Wound healing and repair process

Repair and process of
healing of a wound
Ajay babu gutti MDS 1st yr.
Department of conservative dentistry
and endodontics

1.HEALING DEFINITION
2.REPAIR
3.CLASSIFICATION OF WOUNDS
4. WOUND HEALING
5. HEALING BY FIRST INTENTION
6. HEALING BY SECONDARY INTENTION
7.FACTORS THAT AFFECT WOUND HEALING
8.COMPLICATIONS OF WOUND HEALING
9.WOUND HEALING IN ENDODONTICS
10.REFERENCE

Healing is the body response to injury in an attempt to restore normal structure and function.
Healing involves 2 distinct processes:
Harsh Mohan - Textbook Of Pathology, 6th Edition.
Robbins Basic Pathology (10th Edition).
Lin LM, Rosenberg PA. Repair and regeneration in endodontics. Int J Endod 2011;44: 889–906.
Repair is the replacement of the damaged tissue by different tissue, such as fibrosis or scarring,
and usually causes the loss of biological function of the injured tissue
In contrast, regeneration is the replacement of the damaged
tissue by the same cells with the restoration of the biological
function of the injured tissue

REPAIR
• Repair is the replacement of injured tissue by fibrous tissue. Two processes are involved in
repair:
1. Granulation tissue formation
2. Contraction of wounds
• Repair response takes place by participation of mesenchymal cells (consisting of connective
tissue stem cells, fibrocytes and histiocytes)

1.Granulation Tissue Formation
 The term granulation tissue derives its name from slightly granular and pink appearance of the
tissue.
 The following 3 phases are observed in the formation of granulation tissue :
1. Phase of inflammation.
2. Phase of clearance.
3. Phase of in growth of granulation tissue.
 I) Angiogenesis (neo vascularization).
 ii) Fibrogenesis

1. PHASE OF INFLAMMATION
 Following trauma, blood clots at the site of injury.
 There is acute inflammatory response with exudation of plasma,
neutrophils and some monocytes within 24 hours.
2. PHASE OF CLEARANCE
• Proteolytic enzymes liberated from
neutrophils,
• autolytic enzymes from dead tissues
cells,
• phagocytic activity of macrophages
clear off the
necrotic tissue,
debris and red
blood cells.

3. PHASE OF INGROWTH OF GRANULATION TISSUE.
Angiogenesis
(neovascularisation).
Fibrogenesis.
• Formation of new blood vessels
• Proliferation of endothelial cells from the margins
of severed blood vessels
• oedematous appearance of new granulation tissue
—because newly formed blood vessels are more
leaky,
• Influenced by :
Vascular endothelial growth factor (VEGF) ,
Platelet-derived growth factor (PDGF),
transforming growth factor-β (TGF-β),
basic fibroblast growth factor (bFGF) and
surface integrins
• The newly formed blood vessels are
present in an amorphous ground substance or
matrix
• New fibroblasts originate from fibrocytes
• Collagen fibrils appear by 6th day
• Maturation –more collagen is formed ;
fibroblasts and new blood vessels
decreases

2.Contraction of Wounds
• The wound starts contracting after 2-3 days and the process is completed by the
14th day.
• During this period, the wound is reduced by approximately 80% of its original size.
• Myofibroblasts migration into the wound area and their active contraction
decreases the size of the defect.

 Classification of wounds
Classification based on type of wound :
• Clean inside the wound
• Lacerated wound
• Bruising and contusion
• Hematoma
• Puncture wound
• Abrasion
• Crush injury
• Injuries to bone and joints(may be open or closed)
• Injuries to nerve (either clean cut or crush)
• Injuries to arteries and veins
• Penetrating wound

 Rank and Wakefield classification
• Tidy wounds
• Untidy wounds

Classification based on thickness of wound
 Superficial wound
 Partial thickness wound
 Full thickness
 Deep wounds
 Complicated wounds
 Penetrating wounds

WOUND HEALING
Wound healing can be accomplished in one of the following two ways:
 Healing by first intention (primary union)
 Healing by second intention (secondary union).

HEALING BY FIRST INTENTION (PRIMARY UNION)
This is defined as healing of a wound which has the following characteristics:
i) clean and uninfected;
ii) surgically incised;
iii) without much loss of cells and tissue; and
iv) edges of wound are approximated by surgical sutures.

