Musculoskeletal Growth/Injury and Repair Flashcards
what are ligaments?
dense bands of collagenous tissue that span a joint. they are anchored to bone at both ends
what do ligaments do?
aid joint stability through a range of motion
what are ligaments made from?
type 1 collagen fibres
fibroblasts
what kind of sensory fibres are found in ligaments?
proprioception
stretch
sensory
what allows ligaments to stretch?
crimping
compared to tendons, ligaments have: % collagen, proteoglycans, water, collagen fibres, fibroblasts
less collage
more proteoglycans and water
less organised collagen fibres
rounder fibroblass
when do ligaments rupture?
forces that exceed the strength of the liagment
what determines how much a ligament is ingjured
whether the forcewas expected or not
rate of load
what are the stages of ligament healing?
haemorrhage
proliferative phase
remodelling
healing of ligaments: haemorrhage phase
blood clot
reabsorbed
replaced with a heavy cellular infiltrate
hypertrophic vascular response
healing of ligaments: proliferative phase
production of scar tissue
disorganised collagenous connective tissue
healing of ligaments: remodelling phase
matrix becomes more ligament like
major differences in composition, architecture and function persist
when would you treat ligaments conservatively?
partial
no instability
poor candidate for surgery
when would you treat ligaments operative?
instability
expectation - sportsmen
compulsory- multiple
describe the process of growth and ossification with a diagram
see notes
where is cortical bone found?
diaphysis
where is cancellous bone?
metaphysis
features of cortical bone
resists bending and torsion
laid down circumferentially
less biologically active
features of cancellous bone
resists/absorbs compression
site of longitudinal growth
v biologically active
what are the stages in bone healing?
inflammation
soft callus
hard callus
bone remodelling
stages in bone healing: inflammation
immediately after fracture
haematoma and fibrin clot forms
mesenchymal and osteoprogenitor cells are transformed endothelial cells from medullary canal and/ir periosteum
osteogenic induction of cells from muscle and soft tissues
low oxygen gradient required for angiogenesis
what cells are involved in the inflammatory stage of bone healing?
platelets PMN's neutrophils monocytes macrophages
in bone healing, what are the by products of cell dealth cleared up by?
lysosomal enzymes
what produces angiogenic factors under hypoxic conditions?
macrophages
what factors could alter the first stage in bone healing?
NSAIDs
loss of haematoma (open fractures, surgery)
extensive tissue damage resulting in poor blood supply
what platelet concentrates are implicated in the inflammatory stage of bone healing?
platelet derived growth factor PDGF
transforming growth factor beta TGF-b
insulin like growth factor IGF
vascular endothelial growth factor VEGF
stages in bone healing: soft callus
begins when pain and swelling subside lasts undil bony fragments are united by cartilage or fibrous tissue some stability of the fracture angulation can still occur increased vascularity
what can affect the soft callus formation?
replacing cartilage with demineralised bone matrix
placement of bone grafts
what would the best autogenous cancellous bone graft have?
osteoconductive
osteoinductive
best choice
what is an allograft bone?
cortical cancellous fresh prepared structural osteoconductive not osteoinductive creeping substitution
what risk is there with bone allografts?
disease transmission
stages in bone healing: hard callus
conversion of cartilage to woven bone
in typical long bones there is endochondral and membranous bone formation
increasing rigidity and secondary bone remodelling
can be seen on xray
stages in bone healing: bone remodelling
woven bone converted to lamellar bone
medullary canal reconstituted
Wolff’s law applies
what is delayed union?
when a fracture fails to heal in the expected time
causes of delayed union
- High energy injury
- Distraction results in increased osteogenic jumping
- Instability
- Infection
- Steroids
- Immune suppressants
- Smoking
- Warfarin
- NSAID
- Ciprofloxacin
- Failure of calcification fibrocartilage
- Instability – excessive osteoclasis
- Abundant callus formation
- Pain and tenderness
- Persistent fracture line sclerosis
in delayed union how could you treat it?
different fixation
dynamisation
bone grafting
what is a tendon?
muscle origin from bone muscle belly musculotendinous juntion tendon (? sesamoid bone, ? tendon sheath) tendinous insertion into bone
structure of tendons
longitudinal arragement of cells (tenocytes) and fibres (type 1 collagen)
long narrow spiralling of collagen bundles known as fasicles
what are collagen bundles covered by? (Tendons)
endotenon
what are tendon fascicles covered by?
paratenon
what is a tendon covered with?
epitenon
describe a tendon sheath
Tendons are connected to the sheath by vincula and there is a synovial lining with fluid giving lubrication and nutrition. Thickenings of the tendon sheath form strong annular pulleys. Tendons are flexible structures that are very strong when tensed.
what effect does immobility have on tendons?
reduces water content and glycosaminoglycan concentration and strength
what kind of injuries affect tendons?
degeneration inflammation enthesiopathy traction apophysitis avulsion +/- bone fragment tear - intrasubstance/musculotendinous junction laceration crush ischaemia attrition nodules
injuries to tendons: degenration
intrasubstance mucoid degeneration
may be swollen, painful, tender, may be asymptomatic
?precursors to rupture
what tendon commonly degenerates?
