Wound Healing
• learning objectives:
• Describe the process of healing
• Specify the patterns of wound healing
• Factors influencing wound healing
• Discuss complication of wound healing
• Understand fracture healing
Definition:
• healing-bodies replacement of destroyed
tissue by living tissue
process of healing
• two processes:
-regeneration-by similar tissue
-repair (scar)-by connective tissue (fibrosis)
• tissue damage inflammation
removal of dead tissue and
injurious agent replacement
by: fibrous tissue (scaring) or
specialized tissue
(regeneration) healing
types of cells:
• a .labile cells-have continuous turnover
• excellent replicative capacity e.g. skin, mucosal
cells
• b. stable cells-lower level of replication and few
stem cells.
• undergo division following injury
e.g. smooth muscle cells, fibroblasts, osteoblasts,
endothelial cells , hepatocytes
• good replicative capacity
• c. permanent cells-non dividing cells
e.g.- neurons, striated muscle cells, cells of lens
• regeneration ( generare -bring to life)-
renewal of lost tissue in which the lost cells
are replaced by identical ones.
• regeneration involves two processes:
1. proliferation of surviving cells
2. migration of surviving cells
• the capacity of a tissue for regeneration
depends on:
1. proliferative ability
2. the degree of damage to stromal
framework
3. type and severity of damage
• NB: labile and stable cells proliferate
provided that framework intact.
• Repair (healing by connective tissue)
• repair-orderly process in which lost tissue is
replaced by scar (fibrosis).
• tissues with permanent cells and extensive
stromal injury heal by scar.
• begin with granulation tissue formation
• granulation tissue-is characterized by
proliferation of fibroblasts and in growth of
blood vessels in to the area of injury with
number of inflammatory cells.
• in granulation tissue formation there are 3
phases:
1. phase of inflammation-exudation
2. phase of demolition-digesting or
removing necrotic tissue
3. granulation tissue ingrowth
• fibroblasts-produce extra cellular matrix e.g.
fibronectine, proteoglycans, collagen(type1-
type 4)
• type 1 collagen is the major collagen of mature
scar tissue
• it provides tensile strength of the matrix in a
scar.
• the tensile strength of the wound continuous to
increase many months after the collagen
content has reached a maximum.
Repair by CT(fibrosis)
• Occurs following tissue destruction with
damage to both parenchymal cells and
stromal framework.
Repair by CT(fibrosis)
Four components :
1.Formation of new blood
vessels(angiogenesis)
2.Migration and proliferation of fibroblasts.
3.Deposition of ECM
4.Maturation and organization of the fibrous
tissue ( remodeling ).
Angiogenesis
• Preexisting vessels send out capillary buds or sprouts to
produce new vessels.
Steps :
• Proteolytic degradation of the BM of the parent vessel to
allow formation of capillary sprout and subsequent cell
migration.
• Migration of endothelial cells toward the angiogenic
stimulus.
• Proliferation of endothelial cells, just behind the leading
part of migrating cells.
• Maturation of endothelial cells - inhibition of growth and
remodeling into capillary tubes.
• Recruitment of periendothelial cells i.e. pericytes and
smooth muscle cells.
Fibrosis
• Occurs within the granulation tissue frame
work of new blood vessels and loose
ECM.
Two processes
• Emigration and proliferation of fibroblasts
in the site of injury.
• Deposition of ECM.
two patterns of wound healing
wounds can be-accidental or surgical
(intentional)
based on the amount of tissue damage:
1.healing by first intention(10 union))
2.healing by second intention(20 union)
1. healing by 10 union
• wound edges are approximated by surgical
sutures and healing occurs with minimal
tissue loss.
• the 1st step is formation of scab-dehydrated
clotted blood containing fibrin & blood
cells.
• with in 24hours basal cells mitotic
activity thickened at the cut edge
• by day 3 there will be granulation tissue
formation
• 2nd week leukocyte infiltrate, edema and
increased vascularity
• 1st month-scar tissue covered by an intact
epidermis
• NB: dermal appendages lost permanently
2. secondary union
• more extensive cell and tissue loss large
defect e.g.-infarction, ulceration
• Abundant granulation tissue grows in from
the margin to complete the repair.
