Wound healing after Periodontal procedures

1. Good
Morning

2. WOUND HEALING
AND HEALING AFTER
PERIODONTAL
PROCEDURES
GUIDED BY:
DR. AMIT GOEL
DR. DIVYA JAGGI
PRESENTED BY:
DR.MALVIKA THAKUR
PG II YEAR

3. CONTENTS
1. INTRODUCTION
2. REGENERATION &
REPAIR
3. GROWTH FACTORS IN
WOUND HEALING
4. WOUND HEALING
5. FACTORS INFLUENCING
WOUND HEALING
1. HEALING OF ORAL
WOUNDS
2. WOUND HEALING
FOLLOWING VARIOUS
PERIODONTAL
THERAPIES
3. COMPLICATIONS
4. USE OF LASERS IN
WOUND HEALING
5. CONCLUSION
6. REFERENCES
PART – I PART – II
1/45

4. INTRODUCTION
WOUND
HEALIN
G
Healing is a cell
response to injury in
an attempt to restore
the normal structure
and function.
A wound/Injury is
a disruption of
the anatomic
structure and
function in any
body part.
2/45

5. Wound healing may either take place by:
 Primary Intention
 Secondary Intention
 Tertiary Intention
3/45

6. PROCESS OF HEALING
 It involves 2 distinct processes :
 At times, both the processes take place simultaneously
REGENER-
ATION
REPAIR
4/45

7. REGENERATION
 Natural renewal of a structure, produced by growth &
differentiation of new cells and intercellular substances to form
new tissues or parts which function the same as original tissues.
 Growth from the same type of tissue that has been destroyed or
from its precursors.
 Periodontal tissues are limited in their regenerative capacity.
5/45

8. Regeneration related to periodontal
tissues
Manifested by:
 Mitotic activity in the epithelium of the gingiva and
connective tissue of PDL
 Bone remodelling
 Continuous deposition of cementum
Most gingival and periodontal diseases are chronic
inflammatory process and, as such are, healing lesions.
6/45

9. REPAIR- “HEALING BY SCAR”
 Replacement of one tissue with another tissue, such as fibrous
connective tissue, which may not function the same as the tissue
replaced.
 Two processes are involved in the repair:
1. Granulation tissue formation
2. Contraction of wounds
Phase of inflammation
Phase of clearance
Phase of ingrowth of granulation
tissue
a. Angiogenesis
b. Fibrogenesis
7/45

10. Essential molecules for
regeneration

11. GROWTH FACTORS IN PERIODONTAL WOUND
HEALING
8/45

12. WOUND HEALING
10/45

13. I. THE INFLAMMATORY PHASE
It can be broken down further into :
a) Haemostasis – Clot formation
b) Early inflammation - Chtzd by production of PMNs
c) Late inflammation - Presence of macrophages
Primary contributors to haemostasis include:
 Vasoconstriction
 Platelet Aggregation
 Fibrin Deposition
11/45

14. VASOCONSTRICTION
12/45

15. PLATELET AGGREGATION
13/45

16. COAGULATION CASCADE
14/45

17. Recruitment of PMNs (Early inflammatory phase)
Recruitment of macrophages (Late inflammatory phase)
First infiltrating cells to enter the wound site, peaking at 24 to 48 hours
Migration is stimulated by - ↑ vascular permeability, Local PG release,Presence
of chemotactic substances- complement factors, IL-1, TNF-α, TGF β, platelet
factor 4,or bacterial products.
Following activation - scavenge necrotic debris, foreign material, and bacteria.
Undergo apoptosis once they have completed their tasks - engulfed & degraded
by macrophages.
15/45

18. Key role in transition from inflammation to granulation tissue formation
16/45

19. ECM–growth factor interactions and production of
MMPs in wound
17/45

20. 22/45
MATRIX METALLOPROTEINASES IN WOUND HEALIN

21. II. THE PROLIFERATIVE PHASE
II phase of wound healing & roughly spans days 4 through 12.
It is during this phase that tissue continuity is re-established
The initial fibrin–fibronectin matrix is heavily populated by
inflammatory cells, whereas FIBROBLASTS &
ENDOTHELIAL CELLS will predominate as healing
progresses.
 Cytokines continue to be a part of the process as its release
contributes to:
a) Epithelialization
b) Healing of Connective tissue
18/45

