Transcript Tendon

Shane Hanzlik, MD
2014
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Anatomy
Biomechanics
Injury patterns
Mechanisms of healing
Tendinopathy
Tendon: Basic Function
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Attaches muscle to bone
 Transmits force generated from muscle to
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bone  moves bone/joint
Allows muscle to be at a distance from its point
of action
Allows muscle pull to travel through narrow
areas of body
Allows direction of pull to be changed with a
pulley
Distribute single muscle load to multiple points
Provides proprioceptive feedback
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Complex composite material consisting of
collagen fibrils embedded in a matrix of
proteoglycans
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Water (70% wet weight)
 Changes in water content after injury/inflammation can change the
viscoelastic properties of tendon
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Collagen (86% dry weight)
 Type I (95%)
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Proteoglycans (<5% dry weight)
 Maintain hydration of the tendon
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Glycoproteins
 Tenasin-C: contributes to matrix structure
 Upregulated in tendinopathy
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Tenocytes
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Unsheathed (Paratenon-covered)
 Loose areolar connective tissue
 Majority of tendons (move in a straight line)
 Ex. Patellar tendon, Achilles
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Sheathed
 Tendons that bend sharply
 Sheath acts as a pulley and directs tendon path
 Sliding is assisted by synovial fluid
 Ex. Flexor Tendons
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Paratenon-covered tendons (I.e. Achilles)
 Vessels from surrounding tissue penetrate at any point
along tendon
 Perimysium
 Paratenon
 Periosteal insertion
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Tendons in sheaths (i.e. hand):
 Synovial diffusion
 Osseous insertions
 Proximal mesotenon via vinculae
1.
Fibrous (indirect)
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2.
Metaphysis and diaphysis
Collagen fibers insert into periosteum during
growth
Ex. Pes Anserine
Fibrocartilagenous (direct)
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Epiphysis and apophysis
4 transitional tissues
Ex. RTC
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No nerve fibers within tendon body
Epi- and peritenon contain nerve endings
(sensory)
Golgi tendon organs at musculo-tendinous
junction (proprioceptive)
 Collagen fibrils insert into recesses formed by
myocyte processes
 Weakest point of muscle-tendon unit
 Eccentric contraction
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Enormous tensile strength
Viscoelastic properties
 creep
 stress relaxation
 preconditioning
• Affected by:
– anatomic location
– Stretching and immobilisation
– age
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Load/Elongation Curve
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Direct
 Sharp
 Blunt
Indirect
 Avulsion
 Musculo-tendinous junction tear
▪ Normal tendon can withstand muscle
force
 Weakest link in the chain is MTJ
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 Mid-substance (occurs in degen tendon)
Attrition – inflammatory or not
 3 phases
1. Inflammatory
2. Fibroblastic/Proliferative
3. Remodeling
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Immediate
 blood
 inflammatory products
 fibrin
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1st week
 proliferating tissue from paratenon invade the gap b/w
tendon stumps and fills it with undifferentiated and
disorganized fibroblasts
 disorganised fibroblasts
Granulation
 capillary buds
tissue
 collagen synthesis
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After 2 weeks
 Stumps fused by fibrous bridge
 Fibroblast proliferation and
vascular proliferation in stumps
 Fibrovascular tissue from
paratenon blends with epitenon to
form ‘tendon callus’
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3-4 weeks
 re-orientation of fibrils
 organisation of collagen
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Beyond
 tensile properties increase
 remodelling and further organisation
 minimal histological difference by 20 weeks
 months to regain full strength
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Same 3 phases of healing
2 sources of healing
1. Extrinsic – granulation tissue from tendon
sheath
2. Intrisic – cell invasion from tendon and epitenon
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Mobilized tendons:
 controlled passive motion
 intrinsic response from epitenon predominates
• Immobilized tendons:
– ingrowth of connective
tissue from sheath
– cellular proliferation of
endotenon
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Tendinopathy: Overuse injury of tendons with
resulting pathologic changes in the tendon
 Tendinosis: Degenerative pathologic condition
with lack of inflammatory changes
▪ Much more common
 Tendonitis: Pathologic condition involving
inflammatory changes
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Histologic studies of surgical specimens in
patients with tendinosis show absent or
minimal inflammation
 Hypercellularity
 Loss of tightly bundled collagen appearance
 Increase proteoglycan content
 neovascularization
Rees, J. “Management of Tendinopathy.” AJSM 2009.
Tendon: Tendinopathy
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CAUSES (THEORIES)
 Mechanical
▪ Overload
 Vascular
▪ Poor blood supply in
watershed makes areas
make tendons prone to
injury
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Modify risk factors
 Training error
 Flexibility issues
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Ice/Compression
Exercise
 Eccentric
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Stretching
 Can inc. elongation capability
of muscle/tendon unit
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Massage
Shockwave therapy
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NSAIDS
 Evidence shows analgesic effect of NSAID
 But may delay healing b/c need inflammatory
phase to heal
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Steroid injection
Autologous RBC injection or PRP
Surgery
 Debridement
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“Supraphysiologic” concentration of platelets
Release of growth factors
 PDGF, TGF-B, VEGF, EGF, HGF, IGF, etc
 Multiple protocols and delivery methods
 Ex: Cascade (MTF, NJ)
▪ 18 mL venous blood in 2 tubes loaded with
anticoagulant and polyester separator gel
▪ Inverted 7 times, centrifuge for 6 minutes at 1,100 RCF.
▪ Transfer to glass tube with CaCl, invert 7 times,
centrifuge for 15 min at 1450 RCF.
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Results are inconclusive at best
 Snyder showed a 50% reduction in RTC repair re-
tears on MRI with PRP for tears < 3 cm
 Rodeo showed no change in cuff re-tear rate on
ultrasound (same PRP product).
 Charousset showed no benefit in large or massive
cuff tears using GPS III platelet conc. system
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Electromagnetic coil causes shockwaves and
mechanical micro damage and induce a
healing response
Proposed for treatment of tendonitis,
tendinosis, calcific tendonitis.
High energy and Low energy
 3000 shocks, avg energy of 0.21 mJ/mm2
 3 treatments with energy level of 0.08 mJ/mm2
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Wang et al showed significant improvement
in VAS scores and vascularization on US exa
for patellar tendinopathy
Furia showed improved VAS and a trend to
increased return to sports over control
subjects from 1-12 months
No serious complications