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Healing of oral wounds
Dr.madhusudhanreddy
• CONTENTS
• 1. Healing
– Regeneration
– Repair
• 2. General factors affecting the healing of oral wounds
• 3. Healing of biopsy wound
• 4. Healing of extraction wound
• 5. Complications in the healing of extraction wounds
• 6. Healing of fracture
• 7. Complications of fracture healing
Healing
• Healing is the body’s response to injury in an attempt to
restore normal structure and function.
• The word healing refers to replacement of damaged tissue
by living tissue to restore function
• The process of healing involves 2 distinct processes:
– A. REGENERATION
– B. REPAIR
Regeneration
• Regeneration : Is when healing takes place by proliferation
of parenchymal cells and usually results in complete
restoration of the original tissues.
• To maintain proper structure of tissues, these cells will
under constant regulatory control of the cell cycle.
Repaiir
• Repair : Is when healing takes place by proliferation of
connective tissue elements resulting in fibrosis and
scarring.
• Two processes are involved in repair:
– a. Granulation tissue formation
– b. Contraction of wound
• Cells involved in the process of repair;
– 1. Mesenchymal cells
– 2. Endothelial cells
– 3. Macrophages
– 4. Platelets
– 5. Parenchymal cells of injured organs
General factors affecting the healing of oral wounds
1. Location of wound
– Area with good vascular bed heal more rapidly
– Immobilisation also helps in rapid healing- Corner of
mouth
2. Physical factors
– Severe trauma to tissue slows healing
– Local temperature increases rate of healing through effect
on circulation and cell multiplication.
– Hyperthermia – healing accelerated
– Hypothermia-healing delays
– X-ray radiation
• Low doses stimulates
• High focal doses – suppresses
3.Circulatory factors
– Anemia and dehydration reported to delay wound
healing
4.Nutritional factors
– Hypoproteinemia- delays healing, Slows new fibroblasts
proliferation and multiplication in the wounds
– Scurvy- delays healing
– Interruption in regulation of collagen formation of
normal intercellular ground substance of the connective
tissue and interruption in formation of
mucopolysaccharides A and D- retards healing
5.Age of the patients
– Wounds in younger persons heals rapidly than elderly
persons
6. Infection
– Wounds which are completely protected from bacterial
infection heal considerably more faster than wounds
which are exposed to bacteria or other mild physical
infection.
7. Hormonal factors
– Adrenocorticotropic hormone and cortisone – shows
slow healing
– Growth of granulation tissue was inhibited by
depression of inflammatory reaction –inhibition of
proliferation of new fibroblast ,endothelial sprouts
– Diabetes mellitus- slows healing
Healing of biopsy wound
• Primary healing- healing which occurs after excision of a
small piece of a tissue with close apposition of the edges of
the wound
• Wound heals rapidly
• Occurs in
– Clean and uninfected,
– Surgical incised,
– Without much loss of cells
– Tissue and in which edges of wound are approximated
by surgical sutures.
• Events in primary healing-
– Initial hemorrhage – immediately bleeding which then
clots
– Acute inflammation response- within 24 hours
appearance of polymorphs, which then is replace by
macrophages by the third day
– Epithelial changes- basal layer proliferate and covers
the wounds in 48 hors
– Organization –
• Third day fibroblast invades,
• By fifth day new collagen fibrils starts forming
• Fourth week scar tissue forms and full
epithelialization occurs
• Secondary healing-
– Healing by granulation
– Healing of an open wound
– When there is loss of tissue and the
– Edges of the wound cannot be approximated
• Wounds heals slowly , and forms scar
• Occurs in open wounds with large tissue defect, having
extensive loss of cells and tissues and wounds which are not
approximated by surgical sutures that are open.
