wound Healing/endodontic courses

 By the end of the presentation a learner should
be able to describe:-
 Classification of wounds.
 Phases of Inflammation.
 Healing of fractures.
 Healing of tooth socket.
 Recent advances & future trends.
2www.indiandentalacademy.com

INTRODUCTIO
N
The response to injury is a primitive, yet is
an essential innate host immune response for
restoration of tissue integrity.
The body’s ability to replace injured or
dead cells and to heal tissues after
inflammation is critical to survival.
Healing is the process by which an
organism attempts to reconstitute a tissue
damaged by injury and restore its function.

HISTORY

DEFINITIONS (Robbins)
WOUND : A wound is a breach in the
normal tissue continuum, resulting in a
variety of cellular and molecular sequelae.
HEALING : The process by which tissues
are restored to an anatomic and
physiologic arrangement .

6
REPAIRREPAIR :: Biologic process where by theBiologic process where by the
continuity of the disrupted or lost tissue iscontinuity of the disrupted or lost tissue is
regained by new tissue which does notregained by new tissue which does not
restore structure and functionrestore structure and function
REGENERATIONREGENERATION :: Biologic process byBiologic process by
which the structure and function of thewhich the structure and function of the
disrupted or lost tissue is completelydisrupted or lost tissue is completely
restoredrestored
www.indiandentalacademy.com

DEGENERATION : The deterioration and
loss of specialized function of the cells of a
tissue and organ. The changes may be
caused by a defective blood supply or by a
disease.

8
ULCER : is any breach in the epithelial
surface as a result of molecular events.
SCAR : Any mark left after the healing of
a wound where the damaged tissues fail to
repair themselves completely and are
replaced by connective tissue

ACUTE WOUNDS :
a) Closed wounds : - Bruise/contusion.
- Hematoma.
b) Open wounds : - Puncture wounds and Bites.
- Abrasion and friction burns.
- Lacerations.
c) Complex wounds : - Crush/Avulsion.
- Internal organs.
- War wounds and Gun shot
injuries.
- Tissue loss.
CHRONIC WOUNDS :
- Ulcers.
- Pressure sores.
Classification of woundsBased on their intensity and duration

Abrasion
Bruise
Degloving Puncture
Amputation Incision
LacerationAvulsion
Ulcer
Contusion /

RESOLUTION
It is the repair that occurs in tissues and tissue
spaces with exudates, by digestion of the
exudation and subsequent resorption.
Thus resulting in removal of inflammatory
elements from a tissue or organ resulting in
return to normal structure and function

12
It involves :
1. Reversal of vasodilatation and increased
vascular permeability.
2. Complete removal of inflammatory
exudate and dead cells.
3. Regeneration of tissues.
Resolution can occur when destruction is
not extensive

Replacement of lost tissue by scar tissue
formation, this occurs when the surrounding
specialized cells do not possess the capacity
to proliferate.
Repair response takes place by
participation of mesenchymal cells,
endothelial cells, macrophages, platelets,
and the parenchymal cells of the injured
organ.

14
Replacement of lost tissues by tissue
similar in type. This occurs due to
proliferation of surrounding undamaged
specialized cells.

Replacement of the tissue defects by
undifferentiated cells.
Coordinated regeneration of the several
types of lost tissue resulting in reformation
of the whole organ or limb.

16
Not possible in human beings, though
this is found in lower animals like
amphibians etc.
Reformation of pancreas following
pancreatectomy is the nearest approach to
reconstitution seen in man.

HEALING
The process of healing involves 2 distinct
processes :
1) Regeneration.
2) Repair.
It involves the proliferation of various
cells, and close interactions between cells
and the extracellular matrix (ECM).

O
verlapping
O
verlapping
O
verlapping
O
verlapping

 A) Immediate response
 B) Hemostasis
- Vasoconstriction
- Platelet aggregation
- Thromboplastin makes clot
 C) Inflammation
- Vasodilation
- Phagocytosis

 Clotting takes place in order to obtain
hemostasis, or stop blood loss,
 Various factors are released to attract cells
that phagocytise debris, bacteria, and
damaged tissue and release factors that
initiate the proliferative phase of wound
healing.