• the difference with 10 union
– more intense inflammation
– much granulation tissue formation
– there is more wound contraction
– it takes longer time
wound contraction
• -mechanical reduction in the size of the
defect to 70-80% of original size.
• it is done by myofibroblasts
factors affecting wound healing
• local factors
• systemic factors
local factors:
• type, size and location of the wound
• e.g.-wounds on the face heal fast
• vascular supply
• infection excessive granulation tissue
formation large deforming scar
• movement
• ionizing radiation
systemic factors:
• circulatory status
• infection
• metabolic status
• e.g.-poorly controlled DM delayed
wound healing
• DM atherosclerosis, diabetic neuropathy,
so interferes with normal blood supply or
predisposes to injury respectively.
• nutritional deficiencies
-ed protein ed collagen formation
• vitamin deficiency
e.g.- vit c decreased collagen synthesis scurvy
• -zinc deficiency decreased cell proliferation
(fibroblasts) ed collagen
• hormones
e.g.- corticosteroids -impair wound healing
-ed collagen synthesis
-anti-inflammatory effect.....
• anti-inflammatory drugs
e.g.- aspirin
complications of wound healing
• abnormalities in repair, regeneration and contraction
complication
• 1. infection
• 2. deficient scar formation
• complication- a. wound dehiscence incisional hernias
-b. ulceration
-dehiscence occurs in 0.5-5% of abdominal surgeries
-dehiscence can be due to:-inappropriate surgical
techniques, stress, or infection
Ulceration-defect in the continuity of an epithelial surface
• neuropathic ulcers-in varicose,DM,leprosy,30
syphilis(spinal involvement, tabes dorsalis)
• 3. excessive scar formation
• -failure in 'maturation arrest' or block in the
healing process
– keloid-exuberant scar that tends to progress and recur
after excision
• -frequent after burns
• -common on neck &ear lobes.
• hypertrophic scar-structurally similar to keloid
• but never gets worse after 6 months
• doesn't recur
Keloid
• 4. excessive contraction
• exaggeration of contraction contracture
(cicatrisation)
• results in sever deformity
• palms, soles, and anterior thorax are prone for
contracture (why?)
• follows burn injuries
• it can occur in hollow viscera stricture
• e.g.-urethra, esophagus
• palmar contracture- dupuytren’s contracture
fracture healing
• defect is filled by specialized bone forming
tissue ,unlike scar formation
• so bone is restored nearly to normal
bone structure
• bone is composed of calcified osteoid tissue
consists of collagen fibers embedded in a
mucoprotein matrix (osteomucin)
• based on arrangement of collagen fibers
there are two histologic types:
1. woven, immature or non-lamellar bone
-collagen bundles arranged irregularly
-less abundant osteomucin, less
calcium
2. lamellar or adult bone
-collagen bundles arranged in parallel
sheets
• stages in fracture healing (bone regeneration)
• stage 1-hematoma formation
• stage 2-inflammation
• - hematoma attain a fusiform shape
• stage 3-demolition
• -macrophages remove clot, fibrin, red
cells, exudate & debris
• -fragments of bones by osteoclasts
• stage 4-formation of granulation tissue
• -neovascularization, osteogenesis
• stage 5-woven bone& cartilage formation
- osteoblasts- produce both woven
bone and cartilage
-callus formation, initially soft but will
be hardened
• stage 6-formation of lamellar bone
-provisional callus removed, osteoid
formed and calcified bone
• -collagen fibers arranged in lamellar fashion
concentrically around blood vessels
haversian system formed definitive
lamellar bone merges with the last stage
• stage 7-remodeling
-osteoclastic removal &
osteoblastic lay down of bone material
• -external callus removed
Complications:
• Delayed healing
• Non healing
• Joint involvement - ankylosis
• Abnormal position – arthritis.
• Involucrum formation.
• Pseudoarthrosis
• Thank u

hypertention

  • 1.
