M0307. Healing of Oral Wounds

HEALING OF ORAL
WOUNDS
INTRODUCTION
 “WOUND”
A bodily injury caused by physical means with disruption of

the normal continuity of structures.
 “HEALING”
A process of cure, replacement of destroyed tissue by living
tissue to restore function.
 Repair – replacement with granulation tissue
 Regeneration – replacement with same tissue

Phases of healing
 Early
 Intermediate
 Late
 Terminal
Early wound healing events
 Hemostasis
 Platelet aggregation
 Intrinsic and extrinsic coagulation
 Thrombin, fibrin & Vasoconstriction
 Inflammation
 Vasodilatation
 Vascular permeability
 Chemotaxis & Cellular response
Intermediate wound healing events
Epithelisation
 1 day after injury
 Epithelial spur – connective tissue
 Mediated by cytokines
Mesenchymal cell chemotaxis and proliferation – granulation tissue
Angiogenesis
Late wound healing events
Collagen synthesis
 3-5 days post injury - fibroblasts
 Type 3- seen in early phases of wound healing
 Myofibroblasts - 3-21 day
 Wound contraction
Terminal wound healing events
 Remodeling- Type 3 replaced by type 1 (80 to 90%)
 Day 21- accumulation of wound collagen - stable
Wound Strength
 Week 3-6- greatest rate of increase
 6 weeks- 80-90% of eventual strength.
 6 months maximum strength ( 90% ). Process continues for 12 months
Wounds in the face and oral cavity
1. Accidental
 Jaw fracture, cut in the lips after
accidents
2. Direct physical insult

 Radiation
 Chemical irritation
 Colonization by microorganisms
Wounds in the face and oral cavity
3. Purposely inflicted
Gingivectomy wounds
Biopsy wounds
Extraction wounds
DIFFERENCE IN HEALING OF SKIN AND
ORAL MUCOSA
 In contrast to the skin, the oral mucosa heals in a scarless
manner
 Moist environment in oral cavity = Epithelialization progresses
more rapidly-
 Soft coagulum, easily lost
 Do not exhibit dry exudate (scab)
 growth factors – PGDF, TGF-a, EGF in saliva, KGF
FACTORS AFFECTING WOUND
HEALING
COMPLICATIONS OF WOUND
HEALING
1. Infection
2. Pigmentary changes
3. Keloid & hypertrophic scar
4. Cicatrization
5. Implantation cyst
6. Deficient scar formation
7. Incisional hernia
8. Healing of pulpal disease
9. Healing of periapical disease

HEALING
1. INFECTION
 DM
 Immunosupression
 Nutritional deficiency
2. PIGMENTARY CHANGES
 Hypo/ hyper pigmented areas
 Lichen planus, lichenoid reactions = hyper
3.HYPERTROPHIC SCAR & KELOID
FEATURE HYPERTROPHIC SCAR KELOID SCAR
Type Healing ( remodeling phase ) delayed, Wounds which heal without

More cellular & vascular complications
Red, rasied, itchy & tender Irregular borders & raised
Border Remains within wound Outgrows wound area
Natural history Subsides with time Rarely subsides
Site Flexor surface Face, sternum, shoulder
Etiology Related to tension unknown

HEALING
4.CICATRIZATION
 Late reduction in the wound contraction and distorting
tissue
e.g burns
5. IMPLANTATION CYSTS
6.DEFICIENT SCAR FORMATION

 inadequate formation of granulation tissue
7. INCISIONAL HERNIA
 weak scar, site of bursting open of a wound (wound
dehiscence)
HEALING
 HEALING OF PULPAL DISEASE
 Reparative dentin formation
 Sclerotic dentin formation
 Localized fibrosis
 Pulpal necrosis
 HEALING OF PERIAPICAL DISEASE

