Tendonopathy
NYSAFP Winter Weekend
January 28, 2012
Todd S. Shatynski, MD, CAQSM
tshatynski@caportho.com
Objectives
 Understand the anatomy of a
musculo-tendinous unit and locations
of injury
 Review the process that occurs to
cause tendon degeneration
 Evaluate the current categorization of
tendon pathology
 Assess the current evidence behind
traditional and emerging treatments
Anatomy of a Tendon
 Tight, parallel
collagen bundles
 Transmit forces
muscle -> bone
 Great tensile
strength
 Poor resistance to
compression and
shear forces
 Surrounded by
paratenon +/sheath
Anatomy
 Paratenon – contains tendon
vasculature
 Originates from musculotendinous and
bone-tendon junctions
 Coiled vasculature allows stretch
 Sheath – avascular tendons
 Allows change of direction when crossing
over bony prominences
“Tendonitis”
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Rotator cuff tendonitis
Medial epicondylitis (Golfer’s elbow)
Lateral epicondylitis (Tennis elbow)
Dequervain’s tenosynovitis
Hamstring tendonitis
Adductor tendonitis
Patellar tendonitis (Jumper’s knee)
Achilles tendonitis
Plantar fasciitis
Tendon Overload/Overuse
 Tissue deformation begins as strain
increases due to friction, torsion,
compression
 Most common in tendons with large
mechanical demands (achilles, patellar)
 Originally termed “tendonitis”
implying inflammatory reaction
 Actually spectrum of injury involving
acute and chronic components
Where’s the inflammation?
 “Histologic analysis reveals no
inflammatory cells”
 Nirschl, Clin Sports Med, 1992
 “Microdialysis and gene technology
has clarified there is no chemical
inflammation in Achilles’ tendinosis.”
 Alfredson, Clin Sports Med, 2003
Where is the inflammation?
 Maybe the paratenon…
 Ultrasound guided corticosteroid
paratenon injection of Achilles,
patellar tendonitis (by MRI) provided
significant pain relief compared to
blind placebo
 Ultrasound guidance used to avoid
intratendinous injection
 Fredberg, Scand J Rheumatol, 2004
Biochemical Hypothesis
 Khan, et al. Br J Sports Med, 2000
 Painful tendon reveals fascicles
containing nerve fibers with
sympathetic nerve markers (usually
only seen in nervous system):
 Substance P
 Acetylcholine
 Catecholamines
Molecular analysis
 IL-1 beta induces expression of
cytokines
 Cytokines induce matrix destructive
enzymes (metalloproteases MMP-1, etc)
 Increased lactate (ischemia signal) and
glutamate (pain mediator)
 Chronic overuse leads to degeneration
and premature cell death (apoptosis)
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Tsuzaki, et al. J Ortho Res, 2003; Cook, et al. Phys Sportsmed, 2000; Capasso, et
al. Sports Exerc Inj, 1997; Arnoczky, et al. J Orthop Res, 2002; Yuan, et al. J
Orthop Res, 2002; Alfredson, Clin Sports Med, 2003; Ireland, et al. Matrix Biol,
2001.
Classification
 Tendonopathy = chronic tendon pain
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Tendonitis
Tendonosis
Paratenonitis
Insertional tendonitis
Which one is it?
 “…tendinosis was first used by
German workers in the 1940’s, its
recent usage comes from the work of
Giancarro Puddo in the early 1970’s.”