• Events in secondary healing-
– Initial hemorrhage
– Epithelial changes
– Granulaton tissue formation
– Wound contracture
Healing of the extraction wounds
• Immediate reaction following extraction
• Bleeding and clot formation in the socket RBCs entrapped
in the fine fibrin meshwork ends of torn blood vessels
becomes sealed off
• First 24-48 hrs – vasodilatation and engorgement of BV,
mobilisation of leukocytes
• FIRST WEEK WOUND
• Proliferation of fibroblasts from connective tissue cells in
the remnants of PDL into the clot around the entire
periphery
• Clot is gradually replace by granulation tissue
• Epithelium shows evidence of proliferation at the
periphery
• Crest of alveolar bone shows beginning of osteoclastic
activity
• Endothelial cell proliferation in PDL
• SECOND WEEK WOUND
• New delicate capillaries penetrated to the centre of the clot
• The wall of socket appears frayed due to degeneration of
PDL
• Trabeculae of osteoid can be seen
• Considerable epithelial proliferation over the surface of
wound or completed if small socket is present
• Origin of alveolar socket shows prominent osteoclastic
resorption
• THIRD WEEK WOUND
• Clot is replaced almost completely by organized mature
granulation tissue
• Young trabecuale of osteoid tissue is forming around the
entire periphery
• Crest of alveolar bone rounded off by osteoclasts
• Surface of wound becomes completely epithelized
• FOURTH WEEK WOUND
• Wound is in final stage of healing, there is continuous
deposition and remodelling resorption of the bone filling
the alveolar socket radiographic evidence of bone becomes
prominent after 6th to 8th week.
Complications of extractionwoundhealing
• 1. Dry socket-
– Most common complication
– It is focal osteomyelitis in which the blood clot
disintegrate or lost, with production of a foul odor and
severe pain but no suppuration
– Etiology- difficult or traumatic extractions, in which
there is dislodgement of clot and subsequent infection of
exposed bone
– Clinical feature
– Commonly occurs in lower premolars and molar
sockets
– Extremely painful
– The exposed bone is necrotic there may be
sequestration of fragments
– Foul odor
– Treatment- irrigation of wound by isotonic saline
– Packing the socket with obundent material like ZnOE
paste on iodoform gauze
• 2. Fibrous healing of extraction wound
– Uncommon complication
– Followed by difficult, complicated extraction
– Loss of both the lingual and labial or buccal pates of
bones with loss of periosteum
– Clinical feature- asymptomatic
– Radiographic feature- well circumscribed radiolucent
area in the site of a previous extraction wound
– Histological feature- dense bundles of collagen fibers
with only occasional fibrocytes and few blood vessels
– Treatment- excision of the lesion
Healing of fracture
• Immediate effects of fracture-
• Haversian vessels of the bone, along with vessels of
periosteum and marrow cavity are torn at fracture site
• Loss of local blood supply
• Osteocytes die due to loss of local blood supply
• There is death of bone, and bone marrow adjacent to the
fracture line
1. Procallus formation-
– Hematoma formation
– Inflammatory changes
– Granulation tissue formation
2. Callus formation-
– Callus is the structure which unites the fractured ends
of bone, and it is composed of fibrous tissue, cartilage
and bone
• External callus – new tissue which forms around the
outside of the two fragments of bone
• Internal callus- new tissue arising from marrow cavity
• Periosteum is an important structure in callus formation,
hence its preservation is essential
• Inner layer of periosteum shows osteogenic activity and
forms a collar of callus around or over the surface of the
fracture
3. Osseous callus formation
4. Remodelling
– As there is over abundance of new bone to strengthen
the healing site
– New bone frequently joined with fragment of dead bone
which should be resorbed and replaced by mature bone
Complications of fracture healing
• 1. Nonunion
– Callus fails to meet and fuse or when endosteal
formation of bone is inadequate
– Commonly in elderly , where there is lack of osteogenic
potential of cells
• 2. Fibrous union-
– Due to lack of immobilazation
– Fractured fragments joins by fibrous tissue
– There is failure of ossification
• 3. Lack of calcification

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Healing of Oral Wounds: Regeneration, Repair, and Complications

  • 1. Healing of oral wounds Dr.madhusudhanreddy
  • 2. • CONTENTS • 1. Healing – Regeneration – Repair • 2. General factors affecting the healing of oral wounds • 3. Healing of biopsy wound • 4. Healing of extraction wound • 5. Complications in the healing of extraction wounds • 6. Healing of fracture • 7. Complications of fracture healing
  • 3. Healing • Healing is the body’s response to injury in an attempt to restore normal structure and function. • The word healing refers to replacement of damaged tissue by living tissue to restore function • The process of healing involves 2 distinct processes: – A. REGENERATION – B. REPAIR
  • 4. Regeneration • Regeneration : Is when healing takes place by proliferation of parenchymal cells and usually results in complete restoration of the original tissues. • To maintain proper structure of tissues, these cells will under constant regulatory control of the cell cycle.
