Periodontal wound healing involves four overlapping phases - exudative, resorptive, proliferative, and regenerative. The proliferative phase includes re-epithelialization, fibroplasia, granulation tissue formation, collagen deposition, angiogenesis, and wound contraction. Growth factors play an important role in regulating periodontal wound healing. Healing after periodontal procedures like scaling and root planing, curettage, ultrasonic curettage, and gingivectomy depends on the extent of tissue disruption and follows a timeline of inflammatory response, epithelial migration, granulation tissue formation, collagen deposition and remodeling.

1. HEALING FOLLOWING
PERIODONTAL SURGERY

2. INTRODUCTION
• Conventional periodontal therapy, usually involves
instrumentation in the inflamed dentogingival complex.
• Thus, the consequence of such therapeutic procedures
depends largely on the cellular and molecular events
associated with wound healing.

3. TERMINOLOGIES
• Wound : Disruption of anatomical or functional continuity of
living tissues.
• It can be due to physical, surgical, chemical, thermal,
microbial or immunological insult to the tissues.
• Wound healing: phenomenon by which body attempts to
restore the tissue integrity by formation of new structures
aimed to replace the defect.
• The new structure may more or less match the original
structure.

4. • Repair: refers to the restoration of tissue architecture and
function after an injury.
• Two types of reaction :
• Regeneration : some tissues are able to replace the damaged
components and essentially return to a normal state
• Repair by scarring: if the injured tissue are incapable
complete restitution , or the supporting structures are
severely damaged ,repair occurs by laying down of
connective tissue , a process termed healing that results in
scar formation

6. GENERAL CONCEPTS –
HEALING

7. HEALIING
• A cascade of events that involves the interaction
of various cellular and molecular components
that act in synchrony to effect wound closure
• The process can be understood as progressing
through multiple stages, but realistically takes
place as a continuum.

8. DIFFERENT TISSUES - DIFFERENT
CAPACITIES TO HEAL
• High capacity
• epithelial, lymphoid, hematopoietic, mesenchymal tissues
(fibroblasts, smooth muscle cells, osteoblasts, chrondrocytes, and
endonthelial cells)
• Highly vascularized
• Low capacity
• Nerve, muscle (skeletal and cardiac), cartilage

9. BASED ON THIS CRITERION, THE TISSUES OF
THE BODY ARE DIVIDED INTO THREE
GROUPS
Continuously
dividing tissues
continuously
being lost and
repalced by
maturation from
stem cells and by
proliferation of
mature cells
Stable tissues
Cells- quiescent
and have only
minimal
replicative
activity in their
normal state
capable of
proliferating in
response to
injury
Permanent
tissues
terminally
differentiated
and non
proliferative post
natal

10. TYPES OF HEALING
A. Primary Intention:
• When wound edges are
directly next to one
another
• Little tissue loss
• Minimal scarring occurs

11. B. Secondary Intention:
• The wound is allowed to granulate
• Granulation results in a broader scar
• Healing process can be slower
• Wound care must be performed daily to
encourage wound debris removal to
allow for granulation tissue formation
• examples: gingivectomy,
gingivoplasty,tooth extraction sockets,
poorly reduced fractures.

12. C. Tertiary Intention
• The wound is initially cleaned, debrided and
observed, typically 4 or 5 days before closure.
• Presence of infection

14. The human adult wound healing process can be divided
into 4 distinct but overlapping phases:
1. exudative phase (within hours)
2. resorptive phase (day 0 to 4)
3. proliferative phase (from day 3 up to 2 weeks)
4. regenerative phase (from day 8 up to months)
Phase 1 and 2 -inflammatory phase.

15. EXUDATIVE PHASE

16. 1. COAGULATION & CLOT FORMATION
• Hemostasis
• Structural support
• Provisional ECM
• Early source of mediators of healing
•Immediately after a blood vessel is injured- vasoconstriction,
• 10 to 20 minutes post-wounding - vasodilatation ( histamin, kinins,
PGE2 and prostacyclin)
• Porousness of blood vessels increases

17. RESORPTIVE PHASE

18. Recruitment of PMNs (Early inflammatory phase)
Recruitment of macrophages (Late inflammatory phase)
Polymorphonuclear cells
Attracted by fibronectin, growth factors, and kinins.
Phagocytise debris and bacteria.
Cleanse the wound
Undergo apoptosis once they have completed their tasks - engulfed and degraded by
macrophages.

