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Craniofacial and Tooth Biology > 26. Repair and Regeneration > Flashcards

26. Repair and Regeneration Flashcards

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1
Q

Why do we need to understand repair?

A
  • normal oral tissue development and function helps us understand abnormal control and disease response
  • cells, genes and molecules control response to development, structure and function AND ageing, injury and disease so repair can be a treatment between
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2
Q

What is regenerative medicine?

A
  • to develop novel therapies to repair and regenerate tissues and organs
  • which have been damaged by injury, ageing, cancer, disease
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3
Q

Define ‘repair’

A

restoration of tissue function but with impaired tissue architecture

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4
Q

Define ‘regeneration’

A
  • complete restoration of tissue architecture and function
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5
Q

Problem with regenerative medicine

A
  • full regenerative capacity is lost in humans
  • current use of organ transplants and artificial devices is limited to incomplete restoration of original tissue function
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6
Q

Solutions to improve regenerative medicine

A
  • cellular therapy (using exogenous stem/progenitor cells or stimulating own body’s stem cells to repair defective tissue)
  • tissue engineering (biomaterials)
  • biomedical engineering
  • gene therapy
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7
Q

Aims for regenerative medicine

A
  • better clinical outcomes (shorter rehab, better QOL)
  • improved health-related cost-effectiveness
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8
Q

List stages of tissue regeneration

A
  • morphallaxis
  • epimorphosis
  • compensatory regulation
  • stem cell-mediated regeneration
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9
Q

What happens in morphallaxis?

A
  • repatterning of existing tissue with little new growth
  • for example Hydra (freshwater polyp, 0.5cm, sticks to rocks, filter feeder, asexual reproduction)
  • all cells are constantly dividing and migrating and eventually shed at head or foot region - asexual reproduction budding at 2/3 body axis
  • morphogen gradients specifying head and foot - each piece of cut hydra will form a small hydra with head and foot
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10
Q

What happens in epimorphosis?

A
  • dedifferentiation of cells at wound site
  • formation of undifferentiated cells that redifferentiate to form lost structure
  • for example planarian flatworms, amphibian limbs
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11
Q

What happens in compensatory regulation?

A
  • differentiated cells divide
  • they maintain their identity and specialised functions
  • e.g liver regeneration
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12
Q

Explain how the liver regenerates using compensatory regulation

A
  • sensing of liver damage by increase of gut-derived LPS in blood
  • activates Kupffer and stellate cells
  • paracrine secretion of mediators stimulates hepatocyte cell proliferation
  • size of liver restored 1 week after surgery (mice)
  • chronic injury leads to liver fibrosis
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13
Q

What happens in stem cell-mediated regeneration?

A
  • replacement of lost tissue by stem cell activity
    e.g
  • hair growth from follicular stem cells in hair bulge - concept of ‘niche’
  • continuous blood cell replacement by haematopoietic stem cells
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14
Q

What are stem cells?

A
  • unspecialised, undifferentiated cells that can self-renew and can differentiate into other cell types
  • for development and regeneration
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15
Q

Totipotent stem cells can …

A
  • form all cell types
    e.g fertilised eggs
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16
Q

Pluripotent stem cells can form …

A
  • all cell types of the three embryonic germ layers
  • e.g embryonic stem cells
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17
Q

Multipotent stem cells can form …

A
  • many cell types
  • e.g haematopoietic stem cells or mesenchymal stem cells
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18
Q

Oligopotent stem cells can form ..

A
  • few cell types
  • e.g myeloid precursors that form five blood cell types
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19
Q

Quadripotent stem cells form …

A

4 cell types
e.g mesenchymal progenitor cells (cartilage, bone, stroma, fat)

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20
Q

Unipotent stem cells can form …

A

one cell type
e.g mast cell precursors

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21
Q

Problem with stem cells in regenerative medicine

A
  • stem cell biology not fully understood
  • e.g small number, quiescence, niche, identification, genetic control
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22
Q

What’s a potential use of stem cells that is crucial to dentistry?

A

for missing teeth

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23
Q

Steps of wound healing in oral mucosa or after tooth extraction

A
  • haemostasis
  • inflammatory response
  • epithelial and connective tissue repair
24
Q

Repair of periodontal tissues is …

A
  • more complex
  • restoration of funtional unit
25
Q

Why do we need a wound healing system in oral mucosa?