  • 2.
    • learning objectives: •Describe the process of healing • Specify the patterns of wound healing • Factors influencing wound healing • Discuss complication of wound healing • Understand fracture healing
  • 3.
    Definition: • healing-bodies replacementof destroyed tissue by living tissue process of healing • two processes: -regeneration-by similar tissue -repair (scar)-by connective tissue (fibrosis)
  • 4.
    • tissue damageinflammation removal of dead tissue and injurious agent replacement by: fibrous tissue (scaring) or specialized tissue (regeneration) healing
  • 5.
    types of cells: •a .labile cells-have continuous turnover • excellent replicative capacity e.g. skin, mucosal cells • b. stable cells-lower level of replication and few stem cells. • undergo division following injury e.g. smooth muscle cells, fibroblasts, osteoblasts, endothelial cells , hepatocytes • good replicative capacity • c. permanent cells-non dividing cells e.g.- neurons, striated muscle cells, cells of lens
  • 6.
    • regeneration (generare -bring to life)- renewal of lost tissue in which the lost cells are replaced by identical ones. • regeneration involves two processes: 1. proliferation of surviving cells 2. migration of surviving cells
  • 7.
    • the capacityof a tissue for regeneration depends on: 1. proliferative ability 2. the degree of damage to stromal framework 3. type and severity of damage • NB: labile and stable cells proliferate provided that framework intact.
  • 8.
    • Repair (healingby connective tissue) • repair-orderly process in which lost tissue is replaced by scar (fibrosis). • tissues with permanent cells and extensive stromal injury heal by scar. • begin with granulation tissue formation
  • 10.
    • granulation tissue-ischaracterized by proliferation of fibroblasts and in growth of blood vessels in to the area of injury with number of inflammatory cells. • in granulation tissue formation there are 3 phases: 1. phase of inflammation-exudation 2. phase of demolition-digesting or removing necrotic tissue 3. granulation tissue ingrowth
  • 11.
    • fibroblasts-produce extracellular matrix e.g. fibronectine, proteoglycans, collagen(type1- type 4) • type 1 collagen is the major collagen of mature scar tissue • it provides tensile strength of the matrix in a scar. • the tensile strength of the wound continuous to increase many months after the collagen content has reached a maximum.
  • 12.
    Repair by CT(fibrosis) •Occurs following tissue destruction with damage to both parenchymal cells and stromal framework.
  • 13.
    Repair by CT(fibrosis) Fourcomponents : 1.Formation of new blood vessels(angiogenesis) 2.Migration and proliferation of fibroblasts. 3.Deposition of ECM 4.Maturation and organization of the fibrous tissue ( remodeling ).
  • 14.
    Angiogenesis • Preexisting vesselssend out capillary buds or sprouts to produce new vessels. Steps : • Proteolytic degradation of the BM of the parent vessel to allow formation of capillary sprout and subsequent cell migration. • Migration of endothelial cells toward the angiogenic stimulus. • Proliferation of endothelial cells, just behind the leading part of migrating cells. • Maturation of endothelial cells - inhibition of growth and remodeling into capillary tubes. • Recruitment of periendothelial cells i.e. pericytes and smooth muscle cells.
  • 17.
    Fibrosis • Occurs withinthe granulation tissue frame work of new blood vessels and loose ECM. Two processes • Emigration and proliferation of fibroblasts in the site of injury. • Deposition of ECM.
  • 18.
    two patterns ofwound healing wounds can be-accidental or surgical (intentional) based on the amount of tissue damage: 1.healing by first intention(10 union)) 2.healing by second intention(20 union)
  • 19.
    1. healing by10 union • wound edges are approximated by surgical sutures and healing occurs with minimal tissue loss. • the 1st step is formation of scab-dehydrated clotted blood containing fibrin & blood cells. • with in 24hours basal cells mitotic activity thickened at the cut edge
  • 20.
    • by day3 there will be granulation tissue formation • 2nd week leukocyte infiltrate, edema and increased vascularity • 1st month-scar tissue covered by an intact epidermis • NB: dermal appendages lost permanently
  • 22.
