MSK growth, injury and repair Flashcards

1
Q

Decsribe cortical bone

A
○ Diaphysis
○ Resists
- Bending
- Torsion
○ Laid down circumferentially
○ Less biologically active
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2
Q

Describe cancellous bone

A
○ Metaphysis
○ Resists/absorbs
- compression
○ Site of  longitudinal growth (physis)
○ Very biologically active
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3
Q

What is a fracture?

A

○ Break in structural continuity of bone
○ May be a crack, break, split, crumpling, buckle
○ ( # = shorthand sign for a fracture )

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4
Q

Why do bones fail?

A
○ High energy transfer in normal bones
-Takes a lot
○ Repetitive stress in normal bones
- Stress fracture
○ Low energy transfer in abnormal bones
- Osteoporosis
- Osteomalacia, metastatic tumour
			§ Other bone disorders
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5
Q

What haens in a fracture

A
○ Mechanical and structural failure of bone
○ Disruption of blood supply
○ Regenerative process
- No scar
- Four stages
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6
Q

What is strain and how does it affect healing?

A

□ Degree of instability is best expressed as magnitude of strain (% change of initial dimension)
□ If strain is too low mechanical induction of tissue differentiation fails
□ Too high and healing process does not progress to bone formation

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7
Q

What happens in stage 1 of bone healing?

A
  • Begins immediately after fracture
  • Hematoma and fibrin clot
  • Platelets, PMN’s, Neutrophils, Monocytes, Macrophages
  • Massive increase in blood supply in the first few days
  • By products of cell death: lysosomal enzymes
  • Starts off with muscle contraction for initial stability
  • Fibroblasts come in to stabilise the bone
  • Mesenchymal & Osteoprogenitor cells
    □ Transformed endothelial cells from medullary canal and/or periosteum
    □ Osteogenic induction of cells from muscle and soft tissues
  • Angiogenesis
    □ Oxygen gradient required (low)
    □ Macrophages: produce angiogenic factors under hypoxic conditions
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8
Q

How might stage 1 be affetced?

A
□ NSAIDs
® Potential to slow down fracture repair
□ Loss of haematoma 
® Open fractures
® Surgery
□ Extensive tissue damage
® Fewer live cells to grow back in again
® Poor blood supply
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9
Q

What happens in stage 2 of bone healing?

A
  • Begins when pain and swelling subside
  • Lasts until bony fragments are united by cartilage or fibrous tissue
  • Some stability of fracture
  • Angulation can still occur
  • Continued increase in vascularity
    □ Falls off after 2 weeks
    □ Less so than stage 1
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10
Q

How might stage 2 be affected?

A
□ Replace cartilage 
® DMB (Demineralised bone matrix)
□ Jump straight to bone
® Bone graft
® Bone substitutes
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11
Q

What happens in stage 3 of bone healing?

A
  • Fibroblasts convert to osteocyte
  • Conversion of cartilage to woven bone
  • Typical long bone fracture
    □ Endochondral bone formation
    □ Membranous bone formation
  • Increasing rigidity
    □ Secondary bone healing (natural healing)
    □ Obvious callus
  • Primary bone healing is when you use surgery to insert a plate
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12
Q

What happens in stage 4 of bone healing?

A
  • Conversion of woven bone to lamellar bone
  • Medullary canal is reconstituted
  • Bone responds to loading characteristics Wolff’s Law
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13
Q

What are Platelet concentrates?

A

○ “Buffy coat”
○ Platelet-derived growth factor (PDGF)
○ Transforming growth factor- beta (TGF-B)
○ Insulin like growth factor (IGF)
○ Vascular endothelial growth factor (VEGF)
○ Squirt it in in situations where patients have lost their own haematoma to encourage bone repair

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14
Q

hat is autogenous cancellous bone grafts?

A

○ Gold standard
○ The patient’s own bone
○ Osteoconductive: bone regrows through it
○ Osteoinductive: stimulates bone growth
○ Best choice for the majority of bone graft needs

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15
Q

What is allograft bone

A
○ From the bone bank		
○ Cortical
○ Cancellous
○ Fresh
○ Prepared
○ Structural
○ Osteoconductive 
○ Not osteoinductive
○ Creeping substitution
- The osteoclasts work their way through eating the dead bone
- The osteoblasts come in and replace the bone
○ Risk of Disease transmission
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16
Q

What is delayed union of bone?

A

failure to heal in the expected time

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17
Q

What might cause delayed union in bone healing?

A
○ high energy injury
○ distraction (increased osteogenic jumping!)
○ instability
○ infection
○ steroids
○ immune suppressants
○ Diabetics 
○ Smoking (fracture will take 50% longer time to heal if they smoke when they are healing)
○ warfarin
○ NSAID
○ Ciprofloxacin
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18
Q

What might cause non-union failure in bones?

A
○ failure calcification fibrocartilage 
○ instability 
- excessive osteoclasts 
○ abundant callus formation
○ pain + tenderness
○ persistent fracture line
○ sclerosis
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19
Q

What should you do if there is delayed bone healing?