  • 5. Repaiir • Repair : Is when healing takes place by proliferation of connective tissue elements resulting in fibrosis and scarring. • Two processes are involved in repair: – a. Granulation tissue formation – b. Contraction of wound • Cells involved in the process of repair; – 1. Mesenchymal cells – 2. Endothelial cells – 3. Macrophages – 4. Platelets – 5. Parenchymal cells of injured organs
  • 6. General factors affecting the healing of oral wounds 1. Location of wound – Area with good vascular bed heal more rapidly – Immobilisation also helps in rapid healing- Corner of mouth 2. Physical factors – Severe trauma to tissue slows healing – Local temperature increases rate of healing through effect on circulation and cell multiplication. – Hyperthermia – healing accelerated – Hypothermia-healing delays – X-ray radiation • Low doses stimulates • High focal doses – suppresses
  • 7. 3.Circulatory factors – Anemia and dehydration reported to delay wound healing 4.Nutritional factors – Hypoproteinemia- delays healing, Slows new fibroblasts proliferation and multiplication in the wounds – Scurvy- delays healing – Interruption in regulation of collagen formation of normal intercellular ground substance of the connective tissue and interruption in formation of mucopolysaccharides A and D- retards healing
  • 8. 5.Age of the patients – Wounds in younger persons heals rapidly than elderly persons 6. Infection – Wounds which are completely protected from bacterial infection heal considerably more faster than wounds which are exposed to bacteria or other mild physical infection. 7. Hormonal factors – Adrenocorticotropic hormone and cortisone – shows slow healing – Growth of granulation tissue was inhibited by depression of inflammatory reaction –inhibition of proliferation of new fibroblast ,endothelial sprouts – Diabetes mellitus- slows healing
  • 9. Healing of biopsy wound • Primary healing- healing which occurs after excision of a small piece of a tissue with close apposition of the edges of the wound • Wound heals rapidly • Occurs in – Clean and uninfected, – Surgical incised, – Without much loss of cells – Tissue and in which edges of wound are approximated by surgical sutures.
  • 10. • Events in primary healing- – Initial hemorrhage – immediately bleeding which then clots – Acute inflammation response- within 24 hours appearance of polymorphs, which then is replace by macrophages by the third day – Epithelial changes- basal layer proliferate and covers the wounds in 48 hors – Organization – • Third day fibroblast invades, • By fifth day new collagen fibrils starts forming • Fourth week scar tissue forms and full epithelialization occurs
  • 11.
