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TISSUE REPAIR
LEARNING OBJECTIVES:
• Repair, steps involved in it.
• Granulation tissue
• Types of wound healing
• Complications
• Factors influencing
• Fracture healing
• REGENERATION is restoration to original tissue by
proliferation of parenchymal cells
Structure and function is retained
• REPAIR is healing of proliferation of connective tissue
resulting in fibrosis and scaring
Only structure is preserved.
REPAIR
The replacement of injured tissue by fibrous tissue.
Two processes are involved in repair:
1. Granulation tissue formation
2. Contraction of wounds
STEPS INVOLVED IN REPAIR:
• Formation of blood clot
• Inflammation
• Granulation tissue formation
• Fibroblast proliferation and matrix accumulation
• Angiogenesis
• Wound contraction
• Remodelling
GRANULATION TISSUE
• Migration and proliferation of fibroblasts & deposition of loose
connective tissue, together with vessels and leukocytes
• New connective tissue with microscopic blood vessels that forms the
surface of the wound during healing process.
• Grows from the base of the wound and fill out the wound.
• Gross – pink, soft, granular, seen beneath scab of skin wound.
• Microscopically – fibroblast proliferation, capillaries, loose
extracellular matrix, inflammatory cells & macrophages.
Classification of Wounds Closure
• Healing by Primary Intention:
– All Layers are closed. The incision that heals by first
intention does so in a minimum amount of time, with no
separation of the wound edges, and with minimal scar
formation.
• Healing by Secondary Intention:
– Deep layers are closed but superficial layers are left to
heal from the inside out. Healing by second is
appropriate in cases of infection, excessive trauma,
tissue loss, or imprecise approximation of tissue.
• Healing by Tertiary Intention:
– Also referred to as delayed primary closure.
WOUND HEALING
• 2 TYPES
PRIMARY INTENTION
SECONDARY INTENTION
PRIMARY INTENTION
• CHARACTERISTICS OF WOUND:
CLEAN AND UNINFECTED
SURGICALLY INCISED
WITHOUT MUCH LOSS OF CELLS AND TISSUE
EDGES OF WOUND APPROXIMATED BY SURGICAL SUTURES
• END RESULT
RAPID HEALING
NEAT SCAR
PRIMARY INTENTION
• SEQUENCE
1. INITIAL HEMORRHAGE
2. ACUTE INFLAMMATION RESPONSE
3. EPITHELIAL CHANGES
4. ORGANISATION
5. SUTURE TRACKS
PRIMARY INTENTION
1. INITIAL HEMORRHAGE
SPACE B/W APPROXIMATED SURFACES IS FILLED WITH BLOOD
BLOOD CLOTS
WOUND IS SEALED
PRIMARY INTENTION
2. ACUTE INFLAMMATION RESPONSE
WITHIN 24 HRS
APPEARANCE OF POLYMORPHS
BY 3rd DAY – REPLACED BY MACROPHAGES
PRIMARY INTENTION
3. EPITHELIAL CHANGES
PROFILERATION OF BASAL CELLS OF EPIDERMIS
MIGRATING TOWARDS INCISIONAL SPACE
MIGRATED EPIDERMAL CELLS SEPARATE THE UNDERLYING
VIABLE DERMIS FROM OVERLYING NECROTIC DEBRIS AND CLOT BY
FORMING A SCAB.
NEW EPIDERMIS IS FORMED BY THE 5th DAY.
PRIMARY INTENTION
4 . ORGANISATION
BY 3RD DAY - INVASION OF FIBROBLASTS.
BY 5TH DAY - INVASION OF COLLAGEN FIBRILS
PRIMARY INTENTION
5 . SUTURE TRACKS
EACH SUTURE TRACK IS A SEPARATE WOUND.
AND UNDERGOES THE SAME PHENOMENA.
7TH DAY – SUTURE IS REMOVED.