1. Initial haemorrhage
• the space between the approximated surfaces of incised wound is filled with
blood
• which then clots and seals the wound(from infection & dehydration)
2. Acute inflammatory response.
within 24 hours appearance of polymorphs
By 3rd day, polymorphs are replaced by macrophages.
3. Epithelial changes
 The basal cells of epidermis ,start proliferating and migrating towards incisional space in
the form of epithelial spurs
 The migrated epidermal cells separate the underlying viable dermis from the overlying
necrotic material and clot, forming scab which is cast off.
 By 5th day, a multilayered new epidermis is formed

4. Organisation.
• 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 scar tissue with scanty cellular and vascular elements, a few
inflammatory cells and epithelialized surface is formed.
5. Suture tracks
• Each suture track is a separate wound and incites the same phenomena as in healing of
the primary wound
i.e. ,filling the space with hemorrhage, some inflammatory cell reaction,
epithelial cell proliferation along the suture track from both margins,
fibroblastic proliferation and formation of young collagen
• 7th day, much of epithelialized suture track is avulsed and the remaining epithelial tissue
in the track is absorbed

HEALING BY SECOND INTENTION (SECONDARY UNION)
This is defined as healing of a wound having the following
characteristics:
i) open with a large tissue defect, at times infected;
ii) having extensive loss of cells and tissues; and
iii) the wound is not approximated by surgical sutures but is left open.

1. Initial hemorrhage.
As a result of injury, the wound space is filled with blood and fibrin clot which dries.
2. Inflammatory phase.
There is an initial acute inflammatory response followed by appearance of macrophages which
clear off the debris as in primary union.
3. Epithelial changes.
As in primary healing, the epidermal cells from both the margins of wound proliferate and
migrate into the wound in the form of epithelial spurs
proliferating epithelial cells don't cover the surface fully until granulation tissue from base has
started filling the wound space .
4. Granulation tissue.
Granulation tissue is formed by proliferation of fibroblasts and neovascularization from
the adjoining viable elements.
newly-formed granulation tissue deep red, granular and very fragile

5. Wound contraction
 important feature of secondary healing not seen in primary healing.
 wound contracts to one-third to one fourth of its original size action of
myofibroblasts
6. Presence of infection
 Bacterial contamination of an open wound delays the process of healing due to release of
bacterial toxins that provoke necrosis and thrombosis.
 Surgical removal of dead and necrosed tissue, debridement, helps in preventing the
bacterial infection of open wounds.

Healing by first intention/ Primary
wound healing
Healing by second
intention/secondary wound healing
• Primary union • secondary union
• Clean and uninfected •Unclean and at times infected
• Surgically incised • Open wound
• Edges of wound are approximated
by surgical sutures
The wound is not approximated by
sutures but is left open.
• Without much loss of cells and
tissues
• Having extensive loss of cells and
tissues
• Scanty granulation tissue between
incised margins and along the suture
tracks
•Abundant granulation tissue grows
in from the margin
• Linear scar •Contracted irregular wound
•Infrequent complications •Frequent complications
Primary wound healing vs secondary wound healing

FACTORS INFLUENCING HEALING
1. Infection is one of the most important causes of delayed healing; it prolongs inflammation and
potentially increases the local tissue injury.
2. Poor blood supply to wound slows healing
3. Foreign bodies including sutures interfere with healing and cause intense inflammatory reaction
and infection.
4. Movement delays wound healing.
5. Exposure to ionizing radiation delays granulation tissue formation.
6. Exposure to ultraviolet light facilitates healing.
7. Type, size and location of injury determines whether healing takes place by resolution or
organization.
LOCAL FACTORS:

INFECTIONS
 Endotoxins release pro-inflammatory cytokines such as interleukin-1 (IL-1) and
TNF-α
prolongs the inflammatory phase.
Increases MMPS

Oxygenation
 It prevents wounds from infection
 Induces angiogenesis
 Increases keratinocyte differentiation
 Migration, and re-epithelialization
 Enhances fibroblast proliferation
 Collagen synthesis
 Promotes wound contraction

IMMOBILIZATION
Constant movement wound
Disruption of Formation of the new connective tissue
Delayed healing.
delayed bony union
Healing of bone fracture fibrous union
no union

Age related changes in healing capacity
 Enhanced platelet aggregation
 Increased secretion of inflammatory mediators
 Delayed infiltration of macrophages and lymphocytes
 Impaired macrophage function
 Decreased secretion of growth factors
 Delayed re-epithelialization
 Delayed angiogenesis and collagen deposition
 Decreased wound strength.