 New bone formation
 Fibrosis
HEALING OF BIOPSY WOUND
 Two types of healing of wounds :-
1. Healing by Primary intention
 Primary union with close approximation of wound
margins
2. Healing by Secondary intention
 Loss of tissue and edges of wound cannot be
approximated
Oral Wounds
Ulcers ( e.g. Traumatic)
Diagnostic (e.g. Biopsy)
Treatment ( e.g. Extraction)
Wound Healing..
 Biopsy Wound…
Primary Intention
 Close apposition – by sutures
 Clot = Fibrin and leukocytes
 Connective tissue – Fibroblast +angiogenesis
 Epithelium proliferates on surface
 Small depressed area of mucosa
Wound Healing..
 Biopsy Wound…
 Secondary Intention
 Site – Alveolar Ridge & Palate
 More amount of Granulation tissue
 Fibroblasts & Capillaries – migrate greater distance
 More fibrous tissue – Only depressed area formation
HEALING OF WOUNDS
IMMEDIATE 24 HOURS- 2 DAYS
3-7 DAYS WEEKS

HEALING BY PRIMARY INTENTION
Primary union with close approximation of wound margins
24 hours
Edges held in place

Blood clots
by sutures
Mobilization of leukocytes in that area

3-7 DAYS WEEKS
Transformation of connective New fibroblasts migrate into the line of

tissue cells into fibroblasts incision
Form delicate collagen fibrils

Mitotic division of fibroblasts
 Collagen fibrils interwine and coalesce into thick

bundles
 Endothelial cells proliferate and capillaries bud out
 Collagen fibrils contract
 Close approximation  so no defect  so wound
heals rapidly
HEALING BY SECONDARY INTENTION
 Process in which wound granulates in, occurs in area

where wound margins cannot be approximated
 Identical to primary, except that fibroblasts and
capillaries migrate to greater distance
HEALING BY SECONDARY INTENTION
PMNs , lymphocyte &

mononuclear phagocytes
migrates into granulation tissue
More granulation tissue

Cellular proliferation Condensation of collagen
around wound periphery Vascularity decreases
Surface of granulation tissue
epithelialized
HEALING OF EXTRACTION WOUND
 5 phases :-
1. Immediate reaction
2. First week wound
3. Second week wound
4. Third week wound
5. Fourth week wound
HEALING OF EXTRACTION WOUND
1. IMMEDIATE REACTION
Removal of tooth
Blood fills the socket &coagulates.
Within 24 – 48 hours
Vasodilatation and engorgement of blood
vessels, mobilization of leukocytes.
Surface of the blood clot is covered by a thick

layer of fibrin
2. FIRST WEEK WOUND
Fibroblastic proliferation around the periphery
Clot – acts as a scaffold
Replaced by granulation tissue
Epithelium at periphery proliferates
Clot undergoes organization- in growth of fibroblasts and

capillaries
3. SECOND WEEK WOUND
Fibroblasts grow into the clot
New delicate capillaries–clot center
Extensive epithelial proliferation over the surface
Margins of alveolar socket - osteoclastic resorption
Bone fragments(necrotic) - resorption or sequestration

4. THIRD WEEK WOUND
Original clot organized
Young trabeculae of osteoid 

entire wound periphery
Osteoblasts – Cells of PDL
Crest of alveolar bone- rounded off by osteoclastic

resorption
5. FOURTH WEEK WOUND
Continued deposition and remodeling resorption
Fills the alveolar socket
Radiographic evidence = 6 to 8 weeks
Crest of healed socket – below that of adjacent teeth
Loss of bone from the crest
Significant in preparation of prosthetic appliance

Immature
Organizati Mature
Blood Clot bone/oste
on of clot bone
oids
COMPLICATIONS OF EXTRACTION
DRY SOCKET
 Most common complication
 Focal osteomyelitis
 Disintegration of the blood clot
 Foul odour, severe pain, no suppuration
 Appearance of exposed bone
DRY SOCKET PATHOGENESIS
Traumatic extractions
Mandibular 3rd molars
Smoking after extraction

Rinsing after extraction
Food impacted after extraction
Limited local Blood supply
Excessive vasoconstrictors in LA
Osteosclerotic bone disease 3-4 days after extraction
Oral contraceptives
Previous radiotherapy
Pre-existing perocoronitis
DRY SOCKET PATHOGENESIS
Trauma/infection
Inflammation of bone marrow
Release of tissue activators
Steptokinase Plasminogen Plasmin
Lysis of clot (dissolution) (Birn’s hypothesis)

Dry Socket
 C/f
 3 – 5 days after extraction
 Severe Pain
 Foul smell – presence of some necrotic clot
 Intra – Oral examination

 Absence of clot, no pus
 Necrotic Bone
Treatment of dry socket
 Symptomatic treatment :-
Local debridement
Peroxide rinses
 Intrasocket medicaments :-
ZoE AND Iodoform
Antibiotics :-
Metronidazole- 400mg TID (5days)
HEALING OF FRACTURE
 Minor alveolar process to destructive fractures.