PROLIFERATIVE PHASE

 About two or three days after the wound
occurs, fibroblasts begin to enter the
wound site, marking the onset of the
proliferative phase even before the
inflammatory phase has ended.
 As in the other phases of wound healing,
steps in the proliferative phase do not
occur in a series but rather partially
overlap in time.

REMODELLIN
G PHASE

 When the levels of collagen production
and degradation equalize, the maturation
phase of tissue repair is said to have
begun.
 The maturation phase can last for a year
or longer, depending on the size of the
wound and whether it was initially
closed or left open.

26
 During Maturation, type III collagen, which
is prevalent during proliferation, is gradually
degraded and the stronger type I collagen is
laid down in its place.
 As the phase progresses, the tensile strength
of the wound increases, with the strength
approaching 50% that of normal tissue by
three months after injury and ultimately
becoming as much as 80% as strong as
normal tissue.
 Blood vessels that are no longer needed are
removed by apoptosis.

• Growth factors play a prominent role in the
regulation of chemotaxis and wound healing.
• These polypeptides are released by a variety of
activated cells at the wound site.
• They act in either paracrine or autocrine
fashion to stimulate or inhibit protein synthesis
by cells in the wound, and many have
overlapping functions.

Growth Factors stimulate cells in
a number of ways
1)Act as mitogens to stimulate cells to proliferate
2) Induce differentiation
3) Stimulate synthesis and secretion of proteins
4) Facilitate attachment of cells
5) Alter the shape of the cells
6) Stimulate the cells to migrate 28www.indiandentalacademy.com

30
Incised wounds
 Focal disruption of epithelial
basement membrane continuity
 Death of a relatively few epithelial
and connective tissue cells.
 As a result epithelial regeneration
predominates over fibrosis.

 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.

 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.

33
 Acute inflammatory response.
this occurs within 24 hours with
appearance of polymorphs from
the margins of incision.
 By 3rd day, polymorphs are
replaced by macrophages.

34
 Epithelial changes. 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.

35
 The migrated epidermal cells separate
the underlying, viable dermis from the
overlying necrotic material and dot
forming scab which is cast off. The
basal cells from the margins continue to
divide by 5th day, a multi-layered new
epidermis is formed which is
differentiated into superficial and deeper
layers.

 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 tear
tissue with scanty cellular and
vascular elements, a few
inflammatory cells and epithelialised
surface is formed.

37
Suture tracks. Each suture track is a
separate wound and inicites the
same phenomena as in healng of
the primary wound i.e. filling the
space with haemorrhage, some
inflammatory cell reaction,
epithelial cell proliferates along the
suture track from both margins,

38
Fibro-blastic proliferation and formation
of young collagen. When sutures are
removed around 7th day, much of
epithealised suture track is avulsed and
the remaining epithelial tissue in the
track is absorbed.

 Healing of a wound having the
following characteristics:
Open with large tissue defect, at times
infected;
Having extensive loss of cells and tissues;
The wound is not approximated by surgical
sutures but is left open

The basic events in secondary union are
similar to primary union but differ in
having a larger tissue defect which
has to be bridged.
 Hence healing takes place from the
base upwards. As well as from the
margins inwards.
 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. 41www.indiandentalacademy.com

 Initial haemorrhage. As a result of
injury, the wound space is filled
with blood and fibrin clot which
dries.

43
Inflammatory phase. there is an
initial acute inflammatory response
followed by appearance of
macrophages which clear off the
debris as in primary union,
Epithelial changes. as in primary
healing, the epidermal cells migrate
from both the margins of wound

 Granulation tissue. Granulation tissue is
formed by proliferation of fibroblasts and
neovascularisafion from the adjoining viable
elements.
 Increase in collagen and decrease in
vascularity. The specialised structures of skin
like hair follicles and sweat glands are not
replaced unless their viable residues remain
which may regenerate.

45
 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.