  • 12. • Secondary healing- – Healing by granulation – Healing of an open wound – When there is loss of tissue and the – Edges of the wound cannot be approximated • Wounds heals slowly , and forms scar
  • 13. • Occurs in open wounds with large tissue defect, having extensive loss of cells and tissues and wounds which are not approximated by surgical sutures that are open. • Events in secondary healing- – Initial hemorrhage – Epithelial changes – Granulaton tissue formation – Wound contracture
  • 14. Healing of the extraction wounds • Immediate reaction following extraction • Bleeding and clot formation in the socket RBCs entrapped in the fine fibrin meshwork ends of torn blood vessels becomes sealed off • First 24-48 hrs – vasodilatation and engorgement of BV, mobilisation of leukocytes
  • 15. • FIRST WEEK WOUND • Proliferation of fibroblasts from connective tissue cells in the remnants of PDL into the clot around the entire periphery • Clot is gradually replace by granulation tissue • Epithelium shows evidence of proliferation at the periphery • Crest of alveolar bone shows beginning of osteoclastic activity • Endothelial cell proliferation in PDL
  • 16. • SECOND WEEK WOUND • New delicate capillaries penetrated to the centre of the clot • The wall of socket appears frayed due to degeneration of PDL • Trabeculae of osteoid can be seen • Considerable epithelial proliferation over the surface of wound or completed if small socket is present • Origin of alveolar socket shows prominent osteoclastic resorption
  • 17. • THIRD WEEK WOUND • Clot is replaced almost completely by organized mature granulation tissue • Young trabecuale of osteoid tissue is forming around the entire periphery • Crest of alveolar bone rounded off by osteoclasts • Surface of wound becomes completely epithelized
  • 18. • FOURTH WEEK WOUND • Wound is in final stage of healing, there is continuous deposition and remodelling resorption of the bone filling the alveolar socket radiographic evidence of bone becomes prominent after 6th to 8th week.
  • 19.
  • 20.
  • 21. Complications of extractionwoundhealing • 1. Dry socket- – Most common complication – It is focal osteomyelitis in which the blood clot disintegrate or lost, with production of a foul odor and severe pain but no suppuration – Etiology- difficult or traumatic extractions, in which there is dislodgement of clot and subsequent infection of exposed bone
  • 22. – Clinical feature – Commonly occurs in lower premolars and molar sockets – Extremely painful – The exposed bone is necrotic there may be sequestration of fragments – Foul odor – Treatment- irrigation of wound by isotonic saline – Packing the socket with obundent material like ZnOE paste on iodoform gauze
  • 23. • 2. Fibrous healing of extraction wound – Uncommon complication – Followed by difficult, complicated extraction – Loss of both the lingual and labial or buccal pates of bones with loss of periosteum – Clinical feature- asymptomatic – Radiographic feature- well circumscribed radiolucent area in the site of a previous extraction wound – Histological feature- dense bundles of collagen fibers with only occasional fibrocytes and few blood vessels – Treatment- excision of the lesion
  • 24. Healing of fracture • Immediate effects of fracture- • Haversian vessels of the bone, along with vessels of periosteum and marrow cavity are torn at fracture site • Loss of local blood supply • Osteocytes die due to loss of local blood supply • There is death of bone, and bone marrow adjacent to the fracture line
  • 25. 1. Procallus formation- – Hematoma formation – Inflammatory changes – Granulation tissue formation 2. Callus formation- – Callus is the structure which unites the fractured ends of bone, and it is composed of fibrous tissue, cartilage and bone
  • 26. • External callus – new tissue which forms around the outside of the two fragments of bone • Internal callus- new tissue arising from marrow cavity • Periosteum is an important structure in callus formation, hence its preservation is essential • Inner layer of periosteum shows osteogenic activity and forms a collar of callus around or over the surface of the fracture
  • 27. 3. Osseous callus formation 4. Remodelling – As there is over abundance of new bone to strengthen the healing site – New bone frequently joined with fragment of dead bone which should be resorbed and replaced by mature bone
  • 28.
  • 29. Complications of fracture healing • 1. Nonunion – Callus fails to meet and fuse or when endosteal formation of bone is inadequate – Commonly in elderly , where there is lack of osteogenic potential of cells • 2. Fibrous union- – Due to lack of immobilazation – Fractured fragments joins by fibrous tissue – There is failure of ossification • 3. Lack of calcification