wound, wound healing, periodontal healing, factors, healing after scaling and root planing, gingivectomy, flap surgery, types of healing, factors affecting healing, newer ways, management

1. Presented By:- Dr. Abhilasha
Moderated By:- Dr. Shivaprasad
Department Of Periodontics
M. R. Ambedkar Dental College, Bangalore
1

2. CONTENTS
• WOUND
– Definition
– Classification
• HEALING
– Definition
– Process of wound healing
• TYPES OF WOUND HEALING
• HEALING OF SPECIALIZED TISSUES
• FACTORS AFFECTING WOUND
HEALING
• COMPLICATIONS
• HEALING FOLLOWING PERIODONTAL
THERAPY
• HEALING AFTER IMPLANT PLACEMENT
• COMMONLY USED WOUND HEALING
MATERIALS
• NEW CONCEPTS
• RELATED STUDIES
• CONCLUSION
• REFERENCES
2
PART 1 PART 2

3. WOUND
DEFINITION
 It is a circumscribed injury which is caused by external force and it can involve any
tissue and organ.
A wound is a break in the integrity of the skin or tissues often, which may be associated with
disruption of the structure and function.
(SRB Manual Of Surgery 5TH EDITION)
A cut or break in the continuity of any tissue, caused by injury or operation.
(BAILLIÈRE’S 23RD ED)
3

4. CLASSIFICATION
4
1. ACCORDING TO RANK & WAKEFIELD

5. CLASSIFICATION
Acute Wound
• Defined as those that progress
through the normal phases of
healing and typically show signs of
healing in less than 4 weeks
• Examples are—surgical or traumatic
or burn wounds
Chronic wound
• Defined as those that do not follow
the normal healing process and show
no signs of healing in 4 weeks.
• Diabetes, venous/arterial diseases,
nutritional deficiencies are the
causes.
3. BASED ON TIME ELAPSED
5

6. CLASSIFICATION
Clean Wound
-Herniorrhaphy.
-Excisions.
-Infective rate is
less than 2%.
Clean
Contaminated
Wound
-Appendicectomy.
-Bowel surgeries,
-Infective rate is
10%.
Contaminated
Wound
-Acute abdominal
conditions.
-Open fresh
accidental wound
-Infective rate is
15–30%.
Dirty infected
wound
-Abscess drainage
-Pyocele.
-Infective rate is
40–70%.
6
4. BASED ON DEGREE OF CONTAMINATION

7. HEALING
7
Wound healing is a complex physiological process that is dependent on a number of
inter-related factors.
DEFINITION
Wound healing is complex method to achieve anatomical and functional integrity of
disrupted tissue by various components; in an organised staged pathways.
(SRB Manual Of Surgery 5TH EDITION)
Wound healing can be defined as physiological processes by which the body replaces
and restores the function of damaged tissue.
(FLANAGAN, 1997)

8. PROCESS OF WOUND HEALING
REGENERATION REPAIR
8
All tissues in the body are capable of healing by one of two mechanisms.
At times, both the processes take place simultaneously.
&

9. REGENERATION
• Regeneration occurs when healing takes place by proliferation of parenchymal cells
and usually results in complete restoration of the original tissues.
• The goal of all surgical procedures should be regeneration which returns the tissues
to their normal microstructure and function.
• 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 the period between two successive cell divisions.
9

10. Cell Cycle
10
ROBBIN’S and COTRAN PATHOLOGIC BASIS OF DISEASE, 9TH EDITION, pg 25

11. 11
CELL TYPES
 LABILE CELLS
 STABLE CELLS
 PERMANENT CELLS
 continue to multiply through out life under normal physiologic
conditions
 Example- epithelial cells of epidermis, alimentary canal
 cells decrease / loose their ability to proliferate after adolescence
but retain their capacity to multiply in response to stimuli
throughout life.
 Example- parenchymal cells of organs like lungs, kidneys, liver and
mesenchymal cells like vascular endothelium.
 these cells loose their capacity to proliferate around time of birth.
 Example- neurons and cardiac muscles

12. 12

13. Regulation of cell population
13
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.
ROBBIN’S and COTRAN PATHOLOGIC BASIS OF DISEASE, 9TH EDITION, pg 27