PRIMARY INTENTION
SECONDARY INTENTION
• CHARACTERISTICS OF WOUND:
• LARGE TISSUE DEFECT
• EXTENSIVE LOSS OF CELLS AND TISSUES
• WOUND NOT APPROXIMATED BY SUTURES AND LEFT OPEN
• END RESULT:
LONGER TIME TAKEN FOR HEALING
LARGE SCAR
SECONDARY INTENTION
• SEQUENCE
1. INITIAL HEMORRHAGE
2. INFLAMMATION RESPONSE
3. EPITHELIAL CHANGES
4. GRANULATION TISSUE
5. WOUND CONTRACTION
SECONDARY INTENTION
1. INITIAL HEMORRHAGE
SPACE B/W APPROXIMATED SURFACES IS FILLED WITH BLOOD
BLOOD CLOTS
WOUND IS SEALED
SECONDARY INTENTION
2. ACUTE INFLAMMATION RESPONSE
APPEARANCE OF POLYMORPHS INITIALLY
REPLACED BY MACROPHAGES WHICH CLEARS OFF THE DEBRIS
SECONDARY INTENTION
3. EPITHELIAL CHANGES
PROFILERATION OF BASAL CELLS OF EPIDERMIS
MIGRATING TOWARDS INCISIONAL SPACE
BUT GRANULATION TISSUE FROM BASE ALSO FILLS THE WOUND
SPACE.
REGENERATED EPIDERMIS BECOMES STRATIFIED AND
KERATINISED.
SECONDARY INTENTION
4. GRANULATION TISSUE
FORMED BY PROLIFERATION OF FIBROBLASTS AND
NEOVASCULARISAION.
NEW- RED, GRANULAR, FRAGILE
OLD- PALE, WHITE
NO REPLACEMENT OF HAIR FOLLICLES AND SWEAT GLANDS.
SECONDARY INTENTION
5. WOUND CONTRACTION
BY ACTION OF MYOFIBROBLASTS.
CONTRACTS TO 1/3RD TO 1/4TH OF ORIGINAL SIZE.
• PRESENCE OF INFECTION:
DUE TO BACTERIAL TOXINS
LEADS TO NECROSIS, SUPPURATION, THROMBOSIS
DELAYED HEALING
NEED FOR DEBRIDEMENT
SECONDARY INTENTION
S.NO FEATURES PRIMARY INTENTION SECONDARY INTENTION
1 CLEANLINESS CLEAN UNCLEAN
2 INFECTION MOSTLY UNINFECTED MAY BE INFECTED
3 MARGINS SUGICAL CLEAN MARGINS IRREGULAR
4 SUTURES USED NOT USED
5 HEALING SCANTY GRANULATION
TISSUE IN THE GAP
EXUBERANT GRANULATION
TISSUE IN THE GAP
6 OUTCOME NEAT LINEAR SCAR CONTRACTED IRREGULAR
WOUND
7 COMPLICATIONS EPIDERMAL INCLUSION CYST SUPPURATION
COMPLICATIONS OF WOUND HEALING:
• DELAYED HEALING:
• INFECTION:
• DEFICIENT SCAR FORMATION: inadequate granulation tissue
• INCISIONAL HERNIA:
HYPERTROPHIED SCAR & KELOID:
excessive formation of collagen in
healing leads to keloid
• EXCESSIVE CONTRACTION: exaggeration of wound contraction results
in formation of contractures. Eg- dupuytren’s contracture
• NEOPLASIA: Eg- squamous cell carcinoma in Marjolin’s ulcer.
• EPIDERMAL CYST: persistence of epithelial cells in the wound after
healing
• PIGMENTATION: due to staining with haemosiderin
FACTORS INFLUENCING HEALING:
• LOCAL
1. INFECTION
2. POOR BLOOD SUPPLY
3. FOREING BODIES
4. MOVEMENT
5. IONISING RADIATION
6. ULTRAVIOLET LIGHT
7. TYPE, SIZE AND LOCATION OF INJURY
FACTORS INFLUENCING HEALING:
• SYSTEMIC
1. AGE
2. NUTRITION
3. ADMINISTRATION OF GLUCOCORTICOIDS
4. UNCONTROLLED DM
5. SYSTEMIC INFECTION
6. HEMATOLOGICAL ABNORMALITIES
FRACTURE HEALING:
• Depends on
i. Nature of fracture – traumatic or pathological
ii. Type of fracture – complete or incomplete
iii. Simple (closed), comminuted (splintering of bone), compound
(communicating to skin surface)
STAGES OF FRACTURE HEALING
• PRIMARY UNION
• SECONDARY UNION
• PROCALLUS FORMATION
• OSSEOUS CALLUS FORMATION
• REMODELLING
PRIMARY UNION
• Ends of fracture are approximated
• By application of compression clamps
• Union takes place by the formation of Medullary callus without
periosteal callus formation
• Seen only in special conditions
SECONDARY UNION
• More common process
• Continuous
• It includes:
• PROCALLUS FORMATION
• OSSEOUS CALLUS FORMATION
• REMODELLING
PROCALLUS FORMATION
• It includes:
1) HAEMATOMA
2) LOCAL INFLAMMATORY RESPONSE
3) INGROWTH OF GRANULATION TISSUE
4) CALLUS COMPOSED OF WOVEN BONE AND CARTILAGE
HAEMATOMA
• Bleeding from torn vessels
• Fills the space
• Loss meshwork by blood and fibrin clot is formed
• This acts as framework for granulation tissue formation
LOCAL INFLAMMATORY RESPONSE
• Exudation of fibrin, polymorphs & macrophages.
