This document discusses wound healing and the healing process after tooth extraction. It defines a wound and classifies wounds based on origin, contamination, and depth. The two main processes of healing are regeneration and repair. Repair involves granulation tissue formation and wound contraction. There are two types of wound healing: primary intention and secondary intention. Healing after tooth extraction involves blood clot formation, fibroblast proliferation, angiogenesis, and bone remodeling over 4 weeks. Complications can include dry socket and fibrous union.

1. DR. GAURAV S. SALUNKHE
PG-STUDENT
ORAL & MAXILLOFACIAL PATHOLOGY
DR. D Y. PATIL DENTAL COLLEGE & HOSPITAL
WOUND HEALING

2. WHAT IS WOUND ?
 It is a circumscribed injury which is caused by
external force and it can involved any tissue and
organ.

3. Margins of wound
Wound edge
Wound corner
Surface of wound
Base of wound
Cross section of the wound
Wound edge
Wound depth
Surface of wound
Base of the wound

4. It can be classified based on
1) Origin of the wound.
2) Contamination of the wound.
3) Depth of the wound.

5. Based on origin
Mechanical
1. Abraded wound
2. Punctured wound
3. Incised wound
4. Cut wound
5. Crushed wound
6. Torn wound
7. Bite wound
8. Shot wound
Chemical
Acid & base
Radiation
Thermal
Burning & freezing
Special
Toxins & venoms

6.  Abrasions. They occur when the skin is rubbed away by friction against
another rough surface (e.g. rope burns and skinned knees).
 Avulsions. Occur when an entire structure or part of it is forcibly pulled
away, such as the loss of a permanent tooth or an ear lobe. Explosions,
gunshots, and animal bites may cause avulsions.
 Contusions. Also called bruises, these are the result of a forceful trauma
that injures an internal structure without breaking the skin. Blows to the
chest, abdomen, or head with a blunt instrument (e.g. a football or a fist)
can cause contusions.
 Crush wounds. Occur when a heavy object falls onto a person, splitting
the skin and shattering or tearing underlying structures.
 Cuts. Slicing wounds made with a sharp instrument, leaving even edges.
They may be as minimal as a paper cut or as significant as a surgical
incision.
 Lacerations. Also called tears, these are separating wounds that produce
ragged edges. They are produced by a tremendous force against the body,
either from an internal source as in childbirth, or from an external source
like a punch.
 Missile wounds. Also called velocity wounds, they are caused by an
object entering the body at a high speed, typically a bullet.
 Punctures. Deep, narrow wounds produced by sharp objects such as
nails, knives, and broken glass.

7. Contusions
Crushed wound
Punctures
Avulsions
Burns

8. Based on contamination
1. Clean wound
2. Clean & contaminated wound
3. Contaminated wound

9. Based on the depth
1. Superficial wound – only epidermis.
2. Partial thickness wound = epidermis + dermis.
3. Full thickness wound= epidermis + dermis +
subcutaneous fats
4. Deep wound = epidermis + dermis +
subcutaneous fats + exposed muscles, bone
connective tissue, organs etc.

10. Superficial
Partial thickness
Full thickness
Deep wound

11. HEALING
Healing is the body’s response to injury in an
attempt to restore normal structure and function.
The process of healing involves 2 distinct processes:
a. REGENERATION
b. REPAIR

12. REGENERATION
 Regeneration : Is when healing takes place by
proliferation of parenchymal cells and usually
results in complete restoration of the original
tissues.
 To maintain proper structure of tissues, these
cells are under constant regulatory control of
the cell cycle.