19. Macrophages in healing:
Growth factors - PDGF,VEGF,EGF,TGFB,FGF,IGF
[M2 phenotype] - attract & support proliferation of
fibroblasts, smooth muscle cells &
endothelial cells
- promotes matrix production &
angiogenesis
Key role in transition from inflammation to granulation tissue
formation
 Phagocytose - PMNs, foreign & tissue debris, bacteria

20. PROLIFERATIVE PHASE
• Epithelial healing
• Connective tissue healing
• Fibroplasia
• Formation of granulation tissue
• Collagen deposition
• Angiogenesis
• Wound Contraction

21. EPITHELIAL HEALING
• Mobilization of cells: achived by 2 distinct processes
• Migration: locomotion of epithelia cells
• Mitosis: mitotic growth of cells

22. • Regeneration of small wounds occur by migration alone
• Large wounds need cell migration as well as new cell
supply by mitosis

23. Re-epithelialization
suprabasal keratinocytes
are the first migratory cells sliding over the
basal keratinocytes.

24. • Basal and suprabasal cells from both the cut margins undergoes
dedifferentiation and acquire potential for amoeboid movement
• Start proliferating and migrating towards the incisional space in the
form of epithelial spurs.
• The movement of monolayer or sheets of cells during this migration is
termed “streaming”
• Pattern: caterpillar track, frog leap phenomemon, sliding model
First keratinocytes to migrate- phagocytic

25. • Migration and proliferation of epithelial cells -Begins within 24
hours and Well approximated wound is covered by a layer of
epithelium in 48 hours.
• For excised wound time depends upon its surface area
• Cell migratory rate: 0.5-1mm/day
• contact from opposing edges: epithelial seal
• Once seal is established- mitosis and definitive layers of
stratified squamous epithelium forms

26. CLINICAL SIGNIFICANCE
• Undisturbed healing of underlying C.T.
• Inhibits loss of tissue fluid necessary for C.T. cells and
may affect repair
• Tremendous increase in wound strength

28. B3 - inhibits the growth of primary human keratinocytes
b1- stimulate keratinocyte motility by switching the cells from
the differentiating to regenerative phenotype

29. CONNECTIVE TISSUE HEALING
• 4 processes
• Production of new fibroblasts
• Migration of these cells into the wounded area
• Formation of new extracellular matrix
• Remodeling of the extracellular matrix into the wound

30. FIBROPLASIA
• Fibroblasts proliferate and migrate to the wound area,
adhering to fibronectin, deposit ground substance (later
collagen) into the wound bed, secrete growth factors that
attract epithelial cells to the wound site
• Granulation tissue begins to appear in the wound even
during the inflammatory phase, and continues growing
until the wound bed is covered, consists of new blood
vessels, fibroblasts, endothelial cells, myofibroblasts,
and the components of a new extra cellular matrix (ECM)

31. GRANULATION TISSUE FORMATION
• Begins with the formation of the epithelial seal
• According to Gillman (1955)
• In shallow wound: onset of fibrogenesis occurs after
migration of the epithelial cells
• Deep excised wound: first granulation tissue is built up from
the base and then epithelial migration occurs on this new
C.T.

32. Granulation tissue formation
•Transient specialized organ of repair ,which replaces the PECM
• Microscopically,
Fibroblasts + RBCs matrix + patent single cell lined capillaries
surrounded by fibroblasts & inflm cells
•Fluid rich, source of growth factors & defensins

33. • On the granulation tissue frame work
Migration & proliferation of fibroblasts
Deposition of ECM by fibroblast
• Driven by PDGF, FGF-2,TGF-β ----- Inflammatory cells
Activated endothelial cells
• Cytokines like IL-1 & TNF
• Origin of matrix producing cells:
 Surrounding CT
 Pericytes
 Bone marrow

34. • ‘Peripheral blood fibrocytes’
-Accumulate in early a/c phase
-Antigen presenting cells
-Secrete cytokines
[immune response.hematopoesis,ECM synthesis]

35. COLLAGEN DEPOSITION
• one of fibroblast's most important duties is the production of
collagen starting by the third post-wounding day
• collagen deposition increases the strength of the wound
providing more resistance to traumatic injury
• cells involved in inflammation, angiogenesis, and connective
tissue construction attach to, grow and differentiate on the
collagen matrix
• Type III collagen predominates initially : 15-20% type III collagen

36. ANGIOGENESIS
• Functions of new formed blood vessels
• supply of oxygen and nutrients
• transport of degradation products
• cell settlement
• Angiogenesis process
• stimulation by chemical signals or hypoxia
• endothelial cell proliferation
• directional migration of endothelial cells
• organisation and differentiation to form capillary tubes

37. At its peak, gran. tissue has more capillaries/unit vol than any
other tissue
Growth factors inducing angiogenesis ----- VEGF,TGFB
Factors stabilizing vessels ----- Angiopoetin 1 &2
PDGF & TGFB

38. CONTRACTION
• Dehydration: removal of fluid by drying wound
• Contraction of collagen
• Discovery of myofibroblasts:

39. MYOFIBROBLAST
• Myofibroblasts move along fibronectin linked to fibrin in the
provisional ECM in order to reach the wound edges and
form connections to the ECM and they attach to each
other and to the wound edges
• As the actin in myofibroblasts contracts, the wound edges
are pulled together and fibroblasts lay down collagen to
reinforce the contracted wound