• Macrophages clears the fibrin, red cells, exudate and debris and
necrosed bone
INGROWTH OF GRANULATION TISSUE
• Neovascularisation
• Proliferation of mesenchymal cells from periosteum and endosteum
• Results in soft tissue callus
CALLUS COMPOSED OF WOVEN BONE AND
CARTILAGE
• Cells of periosteum lays down collagen and osteoid matrix in
granulation tissue
• Osteoid matrix undergoes calcification – woven bone callus. This
covers the fracture end on both sides and bridges the gap.
OSSEOUS CALLUS FORMATION
• Procallus acts as scaffolding on which osseous callus is formed.
• Woven bone is cleared by incoming osteoclasts
• Calcified cartilage disintegrates.
• These are replaced by new blood vessels and osteoblasts which in
turn forms lamellar bone by developing Haversian system around the
blood vessels.
REMODELLING
• Osteoblastic laying and osteoclastic removal takes place
simultaneously.
• External callus is cleared away
• Compact bone is formed in place of callus
• Bonemarrow cavity develops
COMPLICATIONS:
• FIBROUS UNION: when immobilization is not done.
• NON-UNION: if soft tissue is interposed b/w fractured ends.
• DELAYED UNION: due to infection, inadequate blood supply, poor
nutrition, old age.
THANKYOU

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Ug wound healing

  • 2. LEARNING OBJECTIVES: • Repair, steps involved in it. • Granulation tissue • Types of wound healing • Complications • Factors influencing • Fracture healing
  • 3. • REGENERATION is restoration to original tissue by proliferation of parenchymal cells Structure and function is retained • REPAIR is healing of proliferation of connective tissue resulting in fibrosis and scaring Only structure is preserved.
  • 4. REPAIR The replacement of injured tissue by fibrous tissue. Two processes are involved in repair: 1. Granulation tissue formation 2. Contraction of wounds
  • 5.
  • 6. STEPS INVOLVED IN REPAIR: • Formation of blood clot • Inflammation • Granulation tissue formation • Fibroblast proliferation and matrix accumulation • Angiogenesis • Wound contraction • Remodelling
  • 7.
  • 8.
  • 9. GRANULATION TISSUE • Migration and proliferation of fibroblasts & deposition of loose connective tissue, together with vessels and leukocytes • New connective tissue with microscopic blood vessels that forms the surface of the wound during healing process. • Grows from the base of the wound and fill out the wound. • Gross – pink, soft, granular, seen beneath scab of skin wound. • Microscopically – fibroblast proliferation, capillaries, loose extracellular matrix, inflammatory cells & macrophages.
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  • 15. Classification of Wounds Closure • Healing by Primary Intention: – All Layers are closed. The incision that heals by first intention does so in a minimum amount of time, with no separation of the wound edges, and with minimal scar formation. • Healing by Secondary Intention: – Deep layers are closed but superficial layers are left to heal from the inside out. Healing by second is appropriate in cases of infection, excessive trauma, tissue loss, or imprecise approximation of tissue. • Healing by Tertiary Intention: – Also referred to as delayed primary closure.
