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basic oral and dental care > symposium on wound healing > Flashcards

symposium on wound healing Flashcards

1
Q

Why is wound healing important?

A 
Essential 
Trauma, injury, surgery
Most commonly skin
£180M to £2B per year to NHS
Research ongoing
Cosmetic Industry
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2
Q

What is healing?

A

Follows tissue damage
Attempts to restore integrity to an injured tissue
Over overlaps the inflammatory process

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3
Q

What does resolution mean?

A

Return to normal

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4
Q

What does regeneration mean?

A

Lost tissue replaced by same type to restore tissue

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5
Q

What does repair mean?

A

Tissue lost is replaced by fibrous scar

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6
Q

What determines whether tissue will be regenerate or repair?

A
  1. Cell type involved-
    ~labile- continual cell division eg. Liver
    ~stable- infreq cell division but can increase eg. Muscle
    ~permanent- no cell division possible eg. Nerve
  2. Tissue architecture-
    ~simple
    ~complex
  3. Amount of tissue lost-
    ~small
    ~large- esp if basement membrane/ECM lost
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7
Q

What does the repair process involve?

A

The formation of a fibrous scar via granulation tissue
~endothelial cells and fibroblasts at edges
~these migrate into area forming loose c. tissue- granulation tissue
~increase in blood vessels and collagen
~vascularity decreases and scar formed

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8
Q

What is granulation tissue?

A 
Named due to appearance in skin
Cells in repair process-
~macrophages (phagocytosis and secretion)
~fibroblasts (collagen and other tissue support)
~endothelial cells (nutrition)
Chronic inflammation is concurrent
Often covered with fibrin slough
Not to be confused w granuloma
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9
Q

What does granulation tissue look like histologically?

A

Fibroblasts- spindle shaped
Macrophages- larger, pale stained
Endothelial cells- blood vessels

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10
Q

How does the appearance of granulation tissue change?

A

3 layers- like a trifle

Top layer- fibrin slough and acute inflammatory cells (neutrophils)
Middle layer- granulation tissue, mainly macrophages and endothelial cells- blood vessels
Bottom layer- more mature granulation tissue, more fibroblasts

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11
Q

What does normal skin look like?

A

3 layers

Top layer- epidermis- keratinocytes
Middle layer- dermis- fibroblast and supporting layer
Bottom layer- hypodermis- fatty subcutaneous layer

However on top of all this- dead cells

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12
Q

What are the phases of wound healing?

A

Haemostasis
Inflammation
Proliferation
Remodelling

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13
Q

What is haemostasis?

A

Vessel rupture- bleeding

Coagulation cascade activated

Vasoconstriction- 5-10mins due to serotonin, adrenaline etc

Blood components (esp platelets) come into contact w exposed ECM to form thrombus (fibrin and fibrinogen glue wound together)

Cytokines and growth factors released from platelets (PDGF and TGF- beta) which act as chemo-attractants

Vasodilation

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14
Q

What is PDGF?

A

Platelet derived growth factors

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15
Q

What is TGF-beta?

A

Transforming growth factor- beta

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16
Q

What is inflammation?

A

Neutrophils- recruited from circulation (by PDGF etc), remove bacteria and foreign material by phagocytosis and enzymes, short lived (2 days)

Macrophages- recruited as monocytes or already resident, phagocytose remaining debris

Both further secrete cytokines and growth factors (cascade)

17
Q

What is proliferation?

A

Granulation tissue forms

Fibroblasts proliferate, migrate and become myofibroblasts which synthesise matrix proteins (eg. Type III collagen)
Then proliferation and migration of cells over wound bed

Keratinocytes- re-epithelialisation and angiogenesis (new blood vessel formation)

18
Q

What is remodelling?

A

2 weeks onwards
Provisional matrix remodelled
Reduction in cell and capillary density so less red
Proteases (collagenases) required
Wound contraction
Type III collagen (quickly made) replaced by stronger bundles of Type I
Strength relies on cross-linked Type I aided by Vit C (activates myofibroblasts to produce)
7-10 days- wound=10% strength
2-3 months- wound=70-80%

19
Q

Why is wound healing considered dynamic?