40. MYOFIBROBLAST
• Differentiation of myofibroblasts - 6 - 15 days
• 70% of fibroblasts show α-smooth muscle actin
• Shape – fibroblasts
Action – smooth muscle cells
• Reduces wound size by 40-80%
• After contraction –apoptosis →New normal CT fibroblasts
emerge
Apoptosis begins at day 12, peaks at day 20 and
resolves by day 60 after wounding

41. REGENERATIVE PHASE
• Regenerative Phase,
also called
Remodeling or
Maturation
Phase includes:
• collagen remodeling
• blood vessel
apoptosis

42. TISSUE REMODELING
• About 14 days post operatively wound is filled with fibers that
run in all direction and remodeling begins
• Decrease in fibroblasts
• Decrease in vascularity
• Remodeling consist of 2 distinct processes (homes,1959)
• Resorption and changing of the orientation of these first deposited
fibers
• Enlarging or increasing the numbers of oriented fibers
• Long lasting phase of repair

43. • Type III collagen, which is prevalent during proliferation,
is gradually degraded and the stronger type I collagen
is laid down
• Originally disorganized collagen fibers are rearranged,
cross linked, and aligned along tension lines, the tensile
strength of the wound increases
• After tissue remodeling is finished redundant blood
vessels undergo apoptosis

44. GROWTH FACTORS IN PERIODONTAL
WOUND HEALING
• Growth factors are polypeptide molecules, released by cells in
the inflamed area, that regulate events in wound healing.
• Regulates connective tissue cell migration and proliferation
and synthesis of proteins and other components of extra
cellular matrix.
• Growth factors can be used to control events during
periodontal wound healing (example: Promoting proliferation
of fibroblasts from the periodontal ligament and favoring bone
formation.)

46. HEALING AFTER PERIODONTAL PROCEDURES

47. CLINICAL REQUIREMENTS FOR
EFFECTIVE HEALING
• The application of initial therapy prior to surgical intervention
• The selection of surgical approach specific for the cure of the
particular inflammatory lesion
• The type of tissue environment that exists after surgery
• The degree of fibrosis of gingiva prior to and after surgery
• The method by which the surgical wound is protected in the
postoperative period
• The maintenance of the dentition and the periodontium by the
patient and the dentist daily and in periodic visits

48. SCALING AND ROOT PLANING
• Removes surface accretions
• Retards further accumulation of deposits

49. HEALING AFTER SRP
Day 0
• Bleed and exudation of GCF will remove irritants
• Epi attachement is severed, acute inflammatory rxn in C.T
Day 1
• After an initial lag of 12-24 hrs, epi migration begins
Day 2
• Inflammation ↓, epithelialialization enhanced.
Day 5. • New epithelial attachment
1-2 wks
• Residual retepegs involute
• Clinically- gingival health

50. CURETTAGE(BLASS & LITE 1959)
• Involves removal of pocket wall
• Chemical and mechanical.
• The sharp curet or blade , however, has
remained the method of choice

51. DURATION Connective tissue
changes
Epithelial
changes
Clinical changes
Immediately • Haemorrhage
• a/c inflamm reac
• Removal of epthelial
lining
• Few cells may remain
• Blood&exudate
1st day • Marked inflamm • Epithelial migration
begins (0.5-1mm/day)
• Edematous
• Dislcoloration persists
2nd day • Inflamm 
• Vasularity 
• Epithelium begins to
cover the gingival corium
•Discoloration 
• Edema still +nt
4th-6th day • Chr inflamm
• Collagenation
• Matrix formation
• restoration of junctional
&sulular epithelium -
7th-10th day •  Collagen formation&
organisation
• Epithelium formation is
complete
• Edema 
• Rigid&well adapted
ginival wall
10th-14th day • Repair of conn tissue
•  vascularity
• Surface keratinization  • Normal color
• Stippling appears
• Gingival shrinkage
After 2 weeks • Mature collagen
• New subsulcular &
marginal vessels
-
• Color,contour,
consistency, texture.
• Well adapted marginal
gingiva

52. ULTRASONIC CURETTAGE
• Epithelium- heat coagulation
• Immediately after – areas of coagulation
– tissue discontinuity
– fused collagen
• Narrow band of necrotic tissue strips off the inner lining
of pocket
• 3 days – epithelialisation occurs
– lesser inflammation
• 2 weeks – shorter & thinner epithelium
– fewer rete pegs
• Goldman (1980) – more satisfactory healing
– healing is faster

53. CHEMICAL CURETTAGE
• Sodium sulphite, alkaline sodium hypochlorite, phenol.
• No control over magnitude of tissue destruction
• More severe damage to underlying connective tissue &
bone
• Delayed healing