14. Molecular Events Involved
 Although many chemical mediators affect cell growth, POLYPEPTIDE GROWTH
FACTORS (GF)… are most important for growth.
 GF have a Pleiotropic role :
– Cellular proliferation and differentiation : affecting the expression of the genes
involved in growth control pathways.
– Tissue re-modelling.
14
1. CELL GROWTH

15. 15
ROBBIN’S and COTRAN PATHOLOGIC BASIS OF DISEASE, 9TH EDITION, pg 19

16. Molecular Events Involved
• Polypeptide growth factors bind to and activate their receptors, many of which
posses intrinsic kinase activity.
• Subsequently they phosphorylate a number of substrates involved in signal
transduction and generate 2nd messengers like ras.
• The resultant kinase cascade leads to the activation of nuclear transcription factors,
initiates DNA synthesis and ultimately culminates in cell division.
• 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 .
16
2. CELL DIVISION

17. 17

18. Molecular Events Involved
 Functions
 Mechanical support for cell anchorage
 Control of cell proliferation
 Scaffolding for tissue renewal
 Establishment of tissue microenvironments
 ECM consists of 3 components
1. Collagen
2. Adhesive glycoproteins : fibronectin, integrins , laminin.
3. Proteoglycans.
3. EXTRACELLULAR MATRIX
18
Midwood et al. and Badylak

19. ROBBIN’S and COTRAN PATHOLOGIC BASIS OF DISEASE, 9TH EDITION, pg 21 19

20. To summarize, cell growth and differentiation involves
at least two types of signals acting in concert.
1. One derives from the soluble molecules such as
polypeptide growth factors and growth inhibitors.
2. Other involves insoluble elements of ECM interacting
with cellular integrins.
20

21. REPAIR
• Healing of a wound by tissue that does not fully restore the architecture or function
of the part.
• It 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.
21
(AAP, Glossary of periodontal terms).

22. • 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 :
22
1. Granulation Tissue Formation
2. Wound Contraction

23. REPAIR
• 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.
1. Granulation Tissue Formation
Granulation
Tissue Formation
Phase of
INFLAMMATION
Phase Of
CLEARANCE
Phase Of
INGROWTH of
granulation tissue
ANGIOGENESIS
FIBROGENESIS
23
CALIN et al

24. • PHASE OF INFLAMMATION
– Following trauma blood clots at site of injury.
– There is acute inflammatory response with exudation of plasma , neutrophils
and some monocytes within 24 hours.
– Moreover, the macrophages, upon secreting chemotactic factors, attract other
inflammatory cells to the wound area.
NORMAL TISSUE INJURY INFLAMMATION
24

25. • PHASE OF CLEARANCE
– Combination of Proteolytic enzymes liberated by neutrophils
– Autolytic enzymes from the dead tissue cells
– Phagocytic activity of the macrophages .
All the above processes leading to clearance of the necrotic tissue ,debris and
RBCs .
NEUTROPHIL DEAD CELL MACROPHAGE 25

26. • PHASE OF INGROWTH OF GRANULATION TISSUE
• Angiogenesis is the process of new blood vessel development from existing vessels.
• Angiogenesis involves sprouting of new vessels from existing ones with the help of
several signalling pathways, cell-cell interactions, extracellular matrix proteins and
tissue enzymes.
• Initially, the proliferated endothelial cells are solid buds but within a few hours
develop a lumen and start carrying blood.
ANGIOGENESIS
26

27. 27

28. • PHASE OF INGROWTH OF GRANULATION TISSUE
• The newly formed blood vessels are present in an amorphous ground substance or
matrix.
• The new fibroblasts have features intermediate between those of fibroblasts and
smooth muscle cells (myofibroblasts).
• Collagen fibrils begin to appear by about 6th day.
FIBROGENESIS
28
-MEDRADO et al

29. • The myofibroblasts have surface receptors for fibronectin molecules which form
bridges between collagen fibrils.
• As maturation proceeds, more and more collagen is formed while the number of
active fibroblasts and new blood vessels decreases.
• This results in formation of inactive looking scar; this process is known as
cicatrisation.
29

30. • 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.
2. Wound Contraction
MECHANISM
OF WOUND
CONTRACTION
Contraction Of Collagen
Myofibroblasts Dehydration
30

