dentist in pune.(bds. mds) - dr. amit t. suryawanshi. wound healing in dentistry
DESCRIPTION
entist in pune. (BDS. MDS) - Dr. Amit T. Suryawanshi. Seminar- Wound healing in dentistry. Email ID- [email protected] Contact -Ph no.-9405622455 Subscribe our channel on youtube - Copy and paste this URL. https://www.youtube.com/channel/UC_gylEXTrjmEbbOTSXjuZ4Q/videos?view_as=public Follow us on Slideshare.TRANSCRIPT
Contact details :Email ID - [email protected] No - 9405622455
Dr. Amit T. Suryawanshi
Dentist & Oral and
Maxillofacial Surgeon
Pune, India
Introduction
Definition of wound healing
Process of wound regeneration
Process of wound repair
Types of wound healing
Pathological aspects of wound healing
Healing in specialised tissue
References.
Wound healing is fundamental to surgery.
“HEALING”
Wound Healing- It is referred to the process
of repair or regeneration of injured, lost or
surgically treated tissue.
The replacement can happen in two ways:
-By Regeneration
-By Repair
Mostly healing takes place using a mixture of
both mechanism
The classic model of wound healing is divided
into three or four sequential, yet overlapping,
phases:
1) Hemostasis
2) Inflammatory
3) Proliferative
4) Remodeling.
Regeneration is the growth and differentiation
of new cells and intercellular substances to
form new tissues or parts.
Regeneration is when the healing takes place
by proliferation of parenchymal cells and
usually results in complete restoration of the
original tissues.
Some parenchymal cells are short lived and
while others are long lived.
Under constant regulatory control of their cell
cycle.
These include growth factors. Eg.
a. Epidermal growth factor
b. Fibroblast growth factor.
c. Platelet derived.
d. Endothelial growth factor.
Defined as the period between two successive
cell divisions and is divided into 4 unequal
phases.
M phase- phase of mistosis.
G1 phase- daughter cell enter G1 phase after
mitosis.
S phase- synthesis of nuclear DNA takes place.
G2- after completion of nuclear DNA
duplication.
G0- resting phase.
TYPES OF CELLS
LabileContinuously dividing; readily regenerate after injury
StableMinimal replicative activity ; limited capacity to regenerate after injury
PermanentNon-proliferative ; repair by scar formation
Repair -It is the process when healing is
accomplished by the non-specialized elements of
connective tissue resulting in fibrosis and
scarring.
-INFLAMMATION
-EPITHELIZATION
-FORMATION OF GRANULATION TISSUE
Angiogenesis
Proliferation of fibroblasts
-SCAR FORMATION
-EXTRACELLULAR MATRIX
MATURATION & REMODELLING
Injury
-Focal disruption of basement membrane continuity
Hemorrhage
- Followed by fibrin clot formation
Temporarily protects denuded tissues
Acute inflammatory response
-Within 24 hours – appearance of polymorphs
3rd day – replaced by macrophages
Cells migrate from wound margins
Re-epithelize gap
Scab cast off
Regenerated epithelium
Fibroblasts and endothelial cell proliferation
Granulation tissue
Gross appearance – granular, pink, soft
Histological appearance
– New delicate capillaries
– Proliferation of fibroblasts
Granulation tissue
Occurs in 2 phases:
Angiogenesis
Fibrogenesis.
Blood vessels are assembled by two
processes:
Vasculogenesis, in which the primitive
vascular network is assembled from
angioblasts (endothelial cell precursors) during
embryonic development and
Angiogenesis, or neovascularization, in which
pre-existing vessels send out capillary sprouts
to produce new vessels
Angiogenesis resulting from- mobilization of
bone marrow endothelial precursor cells
(EPCs).
Angiogenesis from the pre-existing vessels at the site
of injury.
The main steps that occur in angiogenesis from
pre-existing vessels are listed below:
VASODILATATION
MIGRATION OF ENDOTHELIAL CELLS
TOWARD THE AREA OF TISSUE INJURY:
o EPCs can be mobilized from the bone marrow and
migrate to the site of injury.
o At these sites EPCs differentiate and form a mature
network of linking with pre-existing vessels.