54. GINGIVECTOMY
• Elimination of suprabony pockets when underlying bone does
not require therapy
• Elimination of gingival enlargements
• Surgical – scalpel
– electrode
• Produces an open surface wound
• Heals by secondary intention

55. Duration Connective tissue Epithelium Bone
Immediately Hemorrage,exudate
Blood clot
Necrosis at wound margin -
Few hours a/c inflamm reac Wound margin
-Changes in prickle cell
layer -
9-18 hours - Migration from prickle cell
layer begins -
1st day Polyband
Collagen fragmentation
Angioblasts
Epithelialisation-centripetal
fashion -
1st-3rd day - Hemidesmosomes
&basement lamina
-
3rd-4th day Loss of clot
Granulation tissue
- -
5th-14th day Disorganised conn tissue
dilated blood vessels
Anastomis betw periodontal
and gingival vessels
Epithelialisation~ complete
No rete pegs
Transient surface resorption
(7-12 days)
14th-16th day Vascularity 
-
Reversal lines
Resorption continues
3-4 weeks Collagen formation
Organisation
Rete pegs
Dentogingival unit
New sulcus
Resorption ceases
Crestal bone level re-
established
4-5 weeks - Complete repair -
By 7 weeks Complete repair - -

56. ELECTRO-SURGERY GINGIVECTOMY
• Pope (1968)- delayed epithelialisation (by 4 days)
- lack of bleeding and clot formation
• Glickman&Imber(1970)- delayed healing
- bone necrosis
• Schneider&Zaki(1974)- no bleeding
- transiently hyalinised C.T
• Wilhelmsen et al(1976)- avoid contacting cemetum or bone
• Healing – fully rectified = conventional

57. LASER GINGIVECTOMY
• Advantages – minimal disturbance of surrounding
tissues
– hemostatic effect
– edema &pain
– sterelisation of wound
– minimal scarring
• Healing – delayed re epithelialisation
– lesser inflammatory response
– thermal necrosis
– decreased wound contraction

58. CHEMOSURGERY GINGIVECTOMY
• Chemicals – phenols
– paraformaldehyde
– potassium hydroxide
• Incomplete gingival remodelling
• Delayed epithelialisation, connective tissue repair
• Increased inflammation after chemical trauma
• No control over the depth of action

59. FLAP SURGERY
• Periodontal flap – a section of gingiva and/or mucosa
surgically elevated fron the underlying tissue to provide
visibility and access to the root and bone surface.
• Healing – both primary & secondary

60. • Reflection of epithelium and
a layer of connective tissue
• Bone remains covered by a
layer of connective tissue
including periosteum
• Soft tissue including the
periosteum is reflected to
expose the underlying bone

61. FULL THICKNESS FLAP
• Caffese ,Ramfjord& Nasjeleti (1968)
• Healing –
1st intention Ideal flap adaptation
Minimal surgical
trauma
No intervening
granulation tissue
Complete within 21
days
2nd intention Intervening
granulation tissue
Common in well
adapted flaps
3rd intention Poor flap adaptation
Delayed healing with
complications
Not complete even
after 72 days.

62. Duration Healing
2 hours • No crevicular epithelium or epithelial attachment
• Narrow zone of necrosis on surgical surface of flap
• Blood clot
• Superficial necrotic changes on alveolar surface-empty lacunae
24 hours • Thick band of PMNL cells
• Bone appears vital
2 days • Epithelial cells have started migrating
• Blood clot & PMNL cells
• Angioblasts & fibroblasts at alveolar crest
• Superficial necrosis of bone
• Cementoblasts -deranged for 1mm from wound surface
3 days • Epithelium makes contact with teeth surface
• Thin blood clot
• Inflammation
• Connective tissue grows betw flap and bone
• Collagen fibres within flap undergo necrosis
• Granulation tissue starts forming
5 days • Granulation tissue is present
• Osteoclasts (from marrow) – for 1mm over pdl membr side of
bone
• Cementoblasts – missing for 1mm apical to alv crest

63. Duration Healing
7 days • Formation of epithelial attachment begins
• Granulation tissue adheres the flap to underlyng bone
• Severe osteoclastic activity (for 2-3 mm)
9 days • Crevicular epithelium & new epithelial attachment
• Some cementoclastic activity
• Osteoclastic activity over alveolar crest
• Periodontal fibres replaced by vascular granulation tissue
14 days • Band of connective tissue betw flap & underlying bone
• Free gingiva – vascular granulation tissue, no functional orientation
• Alternative osteoclastic& osteoblastic activities
• New periosteum – connective cells surrounded by immature collagen
21 days • Fully Epithelialised Gingival Crevice
• Well Defined Epithelial Attachment
• Functional Arrangement Of Supracrestal Fibres
• Osteoblastic activity
• Cementoblasts are normally arranged
35 days • Gingival Adaptation
• Chronic inflammation in connective tissue
72 days • Total crevicular depth = 1mm
• Parakeratinized free gingival margin
• Periosteum appears normal
• Functional orientation of gingival fibres(immature collagen)
• Newly formed bone on tip of alveolar crest