22. A) RE-EPTHELIALIZATION
• After the epithelium has been disrupted by tissue injury, re-
epithelialization must occur as rapidly as possible in order to re-
establish Tissue Integrity.
• Keratinocytes start moving into the defect about 24 hours after the
injury.
• The keratinocytes use receptors on their surface, known as
Integrins to bind to laminin in the basal lamina.
• Mobilization of cells: achived by 2 distinct processes
• Migration: locomotion of epithelial cells
• Mitosis: mitotic growth of cells
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23. Re-epithelialization
20/45
Suprabasal keratinocytes are the first migratory cells
sliding over the basal keratinocytes.

24.  Integrins play a crucial role in the fibrin clot removal
 The two activators, tissue-type plasminogen activator and
urokinase-type plasminogen activator along with its receptor, are
upregulated in the migrating keratinocytes.
 Creation of a migrating path for keratinocytes : achieved by the
dissolution of the fibrin barrier by the enzyme plasmin.
 Migrating keratinocytes express:
 MMP-1 degrades native collagens and aids cell migration by destroying
collagens I and III.
 MMP-9 can cleave the collagen in basal lamina (type IV) and the collagen
that forms the anchoring fibrils (type VII)
 MMP10 is also expressed in wounds and is thought to have a wide spectrum
of substrate specificity for collagen
21/45

25. • As the basal keratinocytes at the wound margin are exposed to
the new provisional matrix, the phenotype of the cells is
changed from stationary to migratory.
• In this process, keratinocytes detach themselves from the
basement membrane, migrate laterally into the wound bed and
finally regenerate the basement membrane.
• The components of the basement membrane zone such as Type
IV and VII collagens, laminin-1 and heparan sulfate
proteoglycan are missing underneath migrating keratinocytes.
• Laminin-5, however, appears to be always deposited against the
wound bed matrix by keratinocytes during migration
23/45

26. FIG : Keratinocytes express a number of integrin receptors (a2b1 to a6b4) and
extracellular matrix proteins (LM5: laminin-5; TN: tenascin-C; FN ED-A:
fibronectin isoform EIIIA) while they migrate through wound provisional
matrix.FC: fibrin clot; CT: connective tissue; E: epithelium. +++ refers to the
strong immunoreaction at this stage of healing.
24/45

27. 27/45

28. β3 - inhibits the growth of primary human keratinocytes
β1- stimulate keratinocyte motility by switching the cells
from the differentiating to regenerative phenotype and by
inducing their production of fibronectin & laminin-5
28/45

29. • 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 are highly phagocytic
25/45

30. • 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.
26/45

31.  Connective tissue repair by:
1. Activation of FIBROBLASTS
2. Formation of GRANULATION TISSUE
3. ANGIOGENESIS
4. CONTRACTION of the wound by Myofibroblasts.
B. HEALING OF CONNECTIVE
TISSUE
29/45

32.  Wound repair involves phenotypic change of fibroblasts from
quiescent - proliferating cell - to migratory - to stationary matrix
producing and contractile cells.
 In the connective tissue, fibroblasts are surrounded by a matrix that
contains collagen and cellular fibronectin as the major
components.
 Consequently, quiescent fibroblasts express collagen receptors
α1β1 and α2β1 and the major fibronectin receptor α5β1 integrin
which they use for adhesion to the matrix.
1. ACTIVATION OF FIBROBLASTS
30/45

33. Fibrin –
fibrinogen
matrix
Macrophages
Growth
Factors
Fibroblasts
Will migrate
Factors
stimulating
migration –
PDGF,TGF-B,
EGF
Fibroblasts
will require
Cell
membrane
bound
integrins,to
be bound to
Fibronectin
in the ECM
Migrating
cells develop
lamellopodia
Extend until
2nd site is
detected in
the matrix.
Cell migrates,
using the new
site as an
anchor
Cell
migration
may be
impeded by
residual
debris
To facilitate
migration
through such
debris
Fibroblasts secrete several
proteolytic enzymes : MMP-1,
MMP-2, MMP-3 under the
influence of TGF-β
31/45