PROLIFERATION OF ENDOTHELIAL CELLS:
From pre-existing vessels endothelial cells become
motile and proliferate to form capillary sprouts.
INHIBITION OF ENDOTHELIAL CELL
PROLIFERATION AND REMODELLING INTO
CAPILLARY TUBES.
New vessels formed during angiogenesis are
leaky
Hence granulation tissue is often oedematous.
Structural ECM proteins participation.
Non-structural ECM proteins.
Growth Factors Involved in Angiogenesis
Several factors induce angiogenesis, but the
most important are :
1. VEGF (Vascular Endothelial Growth Factor)
VEGFs constitute a family of growth factors that
include VEGF-A, -B, -C, and -D.
2. Basic fibroblast growth factor (FGF).
2. Migration of Fibroblasts and ECM
Deposition(Scar Formation)
Scar formation
It occurs in two steps:
(1) migration and proliferation of fibroblasts into
the site of injury
(2) deposition of ECM by these cells.
The recruitment and stimulation of fibroblasts is
driven by many growth factors, including
PDGF, FGF-2 and TGF-β.
Source of these factors is the activated
endothelium and inflammatory cells.
Macrophages are important cellular
constituents of granulation tissue, and besides
clearing extracellular debris and fibrin at the
site of injury, they elaborate a host of mediators
that induce fibroblast proliferation and ECM
production.
Sites of inflammation are also rich in mast
cells, and with them chemotactic lymphocytes
may also be present.
Collagen synthesis is critical to the development
of strength in a healing wound site.
Collagen synthesis by fibroblasts begins early in
wound healing (days 3 to 5) and continues for
several weeks, depending on the size of the
wound.
Same growth factors that regulate fibroblast
proliferation also participate in stimulating
ECM synthesis.
FIBROGENSIS
Ultimately, the granulation tissue evolves into a
scar composed of largely inactive, spindle-
shaped fibroblasts, dense collagen, fragments of
elastic tissue, and other ECM components .
As the scar matures, there is progressive vascular
regression, which eventually transforms the
highly vascularized granulation tissue into a pale,
largely avascular scar.
Remodelling of the connective tissue takes place to
repair the defect.
Collagen are degraded by a family of
metalloprotienases which catabolize a variety of
ECM constituents- proteoglycans, amorphous
collagen etc.
TYPES OF HEALING
-PRIMARY INTENTION
- SECONDARY INTENTION
-TERTIARY INTENTION
42
CHARACTERISTICS of wound :
1. Clean and uninfected.
2. Surgically incised.
3. Without much loss of cells and tissues.
4. Edges of wound are approximated by surgical
sutures.
• Epithelial regeneration predominates over
fibrosis
• Healing is fast, with minimal
scarring/infection
• Examples:
-Paper cuts
-Well-approximated surgical incisions
-Replaced periodontal flaps
• By 24 hours
• By 2-3days
• By 4-5 days
• Second week
Healing by First Intention:
• By 24 hours
clot forms
neutrophils – in the incision margin and
towards the fibrin clot.
epithelial cells from both the edge begins to
migrate and proliferate along the dermis,
depositing basement membrane components as
they progress.
Continuous epithelial layer
By 2-3 days
macrophages come in
granulation tissue formation starts
- new blood vessels
- fibroblasts
collagen begins to bridge incision
epithelium increases in thickness
4-5 days:
Neovascularization reaches its peak.
Collagen fibrils become more abundant.
Epidermis recovers its normal thickness.
Collagen deposition further increases leading
to scar formation.
Regression of the vascular channels.
6 hours 24 hours
2 days
1 week
Wound characteristics :
1. Open with a large tissue defect.
2. Infected.
3. Extensive loss of cells and tissues.
4. Not approximated by surgical suture.
HEALING BY SECOND
INTENTION
Examples:
-Infarction
-Large burns and ulcers
-Extraction sockets
-External-bevel gingivectomies
More inflammation
More granulation tissue
Wound contraction
Second intention healing has:
WOUND CONTRACTION:
Generally occurs in large surface wounds.
Helps to close wound by decreasing gap between
dermal edges and reducing wound surface area.
Due to the action of myofibroblasts present in
granulation tissue, the wound contracts to one-
third to one-fourth of its original size.