64. PARTIAL THICKNESS FLAPS
• Lesser physical, biological & infective insult
• Higher proliferative capacity of retained periosteum
• Greater post-op edema
• Healing depends on nature & thickness of periosteum and
retained connective tissue (min -0.5mm)
• Heals faster with lesser destruction of alveolar bone
• Ramjford & Costich (1968)

65. Duration Healing
1 weeks • Epithelium extends to margin of the clot and necrotic debries
• Rapid proliferation of granulation tissue
• Rapid bone resorption
2 weeks • Complete epithelial coverage
• Gingiva – vascular granulation tissue with subacute inflammation
3 weeks • Parakeratosis of gingival surface
• Shallow new gingival crevice
• Connective tissue parallel to root surface
• Gingival fibers- no functional orientation
• Diffuse chronic inflammation
• Alternate areas of bone resorption and regeneration
4 weeks • Completely regenerated gingival tissue
• Reparartive osteoblastic activity
• Resorption lacunae on root surface- may extend into dentin
9 weeks • New epithelial attachment
• Mild chronic inflammation
• Bone formation continues
13 weeks • Epithelial covering is normal
• Periosteal fibers – compressed & parallel to root surface
• Slight resorption of cementum; undergoing repair

66. EFFECT OF THICKNESS OF BLOOD CLOT
• A thick coagulum has been associated with incomplete
or imperfect adaptaion of soft tissue to the underlying
bone
• Since the clot must be resorbed and replaced by
connective tissue during healing thinner clot is more
desirable than thick which retards the rapid attachment
• The weakest part of adherence b/w flap and bone occurs
in area of the fibrin clot – not substantial enough to hold
them together

67. APICALLY DISPLACED FLAP
• Introduced in 1950s – pocket elimination
– bone recontouring
– ing width of attached gingiva
• Can be partial/full thickness
• Costich & Ramjford (1968)

68. Healing
sequence
1
week
2
weeks
3
weeks
6
weeks
Granulation starts covering the exposed bone
Surface – acute inflammation
Periodontal membrane – chronic inflammation
Active bone resorption starts
Thin layer of epithelium
Granulation tissue covers the
wound surface
Severe osteoclastic activity
Gingiva – parakeratinised epithelium
Appearance of shallow gingival crevice and epithelial
attachment
Connective tissue – vasculat, young fibroblasts
Osteoclasis &osteoblastosis
Numerous resorption lacunae on cemental surface
Partially regenerated gingival
tissue
Osteoblastic activity
Areas of root resorption
undergoing repair

69. PEDICLE GRAFTS (WILDERMAN & WENTZ
1965)
Coronally
displaced flap
Lateral
pedicle
Double
papilla

70. STAGE HEALING
Adaptaion
(0-4 days)
Clot & thin fibrinous exudate betw flap and root surface
PMNLs in clot & connective tissue
Epithelium at margins of flap proliferate – may contact tooth
surface
Proliferation
(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) - by 14th day
Slight cemental resorption
Attachment
(21-28 days)
Collagen fibers insert into new cementum
Cementoid deposition(by 28th day – along the entire root)
Connective tissue attachment
New gingival margin, sulcuc & epithelial attachment
Osteoblastic activity
Maturation
(28-90 days)
Completely formed gingival sulcus and epithelial attachment
Bone apposition at alveolar crest

71. DONOR SITE
Full thickness Split thickness
Healing starts from periphery of
wound
Sparing marginal gingiva of donor
tooth prevents recession there
Recieves blood supply only through
pdl vessels
Granulation tissue covers the wound
Osteoclastic resorption on the pdl
side
Dehiscence if thin cortical plates
Epthelialisation(centripetal fashion)
– complete by 3 weeks
Retained periosteum and a layer of
connective tissue
Intact supraperiosteal vasculature
Faster healing
Minimal bone resorption

72. FREE GINGIVAL GRAFT
Bjorn (1963) , Sullivan & Atkins (1968)
 s zone of attached gingiva
 can also be used over an extraction socket or osseous graft
(Ellegaard et al 1974).
 success depends on survival of connective tissue
 Oliver, Loe & Karring described the healing into 3 phases

73. Initial phase
(0-3 days)
• Thin layer of exudate
Avascular plasmatic circulation(Foman 1960; Reese
&Stark 1961)
• Epithelium gets desquamated
Revascularisation
(2-11 days)
• Anastomosis betw graft & recipient site blood vessels
• Capillaries proliferate in the graft tissue
• Fibrous union betw graft & conn tissue bed
• Re epithelialisation of the graft
Tissue maturation
(11-42 days)
• Blood vessels in the graft reduce in no
• Epithelium matures-gets keratinised
• Functional integration – by 17th day
• Morphologically distinguishable for several months