STRESS

B. SYSTEMIC FACTORS:
1. Age. Delayed wound healing in the aged is associated with an altered inflammatory response, reduced
macrophage phagocytic capacity.
2. Nutritional status has profound effects on repair; protein malnutrition and vitamin C deficiency, for
example, inhibit collagen synthesis and retard healing.

3. Administration of glucocorticoids has anti-inflammatory effect and their administration may result in
weak scars because they inhibit TGF-β production and diminish fibrosis
4. Uncontrolled diabetics are more prone to develop infections and hence delay in healing.
5. Hematologic abnormalities like defect of neutrophil functions (chemotaxis and phagocytosis), and
neutropenia and bleeding disorders slow the process of wound healing

Diabetes

Complications of Wound Healing
During the course of healing, following complications may occur:
1. Infection of wound due to entry of bacteria delays the healing.
2. Implantation (epidermal) cyst formation may occur due to persistence of epithelial cells in the
wound after healing.
3. Pigmentation. Healed wounds may at times have rust-like color due to staining with hemosiderin.
Some colored particulate material left in the wound may persist and impart color to the healed
wound.
4. Deficient scar formation. This may occur due to inadequate formation of granulation tissue.

6. Hypertrophied scars and keloid formation.
Excessive formation of collagen in healing may result in keloid (claw-like) formation.
Hypertrophied scars differ from keloid in that they are confined to the borders of the initial wound while
keloids have tumors-like projection of connective tissue.
7. Excessive contraction. An exaggeration of wound contraction may result in formation of contractures or
cicatrisation
8. Neoplasia. Rarely, scar may be the site for development of carcinoma later.

Repair & healing in endodontics

HEALING AFTER INDIRECT PULP CAPPING
Indirect pulp capping is a procedure in which a material is placed on a thin partition of
remaining carious dentine that, if removed, might expose the pulp in immature permanent
teeth (AAE 2003).
 Once dentine is damaged by caries or trauma, the integrity of the dentin–pulp complex is
compromised because damaged dentine cannot be regenerated by primary odontoblasts.
 Indirect pulp capping is intended to protect primary odontoblasts and the pulp from further
injury.
 It promotes reactionary dentine formation at the pulp–dentine junction.
Lin LM, Rosenberg PA. Repair and regeneration in endodontics. Int J Endod 2011;44: 889–

*Reactionary dentinogenesis is usually caused by milder injury of the dentine–pulp complex
• Slowly progressing caries,
• Cavity preparation
• Biomaterials used as indirect pulp capping agents
Lin LM, Rosenberg PA. Repair and regeneration in endodontics. Int J Endod 2011;44: 889–9

Treatment of an exposed vital pulp is accomplished by sealing the pulpal wound with a material
such as calcium hydroxide or mineral trioxide aggregate (MTA) to facilitate the formation of
reparative dentine and the maintenance of a vital pulp
Direct pulp capping is a dental material placed directly on a mechanical or traumatic
vital pulp exposure (AAE 2003).
HEALING AFTER DIRECT PULP CAPPING
Lin LM, Rosenberg PA. Repair and regeneration in
endodontics.
Int J Endod 2011;44: 889–906.

HEALING AFTER PULPOTOMY
Pulpotomy is the surgical removal of the coronal portion of a vital pulp as a means of
preserving the vitality of the remaining radicular portion (AAE 2003).
uninfected radicular vital pulp calcium hydroxide to encourage dentine bridge
formation
SEALED
≈
reparative dentine
Lin LM, Rosenberg PA. Repair and regeneration in endodontics. Int J
Endod 2011;44: 889–906.

HEALING AFTER PULPECTOMY
Pulpectomy is the complete surgical removal of the vital dental pulp (AAE 2003).
The wound healing process
following periapical surgery
is similar to that following
nonsurgical root canal
treatment
Lin LM, Rosenberg PA. Repair and regeneration in endodontics. Int J Endod 2011;44: 8

HEALING AFTER APEXOGENESIS
Apexogenesis is a vital pulp therapy procedure performed to encourage continued
physiological development and formation of the root end (AAE 2003).
 Apexogenesis is similar to pulpotomy and indicated in immature permanent teeth with vital pulp
 The cellular and molecular mechanism of dentine bridge formation in Apexogenesis is similar to that in
pulpotomy
 Dentine bridge formation following Apexogenesis is a reparative process of the dentine–pulp complex.
 However, the continued root development is a normal physiological process.