31. • With the closure of the wound, type III collagen undergoes degradation, and
synthesis of type I collagen increases.
• Sampaio & Riviti, have confirmed that, in the final stage, the collagen fibers become
thicker and are placed in parallel, resulting in an enhanced tensile strength for the
tissue.
31

32. TYPES OF WOUND HEALING
PRIMARY WOUND HEALING
SECONDARY WOUND HEALING
TERTIARY WOUND HEALING
32

33. PRIMARY WOUND HEALING
 Also known as HEALING BY FIRST INTENTION (PRIMARY UNION).
 This is defined as healing of a wound which has the following characteristics:
– clean and uninfected;
– surgically incised;
– without much loss of cells and tissue; and
– edges of wound are approximated by surgical sutures.
33

34. 1. INITIAL HAEMORRHAGE
• Immediately after injury, the space between the
approximated surfaces of incised wound is filled
with blood which then clots and seals the
wound against dehydration and infection.
2. ACUTE INFLAMMATORY RESPONSE
• Occurs within 24 hours with appearance of
polymorphs from the margins of incision.
• By 3rd day, polymorphs are replaced by
macrophages.
Sequence in Primary Intention:-
34

35. 3. EPITHELIAL CHANGES
• The basal cells of epidermis from both
the cut margins start proliferating and
migrating towards incisional space in
the form of epithelial spurs.
• A well approximated wound is
covered by a layer of epithelium in 48
hours.
• By 5th day, a multi-layered new
epidermis is formed which is
differentiated into superficial and
deeper layers.
35

36. 4. ORGANISATION
• By 3rd day, fibroblasts also invade the
wound area.
• By 5th day, new collagen fibrils start
forming which dominate till healing is
completed.
• In 4 weeks, the scar tissue with scanty
cellular and vascular elements, a few
inflammatory cells and epithelialized
surface is formed.
36

37. SECONDARY WOUND HEALING
 Also known as HEALING BY SECOND INTENTION (SECONDARY UNION)
 This is defined as healing of a wound having the following characteristics:
– open with a large tissue defect, at times infected;
– having extensive loss of cells and tissues; and
– the wound is not approximated by surgical sutures but is left open.
 Healing by second intention is slow and results in a large, at times ugly, scar as
compared to rapid healing and neat scar of primary union.
37

38. • The basic events in secondary union are
similar to primary union which involves:-
1. INITIAL HAEMORRHAGE
2. INFLAMMATORY PHASE
3. EPITHELIAL CHANGES
-Healing takes place from the base upward and
also from the margins inwards.
- Epidermal cells from both the margins of
wound proliferate and migrate into the wound in
the form of epithelial spurs till they meet in the
middle and re-epithelialize the gap completely.
38

39. 4. GRANULATION TISSUE
• Main bulk of secondary healing is by
granulations.
• Granulation tissue is formed by
proliferation of fibroblasts and
neovascularisation from the adjoining
viable elements.
• The newly-formed granulation tissue is
deep red, granular and very fragile.
39

40. 5. WOUND CONTRACTION
• Contraction of wound is an important
feature of secondary healing, not
seen in primary healing.
• Due to the action of myofibroblasts
present in granulation tissue, the
wound contracts to one-third to
one-fourth of its original size.
40

41. 41

42. TERTIARY WOUND HEALING
• Utilized when there are high chances of wound infection.
• Wound left open for few days
• Late suturing done to allow healing by primary intention.
42

43. HEALING OF SPECIALIZED TISSUES
Healing of the skin wound provides an example of
general process of healing by regeneration and repair.
However, in certain specialised tissues, either
regeneration or repair may predominate.
43

44. • Basic events in healing of any type of fracture are similar and resemble healing of
skin wound to some extent.
 Primary union of fractures
 occurs when the ends of fracture are approximated surgically.
 bony union takes place with formation of medullary callus without periosteal
callus formation.
 The patient can be made ambulatory early
1. FRACTURE HEALING
44

45.  Secondary union of fractures
– More common form of fracture healing when the plaster casts are applied for
immobilisation of a fracture.
– Though it is a continuous process, secondary bone union is described under the
following 3 headings:
A. Procallus formation
B. Osseous callus formation
C. Remodelling
45