74. HEALING FOLLOWING SOFT TISSUE
GRAFTS

75. Initial phase
(0-3 days)
Revascularisation
(2-11 days)
Tissue
maturation
(11- 42 days)
Pale – empty graft vesselsPink – vascularisation begins
Smooth & shiny – loss of epithelium
Thin grey veil like surface – new epithelium
Normal features – maturation of epithelium

76. SECONDARY CONTRACTION
• Upon healing, the graft may shrink by as much as 33% (Egli
et al. 1975)
• Due to cicatrisation of tissues that unites it to the recipient bed
• Thick graft on a rigid bed – maximum resistance to shrinkage

77. Graft mobility
• Improper bed preparation - Too much loose tissue or
muscle fibers left above the periosteum.
• At this point, it is not necessary to redo the graft.
• Raising a partial thickness flap that includes the graft,
removing the loose tissues above the periosteum, and
resuturing generally solves the problem.

78. BRIDGING PHENOMENA
• Collateral circulation
• Essential for graft survival over the avascular area (root
surface)

79. CREEPING ATTACHMENT
• Goldman (1964)
Post operative migration of gingval marginal tissue in
a coronal direction over a portion of previously
denuded root.
• 0.12-3.5 mm ~ 2 years
• Favourable factors – narrow defect
– +nce of interproximal bone
– no gross malpositioning of tooth
– adequate plaque control

80. THICK VS THIN GRAFT
Sullivan and atkins- The two point collateral circulation
present toward the coronal portion of a free graft over
avascular root surface was insufficient to maintain
tissue viability particularly in deep wide recessions
• Graft thickness would determine its behaviour during
healing and its final character
• Thinner grafts (0.5-0.7mm) enhanced survival

81. • Thick graft with a thicker lamina propria → greater
primary contraction causing blood vessels to collapse ,
retarding revascularization and reducing the likelihood
of bridging.
• Once healed thicker grafts show superior resistance to
frictional stress. Are recommended for areas with high
susceptibility for gingival recession.

82. CONNECTIVE TISSUE GRAFTS
• Healing is similar to FGG
Increased vasularity of connective
tissue compared to FGG
Double blood supply (combined
techniques)
Recipient bed & overlying flap
Faster healing

83. HEALING OF CTG
• 2nd day - epithelialization commences
• 7 – 10 days - initial epithelialization completed
• 4 weeks - keratinization commences

84. HEALING FOLLOWING GUIDED
TISSUE REGENERATION
• GTR based on the principle of guiding the proliferation of
the various periodontal tissue components during healing
following periodontal surgery. (MELCHER)
• Placement of barrier covering the periodontal defects in
such a way that gingival tissues are prevented from
contacting the root surface during healing .
• Same time, space is formed between the barrier and root
allowing periodontal ligament cells to produce new
connective tissue attachment and bone cells to form new
bone.

85. SANDER ET AL (1995) DESCRIBED HEALING OF
PERIODONTAL LESIONS IN MONKEYS FOLLOWING THE
GTR
1week
• Coronal border of membrane - slightly exposed
• Histological examination → furcation and proximal defects
contained partly disintegrated blood clot.
• Most apical part of the defects → granulation tissue containing
inflammatory cells and blood vessels present.
• Mean coronal regrowth of granulation amounted 0.9mm or 20% of
the maximal defects height and 1.5mm or 30% on the average in
interproximal defects.
• A few collagen fibres were encountered in the tissue in the notch,
but no instances were the collagen fibres inserted in to the newly
formed cementum.

86. • At 3 week:
• Histological examination: Newly formed tissue which has
proliferated considerably more coronally than in the one
weeks specimens, but with great variation from one defect to
another.
• Newly formed tissue in the central portion of the defects had
primarily proliferated from the bone marrow of the
interproximal and interradicular bone septum,
• Tissue adjacent to the root surfaces seem to originate from
the periodontal space.

87. At 4 week:
• Partly filled with new connective tissue ,some inflammatory
cells.
• New cementum in continuity with the old cementum .
• New collagen fibres were inserted in to the newly formed
cementum
• Notched area → inserting perpendicular to the surfaces, in
most apical part of the defects.,
• Bundles of collagen fibers were oriented in a mesiodistal
direction apically, where as those in the coronal part had no
particular orientation.]

88. 9 weeks:
• Gingiva normal → consistency and color
• Bifurcation defects - partly or completely filled with
new connective tissue + thin epithelial lining (coronal
part of the defects. )
• New cementum with fibers inserting perpendicular to
the surface had formed in the notch and to a varying
degree also on the root surface coronally to the notch

89. HEALING FOLLOWING OSSEOUS
SURGERY
REGENERATIVE RESECTIVE

90. OSSEOUS AND MARROW
AUTOGRAFTS
:
The process of repair of contiguous osseous autografts :
• Ankylosis
• Reattachment
• Transplant resorption for the formation of new bone.
Grafts: compact bone, cancellous bone and
hematopoietic bone marrow.