achilles
injuries to tendons: inflammation
de Quervain’s stenosing tenovaginitis
tendons of EPB and APL passing through common tendon sheath at radial aspect of wrist
swollen, tender, hot, red
positive Finklestein’s test
injuries to tendons: enthesiopathy
inflammation at insertion to bone muscle/tendon
usually at muscle origin rather than tendon insertion e.g. lateral humeral epicondylitis (Tennis elbow)
give an example of enthesiopathy in a ligament
plantar fasciitis
injuries to tendons: traction apophysitis
Osgood Schlatter's disease insertion of patellar tendon into anterior tibial tuberosity adolescent active boys recurrent load inflammation
injuries to tendons: avulsion treatment
conservative - limited application, retraction tendon
operative - reattchment tendon through bone, fixation bone fragment
injuries to tendons: intrasubstance rupture
achilles load exceeds failure strength mechanism of rupture: 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 o Treatment ▪ Conservative • Where ends can be opposed o Mobilise (partial rupture) e.g. medial ligament of knee o Splint Figure 5 Pulley System in Digits • Where healing will occur o Not intraarticular ▪ Operative • High risk rerupture • High activity • Ends cannot be opposed
injuries to tendons: tear at musculotendinous junction
medial head of gastrocnemius at musculotendinous junction with achilles
mis called plantaris syndrome
often partial
injuries to tendons: laceration
E.g. finger flexors (FDS and FDP) ▪ Common ▪ Males > females ▪ Young adults ▪ Repair surgically and early but beware old injuries ▪ Technically challenging
describe a peripheral nerve
This is the part of a spinal nerve distal to the roots. They are bundles of nerve fibres that range in diameter from 0.3-22𝜇m. Schwann cells form a thin cytoplasmic tube around the nerves. Larger fibres are found in multi-layered insulating membranes known as myelin sheaths. There are multiple layers of connective tissue surrounding axons.
A peripheral nerve is a highly organised structure comprised of nerve fibres, blood vessels and connective tissue. Axons are coated with endoneurium and grouped into fasicles covered with perineurium and grouped into nerves covered with epineurium.
function of Aa nerve fibres (IA, IB)
large motor axons
muscle stretch
tension sensory axons
function of Ab nerve fibres (II)
touch pressure vibration joint proprioception sensory axons
function of Ay nerve fibres
efferent motor axons
function of Ad nerve fibres (III)
sharp pain
very light touch
temperature
function of B nerve fibres
sympathetic preganglionic motor axons
function of C nerve fibres
dull, aching,burning pain
temperature
types of injury to nerves
compression
trauma
examples of nerve compression injury
o Entrapment
o Carpal tunnel syndrome – median nerve at wrist
o Sciatica – spinal root by IV disc
o Morton’s neuroma – digital neuroma in 2nd or 3rd web space of forefoot
examples of direct nerve trauma
blow
laceration
examples of indirect nerve trauma
avulsion
traction
what can nerve trauma result in?
neurpraxia
axonotmesis
neurotmesis
describe neurapraxia
▪ Nerve in continuity
▪ Stretched (8% will damage microcirculation) or bruised
▪ Revisable conduction block – local ischaemia and demyelination
▪ Prognosis good (weeks or months)
describe axonotmesis
▪ Endoneurium intact (tube in continuity) but disruption of axons; more severe injury
▪ Stretched ++ (15% elongation disrupts axons) or crushed or direct blow
▪ Wallerian degeneration follows
▪ Prognosis fair
• Sensory recovery better than motor
• Often not normal but enough to recognise pain, hot, cold, sharp, blunt
describe neurotmesis
Complete nerve division
▪ Laceration or avulsion
▪ No recovery unless repaired by direct suturing or grafting
▪ Endoneural tubes disrupted so high chance of miswiring during regeneration
▪ Prognosis poor
clinical features of nerve injury
• Sensory features o Dysaethesiae (disordered sensation) ▪ Anaesthetic ▪ Hypo + hyper aesthetic ▪ Paraesthetic • Motor Figure 6 Peripheral Nerve Regeneration Figure 7 Sunderland Grading of Nerve Injury o Paresis (weakness) o Paralysis ± wasting o Dry skin – loss of tactile adherence since sudomotor nerve fibres not stimulating sweat glands in skin • Reflexes o Diminished or absent
healing of nerve injuries
Healing of nerve injuries is very slow. It starts with initial death of axons distal to the site of injury, Wallerian degeneration and then degradation myelin sheath. Proximal axonal budding occurs after about 4 days. Regeneration proceeds at a rate of about 1mm/day (or 1 inch/month), but in children 3-5mm/day is possible. Pain is the first modality to return. Prognosis for recovery depends on whether the nerve is “pure” (only sensory or motor) or “mixed” and how distal the lesion is (proximal is worse).
how can you measure nerve healing?
Tinel’s sign can monitor recovery. Tap over the 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.
describe the rule of 3 for surgical timing in traumatic peripheral nerve injury
- 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, for closed injuries
UMN lesions: strength
increased
UMN lesions: tone
increased
UMN lesions: reflexes
increased
UMN lesions: clonus
present
UMN lesions: babinski
present
UMN lesions: atrophy
absent
LMN lesions: strength
decreased
LMN lesions: tone
decreased
LMN lesions: reflexes
decreased
LMN lesions: clonus
absent
LMN lesions: babinski
absent
LMN lesions: atrophy
present