34. Migrated Fibroblasts –
Active and increase
protein synthesis
Prominent cell type by 3 to 5
days in clean, noninfected
wounds
Cell division &
proliferation
Synthesis and
secretion of
extracellular
matrix products.
Initial wound
matrix is
provisional -
composed of fibrin,
GAG & hyaluronic
acid
Concomitantly, collagens
types I and III are deposited
onto the fibronectin and GAG
scaffold in a disorganized
array.
Proteoglycan concentration
increases with time in a
manner paralleling collagen.
32/45

35. COLLAGEN production starts by the 3rd post-wounding day
 Synthesis is stimulated by TGF-β, PDGF & EGF
 Collagen deposition ↑ 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 : 30%
Accelerated type III collagen synthesis is correlated with
fibronectin secretion after injury
Collagen synthesis continues at a maximal rate for 2 to 4 weeks and
subsequently begins to slow.
33/45

36. PROTEOGLYCANS binds to proteins and alter their orientation
in a manner that influences their activity.
• Dermatan Sulfate - orients collagen molecules in a manner that
facilitates fibril formation
• Hyaluronan - contributes to tissues viscoelastic properties and
acts as a potent modulator of cellular migration .
• Elastin, an another component of wound matrix that provides
elasticity to normal skin is not synthesized in response to injury
and is the reason for increased stiffness and decreased elasticity of
scar as compared with normal dermis.
34/45

37. 2.GRANULATION TISSUE FORMATION
• New connective tissue begins to form approx. 2–4 days after
wounding.
• 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.
35/45

38. 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
36/45

39. • During the formation of granulation tissue, macrophages,
fibroblasts and new blood vessels grow into the wound space
in a coordinated manner
• 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
37/45

40. 3.ANGIOGENESIS
Angiogenesis or Neovascularisation is a fundamental process to
healing and becomes active from 2nd day after wounding.
Angiogenesis process
• stimulation by chemical signals or hypoxia
• endothelial cell proliferation
• directional migration of endothelial cells
• organisation and differentiation to form capillary tubes
Functions of new formed blood vessels
• supply of oxygen and nutrients
• transport of degradation products
• cell settlement
38/45

41. • At its peak, granulation tissue has more capillaries/unit vol
than any other tissue
Growth factors inducing angiogenesis ----- VEGF, bFGF
Factors stabilizing vessels ----- Angiopoetin 1 &2
PDGF & TGFB
39/45

42.  It starts after 2-3 days and the process is completed by the 14th day.
 Wound is reduced by 80% of its original size which helps in rapid
healing since lesser surface area of the injured tissue has to be
replaced.
MECHANISMS OF
WOUND
CONTRACTION
DEHYDRATION
MYOFIBROBLASTS
CONTRACTION
OF COLLAGEN
4. CONTRACTION
40/45

43.  MYOFIBROBLAST
• Modified fibroblasts - described by Gabbiani et al (1971)
• Appear 4 to 6 days after injury & seen in the wound during the later
2 to 3 weeks.
• Move along fibronectin linked to fibrin in the provisional ECM in
order to reach the wound edges & form connections to the ECM and
attach to each other & 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.
• Reduces wound size by 40-80%
• After contraction –apoptosis →New normal CT fibroblasts emerge
41/45

44. III. THE REGENERATIVE PHASE
Phase includes:
• Collagen Remodeling
• Blood Vessel Apoptosis
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 & change in orientation of the first deposited fibers
• Enlarging or increasing the numbers of oriented fibers
42/45

45. • 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.
43/45

46. FACTORS INFLUENCING
HEALING
LOCAL FACTORS
• Oxygenation
• Infection
• Foreign Body
• Venous Insufficiency
• Exposure To UV Light Facilitates Healing
• Exposure To Ionizing Radiation
44/45

47. SYSTEMIC
FACTORS
• Age and gender
• Sex hormones
• Stress
• Diseases: diabetes, keloids,
fibrosis.hereditary healing
disorders.Jaundice.
• Obesity
• Alcoholism
• Smoking
• Medications: glucocorticoid
steroids, NSAIDS,
chemotherapeutic drugs.
• Immunocompromised
conditions: cancer, radiation
therapy, AIDS
• Nutrition
45/45

49. TO BE CONTINUED…

50. HEALING AFTER
PERIODONTAL
PROCEDURES - II
GUIDED BY:
DR. AMIT GOEL
DR. DIVYA JAGGI
PRESENTED BY:
DR.MALVIKA THAKUR
PG II YEAR

