ugly and painful.Excessive formation of
collagen in healing may result in keloid (claw like) formation
• Excessive contraction exaggeration of wound contractures or
cicatrisation
• Neoplasia rarely ,scar may be the site for development of
carcinoma later eg : squamous cell carcinoma in marjolins
ulcer i.e a scar formed following burns on skin

49. EXTRACELLULAR MATRIX –WOUND STRENGTH
• The wound is strengthened by proliferation of fibroblast and
myofibroblast which get structural support from the extracellular
matrix
• In addition ECM can direct cell migration ,attachment ,
differentiation and organization
• ECM has five main components
1)collagen
2)adhesive glycoprotein
fibronectin - plasma
tissue
tenascin or cytotactin
thrombospondin
3) basement membrane
4)elastic fibres

50. • 5)proteoglycans
chondroitin sulphate
heparin sulphate
dermatin sulphate
keratin sulphate
hyaluronic acid

51. Factors influencing healing
Local factors :
 Infection
 Poor blood supply
 Foreign bodies
 Movement
 Exposure to ionizing radiation
 Exposure to uv light facilitates healing
 Type, size and location of the wound-determines
whether the wound heals by resolution or
organisation

52.  Systemic factors
 Age
 Nutrition
 Systemic infection
 Administration of drugs eg. Glucorticoids
 Uncontrolled diabetes
 haematological abnormalities.

53. HEALING IN SPECIALIZED TISSUES
FRACTURE HEALING:
However, basic events in healing of any type of fracture
are similar and resemble healing of skin wound to some
extent.
The process of fracture healing can occur in two ways:
- Direct or primary bone healing occurs without
callus formation.
- Indirect or secondary bone healing occurs with a
callus precursor stage

54. • Primary union of fractures involves a direct attempt by the
cortex to re-establish itself after interruption.
• Bone on one side of the cortex must unite with bone on the
other side of the cortex to re-establish mechanical continuity.
• This process seems to occur only when anatomic restoration of
the fracture fragments takes place,
• by rigid internal fixation,
• and when the stability of fracture reduction is ensured by a
substantial decrease in interfragmentary strain.

55. • Under these conditions, bone-resorbing cells on one side of the
fracture show a tunnelling resorptive response, whereby they
re-establish new haversian systems by providing pathways for
the penetration of blood vessels .
• Secondary union is the more common process of fracture
healing it is described under three headings
i) Procallus formation
ii) Osseous callus formation
iii) Remodelling

56. PROCALLUS FORMATION:Steps involved in the formation of
procallus are as follows
• Haematoma forms due to bleeding from torn blood vessels,
filling the area surrounding the fracture. Loose meshwork is
formed by blood and fibrin clot which acts as framework for
subsequent granulation tissue formation
• Local inflammatory response occurs at the site of injury with
exudation of fibrin, polymorphs and macrophages. The
macrophages clear away the fibrin, red blood cells,
inflammatory exudate and debris. Fragments of necrosed
bone are scavenged by macrophages and osteoclasts.

57. • Ingrowth of granulation tissue begins with neovascularisation
and proliferation of mesenchymal cells from periosteum and
endosteum. A soft tissue callus is thus formed which joins the
ends of fractured bone without much strength.
• Callus composed of woven bone and cartilage starts within
the first few days. The cells of inner layer of the periosteum
have osteogenic potential and lay down collagen as well as
osteoid matrix in the granulation tissue.The osteoid
undergoes calcification and is called woven bone callus

58. • In poorly immobilised fractures (e.g. fracture ribs), the
subperiosteal osteoblasts may form cartilage at the fracture
site. At times, callus is composed of woven bone as well as
cartilage, temporarily immobilising the bone ends. This stage
is called provisional callus or procallus formation and is
divided into
• external procallus
• intermediate procallus
• Internal procallus.

