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MFMII > Wound Repair, Tissue Renewal, Regeneration and Repair > Flashcards

Wound Repair, Tissue Renewal, Regeneration and Repair Flashcards

1
Q

how is regeneration achieved?

A
  1. proliferation of remaining mature cells 2. adult stem cells may regenerate lost tissue
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2
Q

what is regeneration?

A

complete restoration of lost or damaged tissues

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3
Q

what is repair?

A

combination of regeneration and scar formation

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4
Q

what does the contribution of regeneration and scar formation in repair depend on?

A

the ability of the type of injured tissue to regenerate and the extent of the injury

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5
Q

what are the cell categories according to their proliferative activity?

A
  1. labile tissues 2. stable tissues 3. permanent tissues
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6
Q

what are labile tissues?

A

continuously dividing tissues that are continuously being lost and replaced by proliferating mature cells and maturing tissue stem cells (short G0) – usually contain stem cells which have unlimited capacity to proliferate

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7
Q

what are stable tissues?

A

quiescent tissues that are in a G0 stage of the cell cycle but with growth factor signals at the site of injury, the residual cells will proliferate and new cells will develop from tissue stem cells. there is a limited ability to regenerate (except liver). low level of replication.

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8
Q

what are permanent tissues?

A

terminally differentiated and nonproliferative cells – have left cell cycle forever and CANNOT undergo mitosis postnatally

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9
Q

what tissues are labile?

A

epidermis of skin, GI, hematopoietic cells

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10
Q

what tissues are stable tissues?

A

limited ability to regenerate (except for liver) 1. parenchymal cells of liver, pancreas, kidney 2. fibroblasts, chondroblasts, osteocytes, smooth muscle 3. vascular endothelial cells

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11
Q

what tissues are permanent tissues?

A

neurons, mature skeletal muscle cells (may regenerate through satellite cells), cardiac muscle

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12
Q

what is G1 stage?

A

presynthetic phase

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13
Q

what is S stage?

A

cell actively synthesizing DNA

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14
Q

what is G2 stage?

A

postsynthetic premitotic stage

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15
Q

what is G0 stage?

A

intermitotic stage, resting cell can go into G1 stage then S, then G2 then M

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16
Q

what are stem cells characterized by?

A
  1. self renewal 2. asymmetric division (one daughter cell differentiates into mature cell, other remains stem cell)
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17
Q

2 main categories of stem cells

A
  1. embryonic stem cells (pluripotent) 2. somatic/adult stem cells (restricted in cell types)
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18
Q

where are adult stem cells located?

A

special microenvironments (niches) 1. isthmus of gastric glands 2. crypt cells in intestines 3. bulge area of hair follicle 4. limbus of cornea 5. canals of hering in liver

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19
Q

where are adult stem cells present?

A

continuously dividing tissue like bone marrow, skin, lining of GI tract, others

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20
Q

more examples of labile tissues

A
  1. surface epithelium like skin, oral cavity, vagina, cervix 2. columnar epithelium of GI tract and uterus 3. lining mucosa of excretory ducts (salivary glands, pancreas, biliary tract) 4. transitional epithelium of urinary tract 5. bone marrow
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21
Q

stem cell niches in the skin hair follicle bulge but also ?

A

interfollicular stem cells also scattered throughout surface epidermis and sebaceous gland

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22
Q

what are stem cell in skin hair follicle bulges involved in?

A

regeneration of hair follicle cells as well as surface epidermis of skin after injury

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23
Q

where are crypt cells and what do they do

A

stem cells in the crypts of intestines for regeneration of gut epithelium

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24
Q

2 mechanisms that liver can regenerate

A
  1. proliferation of surviving hepatocytes after injury triggered by cytokines and GF 2. liver stem cells (oval cells) in niches (canals of hering)
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25
Q

what is required for liver regeneration?