51. CONTENTS
1. INTRODUCTION
2. TERMINOLOGIES
3. REGENERATION &
REPAIR
4. GROWTH FACTORS IN
WOUND HEALING
5. WOUND HEALING
6. FACTORS INFLUENCING
WOUND HEALING
1. HEALING OF ORAL
WOUNDS
2. WOUND HEALING
FOLLOWING VARIOUS
PERIODONTAL
THERAPIES
3. EFFECT OF SUTURES,COE
PAK & CYNOACRYLATE
4. USE OF LASERS IN
WOUND HEALING
5. CONCLUSION
6. REFERENCES
PART – I PART – II
01/54

52. 02/54

53. HEALING OF ORAL WOUNDS
Oral wounds heal faster and with less scarring than extra oral
wounds
It is mainly due to:
Ref : Cell Biology Of Gingival Wound Healing, Periodontology 2000, Vol. 24, 2000, 127–152
FACTOR MECHANISM
Saliva Moisture, ionic strength, ions – Mg & Ca
Growth factors(EGF,VEGF, TGFΒ,FGF,IGF)
Bacteria Stimulation of macrophage influx,
Direct stimulative action on keratinocyte and fibroblast
Phenotype of
cells
Fetal like fibroblasts with unique response,
Specialized epithelium & Connective tissue
03/54

54. HEALING AFTER
PERIODONTAL PROCEDURES
04/54

55. 24 hrs: Widespread infiltration of inflammatory cells and migration of
keratinocytes have been observed, in all areas of the remaining
epithelium
2 hours:
• Numerous polymorphonuclear leucocytes can be seen b/w residual
epithelial cells & crevicular surface.
• Dilation of blood vessels, oedema & necrosis in the lateral wall
of the pocket
HEALING FOLLOWING SCALING &
ROOT PLANING
2 days: Entire pocket is epithelialized.
05/54

56. DURATI-
ON
CONNECTIVE TISSUE
CHANGES
EPITHELIAL CHANGES CLINICAL CHANGES
Immediat
ely
• Hemorrhage
• a/c inflamm reac
• Removal of ep. lining
• Few cells may remain
• Blood & exudate
1st day • Marked inflammation • Epithelial migration
begins (0.5-1mm/day)
• Edematous
• Discoloration persists
2nd day • Inflammation 
• Vascularity 
• Epithelium begins to
cover the gingival corium
•Discoloration 
• Edema still present
4th-6th
day
• Chr inflammation
• Collagenation
• Matrix formation
• Restoration of
junctional & sulcular
epithelium
-
7th-10th
day
•  Collagen formation&
organisation
• Epithelium formation is
complete
• Edema 
• Rigid & well adapted
gingival wall
10th-14th
day
• Repair of conn tissue
•  vascularity
• Surface keratinization  • Normal color
• Stippling appears
• Gingival shrinkage
After 2
weeks
• Mature collagen
• New sub sulcular &
marginal vessels
-
• Color, contour,
consistency,
texture.
• Well adapted marginal
gingiva
HEALING FOLLOWING
CURETTAGE
06/54

57. ULTRASONIC CURETTAGE
• Heat coagulationEpithelium
• Tissue discontinuity
• Fused collagen
• Narrow band of necrotic tissue strips off the
inner lining of pocket
Immediately
after
• Epithelialization occurs
• Lesser inflammation
3 days
• Shorter & thinner epithelium
• Fewer rete pegs
2 weeks
• More satisfactory healing
• Healing is faster
Goldman
(1980)
07/54

58. HEALING AFTER SURGICAL
GINGIVECTOMY
(Reported By Bernier & Kaplan
1947 )
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 Collagen
fragmentation
Angioblasts
Epithelialisation-
centripetal fashion -
1st-3rd day - Hemidesmosomes &
basement lamina
-
3rd-4th day Loss of clot
Granulation tissue
- -
DURATION CONNECTIVE TISSUE EPITHELIUM BONE
5th-14th day Disorganized connective
tissue
dilated blood vessels
Anastomosis b/w
periodontal and gingival
vessels
Epithelialization~
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 appear
Dentogingival
unit
New sulcus
Resorption ceases
Crestal bone level
re-established
4-5 weeks - Complete repair -
By 7 weeks Complete repair - -
08/54