13. REPAIR
 Repair : Is when healing takes place by proliferation of connective
tissue elements resulting in fibrosis and scarring.
 Two processes are involved in repair:
a. Granulation tissue formation
b. Contraction of wound
Cells involved in the process of repair;
1. Mesenchymal cells
2. Endothelial cells
3. Macrophages
4. Platelets
5. Parenchymal cells of injured organs

14. REPAIR OF WOUND

15. GRANULATION TISSUE
Phases in the formation of granulation tissue:
 PHASE OF INFLAMMATION
Following injury blood clots at the site of injury.There is acute inflammatory
response with exudation of plasma, neutrophils, and some monocytes within
24 hours.
 PHASE OF CLEARANCE
Proteolytic enzymes liberated from neutophils, autolytic enzymes from
dead tissue and phagocytic activity of macrophages, clear off the necrotic
tissue, debris and red blood cells.
 PHASE OF IN GROWTH OF GRANULATION TISSUE
This phase consists of two main processes
a. ANGIOGENESIS OR NEOVASCULARISATION
b. FIBROGENESIS

16.  ANGIOGENESIS ( NEOVASCULARISATION)
 Formation of new blood vessels at the site of injury takes place
by proliferation of endothelial cells from the margins of severed
blood vessels.
 The newly formed blood vessels are more leaky accounting for the
more edematous appearance of new granulation tissue.
 Soon these blood vessels differentiate into muscular arterioles,thin-
walled venules and true capillaries.
 Angiogenesis takes place under the influence of :
1. Vascular endotheial growth factor
2. Platelet derived growth factor
3. Transforming growth factor- β
4. Fibroblast growth factor

17.  Vascular endothelial growth factor: elaborated by
mesenchymal cells as the receptors are present on
endothelial cells only.
 Platelet derived growth factor, transforming growth
factor- β, fibroblast growth factor are all associated
with cellular proliferation.

18.  FIBROGNESIS
 The newly formed blood vessels are present in an
amorphous ground substance .The new fibroblasts originate
from the fibrocytes as well as by mitotic division of
fibroblasts.
 Some of these fibroblast has functional and structural
similarities to smooth muscles cell called as myofibroblast.
 Collagen fibrils appear by about 6th day. As maturation
proceeds, more and more of collagen is formed the number
of active fibroblasts and the number of new blood vessels
decreases.
 This result in the formation of inactive looking scare known
as cicatrisation.

19. Granulation tissue

20. CONTRACTION OF WOUND
 The wound starts contracting after 2-3 days and the process is
completed by 14th day. During this period the wound is reduced by
approximately 80% of its original size.
 Contraction of wound helps in rapid healing.
 Factors responsible for wound contraction:
1. Dehydration due to removal of fluids by drying.
2. Contraction of collagen
3. Discovery of myofibroblasts.

21. TYPES OF WOUND HEALING
 HEALING BY FIRST INTENTION also called as
PRIMARY UNION.
 HEALING BY SECOND INTENTION also called as
SECONDARY HEALING.

22. HEALING BY FIRST INTENTION
Healing of wound with following characteristics:
 Clean and uninfected
 Surgically incised
 Without much loss of cells and tissue
 Edges of wound are approximated by surgical sutures.

23. Steps in primary wound healing
 Initial hemorrhage: Immediately after injury, the space between
the surfaces of incised wound is filled with blood which soon
clots, and prevent further infection.
 Acute inflammatory response: This occurs within 24 hours of
appearance of polymorphs from the margins of incision.
 Epithelial changes: The basal cells of epidermis from both cut
margins starts proliferating and migrating towards incisional
space in the form of epithelial spurs. A well approximated
wound is covered by a layer of epithelial cell in 48 hrs. the
migrated epithelial cell separates the necrotic cells and clot
forming a scab which is cast off. The basal cells countinues to
divide. By 5th day new epidermis is formed.

24.  Organisation :by 3rd day, fibroblasts also invades the wound
area. By 5th day new collagen fibrils start forming which
dominate till healing is completed.
In 4 weeks a scar tissue with scanty cellular and vascular
elements, a few inflammatory cells and epithelialised surface is
formed.
 Suture tracks: each suture track is a separate wound and follows
the same steps as in healing of primary wound.
 When sutures are removed around 7th day, much of the
epithelialised suture track is avulsed.