 Bone fractures heal by regeneration, as
this tissue contains undifferentiated
stem cells. Healing depends on whether
the fracture is-
1) Traumatic or Pathological.
2) Complete or Incomplete.
3) Simple, Comminuted and
Compound

 1. Reactive Phase
i. Inflammatory phase
ii. Granulation tissue formation
 2. Reparative Phase
iii. Callus formation
iv. Lamellar bone deposition
 3. Remodeling Phase
v. Remodeling to original bone contour

After fracture, the first change
seen by light and electron
microscopy is the presence of
blood cells within the tissues
which are adjacent to the injury
site.
Within a few hours after
fracture, the extravascular blood
cells, known as a "hematoma",
form a blood clot.

 Within this same
area, the fibroblasts
survive and
replicate. They
form a loose
aggregate of cells,
interspersed with
small blood vessels,
known as
granulation tissue.

 Days after fracture, the cells of the periosteum
replicate and transform.
The periosteal cells proximal to the fracture
develop into chondroblasts and form hyaline
cartilage.
The periosteal cells distal to the fracture gap
develop into osteoblasts and form woven bone
The fibroblasts within the granulation tissue
also develop into chondroblasts and form
hyaline cartilage.

52
 These two new tissues grow in size until
they unite with their counterparts from
other pieces of the fracture. This process
forms the fracture callus. Rarely, if the
callus formation is "hyperplastic" (or
"exuberant"), there may be entrapment
of adjacent tissues. Eventually, the
fracture gap is bridged by the hyaline
cartilage and woven bone, restoring
some of its original strength.

 The next phase is the
replacement of the hyaline
cartilage and woven bone with
lamellar bone. The replacement
process is known as
endochondral ossification .
 Substitution of the woven bone
with lamellar bone precedes the
substitution of the hyaline
cartilage with lamellar bone.
 The lamellar bone begins
forming soon after the collagen
matrix becomes mineralized. 53www.indiandentalacademy.com

54
At this point, "vascular channels" with
many accompanying osteoblasts
penetrate the mineralized matrix.
The osteoblasts form new lamellar
bone upon the recently exposed surface
of the mineralized matrix. This new
lamellar bone is in the form of
trabecular bone.
Eventually, all of the woven bone and
cartilage of the original fracture callus
is replaced by trabecular bone.www.indiandentalacademy.com

 The remodeling process
substitutes the trabecular
bone with compact bone.
 The trabecular bone is
first resorbed by
osteoclasts, creating a
shallow resorption pit
known as a "Howship's
lacuna".

56
 Then osteoblasts deposit compact
bone within the resorption pit.
 Eventually, the fracture callus is
remodelled into a new shape
which closely duplicates the
bone's original shape and
strength.

Fibrous union:
May result instead of osseous union
Non union:
May result if some soft tissue is
interposed between the fractured
ends

58
Delayed union:
May occur in general such as
infection, inadequate blood
supply, poor nutrition, movement
& old age.

 Inflammatory phase
 Bleeding from the
socket.
 Cessation of bleeding.
 Formation of the blood
clot.
 Filling of the socket
with the blood clot.

 Ending of the inflammatory phase
and beginning of the proliferative
phase.
 Blood clot becomes stable.

62
 Proliferation of the
surrounding blood
vessels.
 Innervations of the
organized blood clot
with the granulation
tissue.

 Proliferative
phase.
 Granulation
tissue get laid
down on the
base of the
socket.

64
 Fibroblasts starts innervating
into the area.
 Osteoblasts starts laying down
immature bone or osteoid at the
base of the socket.
 Epithelium at the margins starts
proliferating.

 The granulation
tissue starts
getting replaced
by fibrous
connective
tissue or
fibroblasts.

66
The osteoid starts getting
mineralized.
A thin layer of epithelium
covers the socket.

 Epithelium layer
covering the
connective
tissue starts
thickening.

68
 Granulation tissue by this time is
fully replaced by fibrous
connective tissue (myofibroblast).
 Socket starts getting filled with
immature bone.

 Epithelium covering
the defect becomes
fully thickened.
 The socket becomes
fully filled with
immature bone.
 Phase of remodeling
starts.