59. ELECTROSURGICAL
GINGIVECTOMY
• Malone et al. (1969) and Eisenmann .D et al. (1970) reported
no significant differences in gingival healing by electro surgery
and resection with periodontal knives.
• For deep resections, however electro surgery 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.
09/54

60. • 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) - Permanent periodontal damage -
burning of cementum, loss of connective tissue attachment,
and significant recession of gingival margin. Avoid
contacting cementum or bone.
10/54

61. LASER GINGIVECTOMY
• Advantages – Minimal Disturbance Of Surrounding Tissues
– Hemostatic Effect
– Edema & Pain
– Sterilization Of Wound
– Minimal Scarring
• Healing – Delayed Re-epithelialization
– Lesser Inflammatory Response
– Thermal Necrosis
– Decreased Wound Contraction 11/54

62. CHEMOSURGICAL GINGIVECTOMY
• Chemicals – Phenols
– 5% Paraformaldehyde
– Potassium hydroxide
• Incomplete gingival remodeling
• Delayed epithelialization and connective tissue repair
• Increased inflammation after chemical trauma
• No control over the depth of action
12/54

63. HEALING FOLLOWING
GINGIVAL DEPIGMENTATION
The initial response -
formation of protective
surface clot
The underlying tissues
become acutely
inflamed, with some
necrosis.
Clot is then replaced
by Granulation Tissue
(GT)
Capillaries derived
from blood vessels of
the PDL migrate into
the GT
Within 2 weeks,
capillaries connect
with gingival vessels.
Vascularity increases
initially, then begins to
decrease gradually as
healing takes place .
Vascularity returns to
normal in about 2-3
weeks.
After 5-14 days
surface
epithelialization is
generally complete.
Complete epithelial
repair takes about 1
month.
HEALING FOLLOWING SURGICAL DEPIGMENTATION
13/54

64. Healing following depigmentation by laser:
 During laser depigmentation 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
 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.
14/54

65. • 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
HEALING FOLLOWING
PERIODONTAL FLAP SURGERY
15/54

66. FULL THICKNESS FLAP
• Caffese , Ramfjord & Nasjeleti (1968)
• Healing :
1° intention Ideal flap adaptation
Minimal surgical trauma
No intervening granulation tissue
Complete within 21 days
2° intention Intervening granulation tissue
Common in well adapted flaps
3° intention Poor flap adaptation
Delayed healing with complications
Not complete even after 72 days.
16/54

67. 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 tooth surface
• Thin blood clot
• Inflammation
• Connective tissue grows b/w 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 side of bone
• Cementoblasts – missing for 1mm apical to alveolar crest
DURATION HEALING
7 days • Formation of epithelial attachment begins
• Granulation tissue adheres the flap to underlying bone
• Severe osteoclastic activity (for 2-3 mm)
9 days • Crevicular epithelium & new epithelial attachment
• Some cementoclastic activity
• Osteoclastic activity over alveolar crest
• Periodontal fibers replaced by vascular granulation tissue
14 days • Band of connective tissue b/w 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 Epithelialized Gingival Crevice
• Well Defined Epithelial Attachment
• Functional Arrangement Of Supracrestal Fibers
35 days • Gingival Adaptation
• Chronic inflammation in connective tissue
72 days • Total crevicular depth = 1mm
• Para keratinized free gingival margin
• Periosteum appears normal
• Functional orientation of gingival fibers(immature collagen)
• Newly formed bone on tip of alveolar crest 17/54

68. PARTIAL THICKNESS FLAPS
• Ramjford & Costich (1968)
• Lesser physical, biological & infective insult.
• Higher proliferative capacity of retained periosteum.
• Healing depends on nature & thickness of periosteum and
retained connective tissue (min -0.5mm)
• Heals faster with lesser destruction of alveolar bone.
18/54

69. 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
19/54

70. HEALING OF PEDICLE
AUTOGRAFTS
Coronally
displaced flap
Lateral
pedicle
Double
papilla
• Healing at the site where the pedicle is placed over
the denuded root surface. (Wilderman & Wentz 1965)
20/54