59. OSSEOUS CALLUS FORMATION
procallus acts as scaffolding on which osseous callus
composed of lamellar bone is formed. The woven bone is
cleared away by incoming osteoclasts and the calcified
cartilage disintegrates.
In their place, newly-formed blood vessels and osteoblasts
invade, laying down osteoid which is calcified and lamellar
bone is formed by developing Haversian system concentrically
around the blood vessels.

60. REMODELLING
During the formation of lamellar bone, osteoblastic laying
and osteoclastic removal are taking place remodelling the
united bone ends, which after sometime, is indistinguishable
from normal bone.
The external callus is cleared away, compact bone (cortex) is
formed in place of intermediate callus and the bone marrow
cavity develops in internal callus

61. FRACTURE HEALING
A.Haematoma formation and local inflammatory response at the fracture site
B.Ingrowth of granulation tissue with formation of soft tissue callus
C.Formation of procallus composed of woven bone and cartilage with its charecteristic fusiform
appearance and having three arbitrary componenets-external ,intermediate and internal callus.
D.Formation of osseous callus composed of lamellar bone following clearance of woven bone and
cartilage
E.Remodelling bone ends the external callus cleared away,intermediate callus converted in to
lamellar bone and internal callus in to developing bone marrow cavity

62. • Complication of fracture healing
fibrous union -a false joint (pseudoarthrosis).
non - union -soft tissue is interposed
delayed union - delayed wound healing

63. Healing of Nervous Tissue
CENTRAL NERVOUS SYSTEM
 The nerve cells of the brain, spinal cord and ganglia once
destroyed are not replaced.
 Axons of CNS also do not show any significant regeneration.
 The damaged neuroglial cells, however, may show
proliferation of astrocytes called gliosis.

64. PERIPHERAL NERVOUS SYSTEM
• In contrast to the cells of CNS, the peripheral nerves show
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.
• Degenerated debris are cleared away by macrophages.
Regeneration in the form of sprouting of fibrils takes place
from the viable end of axon.

65. • 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

66. Healing of Muscle
All three types of muscle fibres have limited capacity to
regenerate
SKELETAL MUSCLE
• On injury, the cut ends of muscle fibres retract but are held
together by stromal connective tissue.
• The injured site is filled with fibrinous material, polymorphs
and macrophages.
• After clearance of damaged fibres by macrophages, one of the
following two types of regeneration of muscle fibres can occur

67. • 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.

68. 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.

69. CARDIAC MUSCLE
• Destruction of heart muscle is replaced by fibrous tissue.
• However, in situations where the endomysium of individual
cardiac fibre is intact (e.g. in diphtheria and coxsackie virus
infections), regeneration of cardiac fibres may occur in young
patients.

70. 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.

71. 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

72. Healing of oral wounds
• Oral wounds heals faster and with less scarring than extra
oral wounds
• It is mainly due to :
factors in saliva
specific microflora of the oral cavity
resemblance of fetal fibroblast with gingival fibroblast

73. Factor Mechanism
saliva Moisture ,ionic strength,
Growth factors(EGF,TGFβ,FGF,IGF…)&
unknown factors
bacteria Stimulation of macrophage influx,
Direct stimulative action on keratinocyte and
fibroblast
Phenotype of cells Fetal like fibroblasts with unique response ,
Specialised epithelium &
Connective tissue

74. Role of saliva & gingival crevicular fluid in oral wound healing
• Animals instintly lick their wounds which appear to result in
faster wound healing
• People with xerostomia/sialadenectomised animals show
dealyed healing of oral wounds
• Physico-chemical factors favouring healing are
appropriate PH
ionic strength
calcium and magnisium ions
• Saliva has an efficient capacity to reduce redox activity caused
by transitional metal ions and inhibit the production of free
radicals that may be beneficial for the healing process

