The document provides information on wound healing and healing processes in the oral cavity. It discusses: - The classification of wounds as tidy (healing by primary intention) or untidy (healing by secondary intention). - The stages of healing by primary intention (initial hemorrhage, inflammation, epithelial changes, organization) and secondary intention (granulation tissue formation, wound contraction). - Factors that can affect wound healing like infection, nutrition, medication. - Healing of specific oral wounds like extraction wounds and periodontal wounds, which heal faster due to saliva and oral bacteria. - The difference between wound repair, regeneration and new attachment in periodontal healing. - The

1. PRESENTED BY
DR. SONAL KALE
1st Yr PG
WOUND HEALING
1

2. CONTENTS
 INTRODUCTION
 HEALING BY PRIMARY INTENTION
 HEALING BY SECONDARY INTENTION
 COMPLICATION OF WOUND HEALING
 FACTORS AFFECTING WOUND HEALING
 HEALING OF ORAL WOUNDS
 HEALING OF EXTRACTION WOUNDS
 HEALING AFTER PERIODONTAL PROCEDURES
 EDUCATING THE PATIENT
 CONCLUSION
 REFERENCES
2

3. INTRODUCTION
 Wound is a break in the integrity of skin or tissue
often, which may be associated with disruption of the
structure and function.
 Wound is an injury to the body that is usually
associated with cell death and tissue destruction.
 Common causes are violence, accident or surgery that
typically involves laceration or breaking of a
membrane(skin).
 Healing on the other hand is a cell response to injury
in an attempt to restore the normal structure and
function .
3

4. Classification of wound
1.a)TIDY- Incised, caused by sharp object, no tissue loss, heal
by primary intention.
b)UNTIDY-Crushed, teared, devitalised,burn,tissue loss, heal
by secondary intention.
2.CLOSED WOUND
-Contusion or bruising
-Abrasion
-Haematoma
OPEN WOUND
-Incised
-Lacerated
-Penetrating
-Crushed4

5. 5
Incised wound
contusion
abrasion
Penetrating
wound
Crushed
wound

6. Wound healing
Wound healing is a mechanism where the body
attempts-
 To restore the integrity and function of injured part
 To reform barrier to fluid loss and infection
 Limit further entry of foreign organism and material
 Re-establish normal blood and lymphatic patterns
6

7. Classification of wound healing
1. Healing by first/primary intention
Is defined as a wound which has the following
characters
 Clean and uninfected
 Surgically incised
 Without much loss of cells and tissues
 Edges of the wound are approximated by the
surgical sutures
7

8. Sequence of events involved in healing by primary
intention:
 INITIAL HAEMORRHAGE
 ACUTE INFLAMMATORY RESPONSE
 EPITHELIAL CHANGES
 ORGANIZATION
8

9. INITIAL HAEMORRHAGE
 Immediately after injury, the space between the
opposing surfaces of the skin becomes filled with
blood , due to hemorrhage of the injured vessels .
 Clot forms, which seals the incision against
dehydration and infection .
9

10. ACUTE INFLAMMATORY RESPONSE :
 Occurs within 24 hours .
 Margins are infiltrated by neutrophils, monocytes
and swollen by fluid exudate.
 Autolytic enzymes liberated by dead tissue cells .
 Proteolytic enzymes by the neutrophils .
 Phagocytic activity by monocytes and tissue
macrophages which appear by 3rd day clear away
necrotic tissue debris and RBCs .
10

11. EPITHELIAL CHANGES :
 Basal cells of the epidermis from both the cut margins
start proliferating and migrating towards incisional
space in the form of epithelial spurs
 Well approximated wound gets covered by a layer of
epithelium within 48 hours.
 Migrated epidermal cells separate the underlying viable
dermis.
 By 5th day multilayer epidermis is formed which
differentiates in to superficial and deeper layers.
11

12. ORGANIZATION :
 By the 3rd day : capillary buds
fibroblasts
 New collagen by the 5th day-dominates till healing is
complete.
 4th week Scar tissue with scanty cellular and vascular
elements , few inflammatory cells and epithelialised
surface is formed.
12