A

The phases overlap

20
Q

What is primary intention?

A

Wound edged are apposed (brought together) and held in place by mechanical means eg. Suture

21
Q

What is the secondary intention?

A

Wound left open, edges come together naturally by means of granulation and contraction

22
Q

When should you use primary/secondary intention?

A

Primary- wound clean, straight line, little loss of tissue, wound edges well approximated, rapid, minimal scarring

Secondary- considerable tissue loss, natural healing, longer, more scarring

23
Q

How does bone healing work?

A 
Fracture
~tissue formation- calus (like granulation tissue)
~cells grow into this
~becomes mature and solidifies
~inflam, proliferation, remodelling
Primary intention
24
Q

How does socket healing work?

A

Same principles to bone healing w/o calus
Secondary intention unless underlying haematalogical issues
4 days- residual clot
8 days- granulation tissue
52 days- bony infill
Osteoclast resorption to take away excess

25
Q

What are local factors influencing wound healing?

A 
Type, size and location of wound
Movement within wound
Infection
Presence of foreign/necrotic material
Irradiation
Poor blood supply
26
Q

What are systemic factors influencing wound healing?

A

Age
Nutrition (Vit C, Zinc)
Systemic disease- circulatory, diabetes etc
Drugs, esp steroids

27
Q

How is the healing process controlled?

A

Epithelial cells-
Growth (PGDF, KGF, EGF etc)
Migration (contact inhibition)

Fibroblasts-
Activation to myof. (TGF-beta)
Proliferation (PGDF, FGF etc)
Migration (fibronectin, chemo-attractants)

Cell-ECM interactions (integrins)

Angiogenesis (macrophages secrete proangiogenic factor esp low in O2)

Neutrophils and macrophages (chemotaxis)

28
Q

What is dysregulated healing?

A

Similar to cancer

Keratinocyte proliferation and migration
Fibroblast activation
Angiogenesis
Proteases upregulated
Integrin expression altered

However, this is reversible whereas cancer is irreversible

29
Q

What is a scar?

A

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

30
Q

What is a burn?

A

Tissue melts

Only repair process

31
Q

What is a hypertrophic scar?

A

High risk in darker skin

Tissue sticks out of wound

32
Q

What is a contracture?

A

Muscle/tendon shortening
Muscle not replaced
Tissue filled w fibroblasts so when healed, wound contracts
Very deep wound

33
Q

What is a keloid scar?

A

Gross growth of tissue
Thick bundles of collagen w high levels of Type III
Abnormal cross-linkage and high turnover
Altered cytokine levels

34
Q

What is a neuroma?

A

Eg. Wisdom tooth removal

Nerve bruised/traumatised
Scar tissue forms around nerve
Affects nerve transmission and induction
Potential tingling

Removing scar tissue may return to normal

35
Q

What is a chronic wound?

A 
Stuck in inflam phase
Increased proteases (destroy ECM)
Reduced growth factors (PDGF, FGF, EGF)
Underlying disease (eg. Venous insufficiency, diabetes)
Infection
Necrosis
36
Q

How do oral wounds compare to skin wounds?

A

Oral- heal faster, less inflam

Due to saliva (skin wounds heal faster where moist) (contains peptides and proteins [EGF, VEGF, FGF])
Earlier influx of neutrophils/macrophages
Fibroblasts are heterogenous- produce more KGF, increased ability to contract and more foetal like (younger phenotype- longer telomeres due to more telomerase [protects chromosomes from degradation when cell divides])

Increased keratinocyte proliferation and migration so faster re-epithelialisation

More proteinases to contribute to remodelling

37
Q

What are aids to wound healing?

A

Basic wound care

Assisted wound care- dressings, hyperbaric oxygen, alternative therapies (Maggots and leeches)

38
Q

What are alternative therapies?

A

Maggots- eat dead tissue which is stopping wound from healing

Leeches- encourages circulation, their saliva contains nitric oxide, when they suck blood, they inject the saliva

basic oral and dental care (49 decks)

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