46. 1. HEMATOMA
2. LOCAL INFLAMMATORY RESPONSE
3. GRANULATION TISSUE
FORMATION
4. PROCALLUS FORMATION
46

47.  The Procallus acts as scaffolding
on which osseous callus
composed of lamellar bone is
formed.
 The woven bone is cleared away
by incoming osteoclasts.
 Newly-formed blood vessels and
osteoblasts invade, laying down
osteoid which is calcified.
 Lamellar bone is formed by
developing Haversian system.
47

48.  Osteoblastic laying and
osteoclastic removal leads to
remodelling of united ends.
 External callus cleared away.
 Intermediate callus
converted into lamellar bone
 Internal callus develops into
bone marrow cavity.
48

49. 1. SKELETAL MUSCLES
• 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:
2. HEALING OF MUSCLES
1. If the muscle sheath is intact, in about 3 months time, histiocytes
restores properly oriented muscle fibres.
2. If the muscle sheath is damaged, it forms a disorganised multinucleate
mass and scar composed of fibrovascular tissue. 49

50. 2. SMOOTH MUSCLES
• Non-striated muscle has limited regenerative capacity
• However, in large destructive lesions, the smooth muscle is replaced by permanent
scar tissue.
3. CARDIAC MUSCLES
• Destruction of heart muscle is replaced by fibrous tissue.
50

51. 1. CENTRAL NERVOUS SYSTEM
• The nerve cells of the brain, spinal cord and ganglia are permanent cells, and
therefore once destroyed are not replaced.
2. PERIPHERAL NERVOUS SYSTEM
• The peripheral nerves show limited regeneration, mainly from proliferation of
Schwann cells and fibrils from distal end.
3. HEALING OF NERVOUS TISSUE
51

52. • 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.
4. HEALING OF SOLID EPITHELIAL ORGANS
52

53. FACTORS AFFECTING WOUND HEALING
53

54. LOCAL FACTORS
1) Infection is the most important factor acting locally which delays the process of
healing.
2) Poor blood supply to wound slows healing.
e.g. injuries to face heal quickly due to rich blood supply while injury to
leg with varicose ulcers having poor blood supply heals slowly.
3) Foreign bodies including sutures interfere with healing and cause intense
inflammatory reaction and infection.
infection
54

55. LOCAL FACTORS
4) Movement delays wound healing.
5) Exposure to ionising radiation delays granulation tissue formation.
6) Exposure to ultraviolet light facilitates healing.
7) Type, size and location of injury determines whether healing takes place by
resolution or organisation.
55

56. SYSTEMIC FACTORS
• AGE- Wound healing is rapid in young and somewhat slow in aged and
debilitated people due to:-
• Poor blood supply to the injured area .
• Altered inflammatory response
• Delayed T-cell infiltration into the wound area
• Alterations in chemokine production
• Reduced macrophage phagocytic capacity.
56
(World Health Organization[WHO, www.who.int/topics/ageing]),

57. • NUTRITION. Deficiency of constituents like protein, vitamin C (scurvy),
vitamin A and zinc delays the wound healing.
• SYSTEMIC INFECTION - delays wound healing.
• HAEMATOLOGIC ABNORMALITIES - like defect of neutrophil functions
(chemotaxis and phagocytosis), and neutropenia and bleeding disorders slow the
process of wound healing.
57

58. • UNCONTROLLED DIABETICS are more prone to develop infections and
hence delay in healing.
58

59. • ADMINISTRATION OF GLUCOCORTICOIDS
Anti-inflammatory effects which inhibit wound repair –
 suppression of cellular wound responses, including fibroblast proliferation and
collagen synthesis.
 Systemic steroids cause wounds to heal with incomplete granulation tissue and
reduced wound contraction.
 Topical low-dosage corticosteroid –accelerate wound healing, reduce pain and
exudate, and suppress hyper granulation tissue formation in 79% of cases.
59

60. 60

61. COMPLICATIONS
During the course of healing, following complications may occur:
1. Infection The wound may get infected due to entry of bacteria which delays the
healing.
2. Implantation (epidermal) cyst Formation of implantation epidermoid cyst may
occur due to persistence of epithelial cells in the wound after healing.
61

62. 3. Pigmentation Healed wounds may at times have rust-like colour due to staining
with haemosiderin. Some coloured particulate material left in the wound may persist
and impart colour to the healed wound.
4. Deficient scar formation This may occur due to inadequate formation of
granulation tissue.
5. Incisional hernia A weak scar, especially after a laparotomy, may be the site of
bursting open of a wound (wound dehiscence) or an incisional hernia.
62