    2. secondary union •more extensive cell and tissue loss large defect e.g.-infarction, ulceration • Abundant granulation tissue grows in from the margin to complete the repair. • the difference with 10 union – more intense inflammation – much granulation tissue formation – there is more wound contraction – it takes longer time
  • 23.
    wound contraction • -mechanicalreduction in the size of the defect to 70-80% of original size. • it is done by myofibroblasts
  • 25.
    factors affecting woundhealing • local factors • systemic factors local factors: • type, size and location of the wound • e.g.-wounds on the face heal fast • vascular supply • infection excessive granulation tissue formation large deforming scar • movement • ionizing radiation
  • 26.
    systemic factors: • circulatorystatus • infection • metabolic status • e.g.-poorly controlled DM delayed wound healing • DM atherosclerosis, diabetic neuropathy, so interferes with normal blood supply or predisposes to injury respectively. • nutritional deficiencies -ed protein ed collagen formation
  • 27.
    • vitamin deficiency e.g.-vit c decreased collagen synthesis scurvy • -zinc deficiency decreased cell proliferation (fibroblasts) ed collagen • hormones e.g.- corticosteroids -impair wound healing -ed collagen synthesis -anti-inflammatory effect..... • anti-inflammatory drugs e.g.- aspirin
  • 28.
    complications of woundhealing • abnormalities in repair, regeneration and contraction complication • 1. infection • 2. deficient scar formation • complication- a. wound dehiscence incisional hernias -b. ulceration -dehiscence occurs in 0.5-5% of abdominal surgeries -dehiscence can be due to:-inappropriate surgical techniques, stress, or infection Ulceration-defect in the continuity of an epithelial surface • neuropathic ulcers-in varicose,DM,leprosy,30 syphilis(spinal involvement, tabes dorsalis)
  • 29.
    • 3. excessivescar formation • -failure in 'maturation arrest' or block in the healing process – keloid-exuberant scar that tends to progress and recur after excision • -frequent after burns • -common on neck &ear lobes. • hypertrophic scar-structurally similar to keloid • but never gets worse after 6 months • doesn't recur
  • 30.
  • 31.
    • 4. excessivecontraction • exaggeration of contraction contracture (cicatrisation) • results in sever deformity • palms, soles, and anterior thorax are prone for contracture (why?) • follows burn injuries • it can occur in hollow viscera stricture • e.g.-urethra, esophagus • palmar contracture- dupuytren’s contracture
  • 32.
    fracture healing • defectis filled by specialized bone forming tissue ,unlike scar formation • so bone is restored nearly to normal bone structure • bone is composed of calcified osteoid tissue consists of collagen fibers embedded in a mucoprotein matrix (osteomucin)
  • 34.
    • based onarrangement of collagen fibers there are two histologic types: 1. woven, immature or non-lamellar bone -collagen bundles arranged irregularly -less abundant osteomucin, less calcium 2. lamellar or adult bone -collagen bundles arranged in parallel sheets
  • 35.
    • stages infracture healing (bone regeneration) • stage 1-hematoma formation • stage 2-inflammation • - hematoma attain a fusiform shape • stage 3-demolition • -macrophages remove clot, fibrin, red cells, exudate & debris • -fragments of bones by osteoclasts • stage 4-formation of granulation tissue • -neovascularization, osteogenesis
  • 36.
    • stage 5-wovenbone& cartilage formation - osteoblasts- produce both woven bone and cartilage -callus formation, initially soft but will be hardened
  • 37.
    • stage 6-formationof lamellar bone -provisional callus removed, osteoid formed and calcified bone • -collagen fibers arranged in lamellar fashion concentrically around blood vessels haversian system formed definitive lamellar bone merges with the last stage
  • 38.
    • stage 7-remodeling -osteoclasticremoval & osteoblastic lay down of bone material • -external callus removed
  • 39.
    Complications: • Delayed healing •Non healing • Joint involvement - ankylosis • Abnormal position – arthritis. • Involucrum formation. • Pseudoarthrosis
  • 40.