75. Lubrication of oral mucosa is beneficial for wound healing
 Advantages of moist environment
prevention of tissue dehydration and cell death
accelerated angiogenesis
incremental breakdown of fibrin and tissue debris
 Presence of growth factors - growth factors are produced
by salivary glands or derived from plasma through gingival
crevice
Epidermal growth factor
Transforming growth factorβ
Fibroblast growth factor
Insulin growth factor

76. ROLE OF BACTERIA IN WOUND HEALING
• oral cavity harbours more than 500 bacterial species
• Wound colonize by pathoogic bacteria have delayed wound
healing
• In 1921 carrel reported that wounds of dogs treated with
certain concentrations of staphylococcus aureus healed faster
than untreated wounds
• Inflammatory reaction that is prerequisite for tissue repair is
accentuated by bacterial contamination
• Bacteria present in wound will attract macrophages in to the
area and induce their cytokine secretion

77. • As a consequence blood supply and granulation tissue
formation are accentuated in wound healing
• Proliferation of mesenchymal cells is increased and synthesis
rate of connective tissue component is stimulated leading to
greater tensile strength of the contaminated wounds in the
course of healing
• Depending on the type and concentration of bacteria either
accelerate or delay wound healing

78. Periodontal wound healing
HEALING FOLLOWING SCALING & ROOT PLANING
• Immediately after Scaling of Teeth the epithelial attachment will be
severed, junctional & crevicular epithelium partially removed
• Numerous polymorphonuclear leucocytes can be seen between residual
epithelial cells & crevicular surface in about 2 hrs
• There is dilation of blood vessels, oedema & necrosis in the lateral wall
of the pocket
• The remaining epithelial cells show very little pre-mitotic activity at that
time. 24 hrs after scaling a widespread &intense labeling of the cells have
been observed, in all areas of the remaining epithelium& in 2 days
the entire pocket is epithlialized.

79. • In 4-5 days a new epithelial attachment may appear at
bottom of sulcus. Depending on the severity of inflammation
& the depth of the gingival crevice, complete epithelial
healing occurs in 1-2 weeks
• 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 tissue attachment.

80. HEALING FOLLOWING CURETTAGE
• A blood clot forms between the root surface & the lateral wall
of the pocket, soon after the curettage
• Large number of polymorphonuclear leucocytes appear in
the area shortly after the procedure
• This is followed by rapid proliferation of granulation tissue.
• Epithelial cells proliferate along the sulcus.

81. • Epitheliasation of the inner surface of the lateral wall is
completed in 2-7 days
• The junctional epithelium is also formed in about 5 days
• Healing results in the formation of a long junctional
epithelium adherent to the root surface.

82. Healing after surgical gingivectomy
• Initial response after gingivetomy is the formation of a
protective surface clot
• Underlying tissue becomes acutely inflamed with some
necrosis
• Clot is then replaced by granulation tissue
• By 24 hours there is an increase in new connective tissue cells,
mainly angioblasts just beneath the surface layer of
inflammation and necrosis

83. • By the 3rd day numerous young fibroblast are located In the area
• The highly vascular granulation tissue grows coronally,creating a
new free gingival margin and sulcus
• Capillaries derived from the blood vessels of the periodontal
ligament migrate in to the granulation tissue and within 2 weeks
they connect with gingiva vessels

84. • After 12 to 24 hours ,epithelial cells at the margins of the
wound start to migrate over the granulation tissue,seperating
it from the contaminated surface layer of the clot
• Epithelial activity at the margins reaches peak in 24 to 33
hours
• The new epithelial cells arise from the basal and deeper
spinous layers of the wound edge epithelium and migrate
over the wound over a fibrin layer that is later resorbed and
replaced by a connective tissue bed
• The epithelial cells advances by tumbling action,with cell
becoming fixed to the substrate by heidesmosomes and a new
basement lamina

85. • After 5 to 14 days, surface epithelization is generally completed
• During the first 4 weeks after gingivectomy ,keratinization is less
than it was before surgery
• Complete epithelial repair takes about one month
• Vasodilation and vascularity begin to decrease after fourth day of
healing and appear to be almost normal by the sixteenth day