13. PRIMARY UNION OF SKIN
WOUNDS
13

14. Healing by secondary intention
 When wound is open with a large tissue defect, at
times infected.
 Extensive loss of cells and tissues
 Wound is not approximated by sutures, but is left
open
14

15. Secondary union consists of the following events :
 Initial hemorrhage
 Inflammatory process
 Epithelial changes
 Granulation tissue formation
 Wound contraction
 Presence of infection
Similar to that by primary
intension
15

16. Granulation tissue formation :
 Proliferating fibroblasts and neovascularization
 Newly formed connective tissue: deep red, granular
and very fragile.
 With time scar matures : increased collagen
decreased vascularity
16

17. Wound contraction
 Not seen in primary healing
 Myofibroblasts are the cells responsible for the
contraction of the wound
 13rd to 14th its original size
17

18. secondary union of wound
A. The open wound is filled with blood clot and there is inflammatory response at the
junction of viable tissue
B. Epithelial spurs from the margins of wound meet in the middle to cover the gap
and seperate the underlying viable tissue from necrotic tissue at the surface forming
scab
C. After contraction of the wound ,a scar smaller than the original wound is left
18

19. COMPLICATIONS OF WOUND
HEALING
1. Infection
2. Pigmentation – rust like staining
3. Deficient scar formation  inadequate
granulation tissue
4. Incisional hernia  bulge at the site of surgical
incision.
19

20. 6. Keloid formation  scar formed is excessive, ugly &
painful
 Excessive formation of collagen – claw like
 Common in blacks
7. Hypertrophied scars- confined to borders of initial
wounds ,but rises above the skin level.
8. Excessive contraction
9. Neoplasia  eg: squamous cell carcinoma
20

21. FACTORS INFLUENCING
HEALING
Local factors:
1. Infection
2. Poor blood supply
3. Foreign bodies
4. Movement delays wound healing
5. Exposure to ionizing radiation delays granulation
tissue formation
6. Type, size and location of injury
21

22. Systemic factors:
1. Age
2. Nutrition
3. Systemic infection
4. Administration of corticosteroids has anti-inflammatory
effect
5. Uncontrolled diabetes
6. Haematologic abnormalities – defect of neutrophil function
22

23. Healing of oral wounds
 Oral wounds heals faster and with less scarring
than extra oral wounds
 It is mainly due to :
factors in saliva
specific microflora of the oral cavity
23

24. Factor Mechanism
saliva Moisture ,ionic strength,
Growth factors.
bacteria Stimulation of macrophage influx,
Direct stimulative action on keratinocyte
and fibroblast
24

25. Role of saliva & gingival crevicular fluid in oral
wound healing
 Animals instintly lick their wounds which result in
faster wound healing
 People with xerostomia show dealyed healing of
oral wounds
 Physio-chemical factors favoring healing are
appropriate PH
ionic strength
calcium and magnisium ions
25

26. Lubrication of oral mucosa is beneficial for wound
healing
 Advantages of moist environment
prevention of tissue dehydration and cell
death
accelerated angiogenesis
incremental breakdown of fibrin and tissue
debris
 Presence of growth factors - growth factors are
produced by salivary glands or derived from plasma
through gingival crevice
Epidermal growth factor
Transforming growth factorβ
Fibroblast growth factor
26

27. ROLE OF BACTERIA IN WOUND HEALING
 Oral cavity harbours more than 500 bacterial species
 Wound colonized by pathologic bacteria have
delayed wound healing
 Inflammatory reaction that is prerequisite for tissue
repair is accentuated by bacterial contamination
 Bacteria present in wound will attract macrophages
into the area and induce their cytokine secretion.
27

28.  As a consequence blood supply and granulation
tissue formation are accentuated in wound
healing.
 Proliferation of mesenchymal cells is increased
and synthesis rate of connective tissue
component is stimulated leading to greater tensile
strength of the contaminated wounds in the
course of healing.
28

29. HEALING OF EXTRACTION WOUND
29
IMMEDIATE REACTION FOLLOWING EXTRACTION
 After the extraction, the blood which fills the socket
coagulates, red blood cells being entrapped in the fibrin
meshwork.
 The resultant fibrin meshwork containing entrapped red blood
cells seals off the torn blood vessels and reduces the size of
the extraction of wound.
 Within the first 24-48 hours after extraction there are
alterations in the vascular bed.
 There is vasodilation and engorgement of blood vessels in the
remnants of the periodontal ligament and the mobilization of
leucocytes to the immediate area around the wound.