25. PRIMARY HEALING

27. HEALING BY SECODARY INTENSION
This is defined as the healing of a wound with following features.
i. Open with large tissue defects, at times infected
ii. Having extensive loss of cells and tissues, and
iii. The wound is not approximated by sutures but is left open.
STEPS IN HEALING OF SECONDARY WOUND
 Initial haemorrhage: as a result of injury the wound space is
filled with blood and fibrin clot which dries.
 Inflammatory phase: there is initial acute inflammatory
response followed by appearance of macrophages which clear
off the debris.

28.  Epithelial changes: The epidermal cells from both the margins proliferate and
migrate into the wound in the form of spurs till they meet in the middle and re-
epithelialise the gap completely.
 However, the proliferating epithelial cells do not cover the wound completely
until the granulation tissue from the base has started fill the wound space. In this
way the pre-existing viable connective tissue is separated from the necrotic
material and clot on the surface forming the scab, which is cast off.
 Granulation tissue: The main bulk of secondary healing is by granulations.
Granulation tissue is formed by proliferation of fibroblasts and
neovascularisation. The newly formed granulation tissue is deep red, granular
and very fragile. With time, it becomes pale white due to increased in collagen
and decreased blood supply.
 Wound contraction: this phase is not seen in primary healing. Due to the action
of myofibroblasts present in granulation tissue, the wound contracts to one-third
of its original size. It occurs during the formation of active granulation tissue.

29. SECONDARY WOUND HEALING
(various cells involved)

31. Difference between 1˚ & 2˚ union of wound
FEATURES PRIMARY SECONDARY
CLEANLINESS CLAEN NOT CLEAN
INFECTION NOT INFECTED INFECTED
MARGINS SURGICALLY CLEAN IRREGULAR
SUTURES USEAD NOT USED
HEALING SMALL GRANULATION
TISSUE
LARGE GRANULATION
TISSUE
OUT COME LINEAR SCAR IRREGULAR WOUND
COMPICATION NOT FRQUENT FREQUENT

32. FACTORS AFFECTING WOUND HEALING
Local factors Systemic factors
INFECTION NUTRITIONAL FACTORS
LOCATION OF THE WOUND AGE OF THE PATIENT
IMMOBILISATION SYSTEMIC INFECTION
PHYSICAL FACTORS ADMINISTRATION OF
GLUCOCORTICOIDS
UNCONTROLLED DIABETES

33. FACTORS AFFECTING WOUND
HEALING
LOCAL FACTORS
 INFECTION:
it has been demonstrated that wounds which is completely
protected from bacterial irritation heal considerably more
rapidly than wounds which are exposed to bacteria or other
mild physical irritation.
 LOCATION OF THE WOUND:
wounds in the area in which there is a good vascular bed heal
considerably more rapidly than the area in which is relatively
avascular.

34.  IMMOBILISATION:
If the wound is an area which is subjected to constant movement
so that formation of new connective tissue is continuously
distrupted (e.g.: corner of the mouth) , it will result in delayed
wound healing.
 PHYSICAL FACTORS:
severe trauma to tissues is obviously a determinant in rapid
wound healing.
local temperature in the area of wound influences the rate of
healing. Thus, in environment hyperthermia, wound healing is
accelerated while in hypothermia it is delayed.
circulatory factors: anemia has been reported to delay wound
healing. Similarly dehydration also delays wound healing.

35. SYSTEMIC FACTORS
 NUTRITIONAL FACTORS:
Delay in the healing of wounds may occur in a person who is
deficient in variety of essential foods such as proteins,
vitamins, especially vitamin A, D and B complex.
 AGE OF THE PATIENT:
Wounds in younger persons heals more rapidly than wounds In
elderly persons and the rate of wound healing appears to be in
inverse proportion to the age of the patient.