A

reticulin framework must be intact for regeneration

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26
Q

what 3 conditions are required for healing by regeneration

A
  1. tissue is composed of labile or stable cells 2. area of injury must contain some surviving (viable) cells that are capable of undergoing cell division 3. connective tissue framework must be intact to serve as scaffolding
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27
Q

explain stem cell niches in the brain

A

mature neurons do not undergo cell division but neural stem cells are present in the brain of adult humans but it is unclear if newly generated neurons are integrated into neural circuits

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28
Q

what can neural stem cells do?

A

neural precursor cells are capable of generating neurons, astrocytes and oligodendrocytes

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29
Q

explain stem cell niches in skeletal muscle

A

does not divide after injury, but satellite cells are a reserve pool of stem cells located beneath myocyte lamina with the ability to generate differentiated myocytes after injury

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30
Q

when does healing by scar formation occur?

A

in injured tissues incapable of regeneration due to: 1. tissue consists of permanent non dividing cells 2. no surviving tissue cells remain 3. connective tissue framework is destroyed

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31
Q

what does connective tissue repair involve?

A

ECM

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32
Q

what is part of the ECM?

A
  1. interstitial matrix 2. basement membrane
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33
Q

what is part of the interstitial matrix

A

collagen, elastin, fibronectin (adhesive glycoprotein)

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34
Q

what is part of the basement membrane/

A

collagen type IV, laminin (adhesive glycoprotein)

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35
Q

what part of cell membrane binds to ECM proteins? (the adhesive glycoproteins)

A

integrins

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36
Q

6 functions of the extracellular matrix

A
  1. mechanical support 2. control of cell growth 3. maintenance of cell differentiation (integrins) 4. scaffolding for tissue renewal 5. establishment of tissue microenvironments 6. storage and presentation of regulatory molecules
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37
Q

how does ECM control cell growth

A

can regulate cell proliferation by signaling through cellular integrin receptors

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38
Q

how is ECM used for scaffolding for tissue renewal

A

must be uninjured for regeneration, otherwise scar will occur

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39
Q

how does ECM establish tissue microenvironments/

A

the basement membrane forms a boundary between the epithelium and underlying connective tissue ex. glomerular basement membrane

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40
Q

how does ECM work for storage and presentation of regulatory molecules?

A

some growth factors are secreted and stored in the ECM, allowing for rapid deployment after injury

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41
Q

what are the main components of the ECM

A
  1. fibrous structural proteins like collagen and elastins (tensile strength and recoil) 2. adhesive glycoproteins that connect the matrix elements to one another and cells (fibronectin, laminin) 3. proteoglycans and hyaluronan provide resilience and lubrication
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42
Q

how is collagen made?

A

procollagen is secreted from the cell and cleaved by protease to form basic unit of fibrils

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43
Q

what is fibril formation associated with?

A

oxidation of lysine and hydroxylysine residue by lysyl oxidase, results in cross linking with adjacent molecules

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44
Q

how is vitamin C involved with collagen formation?

A

activates prolyl and lysyl hydroxylases which hydroxylate procollagen.

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45
Q

what happens in vitamin C deficiency?

A

inadequate hydroxylated procollagen cannot acquire a stable helical configuration, results in scurvy

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46
Q

what is scurvy

A

vitamin C deficiency, poor healing and bleeding tendency due to weak vascular basement membrane, children will have skeletal deformities

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47
Q

where is type I collagen

A

ubiquitous in hard and soft tissues

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48
Q

where is type II collagen

A

cartilage, intervertebral disk, vitreous fluid

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49
Q

where is type III collagen

A

hollow organs, soft tissues

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50
Q

where is type IV collagen

A

basement membranes

51
Q

where is type V collagen

A

soft tissues and blood vessels

52
Q

where is type VI collagen?

A

microfibrils

53
Q

where is type VII collagen?

A

anchoring fibrils at dermal epidermal junctions

54
Q

where is type IX collagen?

A

cartilage, intervertebral disks, vitreous fluid

55
Q

where is type XVII collagen?

A

transmembrane collagen in epidermal cells

56
Q

where is type XV and XVIII collagen?

A

endostatin forming collagens, endothelial cells

57
Q

3 phases of cutaneous wound healing?