InfectionInfection
Systemic
Factors that
Affect Wound
Healing
AgeAge
temptemp
radiationradiation
nutritionnutrition
drugsdrugs hormoneshormones
DMDM
SmokingSmoking
MalignancyMalignancy
StressStress
Coagulation
disorder
Coagulation
disorder
70

HydrationHydration
InfectionInfection
Ionizing
Radiation
Ionizing
Radiation
Ultraviolet
light
Ultraviolet
light
Local Factors
that Inhibit
Wound Healing
Foreign
Body.
Foreign
Body.
Poor
Blood
Supply
Poor
Blood
Supply
MovementMovement
HypoxiaHypoxia
71

Exuberant granulation tissue formation:
Here excessive amounts of granulation
tissue protrudes above the level of
surrounding skin and blocks
re-epithelialization.
72
COMPLICATIONS

73
Dermoids and Aggressive Fibromatosis:
Exuberant proliferation of fibroblast and
other connective tissue elements that recur
after excision. These lie in the interface
between benign proliferations and malignant
low grade tumor.
Neoplasia:
Rarely scar may be the site for development
of carcinoma later.
Eg: Squamous cell carcinoma in scar.

KELOID
•Collagen scar deposition
•Outspaces degradation –
claw like growth
•6- 16% African Americans
•Benign skin tumour with
continued slow growth
COMPLICATIONS IN
SCAR FORMATION

75
HYPERTROPHIC
SCAR
•Secondary to excessive
tensile forces
• Seen in extremities,
breast, sternum, neck
•Self healing
•Usually regress

Deficient scar
formation
Large ugly
scars
Painful scar 76www.indiandentalacademy.com

 Pigment alteration
 Tattooing
 Stitch marks
 Stitch abscess

1. Minimal tissue damage.
2. Debridement and cleansing of wound -
Debridement is the removal of dead
tissue and cleansing is removal of
foreign bodies.

79
Debridement can be autolytic
enzymatic, mechanical and surgical.
Cleansing is accomplished by
irrigation with sterile saline.
3. Maximal tissue perfusion and
oxygenation.
4. Prevent further injury and keeping
wound well nourished

5. Maintaining a moist environment for
preservation of the wound exudate,
that contains WBC, lysosomal
enzymes, lymphokines, and growth
factors.
Wounds kept in moist environment
have lower infection rates.

RECENT
ADVANCES AND
FUTURE TRENDS

The new field of
regenerative medicine
has as its main goal the
regeneration and
repopulation of
damaged organs using
adult stem cells which
have the capacity to
differentiate into various
cell types and restore
the tissue.
STEM
CELLS

Wounds occurring in fetuses of early
gestational age can heal without any
scar formation.
FETAL WOUND
HEALING

84
Contributing factors to scarless healing
in fetal wounds are
- The presence of fewer neutrophils
and more monocytes during the
inflammatory period,
- Different concentrations of cytokines,
- A greater proportion of type III
collagen in contrast to adult wounds.

In addition, fibronectin is more abundant in
fetal wounds and has been noted to
accelerate wound healing in fetal rat models.
The study of fetal wound healing is
intriguing and may result in the discovery of
an optimal method that would allow wounds
to heal without scar formation.

• Represents the merger of clinical surgery,
engineering, and biology to restore, sustain, or
enhance tissues or organs
• Engineered living-skin products, which are
FDA approved, are already in use for the
treatment of diabetic and venous stasis ulcers.
TISSUE
ENGINEERING

87
•After transfer to the patient, the host
skin cells replace the
skin product as healing occurs.
• Surgeons, using minimally invasive
surgical skills, can potentially
adapt tissue engineering techniques,
treating disease by
replacement with nearly identical
tissue. www.indiandentalacademy.com

 Wound healing is a complex process
encompassing a number of overlapping
phases, including inflammation,
epithelialization, angiogenesis and matrix
deposition.
 As we continue to develop new
information about the unique biological
markers associated with normal and
pathologic wound healing responses, the
better prepared we will be to develop new
strategies to render efficient treatment.

89
BIBLIOGRAPHY
1) Basic pathology ; Robbins
2) Essential Pathology for Dental
Students; Harsh Mohan
3) Short Practice of Surgery; Bailey
and Love

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