  • 16. WOUND HEALING • 2 TYPES PRIMARY INTENTION SECONDARY INTENTION
  • 17. PRIMARY INTENTION • CHARACTERISTICS OF WOUND: CLEAN AND UNINFECTED SURGICALLY INCISED WITHOUT MUCH LOSS OF CELLS AND TISSUE EDGES OF WOUND APPROXIMATED BY SURGICAL SUTURES • END RESULT RAPID HEALING NEAT SCAR
  • 18. PRIMARY INTENTION • SEQUENCE 1. INITIAL HEMORRHAGE 2. ACUTE INFLAMMATION RESPONSE 3. EPITHELIAL CHANGES 4. ORGANISATION 5. SUTURE TRACKS
  • 19. PRIMARY INTENTION 1. INITIAL HEMORRHAGE SPACE B/W APPROXIMATED SURFACES IS FILLED WITH BLOOD BLOOD CLOTS WOUND IS SEALED
  • 20. PRIMARY INTENTION 2. ACUTE INFLAMMATION RESPONSE WITHIN 24 HRS APPEARANCE OF POLYMORPHS BY 3rd DAY – REPLACED BY MACROPHAGES
  • 21. PRIMARY INTENTION 3. EPITHELIAL CHANGES PROFILERATION OF BASAL CELLS OF EPIDERMIS MIGRATING TOWARDS INCISIONAL SPACE MIGRATED EPIDERMAL CELLS SEPARATE THE UNDERLYING VIABLE DERMIS FROM OVERLYING NECROTIC DEBRIS AND CLOT BY FORMING A SCAB. NEW EPIDERMIS IS FORMED BY THE 5th DAY.
  • 22. PRIMARY INTENTION 4 . ORGANISATION BY 3RD DAY - INVASION OF FIBROBLASTS. BY 5TH DAY - INVASION OF COLLAGEN FIBRILS
  • 23. PRIMARY INTENTION 5 . SUTURE TRACKS EACH SUTURE TRACK IS A SEPARATE WOUND. AND UNDERGOES THE SAME PHENOMENA. 7TH DAY – SUTURE IS REMOVED.
  • 25. SECONDARY INTENTION • CHARACTERISTICS OF WOUND: • LARGE TISSUE DEFECT • EXTENSIVE LOSS OF CELLS AND TISSUES • WOUND NOT APPROXIMATED BY SUTURES AND LEFT OPEN • END RESULT: LONGER TIME TAKEN FOR HEALING LARGE SCAR
  • 26. SECONDARY INTENTION • SEQUENCE 1. INITIAL HEMORRHAGE 2. INFLAMMATION RESPONSE 3. EPITHELIAL CHANGES 4. GRANULATION TISSUE 5. WOUND CONTRACTION
  • 27. SECONDARY INTENTION 1. INITIAL HEMORRHAGE SPACE B/W APPROXIMATED SURFACES IS FILLED WITH BLOOD BLOOD CLOTS WOUND IS SEALED
  • 28. SECONDARY INTENTION 2. ACUTE INFLAMMATION RESPONSE APPEARANCE OF POLYMORPHS INITIALLY REPLACED BY MACROPHAGES WHICH CLEARS OFF THE DEBRIS
  • 29. SECONDARY INTENTION 3. EPITHELIAL CHANGES PROFILERATION OF BASAL CELLS OF EPIDERMIS MIGRATING TOWARDS INCISIONAL SPACE BUT GRANULATION TISSUE FROM BASE ALSO FILLS THE WOUND SPACE. REGENERATED EPIDERMIS BECOMES STRATIFIED AND KERATINISED.
  • 30. SECONDARY INTENTION 4. GRANULATION TISSUE FORMED BY PROLIFERATION OF FIBROBLASTS AND NEOVASCULARISAION. NEW- RED, GRANULAR, FRAGILE OLD- PALE, WHITE NO REPLACEMENT OF HAIR FOLLICLES AND SWEAT GLANDS.
  • 31. SECONDARY INTENTION 5. WOUND CONTRACTION BY ACTION OF MYOFIBROBLASTS. CONTRACTS TO 1/3RD TO 1/4TH OF ORIGINAL SIZE.
  • 32. • PRESENCE OF INFECTION: DUE TO BACTERIAL TOXINS LEADS TO NECROSIS, SUPPURATION, THROMBOSIS DELAYED HEALING NEED FOR DEBRIDEMENT
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  • 35.