63. 6. Hypertrophied scars and keloid formation-
– At times the scar formed is excessive, ugly and painful.
– Excessive formation of collagen in healing may result in keloid (claw-like)
formation, seen more commonly in Blacks.
– Hypertrophied scars differ from keloid in that they are confined to the borders
of the initial wound while keloids have tumour-like projection of connective
tissue.
7. Excessive contraction
– An exaggeration of wound contraction may result in formation of
contractures or cicatrisation
8. Neoplasia- Rarely, scar may be the site for development of carcinoma.
63

64. TO BE CONTINUED…..
END OF PART 1…..
64

65. 65

66. 66

67. Presented By:- Dr. Abhilasha
Moderated By:- Dr. Shivaprasad
Department Of Periodontics
M. R. Ambedkar Dental College, Bangalore
67

68. CONTENTS
• WOUND
– Definition
– Classification
• HEALING
– Definition
– Process of wound healing
• TYPES OF WOUND HEALING
• HEALING OF SPECIALIZED TISSUES
• FACTORS AFFECTING WOUND
HEALING
• COMPLICATIONS
• HEALING FOLLOWING PERIODONTAL
THERAPY
• HEALING AFTER IMPLANT PLACEMENT
• COMMONLY USED WOUND HEALING
MATERIALS
• NEWER CONCEPTS
• RELATED STUDIES
• CONCLUSION
• REFERENCES
68
PART 1 PART 2

69. INTRODUCTION
• 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 foetal fibroblast with gingival fibroblast
69

70. 70
FACTOR MECHANISM
SALIVA
BACTERIA
PHENOTYPE
OF CELLS
• Moisture
• Ionic strength
• Growth factors (EGF, TGF-β, FGF, IGF…)
• Stimulation of macrophage influx,
• Direct simulative action on keratinocyte
• Fibroblast
• Fetal like fibroblasts with unique response
• Specialised epithelium
• Connective tissue

71. • Physio-chemical factors favouring healing are:-
– appropriate PH
– ionic strength
– calcium and magnesium 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.
71
ROLE OF IN ORAL WOUND HEALING

72. • 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
72

73. HEALING FOLLOWING PERIODONTAL
THERAPY
73

74. SCALING AND ROOT PLANING
74

75. 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, edema & necrosis in the
lateral wall of the pocket
The remaining epithelial cells show very little pre-mitotic activity
at that time.
75

76. HEALING FOLLOWING SCALING & ROOT PLANING
24 HRS after scaling a widespread &intense labelling of the cells
have been observed, in all areas of the remaining epithelium
In 2 DAYS the entire pocket is epithelialized
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
76

77. HEALING FOLLOWING SCALING & ROOT PLANING
• Immature collagen fibres occur within 21 days.
• Following scaling & root planning procedure healing occurs with the formation of a
long thin junctional epithelium with no connective tissue attachment.
77

78. 78
POLYMORPHS
CELL
PROLIFERATION
POCKET
EPITHELIALIZATION
NEW EPITHELIAL
ATTACHMENT
2 HRS 24 HRS 2 DAYS 4- 5 DAYS
COMPLETE
HEALING
1-2 WEEKS
E
V
E
N
T
S
TIME TAKEN
HEALING FOLLOWING SCALING & ROOT PLANING

79. CURETTAGE
79

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.
80

81. HEALING FOLLOWING CURETTAGE
Epithelialization 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.
81

82. GINGIVECTOMY
82

83. HEALING AFTER SURGICAL GINGIVECTOMY
By 24 hours there is an increase in new connective tissue cells, mainly
angioblasts just beneath the surface layer of inflammation and necrosis
Clot is then replaced by granulation tissue
Underlying tissue becomes acutely inflamed with some necrosis
Initial response after gingivectomy is the formation of a protective surface clot
83

84. HEALING AFTER SURGICAL GINGIVECTOMY
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
The highly vascular granulation tissue grows coronally,
creating a new free gingival margin and sulcus
By the 3rd day numerous young fibroblast are located In the area
84

