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BODC exodontia yr 2 > wound healing > Flashcards

wound healing Flashcards

1
Q

healing

A

Follows tissue damage

  • attempt to restore integrity to an injured tissue (back to how they were)
  • follows the inflammatory process (often overlaps)
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2
Q

resolution

A

return to normal

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3
Q

regeneration

A

lost tissue replaced by same type of tissue to restore tissue

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4
Q

repair

A

tissue lost replaced by firbois scare (via granulation tissue)

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5
Q

regeneration vs repair headings for comparision

A

cell type involved
tissue architecture
amount of tissue lost

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6
Q

cell type involved (regeneration vs repair )

A

labial continual cell division vs stable infrqeuen cell divison

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7
Q

tissue architecture regeneration vs repair

A

simple vs complex tissue

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8
Q

amount of tissue lost regeneration vs repair

A

small vs large

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9
Q

steps for repair

A

1) endotheoal cells and fibroblasts at edges (form loose meshwork/bridge)
2) these migrate into area forming loose connective tissue, granulation tissue
3) increase in blood vessels and collagen
4) vascularity decreases and fibrous scar formed

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10
Q

cells involved in the repair process

A
  • macrophages (phagocytosis any debris cell ect and secretion to promote wound healing
  • fibroblasts (collagen and other tissue support)
  • endothelial cells (nutrition)
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11
Q

what does slough contain

A

neutrophuils

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12
Q

granulation tissue conposition

A
  • Inflammatory
  • endothelial cells
  • fibroblasts
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13
Q

phases of wound healing

A

1) haemostasis
2) inflammation
3) proliferation
4) remodelling

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14
Q

haemostasis

A

vessel rupture, bleeding

  • activation of coagulation cascade
  • vasoconstriction (5-10 mins serotonin, adrenaline)
  • thrombus formation, fibrin and fibrinogen glue would together
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15
Q

cells involved in inflamamtion

A

neutrophls

macrophages

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16
Q

neutrophils inflammation

A
  • recruited from circulation (why we need vasodilation)
  • remove bacteria and forign material
  • phagocytosis and enzymes
  • short live (2 days)
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17
Q

macrophages inflammation

A
  • recruited from blood monocytes (circulation) and those already resident in the tissue, proliferate locally
  • phagocytose of remaining debris
    Further secretion cytokines and growth factors by both (secret further cytokines)
  • both follow the chemoattracts to where they are needed
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18
Q

proliferation step in wound healing key cells and roles

A

key cell- fibroblast
- proliferate, migrate and become myofibroblast (change phenotype, gives them some contractile properties to pull wound together)
- synthesis of matrix proteins eg collagen
- proliferation and migration of cells over wound bed
Key cell – keratinocyte
- re epithelialisation
- angiogenesis (new blood vessel formation)

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19
Q

remodelling in wound healing steps

A
  • provisional matrix remodelled
  • reduction in cell and capillary density (less red)
  • protases (collagenases) required for remodelling ECM (Scaffold and chemical signalling matrix)
  • wound contraction (using proteins within the cytoskeleton to pull together)
  • type III collagen replaced by bundles of type I
  • strength relies on cross linked collagen I (vitamin C)
  • 7-10 days wound = 10% strength (provisional matrix)
  • 2-3 months 70-80%
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20
Q

types of intention on how to treat the wound

A

primary

secondary

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21
Q

primary intention

A
  • wound edges are apposed (brought together) and held in place by mechanical means (eg sutrues, glue)
  • actively helping process
  • wound that is clean straight
  • no tissue lost
  • just split open due to pressure of tissue
  • bring together with stiches
  • minimal scaring
22
Q

secondary intention

A
  • wound left open
  • edges come together natural by means of granulation and contraction
  • heal by itself
23
Q

secondary intention type of wound

A
  • bigger wound
  • deeper
  • wider
  • tissue has been lost
  • even if you brought it together on the surface, there would be missing skin underneath so the extra pressure would not help healing
  • leave to heal on its own
  • healing will take longer, more like repair, fibroblastic response, more scarring
24
Q

bone fracture healing

A
  • don’t get granulation tissue but similar tissue which forms a bridge/scaffold
  • follows by immature then mature bone
  • resolution process, extra bits of bone taken away by macrophages
25
Q

socket healing steps

A
  • inflammation
  • proliferation
  • remodelling

granulation tisseu formation is then replaced by fibroblasts

26
Q

oral and skin wound healin g is best acheived by

A

primary intention

27
Q

factors influencing wound healing (systemic and local)

A

1) Local
- type(eg clean cut), size and location of wound
- movement within wound
- infection (barrier function of the epithelium) is gone
- presence of forgein/necrotic material
- irradiation (damage cells ability to proliferate)
- poor blood supply (cant bring inflammatory cells in)

2) systemic
- age (longer to heal)
- nutrition
- (vitamin C and Zinc)
- systemic disease – circulatory, diabetes
- drugs (esp steroids, antiinflammaory healing stage interrupted)

28
Q

signals involved in the healing process

A
  • from cells or blood
  • growth factors
  • cytokines and chemokines
  • O2, nutrients etc
  • extracellular matrix
29
Q

cells involved in healing process

A
  • different types (WBC, bone cells, epithelail cells ect interact with each other and the ECM)
  • cell to extracellular matrix interactions (integrins) – sense type of ECM they are in
  • cell- cell interactions
  • correct position of cells
30
Q

mitogenic growth stimuli in epithelail cells

A
  • loss of contact inhibition (cells are tightly packed and normally don’t grow, loss of contact tells epithelial cells they need to grow to replace)
  • growth factor mediated (from platelets and damaged endothelial cells)
31
Q

control of epithelila cell movment

A

Migration of existing cells at wound edge (fibronectin) – proliferating cells move over the wound bed