30. 30
FIRST WEEK WOUND
 Within the first week after tooth extraction, proliferation of
fibroblasts from connective tissue cells in the remnants of the
periodontal ligament is evident, and these fibroblasts begun to
grow into the clot around the entire periphery.
 This clot forms the scaffold on which the cells associated with
healing process may migrate. It is the temporary structure.
 The epithelium at the periphery of the wound grow over the
surface of the organizing clot.
 Osteoclasts accumulate along the alveolar bone crest setting
the stage for active crestal resorption.
 Angiogenesis proceeds in the remnants of the periodontal
ligaments

31. 31
SECOND WEEK WOUND
 During the second week, the blood clot continues to
get organized through fibroplasia and new blood
vessels that penetrate towards the center of the clot.
 Trabeculae of the osteoid slowly extend into the clot
from the alveolus, and osteoclastic resorption of the
cortical margin of the alveolar socket is more distinct.
 The remnants of the periodontal ligament gradually
undergo degeneration and are no longer recognizable.

32. 32
THIRD WEEK WOUND
 As healing continues into the third week , the original clot
appear completely organized by mature granulation tissue and
poorly calcified bone at the wound perimeter.
 The surface of the wound is re-epithelialized with minimum or
no scar formation.
 Very young trabeculae of osteoid bone forms around the entire
periphery of the wound from the socket wall.
 The original cortical bone of the alveolar socket undergoes
remodeling so that it is no longer consist of such a dense layer.
 The crest of the alveolar bone is rounded off by osteoclastic
resorption.

33. 33
FOURTH WEEK WOUND
 During the fourth week the wound begins the final stage of
healing, in which there is continued deposition and
resorption of the bone filling the alveolar socket.
 Much of this early bone is poorly calcified, as is evident
from its general radiolucency on the radiograph.
 Radiographic evidence of bone formation does not become
prominent until the sixth or eighth week after tooth
extraction.

34. 34
1st week 2nd week 3rd week
after 6-8weeks

35. Periodontal wound healing
HEALING FOLLOWING SCALING & ROOT PLANING
 Immediately after Scaling of teeth the epithelial
attachment will be disturbed, junctional & crevicular
epithelium partially removed.
 Numerous polymorphonuclear leucocytes can be
seen between residual epithelial cells & crevicular
surface in about 2 hrs
 There is dilation of blood vessels, oedema & necrosis in
the lateral wall of the pocket
35

36.  In 4-5 days a new epithelial attachment may
appear at bottom of sulcus. Depending on the
severity of inflammation & the depth of
the gingival crevice, complete epithelial healing
occurs in 1-2 weeks
 Immature collagen fibers occur within 21days.
Following scaling, root planning & curettage
procedure healing occurs with the formation of a
long thin junctional epithelium with no connective
tissue attachment.
36

37. 37
 Reduction in pocket depth occurs by two principal
mechanisms:
 1- Recession of the gingival margin due to
resolution of inflammation and subsequent
reduction in swelling and hyperplasia
 2- Reattachment to the root surface. This occurs
primarily by the formation of a long junctional
epithelial attachment. Epithelial cells grow from
the gingival sulcus to repopulate the pocket lining
and attach by hemidesmosomes to the root
surface. This is most likely to occur in the
absence of inflammation

38. 38
Periodontal pocket formation
A- junctional epithelium at CEJ
B- junctional epithelium on cementum, destruction of periodontal
fibres
C-destruction of periodontal fibres and alveolar bone

39. 39

40. Healing following periodontal
procedures
40
During healing 4 type of cells compete to migrate in
the area of wound.
1. Oral epithelium cells
2. Gingival connective tissue cells
3. Bone cells
4. Periodontal ligament cells

41. 41
 Oral epithelium cells- long junctional epithelium
(repair)
 Gingival connective tissue cells- fibres which are
parallel to tooth surface.
 Bone cells- ankylosis
 Periodontal ligament cells- periodontal fibres, new
cementum, new alveolar bone.(regeneration)

42. Healing following periodontal
procedures
42

43. 43
Repair- restores the continuity of diseased marginal
gingiva.
- reestablishes normal gingival sulcus.
-but no gain in alveolar bone height.
- no formation of periodontal fibres.
- by formation of long junctional epithelium.