85. HEALING AFTER SURGICAL GINGIVECTOMY
The epithelial cells advances by tumbling action, with cell becoming fixed to the
substrate by hemidesmosomes and a new basement lamina
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
Epithelial activity at the margins reaches peak in 24 to 33 hours
After 12 to 24 hours ,epithelial cells at the margins of the wound start to migrate
over the granulation tissue, separating it from the contaminated layer of the clot
85

86. HEALING AFTER SURGICAL GINGIVECTOMY
Vasodilation and vascularity begin to decrease after fourth day of healing and appear
to be almost normal by the sixteenth day
Complete epithelial repair takes about one month
During the first 4 weeks after gingivectomy, keratinization is less than it was
before surgery
After 5 to 14 days, surface epithelization is generally completed
86

87. HEALING AFTER SURGICAL GINGIVECTOMY
In patients with physiologic gingival melanosis the pigmentation is
diminished in the healed gingiva
Maximal flow is reached after 1week,coinciding with the time of maximal
inflammation
The flow of gingival fluid in humans is initially increased after gingivectomy
and diminishes as healing progresses
Complete repair of the connective tissue takes about 7 weeks
87

88. 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

89. HEALING FOLLOWING LASER GINGIVECTOMY
• Advantages-
– Minimal disturbance of surrounding tissues
– Hemostatic effects
– Reduced edema
– Minimal scarring
• Healing-
– Delayed re-epithelialization
– Lesser Inflammatory response
– Thermal Necrosis
– Decreased wound contraction
89

90. GINGIVAL DEPIGMENTATION
90

91. HEALING FOLLOWING DEPIGMENTATION OF GINGIVA:
• After surgery it is considered necessary to cover the exposed lamina
propria with periodontal packs for 7 to 10 days. The wound heals
uneventfully.
• After 6 weeks the attached gingiva
regenerate by only a delicate scar present.
• The newly formed gingiva will clinically be non-pigmented.
91
Healing after surgical depigmentation:

92. HEALING FOLLOWING DEPIGMENTATION OF GINGIVA:
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.
92
Healing following cryosurgical depigmentation:

93. HEALING FOLLOWING DEPIGMENTATION OF GINGIVA:
• 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
93
Healing following depigmentation by laser

94. PERIODONTAL FLAP SURGERY
94

95. HEALING FOLLOWING FLAP SURGERY
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 & remnants 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.
95

96. By 1 week after surgery epithelial cells have migrated
&established an attachment to root surface by means of
hemidesmosomes
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
96

97. • By end of one month following surgery the epithelial attachment is well formed &
the gingival crevice is also well epithelialised.
• There is beginning functional arrangement of supracrestal fibres.
97

98. • In cases where MUCOPERIOSTEAL FLAP
• 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.
98

99. OSSEOUS RESECTION
99

100. HEALING FOLLOWING OSSEOUS RESECTION
• 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.
100

101. • The initial loss in bone height is compensated to some extent by the repair and
re-modeling.
• 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 last for long
101

102. Possible Outcome of Periodontal therapy
102
In 1976, Melcher in a review
paper suggested that the
type of cells that repopulate
the root surface after
periodontal therapy
determines the nature of
attachment that will form

103. 103
HEALING AFTER
IMPLANT PLACEMENT

104. • 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.
104

105. • 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
• Lamellar Bone Formation : From 2nd month post-operatively the microscopic
structure of bone changes to lamellar or parallel fibered bone
• Bone Remodelling : It begins around 3rd month postoperatively.
• Initially rapid remodelling occurs which slows down & continuous for rest of the life
• Thus complete healing probably takes longer than 3 to 6 months.
105
STAGES OF HEALING OF IMPLANTS

106. 106

107. Oxidised regenerated cellulose (Surgicel)
• Oxidised regenerated cellulose is used as a haemostatic agent, working primarily by
chemical interaction with blood.
• It forms a gelatinous mass when mixed with blood that functions as an artificial
blood clot.
• Due to its low pH, it may also have some antimicrobial effects.
107

108. Whitehead's varnish
• It prevents capillary oozing, helps in relieving postoperative pain and allowing the
patient to be fed orally.
• Also used as a pack for cystic cavities of the jaw, to reduce pain following wisdom
tooth removal, and with the surgical management of osteomyelitis.
• Constituents of Whitehead's varnish are iodoform, Benzoic acid, Storax, Balsam of
Tolu, Ether.
108