HEALING AFTER APEXIFICATION
Apexification is a method to induce a calcified barrier in a root with an open apex or the
continued apical development of an incompletely formed root in teeth with necrotic pulps
(AAE 2003).

HEALING AFTER APICAL SURGERY
Following apical microsurgery, there is healing in two components:
(1) osseous healing involving trabecular and cortical bone and
(2) dentoalveolar healing that results in repair or regeneration of apical attachment apparatus
(alveolar bone, periodontal ligament, and cementum)
Dapkute, I., Bandelac, G., Safi, C., & Setzer, F. (2017). Periapical Wound Healing. Microsurgery in Endodontics,

slowly replaced by granulation tissue originating from the periodontal ligament and
endosteum
After apical surgery
The resected cavity is occupied by a coagulum
The formation of new bone begins in the internal area and progresses externally toward the
level of the former cortical plate
As newly laid woven bone reaches the lamina propria, the overlying membrane becomes
functional periodontium (osseous healing)

Progenitor cells from the periodontal ligament differentiate into periodontal
ligament cells and cementoblasts to cover the resected root surface and lead to
regeneration of the periodontal ligament (dentoalveolar healing).
113–118.

divided into 4 types by radiographic and histologic
observations :
1. Healing with calcified tissue (Figure A) :
hard tissue found uniting the fragments are
 innermost layer of repair -dentin
 peripheral part of the fracture – cementum
 Radiographically - the fracture line is visible , but
the fragments are in close contact.
2. Interposition of connective tissue (Figure B) :
 periodontal ligament cells dominate
 The fracture surfaces are covered by cementum
 with connective tissue fibers running parallel to the
fracture surface or from one fragment to the other
 Radiographically, peripheral rounding of the fracture
edges and a radiolucent line separating the
fragments
HEALING OF ROOT FRACTURES
Textbook and Color Atlas of Traumatic Injuries to the Teeth, 5th Edition

3. Interposition of connective tissue and bone ( Figure C )
 Interposition of a bony bridge and connective tissue between the apical and coronal fragments, with a
normal periodontal ligament surrounding both fragments
 Radiographically, a bony bridge is seen separating the fragments, with a periodontal space around both
fragments
4. Interposition of granulation tissue without healing ( Figure D )
 Inflamed granulation tissue between the fragments
 Radiographically, widening of the fracture line, loss of lamina dura and rarefaction of the alveolar bone
corresponding to the fracture line
Textbook and Color Atlas of Traumatic Injuries to the Teeth, 5th Edition

Kornfeld has pointed out that the granuloma is not an environment in which bacteria live
but one in which they are destroyed.
• He compared the bacteria in the root canal (Zone I) with an army entrenched “behind
high and inaccessible mountains” the foramina serving as mountain passes.
• The exudative and granulomatous tissues of the granuloma represents a mobilized army
defending the plains (periapex) from the invaders.
• If only a few invaders enter the plain through the mountain pass they are destroyed by
the defenders (leukocytes).
Kornfeld'sMountainPass Concept

• Only complete elimination of the invaders from their mountainous entrenchment will
eliminate the need for a defense force in the “plains”.
• Once this is accomplished the defending army of leukocytes withdraws the local
destruction created is repaired (granulation tissue of zone III) and the environment
returns to with normal pattern.
• Therefore the objective in non-surgical root canal therapy of teeth with periapical
pathoses is elimination of the irritant from the canal and keeping it out by a “Three-
dimensional” filling of the canal. If the contents of the zone of necrosis are eliminated
the granuloma can complete its function of healing and repair.

Reference :
 Harsh Mohan - Textbook Of Pathology, 6th Edition.
 Robbins Basic Pathology (10th Edition).
 Lin LM, Rosenberg PA. Repair and regeneration in endodontics. Int J Endod 2011;44: 889–
906.
 Dapkute, I., Bandelac, G., Safi, C., & Setzer, F. (2017). Periapical Wound Healing.
Microsurgery in Endodontics, 113–118.
 Textbook and Color Atlas of Traumatic Injuries to the Teeth, 5th Edition

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