Transcript Tendon
Shane Hanzlik, MD
2014
Anatomy
Biomechanics
Injury patterns
Mechanisms of healing
Tendinopathy
Tendon: Basic Function
Attaches muscle to bone
Transmits force generated from muscle to
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
Complex composite material consisting of
collagen fibrils embedded in a matrix of
proteoglycans
Water (70% wet weight)
Changes in water content after injury/inflammation can change the
viscoelastic properties of tendon
Collagen (86% dry weight)
Type I (95%)
Proteoglycans (<5% dry weight)
Maintain hydration of the tendon
Glycoproteins
Tenasin-C: contributes to matrix structure
Upregulated in tendinopathy
Tenocytes
Unsheathed (Paratenon-covered)
Loose areolar connective tissue
Majority of tendons (move in a straight line)
Ex. Patellar tendon, Achilles
Sheathed
Tendons that bend sharply
Sheath acts as a pulley and directs tendon path
Sliding is assisted by synovial fluid
Ex. Flexor Tendons
Paratenon-covered tendons (I.e. Achilles)
Vessels from surrounding tissue penetrate at any point
along tendon
Perimysium
Paratenon
Periosteal insertion
Tendons in sheaths (i.e. hand):
Synovial diffusion
Osseous insertions
Proximal mesotenon via vinculae
1.
Fibrous (indirect)
2.
Metaphysis and diaphysis
Collagen fibers insert into periosteum during
growth
Ex. Pes Anserine
Fibrocartilagenous (direct)
Epiphysis and apophysis
4 transitional tissues
Ex. RTC
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
Enormous tensile strength
Viscoelastic properties
creep
stress relaxation
preconditioning
• Affected by:
– anatomic location
– Stretching and immobilisation
– age
Load/Elongation Curve
Direct
Sharp
Blunt
Indirect
Avulsion
Musculo-tendinous junction tear
▪ Normal tendon can withstand muscle
force
Weakest link in the chain is MTJ
Mid-substance (occurs in degen tendon)
Attrition – inflammatory or not
3 phases
1. Inflammatory
2. Fibroblastic/Proliferative
3. Remodeling
Immediate
blood
inflammatory products
fibrin
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
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’
3-4 weeks
re-orientation of fibrils
organisation of collagen
Beyond
tensile properties increase
remodelling and further organisation
minimal histological difference by 20 weeks
months to regain full strength
Same 3 phases of healing
2 sources of healing
1. Extrinsic – granulation tissue from tendon
sheath
2. Intrisic – cell invasion from tendon and epitenon
Mobilized tendons:
controlled passive motion
intrinsic response from epitenon predominates
• Immobilized tendons:
– ingrowth of connective
tissue from sheath
– cellular proliferation of
endotenon
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
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
CAUSES (THEORIES)
Mechanical
▪ Overload
Vascular
▪ Poor blood supply in
watershed makes areas
make tendons prone to
injury
Modify risk factors
Training error
Flexibility issues
Ice/Compression
Exercise
Eccentric
Stretching
Can inc. elongation capability
of muscle/tendon unit
Massage
Shockwave therapy
NSAIDS
Evidence shows analgesic effect of NSAID
But may delay healing b/c need inflammatory
phase to heal
Steroid injection
Autologous RBC injection or PRP
Surgery
Debridement
“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.
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
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
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