71. STAGE HEALING
ADAPTAION
STAGE
(0-4 DAYS)
• Clot & thin fibrinous exudate b/w flap and root surface
• PMNLs in clot & connective tissue
• Epithelium at margins of flap starts to proliferate – may contact
tooth surface
PROLIFERATION
STAGE
(4-21 DAYS)
• Connective tissue invades the fibrin layer
• 6-10 days- fibroblasts apposed against root surface
• Collagen within the flap – oriented parallel to root surface
• Thin collagen fibers adjacent to root (no fibrous union)
• Apical proliferation of epithelium- peaks at 10-14 days
• Osteoclastic resorption (peaks at 6th day) - by 14th day
• Slight cemental resorption
ATTACHMENT
STAGE
(21-28 DAYS)
• Collagen fibers insert into new cementum
• Cementoid deposition(by 28th day – along the entire root)
• Connective tissue attachment
• New gingival margin, sulcuc & epithelial attachment
• Osteoblastic activity
MATURATION
STAGE
(28-90 DAYS)
• Continuous formation of collagen fibres
• Completely formed gingival sulcus and epithelial attachment
• Bone apposition at alveolar crest 21/54

72. FULL THICKNESS SPLIT THICKNESS
Healing starts from periphery of wound
Sparing marginal gingiva of donor
tooth prevents recession there
Receives blood supply only through
PDL vessels
Granulation tissue covers the wound
Osteoclastic resorption on the PDL side
Dehiscence if thin cortical plates
Epithelialization (centripetal fashion) –
complete by 3 weeks
Retained periosteum and a layer of
connective tissue
Intact supraperiosteal vasculature
Faster healing
Minimal bone resorption
PEDICLE AUTOGRAFTS
22/54

73. 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 et al (1968), Nobuto et al (1988) described the
healing into 3 phases
23/54

74. PHASE HEALING
INITIAL
PHASE
(0-3 DAYS)
• Thin layer of exudate b/w graft & recipient bed.
•Avascular plasmatic circulation (Forman 1960;
Reese & Stark 1961)
• Epithelium of free graft gets desquamated
REVASCULARI
- SATION
(2-11 DAYS)
• Anastomosis b/w graft & recipient site blood
vessels.
• Capillaries proliferate in the graft tissue
• Fibrous union b/w graft & conn tissue bed
• Re epithelialization of the graft
TISSUE
MATURATION
(11-42 DAYS)
• ↓ in the number of blood vessels to normal by the
14th day.
• Epithelium maturation- formation of keratin layer
• Functional integration – by 17th day
• Morphologically distinguishable for several months
24/54

75. Initial phase
(0-3 days)
Revascularisation
(2-11 days)
Tissue
maturation
(11- 42 days)
Pale – empty graft vessels
Pink – vascularisation begins
Smooth & shiny – loss of epithelium
Thin grey veil like surface – new epithelium
Normal features – maturation of epithelium
25/54

76. • Bissada et al (1978) performed a study to quantitatively assess
FGG with and without periosteum and osseous perforation. They
concluded that there was no difference in the survival or healing
pattern of grafts placed on the periosteum and grafts placed on
bear bone.
• Mormann et al (1981) conducted angiographic studies on the
healing of FGG of varying thickness. They demonstrated that
rapid revascularization can be expected when uniform grafts of
thin to intermediate thickness are placed on a periosteal recipient
site. An uneven, thick graft on a site of denuded bone favored a
prolonged period of re-vascularization and delayed healing.
26/54

77. DONOR SITE
 Granulation tissue fills the donor site.
 Initial healing is usually complete within 2 - 3 weeks after
the removal of a 4 to 5 mm thick graft.
 Patients should wear the surgical stent for about 2 weeks to
protect the healing wound.
 Palate returns to its pre surgical contour after about 3
months.
27/54

78. • FIRST WEEK :
Postoperative swelling
The epithelium of the graft will sough
Ep. cells, together with fibrin form a white film on the
surface of the grafts.
The “white stage” passes in 4 to 7 days.
 Ep. will not cover the grafted tissue until a functional capillary
circulation has been re-established.
 Therefore - RED STAGE (2nd & 3rd Week)
Normal colour as epithelialization is completed
Epithelium thickens via stratification.
RECIPIENT SITE
28/54

79.  The graft reverts to its original volume or remains slightly
larger as the swelling subsides.
 Tissue form is usually stable after 2 months, but some
shrinkage may occur between the 2nd and 4th months after
surgery.
 Final restorative measures should be initiated until after 4 - 6
months.
29/54