  • 36. S.NO FEATURES PRIMARY INTENTION SECONDARY INTENTION 1 CLEANLINESS CLEAN UNCLEAN 2 INFECTION MOSTLY UNINFECTED MAY BE INFECTED 3 MARGINS SUGICAL CLEAN MARGINS IRREGULAR 4 SUTURES USED NOT USED 5 HEALING SCANTY GRANULATION TISSUE IN THE GAP EXUBERANT GRANULATION TISSUE IN THE GAP 6 OUTCOME NEAT LINEAR SCAR CONTRACTED IRREGULAR WOUND 7 COMPLICATIONS EPIDERMAL INCLUSION CYST SUPPURATION
  • 37. COMPLICATIONS OF WOUND HEALING: • DELAYED HEALING: • INFECTION: • DEFICIENT SCAR FORMATION: inadequate granulation tissue • INCISIONAL HERNIA:
  • 38. HYPERTROPHIED SCAR & KELOID: excessive formation of collagen in healing leads to keloid
  • 39. • EXCESSIVE CONTRACTION: exaggeration of wound contraction results in formation of contractures. Eg- dupuytren’s contracture • NEOPLASIA: Eg- squamous cell carcinoma in Marjolin’s ulcer.
  • 40. • EPIDERMAL CYST: persistence of epithelial cells in the wound after healing • PIGMENTATION: due to staining with haemosiderin
  • 41. FACTORS INFLUENCING HEALING: • LOCAL 1. INFECTION 2. POOR BLOOD SUPPLY 3. FOREING BODIES 4. MOVEMENT 5. IONISING RADIATION 6. ULTRAVIOLET LIGHT 7. TYPE, SIZE AND LOCATION OF INJURY
  • 42. FACTORS INFLUENCING HEALING: • SYSTEMIC 1. AGE 2. NUTRITION 3. ADMINISTRATION OF GLUCOCORTICOIDS 4. UNCONTROLLED DM 5. SYSTEMIC INFECTION 6. HEMATOLOGICAL ABNORMALITIES
  • 43. FRACTURE HEALING: • Depends on i. Nature of fracture – traumatic or pathological ii. Type of fracture – complete or incomplete iii. Simple (closed), comminuted (splintering of bone), compound (communicating to skin surface)
  • 44. STAGES OF FRACTURE HEALING • PRIMARY UNION • SECONDARY UNION • PROCALLUS FORMATION • OSSEOUS CALLUS FORMATION • REMODELLING
  • 45. PRIMARY UNION • Ends of fracture are approximated • By application of compression clamps • Union takes place by the formation of Medullary callus without periosteal callus formation • Seen only in special conditions
  • 46. SECONDARY UNION • More common process • Continuous • It includes: • PROCALLUS FORMATION • OSSEOUS CALLUS FORMATION • REMODELLING
  • 47. PROCALLUS FORMATION • It includes: 1) HAEMATOMA 2) LOCAL INFLAMMATORY RESPONSE 3) INGROWTH OF GRANULATION TISSUE 4) CALLUS COMPOSED OF WOVEN BONE AND CARTILAGE
  • 48. HAEMATOMA • Bleeding from torn vessels • Fills the space • Loss meshwork by blood and fibrin clot is formed • This acts as framework for granulation tissue formation
  • 49. LOCAL INFLAMMATORY RESPONSE • Exudation of fibrin, polymorphs & macrophages. • Macrophages clears the fibrin, red cells, exudate and debris and necrosed bone
  • 50. INGROWTH OF GRANULATION TISSUE • Neovascularisation • Proliferation of mesenchymal cells from periosteum and endosteum • Results in soft tissue callus
  • 51. CALLUS COMPOSED OF WOVEN BONE AND CARTILAGE • Cells of periosteum lays down collagen and osteoid matrix in granulation tissue • Osteoid matrix undergoes calcification – woven bone callus. This covers the fracture end on both sides and bridges the gap.
  • 52. OSSEOUS CALLUS FORMATION • Procallus acts as scaffolding on which osseous callus is formed. • Woven bone is cleared by incoming osteoclasts • Calcified cartilage disintegrates. • These are replaced by new blood vessels and osteoblasts which in turn forms lamellar bone by developing Haversian system around the blood vessels.
  • 53. REMODELLING • Osteoblastic laying and osteoclastic removal takes place simultaneously. • External callus is cleared away • Compact bone is formed in place of callus • Bonemarrow cavity develops
  • 54.
  • 55.
  • 56. COMPLICATIONS: • FIBROUS UNION: when immobilization is not done. • NON-UNION: if soft tissue is interposed b/w fractured ends. • DELAYED UNION: due to infection, inadequate blood supply, poor nutrition, old age.