A
  1. inflammation -initial injury has clot formation with platelet adhesion and aggregation 2. proliferation - formation of granulation tissue (prolif of fibroblasts and vascular endothelial cells) 3. maturation and reorganization - ECM deposition, remodeling, wound contraction
58
Q

what occurs in acute inflammation with wound healing

A
  1. activation of coagulation pathways with blood clot form on wound surface 2. growth factors, cytokines, and chemokines are released 3. neutrophils appear within 24hours
59
Q

what causes a scab?

A

dehydration of surface clot

60
Q

what does the clot do?

A

stops bleeding and acts as scaffold for cells migrating into the wound

61
Q

what is one cause of edema in wound healing?

A

VEGF causes edema due to increased vascular permeability

62
Q

what shows up 24hours of injury?

A

neutrophils that release proteolytic enzymes to clear debris

63
Q

what do polypeptide messenger molecules do?

A

bind to specific membrane receptors on target cells to stimulate transcription of genes that may be silent in resting cells

64
Q

how do GF promote cell proliferation?

A

recruit G0 cells into the cell cycle (mitogenic)

65
Q

what else go GF do in wound healing?

A

influence other cell functions like cell differentiation, chemotaxis, angiogenesis

66
Q

what is granulation tissue?

A

pink, soft granular appearance on surface of wounds

67
Q

how much granulation tissue is formed?

A

depends on size of defect and amount of inflammation

68
Q

what forms granulation tissue.

A

proliferation of fibroblasts and vascular endothelial cells in the first 24-72 hours

69
Q

when is granulation tissue maximal?

A

5-7 days, apparent at 3-5 days

70
Q

what is the histology of granulation tissue?

A

blood vessel formation, fibroblast proliferation, edema, macrophages mostly, other inflammatory cells

71
Q

when is collagen synthesis by fibroblasts apparent?

A

days 3-5, continues for several weeks

72
Q

describe what new vessels are like in angiogenesis?

A

are immature and have leaky interendothelial junctions, allows exudate to form, and makes granuation tissue edematous

73
Q

where do new blood vessels originate

A

in part from budding of preexisting blood vessels that are within the area of repair

74
Q

when growth factors are involved in angiogenesis?

A

VEGF and FGF

75
Q

what does notch signaling do in angiogenesis

A

regulates sprouting/branching of new blood vessels

76
Q

how does ECM help in angiogenesis

A

provides scaffolding for vessels and interacts with endothelial cells integin receptors

77
Q

what cell replaces neutrophils in 48-96hours

A

macrophages

78
Q

what is M1

A

classically activated macrophages that secrete mediators of inflammation to clear debris, fibrin and other foreign material

79
Q

what is M2

A

alternatively activated macrophages that promote angiogenesis, activate fibroblasts, and stimulate collagen synthesis

80
Q

how do macrophages assist in debridement and removal of injured tissue and debris

A

phagocytosis, collagenase, elastase

81
Q

how do macrophages have antimicrobial activity

A

secrete nitric acid and ROS

82
Q

how do macrophages help with chemotaxis and proliferation of fibroblasts and keratinocytes

A

secrete PDGF, TGFbeta, TNF, IL-1, KGF-7

83
Q

how do macrophages help with angiogenesis

A

secrete VEGF, FGF-2, and PDGF

84
Q

how do macrophages help with deposition and remodeling of ECM

A

secrete TGFbeta, PDGF, TNF, OPN IL-1, collagenase, and MMPs

85
Q

what is the most important fibrogenic agent?

A

TGFbeta

86
Q

what does TGFbeta do

A

causes: 1. fibroblast migration and proliferation 2. increased synthesis of collagen and fibronectin 3. decreased degradation of ECM by MMP

87
Q

what does the provisional matrix have at first?

A

fibrin, plasma, fibronectin and type III collagen

88
Q

what replaces the type III collagen as wound healing progresses?

A

type I collagen

89
Q

when does epithelialization occur in cutaneous wounds?

A

24-48hours

90
Q

what is epithelialization

A

cells move from the wound’s edge along the cut margins of the dermis and deposit basement membrane as they move, then epithelial cells meet in the midline beneath the scab.