44. 44
 Regeneration- natural renewal of a structure,
produced by growth and differentiation of new
cells and intercellular substance to form new
tissues or parts.
-regeneration occurs through growth from same
type of tissue that has been destroyed.
- formation of new periodontal fibres, new
cementum, new alveolar bone, gingival
epithelium.

45. 45
New attachment- New cementum formation with
inserting collagen fibers on a root previously
denuded of its periodontal ligament.
- New cementum formation, new periodontal
ligament fibres formation. No formation of new
alveolar bone.

46. 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.
46

47.  Epithelisation 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.
47

48. HEALING FOLLOWING FLAPSUR
GERY
 Immediately after suturing of the flap against tooth
surface a clot forms between the 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
By 1 week after surgery
 epithelial cells have migrated &established an attachment
to root surface by means of hemidesmosomes
48

49.  The blood clot is replaced by granulation tissue
proliferating from the gingival connective tissue, alveolar
bone and periodontal ligament
 By 2nd week collagen fibers begins to appear. Collagen
fibers gets arranged parallel to root surface rather than
at right angles. The attachment between soft tissue &
tooth surface is weak
 By end of one month following surgery the epithelial
attachment is well formed & the gingival crevice is also
well epithealised
 There is beginning of functional arrangement of
supracrestal fibres.
49

50. Educating the patients
50
Wounds have less chance of becoming infected and
progress through the healing process faster if they are
kept clean.
Self-care of Burns and Abrasions (Scrapes)
 Keep the bandage(s) dry between changes.
 Wash your hands with soap and water.
 Clean wound(s) with a soapy washcloth. You may do
this in the shower. (Permanent tattooing can occur if all
dirt or asphalt is not totally removed from injured skin.)
 Dry wound(s) gently with a clean towel.
 Apply antibiotic ointment to wound(s).
 Apply a dry, clean bandage

51. Post-extraction precautions to
improve healing
51
Patient should be educated by the dentist to follow these
precautions.
1.Bite tightly on the gauze- pressure application to stop
bleeding.
2. Use an ice pack- reduces bleeding and controls
swelling by constricting blood vessels.
3. Gargle with a warm saline rinse- to prevent
accumulation of debris( which will prolong healing
process).
4. Avoid toothbrush near extraction site- irritation due to
bristles at extraction site will delay healing.
5.Use of mouthwash- will help kill bacteria and prevent
infection.

52. 52
7.Healthy diet has the potential to accelerate oral
wound healing. So the patients should be advised
to take diet rich in calcium, vitamin D, vitamin C.

53. CONCLUSION
The healing wound is a dynamic and changing
process .The early phase is one of inflammation,
followed by a stage of fibroplasia, followed by
tissue remodelling and scarring. Different
mechanisms occur at different times.
The public health professional deals with a large
group of population during health camps during
which lot of extractions and periodontal
procedures are done. So during these camps the
patients can be educated regarding wound
healing and precautions to be taken post wound.
53

54. References
 Mohan H. Healing of tissues. Essential pathology for dental
students, 2nd edition. New Delhi, Jaypee brothers, 2002;126-
134
 Carranza . Scaling and root planing. Clinical
periodontology,10th edition. Elsevier publication, 2010;749-797
 Factors affecting wound healing. Guo S, Dipietro LA. Journal
of dental rsearch . 2010;89:219-229
 Dietary Strategies to Optimize Wound Healing after
Periodontal and Dental Implant Surgery: An Evidence-Based
Review. Lau BY , Johnston BD , Fritz PC and Ward WE. The
Open Dentistry Journal.2013;7:36-4654

55. THANK YOU
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