  • migration stops when cells meet
  • stratification (differentiation) finally occurs
  • basement membrane proteins reappear (between dermis and epidermis)
32
Q

control of neutrophils and macrophages

A

1) margination
- cells line up against the vessel wall
- neutrophils line up against endothelium
2) adhesion
- adhesion molecule expression on endothelium changed
- receptors that respond to this signal
3) emigration
- pseudopodia push through gaps in endothelium
4) chemotaxis
- movement along a chemical gradient
- released in local areas, to bring in blood cells
- bacteria products(exogenous)
- complement
- fragments
- prostaglandins
- leukotrienes
- cytokines
5) phagocytosis and degranulation
- free radicals
- lysozyme (digest and kill bacteria)
- proteolytic enzymes in lysosomes

33
Q

angiogenesis

A

ingrowth of new blood vessels

34
Q

steps for angiogeneiss

A
  • budding from intact vessels at wound edge
  • macrophages secrete angiogenic
  • macrophages secrete angiogenic factors in response to low oxygen (hypoxic, to relief that environment)
  • fibroblast GF and VEGF stimulate protease secretion and growth of endothelial cell
  • anti- angiogenic factors limit vessel formation (towards end of would healing)
  • as inflammation subsides, apoptosis occurs
35
Q

what are fibroblasts activated to form

A

myofibroblasts
change phenotype, express contractile protein
- fibroblast and smooth muscle features
- gives fibroblast cell ability to contract
- pull wound together

36
Q

what is migrtion stimulated by for fibroblasts

A

fibronectin
Chemoattraction by macrophages
secretion of collagen and fibronectin and TGF beta (affects other cells)

37
Q

proliferation of fibroblasts

A
  • PDGF, FGF, TGFalpha, c5a from macrophages, platelets and endothelial cells
  • grow within granulation tissue
38
Q

why is healing complicated

A
  • multiple cell types
  • multpiple control points
  • control is key
  • lots of chemokines
  • all processes are crutial for healing, needs to be tightly regualted
39
Q

dysregulated healing leads to

A

cancer

40
Q

scar

A

macroscopic disturbance of the normal structure and function of the skin architecture resulting from the end product of a healed wound

41
Q

cancer steps in wound healing

A
  • keratinocyte proliferation and migration
  • fibroblast activation
  • angiogenesis
  • proteases unregulated
  • integrin expression altered
42
Q

problems with healing

A
  • burns (lose ECM, can get the repair back by filling the gap but don’t get tissue architecture back)
  • hypertrophic scars (where wound healing takes longer to stop not when it should, scars with stick out of the wound further than they should)
  • contracture
  • keloids
  • neuroma
  • loss of function
  • cosmetic (collagen, fibroblasts)
43
Q

hypertrophic scaring

A

increased incidence of hypertrophic/keloid in those with darker skin

44
Q

contractures

A

Muscle/tendon shortening

45
Q

keloid scar

A
  • thick bundles of collagen with high levels of type III
  • abnormal cross linkage and high turnover
  • altered cytokine levels
46
Q

neuroma

A

scar tissue around nerves

  • nerve bruised or pulled
  • can form scar tissue around it
  • may reduce condition and alter sensation
  • eg may be tingly lower lip
47
Q

chronic wounds and characteristics

A

Stuck in inflammatory phase

  • beyond 3 months
  • increased proteases (destroy ECM)
  • reduced GFs (PDGF, FGF, EGF)
  • fibrin cuffs
  • underling disease (venous insufficiency, diabetes)
  • infection
  • necrosis
48
Q

foetal wounds and mechaism

A

wounds almost scarless and dissolve immediately

  • reduced inflammation, fewer neutrophils
  • fibroblast phenotype different to adults (ECM synthesis, cytokine production, RTK signalling)
  • prompt disappearance of PlatletderivedGF (stimulates the next phase)
  • VEGF increased (more rapid angiogenesis) and FGF – quicker to give nutrients
  • homeobox genes (transcription factors)
49
Q

chronic wounds

A
  • don’t heal due to underlying disease
  • adult skin scarring lasts almost forever
  • can create sig defect in the OC, but will heal without scar (secondary healing without sutres)
50
Q

oral vs skin healing

A

Enviroment
- saliva has antibacterial properties
- protected from other elements
Fibroblasts are heterogeneous
- different in underlying tissue in mouth vs skin
- oral have increased ability to contract
- younger phenotype (telomerase)
- increased secretion of growth factors, change in profile of the messengers, different levels in oral vs skin (KGF, HGF, VEGF)
- increased keratinocyte proliferation, can cover a wound are in a shorter length of time

51
Q

assisted wound healing

A
  • dressings
  • hyperbaric oxygen (can encourage wound healing, cells able to take up oxygen better)
  • maggots and leeches (maggots eat dead things, debride the wound, encourage remaining tissue to grow back, leech good for grafts to encourage circulation
  • negative pressure/vaccum therapy (creates a seal around the wound, vaccum keeps dry and sealed also keeps the wound together)
52
Q

new research into wound healing

A

TGFB

alter ratio of isoforms

BODC exodontia yr 2 (25 decks)

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