A

○ Consider alternative management

  • Different fixation
  • Dynamisation
  • Bone grafting
20
Q

Describe the anatomy of tendons

A
  • longitudinal arrangement of cells (mostly tenocytes) and fibres (collagen type 1 - triple helix)
  • fascicles of long narrow spiralling collagen bundles
    □ COLLAGEN BUNDLES covered by endotenon,
    □ FASCICLES covered by paratenon,
    □ TENDON covered by epitenon
  • tendon sheath - e.g. flexor tendons in distal palm and fingers
    □ tendons connected to sheath by vincula
    □ synovial lining + fluid (gliding lubrication and nutrition)
    □ thickenings which form strong annular pulleys
21
Q

What is the function of tendons?

A
  • flexible and very strong in tension

- movement is life; immobility reduces water content & glycosaminoglycan concentration and strength

22
Q

Why might a tendon degenerate?

A
- Due to aging 
□ Repetitive injuries
□ Poor blood supplies
□ Occurs from 30s onwards
- e.g. Achilles tendon
□ intrasubstance mucoid degeneration
□ may be swollen, painful, tender; may be asymptomatic
□ May precursor to rupture
- (rheumatoid arthritis considered elsewhere)
23
Q

Why might a tendon be inflammed?

A
  • Inflammation of the synovial lining
  • Can be caused by an inflammatory condition or could be caused by repetitive use
  • e.g. de Quervain’s stenosing tenovaginitis
    □ tendons of EPB + APL passing through common tendon sheath at radial aspect of wrist
    □ swollen, tender, hot, red
    □ positive Finklestein’s test
24
Q

What is enthesioathy?

A
§ Repetitive use injury 
			§ Inflammation at insertion to bone
-Muscle/Tendon
□ Usually at muscle origin rather than tendon insertion - e.g. lateral humeral epicondylitis (tennis elbow) - common extensor origin
- Ligament
□ Plantar Fasciitis
25
Q

What is traction apophysitis and give an examle?

A
  • Apophysis is the growing end of a tendon
  • e.g. Osgood Schlatter’s disease
    □ insertion of patellar tendon into anterior tibial tuberosity
    □ adolescent active boys
    □ Recurrent load
    □ Inflammation
    □ No treatment- it is annoying and discomforting you have to decide whether you want to carry on with the activity or not
26
Q

What is avulsion +/- bone fragment?

A
  • Failure at insertion
  • Load exceeding failure strength while muscle contracting
  • Mallet finger
    □ insertion of extensor tendon into dorsum of base of distal phalanx of finger
    □ forced flexion of extended finger
    -Treatment
    □ Conservative (tends to be just in finger)
    ® Limited application
    ® Retraction tendon
    □ Operative (majority)
    ® Reattachment tendon
    ◊ Through bone
    ®Fixation bone fragmen
27
Q

What is intrasubstance (rupture) tear?

A
  • tear - intrasubstance - e.g. Achilles tendon
    - Load exceeds failure strength
    - Mechanism
    □ pushing off with weight bearing forefoot whilst extending knee joint (53%) e.g. sprint starts or jumping movements
    □ unexpected dorsiflexion of ankle (17%) e.g. slipping into hole
    □ violent dorsiflexion of plantar flexed foot (10%) e.g. fall from height
    - Achilles tendon rupture
    □ “positive” Simmond’s (squeeze) test
    □ palpable tender gap
28
Q

Give an example of a musculotendendinous junction tear

A
  • e.g. medial head of gastrocnemius at musculotendinous junction with Achilles tendon
    □ “plantaris syndrome” (mis-called)
    □ often partial
29
Q

What is the treatment for tendon rupture?

A
○ Conservative
			- Where ends can be opposed
				□ Mobilise (partial rupture) e.g. med lig knee
				□ Splint/cast
			- Where healing will occur 
				□ Not intraarticular
		○ Operative
			- High risk rupture
			- High Activity
			- Ends cannot be opposed
30
Q

What are ligaments?

A

○ Dense bands of collagenous tissue (condensations capsule)
○ Span a joint
○ Anchored to the bone at either end
○ Joint stability through range motion
○ Different portions ligament tensioned at different joint positions
○ Multiple

31
Q

Describe ligament structure

A
○ Collagen fibres (type 1)
		○ Fibroblasts  (communicate)
		○ Sensory fibres
			- Proprioception
			- Stretch
			- Sensory
		○ Vessels (surface)
                ○ Crimping (allow stretch)
32
Q

Compare ligaments and tendons

A
○ Composition
			- Compared to tendons, ligaments have
				□ Lower percentage of collagen 
				□ Higher percentage of proteoglycans and water
				□ Less organised collagen fibers
				□ Rounder fibroblasts
33
Q

What happens in ligament rupture?

A
○ Forces exceed strength ligament
			- Expected
			- Unexpected (position/muscle)
			- Rate load
		○ Complete vs incomplete
		○ Stability joint?
		○ Proprioception loss?
34
Q

How do tendons heal?