36.  SYSTEMIC INFECTION
Delays healing of he wound.
 ADMINISTRATION OF GLUCOCORTICOIDS
It has an anti-inflammatory effect thus it delays wound healing.
 UNCONTROLLED DIABETES
Diabetics are more prone to develop infections thus delayed
wound healing takes place.
 HAEMATOLOGIC ABNORMALITIES
There is delayed wound healing

37. HEALING OF EXTACTION WOUND
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.

38. 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 have
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.

39.  Osteoclasts accumulate along the alveolar bone crest setting the
stage for active crestal resoption.
 Angiogenesis proceeds in the remnants of the periodontal
ligaments.

40. 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 resoption 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.

41. 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-epithelised with minimum or no
scar formation.
 Very young trabeculae of osteoid bone forms around the entire
periphery of the wound from the socket wall.

42.  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
resoption.

43. FOURTH WEEK WOUND
 During the fourth week the wound begins the final stage of
healing, in which there is continued deposition and remodeling
resorption of he 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.

44. HEALING AFTER EXTRACTION OF TOOTH
1- immediate reaction after extraction
2-second week after extraction
3-third week after extraction
4-six to eight weeks after extraction( complete healing)

46. COMPLICATION OF HEALING OF
EXTRACTON WOUND
 DRY SOCKET
 FIBROUS UNION
DRY SOCKET
 The most common and painful complication in the healing of
human extraction wound is alveolar osteitis or dry socket.
 It is basically a focal, in which the blood clot has disintegrated
or been lost.
 The condition is extremely painful without suppuration and the
presence of foul odor.

47.  The condition derives its name from the fact that after the clot
is lost the socket has a dry appearance because of the exposed
bone.
 It is more commonly associated with difficult and traumatic
extractions like the removal of impacted third molars.
 Destruction of the clot is caused by the proteolytic enzymes
produced by bacteria or local fibrinolytic activity.

48. DRY SOCKET

49. FIBROUS HEALING OF EXTRACTION WOUND
 It occurs more frequently when the extraction is accompanied
by the loss of both the buccal and the lingual cortical plates of
bone and the loss of periosteum as well.
 On a radiograph the lesion appears as a well circumscribed
radiolucent area in the site of a previous extraction wound .
 There is no certain way of differentiating fibrous healing from
the residual infection like residual cyst or granuloma.
 The areas of fibrous healing consists of dense bundles of
collagen fibrils with occasional fibrocytes and few blood
vessels. The lesion is a fibrous scar tissue with little or no
evidence of ossification.

50. HEALING OF FRACTURE
IMMEDIATE EFFECTS OF FRACTURE
 When fracture of a bone occurs, the haversian vessels of the bone
are torn at the fracture site along with the vessels of the periosteum
and the marrow cavity. This evokes acute inflammation in the soft
tissue adjacent to the fracture line.
 Because of the disruption of the vessels, there is considerable
amount of blood in this general area and at the same time there is
loss of circulation and blood supply.

51.  Three major phase occurs:
1) Reactive phase:
-fracture and inflammation
-granulation tissue formation
2) Reparative phase:
-callus formation
-lamellar bone deposition
3) Remodelling phase:

52. Reactive phase
 Soon after fracture the blood vessels constrict,
stopping any further bleeding.
 Within a few hours after fracture, the extravascular
blood cells forms a blood clot called as Hematoma.
 All of the cells within the blood clot degenerate and
die.
 Some of the cells adjacent to the fracture site also
die, but fibroblast survive and replicate forming a
loose aggregates of cells interspersed with small
blood vessels known as Granulation tissue.

53. Reparative phase
 Days after fracture, the cells of the periosteum
replicates.
 The Periosteal cells proximal (close) to the fracture
gap develops into chondroblasts which forms hyaline
cartilage.
 Periosteal cells distal (far away ) from the fracture
gap develops into osteoblasts which forms woven
bone.
 The fibroblast with in the granulation tissue develops
in to chondroblasts which also forms hyaline
cartilage.

54.  The two new tissue grow in size until they meet their
counter part from other part of fracture.
 This process is called as Callus formation.
 Callus in Latin means overgrowth of hard skin.
 Composed of varied amounts of fibrous tissue, cartilage
and bone.
 The external callus consists of the new tissue which
forms around the outside of two fragments of bone.
 The internal callus is the new tissue arising from the
marrow cavity.