A
  • protective and barrier function of oral mucosa
  • effective repair system to re-establish function after injury (physical, chemical, radiation, microorganisms)
26
Q

Explain haemostasis in wound healing

A
  • essentially the cessation of blood loss
  • happens in minutes
  • vascular damage causes hemorrhaging into tissue defect and results in forming of a blood clot (coagulation - fibrin deposition and aggregation of platelets)
  • forms barrier that unites wound margins and protects exposed tissue
  • provides provisional scaffold for subsequent colonisation by reparative cells
27
Q

What happens in the inflammatory response in wound healing?

A
  • microorganisms and toxins have likely entered and induce acute inflammatory response
  • leakage of plasma proteins (vasodilation and increased vascular permeability) and platelet-derived cytokines and growth factors (TGF-beta, PDGF) stimulate leukocyte migration towards wound (by chemotaxis)
  • neutrophils appear within hours, become activated and kill bacteria (destroy damaged tissue)
  • macrophages and lymphocytes appear after 24 hrs and mediate clearance of cell debris (phagocytosis) and humoral immune response
  • mast cells promote inflammation and vascular changes
28
Q

Explain reparative phase/epithelial response in wound healing

A
  • mobilisation of epithelial cells (widening of intercellular spaces) within 24 hours
  • increased basal cell proliferation and epithelial cells adjacent to wound margin migrate beneath blood clot (24-48 hrs)
  • deposition of basal lamina components facilitates cell movement and epithelial sheet formation
  • migration stops when cells reach opposing wound margin and increased cell proliferation and differentiation leads to stratification and re-establishment of normal epithelial sheet
29
Q

Explain reparative phase/connective tissue response in wound healing

A
  • fibroblasts proliferate and migrate into wounded connective tissue within 24-48 hrs
  • they deposit disorganised collagen fibres, regulated by TBF-beta
  • formation of new blood capillaries from existing vessels (angiogenesis) at wound margin (regulated by VEGF, FGF, TGF-beta)
  • ECM (fibronectin, laminin, collagen) formed by new fibroblasts provides scaffold for forming blood vessels - provides nutrients and oxygen, access to inflammatory cells, stimulates connective tissue formation (endothelial cytokines/growth factors)
  • increased collagen deposition between day 5-20 but reduced tensile strength - initial scar tissue formation but removal of scar tissue by tissue remodelling within 150 days
30
Q

Scar tissue formation in wound healing

A
  • quick restoration of tissue integrity required to prevent damage to whole organism
  • trade-off with inflammatory response - control of infection allows quick wound healing but produces scar tissue of inferior quality
  • in skin, deposition of disorganised collagen fibres leads to immobilisation and rigidity at repair site
  • in oral mucosa, remodelling of scar tissue (mainly collagen fibre remodelling and cross-linking) prevents scar tissue formation
31
Q

How does foetal wound healing differ?

A
  • repair of skin injuries doesn’t involve inflammatory response and results in scar-less healing in foetal development
  • fibroblasts of oral mucosa may resemble these foetal fibroblasts
32
Q

Explain wound contraction in wound healing

A
  • first fibroblasts entering the wound site are contractile myofibroblasts
  • different from connective tissue fibroblasts (pericyte origin?)
  • form connections with each other and align with collagen fibrils
  • cell contraction draws edges of wound together
33
Q

Wound healing after tooth extraction compares to that of oral mucosa except for …

A
  • substantial loss of tissue in extraction
  • dislodgement of blood clot (‘dry socket’) causes painful bone infection
34
Q

Complete epithelialsation of socket occurs in …
What happens then?

A
  • 10 days
  • instead of fibroblasts, osteogenic precursor cells migrate into blood clot
  • after day 10, osteoblasts differentiate and form bone
  • extraction site is filled with bone and indistinguishable after 10-12 weeks
35
Q

How does wound healing at the dento-gingival junction differ to in mucosa?

A
  • day 3, colonisation of gingival wound by epithelial cells and formation of junctional epithelium
  • cells express REE-marker ODAM (odontogenic ameloblast-associated protein)
  • day 5-7, expansion and down-growth of junctional epithelium
  • re-establishment of dento-gingival junction (high regenerative capacity in rodents especially)
36
Q

How does repair of periodontal tissue occur?