80. THICK VS THIN GRAFT
Sullivan and Atkins-(1968)
• Graft thickness would determine behavior of circulation during
healing and its final character.
• Thinner grafts (0.5-0.7mm) enhanced survival
• Thick graft with a thicker lamina propria → greater primary
contraction causing blood vessels to collapse , retarding
revascularization & 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.
30/54

81. HEALING OF CONNECTIVE
TISSUE GRAFTS
• Healing is similar to FGG
• 2nd day - Epithelialization commences
• 7 – 10 days - Initial epithelialization
completed
• 4 weeks - Keratinization commences
31/54

82. HEALING FOLLOWING REGENERATIVE
OSSEOUS SURGERY
• Ellegaard et al. (1973, 1974, 1975, 1976) and Nielsen et al.
(1980)
• Therapeutic bone regeneration approaches uses the
principles of:
Osteogenesis : – Direct formation through osteoblasts
Osteoinduction : – Transformation of mesenchymal
cells to osteoblasts
Osteoconduction Or the Trellis effect : – Stimulation of
attachment, migration & distribution of vascular &
osteogenic cell.
32/54

83. HEALING CANCELLOUS CORTICAL
Blood clot
(1st week) Similar
Revascularization • 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
33/54

84. DRAGOO (1973)
DURATION HEALING
3 days • Vascularity
1 week • Resorption of grafted bone
• No evidence of periodontal membrane
• Union b/w the graft & existing 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 arrangement.
• Sharpeys fibers well inserted
4 months • Root resorption in some areas
• Well oriented periodontal ligament
6 months • Root resorption areas repaired
• Many niduses of bone formation
34/54

85. • 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.
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’s Concept)
35/54

86. • 1976, Melcher - Root surfaces may be repopulated by 4 different
types of cells:
36/54

87. HEALING AFTER RESECTIVE
OSSEOUS SURGERY
• Osteoplasty : reshaping of the alveolar process to achieve
a more physiological form without removal of supporting
bone
• Ostectomy : bone that is part of the attachment apparatus
is removed to eliminate a periodontal pocket and establish
gingival contours that will be maintained .
Friedman 1955
• Wilderman (1970) described the healing after resective
osseous surgery
37/54

88. 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 radicular surfaces
After 6
months
• Slight bone apposition at bone crest, periodontal surface, periosteal surface
• Presence of a definitive periosteum 38/54

89. HEALING FOLLOWING DENTAL
IMPLANTS
• Healing of an osseous wound around a dental implant ,is a
coordinated and sequentially organized repair mechanism.
(Nguyen et al 2009)
OSSEOINTEGRATIO
N
FIBRO-OSSEOUS
INTEGRATION
BIOINTEGRATION
39/54

90. FIBRO-OSSEOUS INTEGRATION
• “Tissue to implant contact with dense collagenous tissue between
the implant and bone”
• Seen in earlier implant systems.
• Initially good success rates but extremely poor long term success.
• Considered a “failure” by todays standards
40/54

91. OSSEO-INTEGRATION
• In 2012, Zarb and Koka defined Osseo integration as “a time-
dependent healing process whereby clinically asymptomatic
rigid fixation of alloplastic materials is achieved and
maintained in bone during functional loading.”
• Success Rates >90%
• Meffert et al (1987)
ADAPTIVE BIOINTEGRATION
OSSEOINTEGRATION
41/54

92. • Stages of osseointegration are divided into three
overlapping steps:
Early Immune-inflammatory Response
 Angiogenesis
Osteogenesis
42/54

93. STAGES OF HEALING OF
IMPLANTS
1. 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 first 4-6 weeks
2. Lamellar Bone Formation :
• From 2nd month post-operatively the microscopic structure
of bone changes to lamellar or parallel fibered bone.
43/54

94. 3. 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.
44/54

95. HEALING IN IMMEDIATE IMPLANT PLACED
IN FRESH EXTRACTION SOCKET
• Vignoletti et al, 2009 described histologically the early phases of
soft tissue healing in implants placed in fresh extraction sockets
in dogs – observed fast apical down growth of the peri implant
J.E within 1st week of healing & a final biological width of
5mm with peri implant J.E measuring 3.0-3.5mm at 8 weeks.
• Rimondini et al 2009 – in mini pigs – 3mm JE after 30 and 60
days
• De Sanctis et al 2009 – in different implant systems in dogs
2.33-2.70 mm JE after 6 weeks
45/54