109. Carnoy's solution
• Carnoy's solution is used in the mouth as a tanning agent in order to facilitate the
removal of cyst linings.
• Commonly used in marsupialization of OKC.
• It is made up of chloroform, acetic acid and ferric sulphate, in an alcohol solvent
109

110. Zinc oxide based dressing
• It used to cover the gingival tissues or extraction sockets.
• These materials function to provide a physical barrier against the entry of food or
other materials.
• They are divided into eugenol-containing and non-eugenol-containing materials
110

111. Alvogyl
• Alvogyl is a proprietary material that has butamben, iodoform and eugenol as its
active ingredients.
• It is primarily used for the treatment of alveolar osteitis. It is placed into an
extraction socket with the aim of reducing pain and infection.
111

112. 112
NEWER CONCEPTS
IN WOUND HEALING

113. Low level laser therapy
• Low-level laser therapy (LLLT) has been promoted for its beneficial effects on tissue
healing and pain relief.
• Abrasions, turf burns, labial herpes, thrush, surgical incisions, and ulcerations.
113

114. Negative-pressure wound therapy (NPWT)
• Negative-pressure wound therapy (NPWT) is a therapeutic technique using a
vacuum dressing to promote healing in acute or chronic wounds and enhance
healing of second and third degree burns.
• The therapy involves the controlled application of sub-atmospheric pressure to the
local wound environment, using a sealed wound dressing connected to a vacuum
pump
114

115. Apligraft
• Apligraft is a unique, advanced treatment for healing. It is created from cells found
in healthy human skin.
• It is used to heal ulcers such as diabetic foot and venous leg ulcers that are not
healing after 3-4 weeks, despite treatment with conventional therapies.
115

116. Alloderm (life cell)
• Processed human cadaver skin with a cellular dermal matrix and intact basement
membrane
• Advantages: Permanently cover full thickness burns and deep ulcers.
• Disadvantages: not suitable for infected wounds.
• In surgery:
– Root coverage
– Gingival augmentation
– Soft tissue ridge augmentation.
– Soft tissue augmentation around implants.
116

117. Tegaderm
• Used for simple shallow wound dressing
• Protects from water loss mechanical injury and drying
117

118. TransCyte
• Allogenic human fibroblasts cultured on nylon mesh coated with porcine collagen
• Advantages: To cover surgically excised full-thickness burns and non-excised partial
thickness burns
• Disadvantages: Temporary (may need skin grafting after 2–3 weeks); not suitable
for infected wounds and patients allergic to porcine collagen.
118

119. ORCEL
• Allogenic cultured skin containing keratinocytes, fibroblasts, and bovine collagen
• Advantages: Acute and chronic deep dermal ulcers, partial-thickness burns and
donor site wounds.
• Disadvantages: Not for infected wounds or patients allergic to bovine collagen
119

120. MAX8 or Novel hydrogel
• A novel hydrogel, used to seal wounds and at the same time deliver an antibacterial
punch
120

121. Platelet Rich Plasma (PRP)
• Platelet-rich plasma (PRP) is a new approach to tissue regeneration and it is
becoming a valuable adjunct to promote healing in many procedures in dental and
oral surgery, especially in aging patients.
• PRP is derived from the centrifugation of the patient's own blood and it contains
growth factors that influence wound healing, thereby playing an important role in
tissue repairing mechanisms
• In regard to periodontal surgery, the use of PRP at injury sites might be able to
promote wound healing and the regeneration of periodontal soft tissues.
121
Albanese A, Licata ME, Polizzi B, Campisi G. Platelet-rich plasma (PRP) in dental and
oral surgery: from the wound healing to bone regeneration. Immunity & Ageing. 2013 Dec 1;10(1):23.

122. 122

123. 123
RELATED STUDIES

124. 124
2014

125. 125
2015

126. 126
2016

127. 127
2019

128. 128
2019

129. 129
2020

130. CONCLUSION
• 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.
130

131. REFERENCES
• Textbook of pathology, harsh mohan
• Principles of pathology, Robbins& Cotran
• 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)
131

132. • 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.
• Wai-Ping Linda Fan, Mamun Rashid, Stuart Enoch,Current advances in
modern wound healing,Wounds uk, 2010, Vol 6, No 3
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133. 133