86. • Complete repair of the connective tissue takes about 7 weeks
• The flow of gingival fluid in humans is initially increased after
gingivectomy and diminishes as healing progresses
• Maximal flow is reached after 1week,coinciding with the time
of maximal inflammation
• In patients with physiologic gingival melanosis the
pigmentation is diminished in the healed gingiva

87. HEALING FOLLOWING ELECTROSURGICAL GINGIVECTOMY
There appears to be little difference in the results obtained
after shallow gingival resection with electrosurgery and that
with periodontal knives. However, when used for deep
resection close to bone, electrosurgery can produce gingival
recession, bone necrosis and sequestration, loss of bone
height, furcation exposure, and tooth mobility, which do not
occur with the use of periodontal knives.

88. HEALING FOLLOWING DEPIGMENTATION OF GINGIVA:
Healing after surgical depigmentation:
• After surgery it was found necessary to cover the exposed lamina
propria with periodontal packs for 7 to 10 days. The wound healed
uneventfully. After 6 weeks the attached gingiva regenerated by
only a delicate scar present. The newly formed gingiva was clinically
non-pigmented.
Healing following cryosurgical depigmentation:
• At 2nd to 3rd day: superficial necrosis becomes apparent and a
whitish slough could be separated from the underlying tissue,
leaving a clean pink surface.
• In 1-2 weeks: normal gingiva
• In 3-4 weeks: keratinization completed.
• No postoperative pain, hemorrhage, infection or scarring seen in
patients.

89. Healing following depigmentation by laser:
• During lasing gingiva gets covered with a yellowish layer, that
could be easily removed by a wet gauze.
• After 1-2 weeks: completion of re-epithelization.
• At 4th week: gingiva is similar to normal untreated gingiva i.e.,
lacking melanin pigmentation completely

90. HEALING FOLLOWING FLAPSURGERY
• Immediately after suturing of the flap against tooth surface a
clot forms between the 2 tissues
• The clot consists of fibrin reticulum with many
polymorphonuclear leukocytes, erythrocytes & remnents of
injured clots
• At edge of flap numerous capillaries are seen
• 1-3days after surgery space between flap & tooth surface &
bone appears reduced & the epithelial cells along border of
the flap start migrating
By 1 week after surgery
• epithelial cells have migrated &established an attachment to
root surface by means of hemidesmosomes

91. • The blood clot is replaced by granulation tissue proliferating
from the gingival connective tissue, alveolar bone and
periodontal ligament
• By 2nd week collagen fibers begins to appear. Collagen fibers
gets arranged parallel to root surface rather than at right
angles. The attachment between soft tissue & tooth surface is
weak
• By end of one month following surgery the epithelial
attachment is well formed & the gingival crevice is also well
epithealised
• There is beginning functional arrangement of supracrestal
fibres.

92. In cases where MUCOPERIOSTEAL FLAP
• has been reflected, superficial bone necrosis have been
observed during first 3 days
• Osteoclastic Resorption occurs in that area which reaches its
peak at 4-6 days
• Osteoblastic Remodelling occurs subsequently
• Loss of alveolar bone height by about 1 mm may be expected
after healing.

93. HEALING FOLLOWING OSSEOUS RES ECTION
• Osseous surgery initiates a inflammatory response
• Elevation of Mucoperiosteal Flap results in
temporary loss of nutrient supply to the bone
• In additition surgical resection of bone also contributes to
inflammatory changes. Necrosis of the alveolar crest &
osteoclastic resorption of the bone takes place initially
• The osteoclastic resorption is followed by bone deposition &
remodeling.