91
Q

what do macrophages do in epithelialization

A

stimulate fibroblasts to produce FGF-7 (keratinocyte GF) and IL-6, enhancing keratinocyte migration and proliferation along with other growth factors

92
Q

what is the most important cytokine for the synthesis and deposition of connective tissue proteins?

A

TGFbeta

93
Q

what is tissue remodeling, what does it involve

A

replacement of granulation tissue with scar tissue, involves both synthesis and degradation of ECM components by MMP

94
Q

what are MMPs dependent on

A

zinc

95
Q

what does a mature scar look like

A
  1. amount of collagen and ECM proteins increases 2. number of fibroblasts and vascularity decreases
96
Q

what does a fully mature scar have

A

practically avascular, has very few cells, no dermal appendages (hair), and has dense collagen

97
Q

what does granulation tissue have that fully mature scars do not

A

numerous blood vessels, edema and loose ECM containing occasional inflammatory cells, minimal mature collagen

98
Q

how long does granulation tissue/healing

A

3-7days

99
Q

what is healing by first intention

A

cutaneous wound healing with wounds with opposing edges like healing of clean, uninfected surgical incision or knife wound where the edges are nicely approximated (sutures, staples)

100
Q

what is healing by second intention

A

cutaneous wound healing with wounds that have separated edges, have more extensive loss of cells and tissue.

101
Q

how does a scalpel blade impact wounds

A

injures a limited number of epidermal cells, injures the underlying connective tissue

102
Q

what occurs within 24 hours of healing by first intention?

A

incisional space immediately fills with clotted blood. cellular evidence of acute inflammation appears within 24hours == neutrophils

103
Q

when does chronic inflammatory response replace acute inflammatory response?

A

by day 3 of wound healing macrophages

104
Q

when does granulation tissue begin forming

A

3 days

105
Q

why does granulation tissue begin formin

A

growth factors secreted by platelets, macrophages, and endothelial cells

106
Q

what do GF incude?

A

regeneration of basal cells of the epidermis

107
Q

when has granulation tissue filled the incisional space>

A

day 5

108
Q

what occurs in the 2nd week of healing by first intention

A

collagen accumulates, leukocytes, edema and increased vascularity begin to disappear

109
Q

what occurs by the end of the 1st month during healing by first intention

A

the connective tissue scar is formed and the epidermis is fully regenerated

110
Q

when does tensile strength of the scar plateau?

A

3 months

111
Q

what is wound contraction unique to?

A

healing by second intention

112
Q

what is different about healing by second intention

A
  1. inflammation reaction is moire intense
  2. much larger amount of granulation tissue
  3. wound contraction by myofibroblasts
  4. substantial scar formation
113
Q

what causes wound contraction?

A

myofibroblasts

114
Q

describe wound strength when sutures are removed after 1 week

A

wound strength is 10% of unwounded skin

115
Q

what systemic factor retards wound healing

A

diabetes

116
Q

what occurs by 3 months of wound healing

A

tensile strength plateaus to 70-80% may never regain 100%

117
Q

local factors of decreased wound healing

A

blood supply

denervation

local infection

foreign body

hematoma

mechanical stress

necrotic tissue

protection

surgical techniques

type of tissue

118
Q

systemic factors that slow wound healing

A

age

anemia

drugs

genetic disorders

malnutrition

obesity

systemic infection

diabetes

temp

trauma

uremia

vitamin C deficiency

trace metal deficiency

119
Q

what are hypertrophic scars

A

raised, red, shiny scars that do not extend beyond the original wound site

120
Q

what causes hypertrophic scars

A

excess fibroblast activity and collagen deposition

121
Q

what are keloids

A

scar grows beyond initial wound site, could grow indefinitely and aggressively and produce tumor like scars

122
Q

what causes keloids

A

excess production of type III collagen

123
Q

what could be a predisposition in keloids

A

more common in African Americans, commonly affects earlobes, face, neck, sternum, forearms

MFMII (29 decks)

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