A

○ Haemorrhage
- Blood clot
- resorbed
- Replaced with a heavy cellular infiltrate.
- hypertrophic vascular response
○ Proliferative phase
- production of “scar tissue“
- disorganised collagenous connective tissue
○ Remodelling.
- Matrix becomes more ligament like
- Major differences in composition, architecture and function persist.
○ Will never be completely normal again
- There will always be a scar

35
Q

How is a tendon injury treated?

A
○ Conservative
			- Partial
			- No instability
			- Poor candidate surgery
		○ Operative
			- Instability
			- Expectation (sportsmen)
			- Compulsory (multiple)
			- Repair
				□ Direct
				□ Augmentation
				□ Replacement
36
Q

What happens in compression (give examples)

A
○ Entrapment
		○ Classical conditions
			- Carpal tunnel syndrome
				□ Median nerve at wrist
		○ Sciatica
			- Spinal root by intervertebral disc
		○ Morton’s neuroma 
			- (digital nerve in 2nd or 3rd web space of forefoot)
37
Q

What is neuropraxia?

A
  • Caused by trauma
  • nerve in continuity
  • stretched (8% will damage microcirculation) or bruised
  • reversible conduction block - local ischaemia and demyelination
  • Nerve fibers are still intact so there is only temporary ischaemia and demyelination
  • prognosis good (weeks or months)
38
Q

What is axonotmesis?

A
  • Caused by trauma
  • endoneurium intact (tube in continuity), but disruption of axons; more severe injury
  • Still a potential for the axon to re-grow
  • stretched ++ (15% elongation disrupts axons) or crushed or direct blow
  • Wallerian degeneration follows
    □ The axon dies back a bit before it starts to recover by re-growing down the tube
  • prognosis fair
    □ Sensory recovery often better than motor - often not normal but enough to recognise pain, hot & cold, sharp & blunt
39
Q

What is neurotmesis?

A
  • Caused by trauma
  • complete nerve division
    -□ Two ends that are separated
    -□ Try to regrow but cannot find the end point as they are blind
  • laceration or avulsion
  • no recovery unless repaired (by direct suturing or grafting)
  • endoneural tubes disrupted so high chance of “miswiring” during regeneration
  • prognosis poor
    □ Very poor without repair
    □ With repair it is by no means certain
40
Q

What are closed nerve injuries and give examples?

A
○ Associated with nerve injuries in continuity
			- neuropraxis
			- axonotmesis
		○ spontaneous recovery is possible 
		○ surgery indicated after 3 months
			- if no recovery is identified
				□ Clinical
				□ Electromyography
			- Measure growth using Tinel's test
				□ Tap the end of the nerve and you get a shooting pain up the limb until the nerve ends
		○ axonal growth rate (1–3 mm/day) 
		○ Examples
			- Typically stretching of nerve
				□ brachial plexus injuries 
				□ Radial Nerve humeral fracture
41
Q

What happens in open nerve injuries?

A

○ Frequently related to nerve division
- neurotmetic injuries
- E.g. knives /glass
○ Treated with early surgery
○ Distal portion of the nerve undergoes Wallerian degeneration
- Occurs up 2 to 3 weeks after the injury

42
Q

What are the clinical features of a nerve injury?

A

○ Sensory
- dysesthesia (disordered sensation)
□ anaesthetic (numb), hypo- & hyper-aesthetic, paraesthetic (pins & needles)
○ Motor:
- paresis (weakness) or paralysis ± wasting
- dry skin
□ loss of tactile adherence since sudomotor nerve fibres not stimulating sweat glands in skin
○ Reflexes:
- diminished or absent

43
Q

Describe nerve injury healing

A

○ very slow!!
○ starts with initial death of axons distal to site of injury
- Wallerian degeneration
- Then degradation myelin sheath
○ proximal axonal budding occurs after about 4 days
○ regeneration proceeds at rate of about 1 mm/day (or 1 inch/month) - poss. 3-5 mm/day in children
- pain is first modality to return

44
Q

What does the prognosis for nerve injury recovery depend on?

A
  • whether nerve is
    □ “pure”
    ® Only sensory or only motor
    ® Quicker recovery
    □ “mixed”
    ® Both sensory and motor within same nerve
    - how distal the lesion is (proximal worse)
45
Q

How can nerve injuries be monitered?

A

○ Tinel’s sign can monitor recovery
- (tap over site of nerve and paraesthesia will be felt as far distally as regeneration has progressed)
○ Injury can be assessed, and recovery monitored
- by electrophysiological Nerve Conduction Studies

46
Q

How can the nerve be repaired?

A
○ Direct Repair
			- Laceration
			- No loss nerve tissue
			- Microscope/Loupes
			- Bundle repair
			- Growth factors
		○ Nerve Grafting
			- Nerve loss
			- Late repair
				□ (retraction)
				□ Sural nerve
47
Q

What is the surgical timing for different traumatic peripheral nerve injuries?

A

○ Immediate surgery within 3 days for clean and sharp injuries
○ Early surgery within 3 weeks for blunt/contusion injuries
○ Delayed surgery, performed 3 months after injury, for closed injuries