94. • The initial loss in bone height is compensated to some extent
by the repair and remodeling.
• Thus final loss in bone height is clinically insignificant
• Osteoblastic activity is even seen after 1 yr. post-operatively
• As mucoperiosteum is sutured back on to alveolar process the
osteoclastic activity doesn’t lost for long

95. Healing after implant placement
• The interface area consists of bone, marrow tissue, and a
hematoma mixed with bone fragments from the drilling process.
• In the early phase of healing, woven bone is formed by osteoblasts
at the surfaces of trabecular and endosteal cortical bone
surrounding the implant.
• The newly 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 increase with time.
• In the late phases of healing, lamellar bone replaces woven bone in
a process of creeping substitution.

96. STAGES OF HEALING OF IMPLANTS
a. Woven Bone Formation: When bone matrix is exposed to
extra-cellular fluid, non-collagenous proteins & growth factors
are set free & initiate repair.
• Woven bone is first formed & bridge a gap within a few days.
• Woven bone formation dominates the first4-6 weeks
b. Lamellar Bone Formation : From 2nd month post-operatively
the microscopic structure of bone changes to lamellar
or parallel fibered bone
c. Bone Remodelling : It begins around 3rd month post-
operatively.Initially rapid remodeling occurs which slows
down & continuos for rest of the life
Thus complete healing probably takes longer than 3 to 6 months.

97. LASERS IN WOUND HEALING
• Lasers employing low-level radiant energy have been claimed
to produce a positive effect on the biological and bio-chemical
processes of wound re-constitution.
• It has been reported that low level radiant energy of lasers
has accelerated wound healing, reduced pain and enhanced
neural regeneration.
• Dermatologic investigations have demonstrated more rapid
epithelialization, enhanced neovascularization, and increased
production of collagen by fibroblasts in vivo by the application
of radiation from argon or helium neon lasers.

98. • Reports have also shown increased synthesis of collagen and
enhanced phagocytic activity of leukocytes after use of low-
level laser irradiance of tissues in vitro.
• At present, majority of laser wound healing literature has
focused on the proliferative phase of wound healing, the
period of 10 to 14 days after wounding that is characterized
by populations of proliferating fibroblasts and the initiation of
the synthesis of collagen.

99. summary
The healing wound, as a prototype of tissue repair, is a dynamic and
changing process .The early phase is one of inflammation, followed
by a stage of fibroplasia, followed by tissue remodelling and
scarring. Different mechanisms occurring at different times trigger
the release of chemical signals that modulate the orderly migration,
proliferation, and differentiation of cells and the synthesis
and degradation of ECM proteins. These proteins, in turn, directly
affect cellular events and modulate cell responsiveness to soluble
growth factors. The magic behind the seemingly precise
orchestration of these events under normal conditions remains
beyond our grasp but almost certainly lies in the regulation of
specific soluble mediators and their receptors on particular cells,
cell-matrix interactions and a controlling effect of physical
factors,including forces generated by changes

100. To conclude with, the ideal healing in periodontics
should lead to the adequate function and
acceptable aesthetics. Thorough knowledge
regarding the nature and relationship of various
periodontal tissues is necessary to achieve
adequate healing.

101. References
• Anderson’ s - basic pathology
• Harshmohan - essential pathology for dentral students
• Jan lindhe - clinical periodontology & implant dentistry
• Carranza - clinical periodontology
• Perio 2000 - vol 1 :periodontal regenaration
(basic consideration in periodontal wound
healing to achieve regeneration)
vol 24:connective tissue of periodontium
(cell biology of wound healing)
• Journel of dental rsearch 2010 march ,89(3),219-229
(factors affecting wound healing)
 Lars Sennerby : Implant Integration and Stability. In : Partick Palacci, Esthetic
implant dentistry, soft and hard tissue management. Germany: Quintessence
Publishing Company, 2001.
 Guy A. Catone, Edward Halusic. Photobiology of lasers in oral and maxillofacial
surgery. In: Guy A. Catone, Charles C. Alling. Lasers applications in oral and
maxillofacial surgery. USA: W.B. Saunders company, 1997.