91. COMPACT BONE :
Osteocytes present die , except the surface osteocytes . due
to their close proximity to functioning capillaries or tissue
fluids. Can possibly contribute to osteogenesis
• osteogenic layer (cambium) of periosteum , endosteum and
marrow form new trabeculae & unite with the graft .
• After union of the graft and host , → resorption and
replacement occur concurrently .
• Resorption - along the outer surface of the transplant and
on the inner surface of haversian canals.

92. CANCELLOUS BONE TRANSPLANT
• Higher chance of osteocyte survival
→covered with osteogenic cells
• High production of surface cells ( osteoblasts) to bone cells (
osteocytes).
• Cancellous fragments →new centers for osteogenesis if
transplanted in to an area with an adequate vascular bed
that provides surface cells with sufficient tissue fluid.

93. Healing Cancellous Cortical
Blood clot
(1st week) Similar
Revascularisation • Occurs within hrs
• Marrow spaces – rapid
degenration
• Space for new channels
• Complete within 2 weeks
• Slower rate
• Not penetrated by vessels till 6th
day
• Complete within 1-2months
Repair • Initiated by osteoblats
• Mesenchymal cell
osteoblast
• Osteoid deposited around
cores of dead bone
• Dead bone removed by
osteoclasts
• Transplant gets replaced by
viable NEW bone.
• Initiated by osteoclasts
• Bone apposition occurs only after
12 weeks

94. DRAGOO (1973)
Duration Healing
3 days • Vascularity
1 week • Resorption of grafted bone
• No evidence of periodontal membrane
• Union betw the graft & existiong bone
• Beginning of osteogenesis (osteoid)
3 weeks • Beginning of cementogenesis
• Areas of calcification in conn tissue
8 weeks • Developing lamina dura and periodontal membrane
• Further resorption of graft material
• Cementogenesis
• Beginning of attachment of sharpeys fibers to bone
3 months • New bone formation
• Maturation of periodontal membrane with functional arangement.
• Sharpeys fibers well inserted
4 months • Root resorption in some areas
• Well oriented periodontal ligament
• Lamina dura
6 months • Root resorption areas repaired
• Many niduses of bone formation

95. RESECTIVE OSSEOUS SURGERY
• Osteoplasty
• Ostectomy
• Wilderman (1970) described the healing after resective
osseous surgery

96. Duration Healing
After 2 days Numerous empty lacunae – initial evidence of bone degeneration
Osteoclasts & osteoblasts undergo enzymatic degradation
After 1 week Osteoclasts begin to appear – resorption
Undermining resorption ie from marrow spaces beneathe the exposed bone
Widening of periodontal space
If bone septum was exposed – gets completely resorbed – lowering of the crest
Few osteoclasts on periosteal surface
After 2 weeks Osteoclastic resorption begins to 
Bone apposition – osteoid deposition
Resorption on periosteal bone surface (2-3 weeks)
After 3 weeks Osteoid formation continues
New bone – with entrapped osteocytes
Woven bone (radicular interproximal, inter radicular)
Waning of resorption
After 4 weeks Restoration of periodontal ligament width
Repair of bone
Restoration of crestal height (interdental & furcation areas)
After 3 months Compact bone partially restored
Loss of bone height on redicular surfaces
After 6 months Slight bone apposition at bone crest, periodontal surface, periosteal surface
Presence of a definitive periosteum

97. HEALING AFTER ELECTROSURGERY
• Epithelium- Incision causes volatalisation of the
cells in the line of delivered high frequency
energy.
• Loss of cellular details secondary to lateral heat
produced
• Subsequent wound healing is not affected
adversely. (Krejci etal 1987)

98. Connective tissue –
• Small denatured zone (100µm) resulting
• Does not interfere with wound healing and gradually
disappear within 14 days (Kalkwarf etal 1981)
• Misuse →delayed healing response ( Krejci etal)

99. HEALING AT IMPLANT SITE
osseointegratio
n
Fibro-osseous
integration
Biointegration

100. Fibro-osseous Integration
“tissue to implant contact- with healthy dense collagenous
tissue between the implant and the bone”
The fibers …

101. Osseo-integration
Direct connection b/w living bone & implant
at light microscopic level
Meffert et al (1987)
Adaptive Biointegration
osseointegration

102. Adaptive osseointegration –
has osseous tissue approximating the surface of the
implant without apparent soft tissue interface at the light
microscope level
Biointegration
is a direct biochemical bone surface attachment
confirmed at the electron microscopic level

103. FACTORS AFFECTING WOUND
HEALING
Local factors
 Infection
 Movement of the wound
 Poor blood supply
 Presence of foreign body
 X-ray irradiation
 Local application of
drugs/ointments
 Effect of smoking
Systemic factors
 Malnutrition
 Metabolic disorders
 Hematologic disorders

104. • Malnutrition
• vitamin C defeciency:
• collagen cross linking and synthesis impaired
• vitamin B6 deficiency:
• poor wound repair
• impairs collagen cross linking
• vitamin E:
• serves as a membrane stabilizer
• plays role in anti bacterial action during healing.