At suture removal: 10%
Rapid increase over next 4 weeks
At third month: 70-80%
Recovery of tensile strength results from excess of
collagen synthesis over collagen degradation and
later from structural modifications of collagen
fibers(cross linking, increased fiber size).
Wound Strength
Delayed primary closure
Infected wound – complex, delayed healing
Wound is cleaned, debrided, observed
Antibiotics may be administered
Infection subsides closure
PATHOLOGIC ASPECTS OF WOUND
HEALING
FACTORS AFFECTING WOUND HEALING
Local factors
Systemic factors
COMPLICATIONS OF WOUND HEALING
59
FACTORS AFFECTING WOUND HEALING
Local factors
Infection-Delays the process of healing.
Poor blood supply-wound healing get slow.
Foreign bodies
Movements
Radiation
Type of tissue injured
Location of the injury-
resolution
organization
Systemic factors
Age- Rate of healing
Nutrition-Deficiency leads to delays healing.
Systemic infection
Administration of glucocorticoids-Anti
inflammatory effect
Uncontrolled diabetes
Hematological abnormalities
COMPLICATIONS OF WOUND HEALING
Infection
Implantation cyst
Pigmentation
Deficient scar formation
“Proud flesh”
Incisional hernia
Hypertrophied scars and keloid formation
Excessive contraction
Bone fracture healing
Extraction socket healing
Healing of nervous tissue
BONE FRACTURE HEALING –
Depends upon some clinical considerations:
-Traumatic or Pathological
-Complete or Incomplete
-Simple or Compound
Primary union of fractures
Secondary union of fractures- more common.
i) procallus formation
ii) osseous callus formation
iii)Remolding
-Complication of fracture healing
1. FIBROUS UNION
2. NON UNION
3. DELAYED UNION
5 stages:
1. HEAMORRHAGE AND CLOT FORMATION
Haemorrhage- occurs immediately after extraction
due to tearing of apical blood vessels and in the
periodontal tissues.
Within half an hour- blot clot forms.
In 24-48 hrs- inflammatory process starts.
2. ORGANIZATION of the clot begins on 2-3rd day.
Characterized by the formation of 2 types of cells:
From periphery of the socket and adjacent bone
marrow spaces, fibroblasts grow into the clot.
Endothelial buds from neighbouring blood vessels to
form capillary network
Blood clots gets replaced by granulation tissue
3. REPLACEMENT of the granulation tissue by the
connective tissue and epithelization of the wound-
Immature fibrillar bone is seen at the base of the
socket
Osteoclastic resorption of the sharp bone edges of
the alveolar crest.
Epithelization of socket begins at the gingival
margin.
4. The socket is usually at least two thirds filled with
coarse fibrillar bone by about the 38th day.
5. Reconstruction of the alveolar process and
replacement of the immature bone by mature bone
tissue .
Central Nervous System
Peripheral Nervous System- have reparative
capacity.
3 types of degenerative processes:
a.WALLERIAN DEGENERATION-
Occurs after transection of the axon
The process of regeneration occurs by sprouting of
axons and proliferation of schwann cells from the
proximal end.
b. AXONAL DEGENERATION:
Degeneration of the axon begins at the peripheral
terminal and proceeds towards the nerve cell body.
Schwann cell proliferation at the site is seen.
Regeneration reaction is limited or absent.
c. SEGMENTAL DEMYELINATION:
It is demyelination of the segment between 2
consecutive nodes of Ranvier, leaving a denuded
axon segment.
Schwann cell proliferation results in remyelination of
the affected axon.
Kumar V.K. 8th edition. Robbins Basic pathology.
Saunders.
Harsh Mohan. Essential Pathology. Jaypee.
Giuseppe Polimeni, Andreas V. Xiropaidis & Ulf M. E.
Wikesjo. Biology and principles of wound
healing/regeneration.
Daniel M Laskin. Oral and maxillofacial surgery. Volume 2
Subscribe our channel on youtube
(Copy and paste this url )-
https://www.youtube.com/channel/UC_gy
lEXTrjmEbbOTSXjuZ4Q/videos?view_as
=public
Follow us on slideshare