 Bone is unique in its ability to heal without scarring
 Constant renewal
 3 phases :-
1. Immediate effects
2. Callus formation
3. Remodeling of callus
HEALING OF FRACTURE
1. IMMEDIATE EFFECTS
 Single blood supply disrupted

 Bone cells of haversian system die
 Dead bone extends away from the fracture area
 Death of bone marrow adjacent to fracture line
IMMEDIATE EFFECTS
 Blood clot –
 Important role in the healing
 Replacement by granulation tissue
 Passive role
 Not necessary for invasion by osteogenic cells
 Necrosis of clot – retards healing process
2. CALLUS FORMATION
 Callus = (Lt : over growth of hard skin)

 Unites the fractures end of bone
 callus = fibrous tissue+ cartilage + bone
2. CALLUS FORMATION
External callus :
New tissue forming around the
bone fragments
Internal callus :
New tissue arising from the
marrow cavity
3. REMODELLING
Periosteum essential for callus formation
Increased proliferation of cells in the cellular

layer
Osteogenic cells – osteoblasts
External callus- irregular trabeculae laid at

right angles
COMPLICATIONS OF FRACTURE
HEALING
NON-UNION
FIBROUS UNION
 Calluses fail to meet

and fuse  Lack of
immobilization
 Lack of osteogenic
potential of cells  Fragments are
united by fibrous
 Seen in elderly
tissue
 Local
 Failure of
infection/presence of
foreign bodies calcification
Thank You

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HEALING OF ORAL

A bodily injury caused by physical means with disruption of

 Regeneration – replacement with same tissue

2. Direct physical insult

3. Keloid & hypertrophic scar

6. Deficient scar formation

8. Healing of pulpal disease

9. Healing of periapical disease

FEATURE HYPERTROPHIC SCAR KELOID SCAR

Type Healing ( remodeling phase ) delayed, Wounds which heal without

Red, rasied, itchy & tender Irregular borders & raised

Border Remains within wound Outgrows wound area

Natural history Subsides with time Rarely subsides

Site Flexor surface Face, sternum, shoulder

Etiology Related to tension unknown

6.DEFICIENT SCAR FORMATION

 HEALING OF PERIAPICAL DISEASE

IMMEDIATE 24 HOURS- 2 DAYS

3-7 DAYS WEEKS

Edges held in place

Mobilization of leukocytes in that area

Transformation of connective New fibroblasts migrate into the line of

Form delicate collagen fibrils

 Collagen fibrils interwine and coalesce into thick

 Process in which wound granulates in, occurs in area

PMNs , lymphocyte &

More granulation tissue

Blood fills the socket &coagulates.

Surface of the blood clot is covered by a thick

Clot – acts as a scaffold

Replaced by granulation tissue

Epithelium at periphery proliferates

Clot undergoes organization- in growth of fibroblasts and

New delicate capillaries–clot center

Extensive epithelial proliferation over the surface

Margins of alveolar socket - osteoclastic resorption

Bone fragments(necrotic) - resorption or sequestration

Young trabeculae of osteoid 

Osteoblasts – Cells of PDL

Crest of alveolar bone- rounded off by osteoclastic

Continued deposition and remodeling resorption

Fills the alveolar socket

Radiographic evidence = 6 to 8 weeks

Crest of healed socket – below that of adjacent teeth

Loss of bone from the crest

Significant in preparation of prosthetic appliance

Mandibular 3rd molars

Smoking after extraction

Inflammation of bone marrow

Release of tissue activators

Steptokinase Plasminogen Plasmin

Lysis of clot (dissolution) (Birn’s hypothesis)

 Intra – Oral examination

 Minor alveolar process to destructive fractures.

 Single blood supply disrupted

 Callus = (Lt : over growth of hard skin)

Periosteum essential for callus formation

Increased proliferation of cells in the cellular

Osteogenic cells – osteoblasts

External callus- irregular trabeculae laid at