55.  The next step is deposition of lamellar bone by
replacing hyaline cartilage and woven bone.
 The replacement process is called endochondral
ossification.
 The lamellar bone begins forming soon after the
collagen matrix of either tissue becomes mineralized.
 The new bone is formed in the form of trabecular
bone.

56. Remodelling phase
 In this, the trabecular bone is replaced by compact
bone.
 It takes 3-5 yrs depending on factors like type of
fracture, age of patient, or general condition of
patients.

57. STAGES IN HEALING OF FRACTURE

58. COMPLICATIONS OF FRACTURE HEALING
 DELAYED UNION OR NON UNION
This results when the calluses of the osteogenic tissue over
each of the two fragments fail to meet and fuse or when
endosteal formation of bone is inadequate.
 FIBROUS UNION
The Fractured ends of fragments are united by fibrous tissue,
but there is failure of ossification.
 LACK OF CALCIFICATION
This may occur in unusual circumstances of dietary deficiency
or mineral imbalance which is seldom seen clinically.

59. HEALING AFTER REPLANTATION
 Following replantation the clot forms between the root surface
and ruptured periodontal ligament.
 Proliferation of the fibroblasts and the endothelial cells occurs
in the periodontal ligament remnants on the side of the
alveolar bone.
 The reconnection of the periodontal ligament is evident by the
extension of collagen fibers from the cementum to the alveolar
bone.

60.  The epithelium is reattached to the tooth at the end of the first
week.
 Complete regeneration of the periodontal ligament takes place
between two to four weeks.
 In the course of time, a number of teeth results in resorption or
ankylosis.

61. OSSEOINTEGRATION OF IMPLANTS
 Osseointegration is a direct structural and functional
connection between ordered living bone and the surface of the
load carrying implant.
 Factors that determine the outcome of the implant treatment
depend on the biocompatibility of the implants, status of the
host tissue, surgical technique, and the loading condition.
 After the implant insertion, a period of 10-12 weeks of healing
is required.

62.  During healing, compact and cancellous bone forms around the
implant together with variable amount of fibrous marrow.
 Implants do not have a direct contact with the bone and a certain
amount of bone marrow and soft tissue are interposed between the
bone and the implant.
 The implant and the mucosal interface serve the similar functions
as the dentogingival.

63.  The connective tissue of the
mucosa forms the intimate
contact with the implant.
 The collagen fibers of the
connective tissue runs
parallel to the long axis of the
implant, and the epithelium is
attached to the implant by
means of basal lamina and
hemidesmosomes.

64. OSSEOINTEGRATION OF IMPLANT

65. COMPLICATIONS OF WOUND HEALING
 INFECTION
Wounds may provide a portal of entry to microorganisms.
Infections of the wound delay the healing process. Systemic
conditions such as diabetes mellitus, immunosuppressive state
etc. make the individual prone to infection.
 KELOID AND HYPERTROPIC SCAR
Keloids are overgrown scar tissues with no tendency for
resolution. They occur in wound, which heal without any
complications.

66. hypertrophic scar occur in wounds where healing is delayed.
These scars are more cellular and vascular.
Keloid and hypertropic scars are not seen in the wounds of the
oral cavity.
 PIGMENTARY CHANGES
These are common in healing of wounds on skin and may appear
and may appear as hyperpigmented and hypopigmeted areas.
In oral cavity hypopigmented scars are less common but some
lesions leave hyperigmentation while healing e.g. lichenplanus,
lichenoid reactions.

67.  CICATRIZATION
Cicatrization refers to late reduction in the size of the scar in
contrast to immediate wound contraction. It a complication due
to burns on the skin.
 IMPLANTATION CYSTS
Epithelial cysts may slide and get entrapped in the wound and
later may proliferate to form implantation cysts.

68. Thank- u