dentist in pune.(bds. mds) - dr. amit t. suryawanshi. wound healing in dentistry

Contact details :Email ID - amitsuryawanshi999@gmail.comMobile 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

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