96. FLAP VERSUS FLAPLESS HEALING OF PERI
IMPLANT MUCOSA
• Kim et al 2009, Investigated vascularity of peri implant mucosa
after flap and flapless implant installation. – increased
vascularity after flapless procedure.
• Muller et al 2010 – smooth neck portion is to be preferred for
flapless approach.
• Lee et al 2010 & Bayounis et al 2011, it seems that flapless
approach has, advantage over flap surgery.
• Blanco et al, 2012, using flapless approach with and without
immediate implant loading found similar soft tissue dimensions
in dog around titanium implants after 3 months.
46/54

97.  RESPONSE TO SUTURES
• Insertion of suture itself entails incisional damage.
• Each suture track is a separate wound
• Incites the same phenomena as in healing of primary wound
• 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 .
HEALING RESPONSE
47/54

98. 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 48/54

99.  RESPONSE TO COE PAK
• Saito et al. 2008 in their histologic study reported tissue
inflammatory reaction to Coe-pack.
• Genovesi et al 2012 -effective for improving the results of non-
surgical treatment of patients and attributed this effect to
enhanced clot stability and decreased risk of bacterial infection.
• Bose et al. 2013 suggested that periodontal dressing leads to
more inflammation immediately post-surgery; which may in
turn delay the wound healing response.
• Sara Soheilifar et al 2015 - No significant difference was noted
b/w sites with & without Coe Pack in terms of swelling,
bleeding, gingival consistency, granulation tissue formation,
gingival color & ease of nutrition
• Post-surgical healing with Coe pack can be beneficial for
reducing post-operative pain.
49/54

100.  RESPONSE TO CYNOACRYLATE
• Tensile strength of the glued wound is similar to that of the
sutured wound during the first 7 postoperative days.
• Less scar formation and rapid wound healing are the main
factors that contribute to the effectiveness of the cyanoacrylates.
• ↓ the incidence of inflammation and infection and the cosmetic
results is superior.
• Shortens operation time as hemostatic properties are superior.
• It also has anti-microbial properties. (Bonutti PM et al 1988 )
50/54

101. USE OF LASERS IN WOUND
HEALING
 LOW-LEVEL laser therapy (LLLT) as a therapeutic modality was
introduced by the work of Mester and colleagues(1971,1975,1982)
who noted improvement in wound healing with application of a
low-energy.
 Lasers employing low-level energy have been claimed to produce a
positive effect on the biological and bio-chemical processes of
wound re-constitution.
 Investigations have demonstrated more rapid epithelialization,
enhanced neovascularization, and increased production of collagen
by fibroblasts, ultimately leading to accelerated wound healing,
reduced pain and enhanced neural regeneration.
51/54

102. • The ability of low-power laser to activate and prime the latent TGF-
β1 complex in healing wounds suggests a key role for TGF-β in
mediating the photobiomodulatory effects of low-power lasers.
(Praveen R. Arany et al,2007).
• The ↑ early active TGF- β1 - ↑ inflammatory infiltrate - reflects a
more rapid onset of inflammation and cascades into a more rapid
onset of succeeding phases of healing .
• Significant ↑ at 14 days in TGF-β1 and - β3,coincided with the ↑
‘‘round cell’’ inflammatory infiltration in the laser-irradiated wounds
Inflammatory cells- monocyte–macrophages - abundant sources of
TGF-β.
• TGF-β3 isoform in these wounds might specifically mediate the scar-
less healing pattern
52/54Ref : Praveen R. Arany et al, 2007

103. CONCLUSION
 Current scientific evidence points to the presence of:
1. Cells originating from the periodontal ligament
2. Wound stability
3. Space provision
4. Primary intention healing
as fundamental biologic and clinical factors that must be met to
obtain periodontal regeneration.
53/54

104.  Wound healing is achieved by a series of coordinated efforts by
inflammatory cells, keratinocytes, fibroblasts and endothelial
cells responding to a complex array of signals.
 Future research will have to be directed towards understanding
in more detail the molecular mechanisms of differential gene
expression in healing wounds.
54/54

105. 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