A
  • restoration of functional unit like cementum, PDL, alveolar bone, gingiva
  • different to oral mucosa as PDL fibres must insert to cementum and bone
  • coordinated repair needs complex regulation at cellular and molecular level
  • normal remodelling has no inflammation e.g tooth movements
  • in injury, inflammatory response required to combat infection and initiate repair
  • chronic inflammation inhibits stem cell activation, cell recruitment, cell proliferation, differentiation
37
Q

Fibroblasts in periodontal repair

A
  • key to remodelling collagen fibres
  • mesenchymal progenitor cells in PDL or perivascular and endosteal fibroblasts
38
Q

Endothelial cells in periodontal repair

A

form new blood vessels from existing vessels (angiogenesis)

39
Q

Cementoblasts cells in periodontal repair

A

perivascular and endosteal fibroblasts
and/or
rest of Malassez

40
Q

Osteoblasts cells in periodontal repair

A

mesenchymal progenitor cells in endosteum or periosteum

41
Q

Molecular approaches to periodontal repair

A
  • application of growth factor cocktails and ECM molecules to root surfaces
  • like EGF, FGF, IGF, PDGF, TBG-beta for PDL and cementum
  • BMP for bone and cementum
  • fibronectin but clinical efficiency is controversial
  • emdogain as enamel matrix proteins stimulate periodontal repair
42
Q

Can we get complete regeneration of enamel?

A
  • no
  • as ameloblasts are lost at the end of development
  • can be remineralised by calcium, phosphate and fluoride ions in saliva
  • acts as a physico-chemical repair process
43
Q

What is the dynamic process of an early caries lesion?

A
  • translucent zone - demineralisation
  • dark zones - remineralisation
  • body of the legion - enamel destruction
  • surface zone - intact enamel (remineralisation caused by ion precipitation from saliva)
44
Q

When is an early caries lesion reversible?

A
  • if surface enamel remains intact and acid producing bacteria are removed
45
Q

Dentine is a living tissue so the reparative process depends on …

A
  • extent and duration of stimulus e.g attrition/cavity prep
  • structural variations in dentine e.g open or accluded dentinal tubules
  • age of tooth - smaller pulp chamber, diminished blood/nerve supply
46
Q

What happens to repair dentine in a slow onset, prolonged insult?
Examples of this

A
  • for example in attrition, early caries
  • occlusion of dentinal tubules (collagen plug or sclerotic dentine)
  • reactionary dentine formed by existing odontoblasts (slow, tubular)
47
Q

What happens to repair dentine in a rapid onset, severe insult?
Examples of this

A

e.g in late stage caries or cavity prep
- reactionary dentine if odontoblasts survive (slow, tubular)
- reparative dentine form by newly differentiated odontoblast-like cells if originals have died (rapid, amorphous, less collagen)
- classic wound healing response - inflammation and repair but no epithelial response

48
Q

Most accessible sources of stem cells for dental regeneration

A
  • primary teeth
  • 3rd molars
49
Q

List sources of dental stem cells

A
  • primary teeth and 3rd molars
  • dental pulp (DPSC)
  • dental pulp from exfoliated primary teeth (SHED)
  • dental follicle of unerupted teeth
  • periodontal ligament (PDLSC)
  • tooth germs
50
Q

Other sources of stem cells in body

A
  • umbilical cord blood
  • bone marrow
  • skin
  • adipose tissue
51
Q

What animal tooth is used as a model for studying tooth regeneration?

A

mouse lower incisor

52
Q

How can you bioengineer replacement teeth?

A
  • add epithelial and mesenchymal cells to a collagen gel to form a high-density reconstituted tooth germ
  • organ culture for 5-7days
  • extraction and wound healing
  • transplantation of the tooth germ, grows tooth
53
Q

How could tissue engineering help dentistry?

A
  • biodegradable scaffolds for cell seeding - 3D printing
  • bioengineering, material sciences and nanotechnology - materials with novel properties, implants with bioactive surfaces allowing for better tissue integration
  • gene therapy - ex and in vivo (CRISPR/Cas9 genome editing tools with RNAi, novel delivery systems)
54
Q

Impact of tissue engineering on dentistry

A
  • conventional treatments like amalgam, composites, metallic implants, tissue grafts
  • have limitations like non-biological, immune rejection, pathogen transmission, lack of remodelling with recipient tissue, donor site morbidity
  • novel approaches like engineering of precise tissue shape using biodegradable scaffolds onto which stem cells can grow and re-establish morphology and function
  • need more translation of basic science findings like clinical trials
55
Q

What did Mao say about this?

A

‘craniofacial tissue engineering is likely to be realised in the foreseeable future and represents an opportunity that dentistry cannot afford to miss’

Craniofacial and Tooth Biology (25 decks)

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