105. • Vitamin A deficiency:
• It is involved in fibroplasia,collagen synthesis and cross
linking&epithelialization.
• Defeciency decreases collagen synthesis and stability
• Protein deficiency:
• It delays healing by intererfering the formation of
granulation tissue& collagen
• Wound lacks tensile strength.
• Synthesis of pro collagen is hampered

106. • Zinc defeciency
• it is necessary for DNA and RNA polymerase enzyme which are
necessary for the replication of the cells.
• it leads to delayed wound healing.
• Metabolic disorder
Diabetes mellitus:
wound healing in diabetes mellitus is delayed due to
1.neuropathy
2.ischemia
3.infection
• Haematological disorder:
• it delays wound healing because of repeated haemmorhage of the
wound the leukopenia or functional abnormalities of leukocytes again
delay the wound healing.

107. COMPLICATIONS
• Retarded epithelialization
• Rough and irregular wound surface and tissue tags
• Foreign substance embedded in the wound
• Donor epithelium required for re-epithelialization is distant to the
wound site with temporal delay in epithelial coverage
• Hyperplastic connective tissue due to production of irregular
granulation tissue or infection
Clinical consequences: bleeding and exudation, necrotic surface
with fibrino- membranous cover, irregular hyperplastic hyperemic
and edematous tissue

108. • Failure of epithelial keratinization
• Connective tissue edge of the incision lies on the alveolar
mucosa
• Direct relationship between the connective tissue density rigidity
and tightness of bond to underlying bone
• When it is associated or in contact with a dental surface or
restoration
• Presence of bacterial plaque or debris
Clinical consequences:
smooth and shiny gingival surface that is hyperemic, the usual
sharp demarcation between attached gingiva

109. • Flap displacement and avulsion
• Retardation or failure of tissue flap to reattach to bone or tooth
and marginal aspect of the periodontal ligament
• Inadequate adaptation of flap due to
• Inadequate no of sutures or improper placement, suture breakage

110. • Bone exposure
• Deficiency of vascularization
• Periodontal abscesses, pyogenic granulomas
• Uncommon complication
• More likely to occur in association with bone exposure ,flap
displacement , accidental impaction of calculus and foreign
bodies
• Presence of systemic disease : diabetes mellitus , atherosclerosis
• Increased tooth mobility

111. APPLIED CLINICAL ASPECTS AND FUTURE
APPROACHES TO ENHANCE WOUND HEALING
• Knowledge of growth factors, cell adhesion molecules
and cytokines in the last two decades, understanding of
the cellular and molecular biology of wound healing has
improved significantly.
• Application of epidermal growth factor and TGF-a to burn
wounds in animal models has been shown to enhance
re-epithelialization
• Keratinocyte growth factor to skin wounds has been
shown to have mitogenic effects on the healing
epithelium

112. • Topical application of fibronectin in periodontal wound
healing
• Systemic conditions such as diabetes → reduction in the
availability of some of the growth factors
→supplementing the appropriate growth factor may be
beneficial.
• Recombinant growth factors to treat osseous defects →
shows promising results
• Photobiomodulation - LLLT

113. BONE MORPHOGENIC PROTEIN
• Urist (1965)
• Protein extracted from bone containing multiple
osseopromoting factors
• Part of transforming growth factor-β superfamily

114. POLYPEPTIDES
• Osteoinducer + osteopromoter
• PepGen P-15 & OSA-117 MV
• Further studies required

115. ENAMEL MATRIX DERIVATIVES
Introduced in 1997
Composite of enamel matrix proteins
• Stimulates fibroblast proliferation
• Enhances growth of PDL cells
• Enhances expression of osteopontin osteoprotegrin, TGF-β1,
bone sialoprotein, BMPs
• Anti-inflammatory effects

116. CONCLUSION
• Wound healing is a complex process especially when
compromised by local and systemic factors
• Only profound understanding of biological and clinical
variables affecting the outcome of periodontal treatment
procedures will allow clinicians to manipulate biological and
clinical factors effectively in order to optimize the clinical
result and increase the predicatbility of therapy.

117. REFERENCES
• Carranza’s clinical periodontology: 10th edition
• Clinical periodontology Jan Lindhe-5th edition.
• Cell biology of gingival wound healing:Periodontology
2000, Vol. 24, 2000, 127–152
• Basic considerations of wound healing. Periodontology
2000 vol19
• General Pathology-Robins
• Basic considerations of wound healing. Periodontology
2000: vol19
• Periodontal therapy: Goldman