 N. Maffuli, Clin J Sports Med, 2003
 “Degenerative tendinosis occurs over
time when tendon damage exceeds
the rate of the tendon’s intrinsic
ability to heal”
 Budoff & Nirschl, Op Techniques in Sp Med, 2001
Histopathology
Khan, Sports Med, 1999
 Tendonitis –
 Symptomatic degeneration with vascular
disruption and inflammatory repair
response
 Collagen disorientation/disorganization
with tear, fibroblastic proliferation,
hemorrhage, and organizing granulation
tissue
 + Inflammatory cells
 Animal models
Histopathology
 Tendonopathy
 Intratendonous degeneration due to
aging, microtrauma, or vascular
compromise
 Collagen disorientation/disorganization
with fiber separation by increased
mucoid ground substance, possibly
neovascularization, focal necrosis or
calcification
 No inflammatory cells
Histopathology
 Paratenonitis
 Inflammation of outer layer of the
tendon (paratenon)
 Acute edema and hyperemia of
paratenon with infiltration of
inflammatory cells
 Production of fibrous exudate in the
tendon sheath
 Mild mononuclear infiltrate
 Inflammatory cells in paratenon only
Histopathology
 Peratenonitis with tendinosis
 Intratendinous degeneration
 Paratenonitis with mucoid degeneration
and scattered inflammatory cells in
paratenon
Appearances…
Healthy
 Glistening white
 Hierarchical, parallel,
tightly packed collagen
fibers
 Reflectivity under
polarized light
 No extracellular matrix
 Vasculature, tenocytes
inconspicuous
Symptomatic
 Grey, amorphous
 Discontinuous,
disorganized collagen
fibers
 No reflectivity under
polarized light
 Mucoid ground
substance present
 Less tenocytes, appear
plump
Microscopy
General Tendon Injury
 Ruptures – Male:Female (4-7xs)
 Wong, et al. Am J Sports Med, 2002
 Anabolic steroids increase rupture
risk
 More common in blood type O, less
common in type A
 Josza, et al. JBJS, 1989; Kujala, et al. Injury, 1992;
Maffuli, et al. Clin J Sports Med, 2000.
 Tendon ruptures increased with oral
quinolone use
 Kibler, et al. Clinics in Sports Med, 2002
Exercise Response
 Tendonopathy improves with exercise
but worsens after
 Allows exercise to continue
 Inhibits healing response
“Tennis elbow”
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Lateral epicondylitis (-osis)
Extensor carpi redialis brevis tendinosis
9x more common than medial
Pain with resisted extension
More common in older players
 Occupational injury very common
 Intensity, conditioning, warm-up, training
changes
 Grip size, string tension, racket size/rigidity
Classic treatment
 Reduce stresses across tissue
 Rest
 Counterforce brace
 Improve quality of tissue and balance
 Strength and endurance
 Eccentric strengthening
 Balanced flexibility
 Optimize technique, equipment,
Treatment
 NSAIDS and Corticosteroids?
 Prolotherapy (irritant injection)
 Dextrose, Sodium morrhuate
 Blood
 Injectable healing factors
 Platelet rich plasma (PRP)
 Stem cells
 Mechanical adjuvants
 Deep massage
 Extracorporeal Ultrasound
 Needle tenotomy
 Surgery
Anti-inflammatory techniques
 Cryotherapy – acutely
 Ultrasound guided paratenon and
bursal injections of corticosteroid may
be temporarily beneficial
 Never inject corticosteroid into
tendon
 Increases risk for rupture
Anti-inflammatory techniques
 Achilles tendonopathy – oral NSAID
(piroxicam) no benefit over placebo
 Astrom, Westlin, Acta Orthop Scand, 1992.
 NSAIDS may permit patient to ignore
pain and cause further injury
 NSAIDS may reduce healing response
Injected Corticosteroid
 Well-established efficacy in short
term relief of pain
 Safe, limited side effects
 Long term degeneration?
 Ineffective if used in isolation without
use of PT modalities
Topicals
 Topical Nitric Oxide
 Not FDA approved
 Topical Glyceryl trinitrate with hand
rehab
 81% asymptomatic (vs 60%) at 6
months
 Less pain, improved strength
 Paoloni, Am J Sports Med, 2003; Paoloni, JBJS, 2004.
Newer concepts:
Anti-antiinflammatory approach
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Deep friction massage
Prolotherapy
Injection of blood or platelets
Hyperbaric oxygen
Injectable growth factors
Radiofrequency coblation
Extracoporeal shockwave therapy
Minimally invasive release/needle
tenotomy/barbotage
Platelet Rich Plasma
 NFL, MLB, MLS, PGA
 Patients own blood extracted, spun in
centrifuge and PRP injected into
diseased tissue
 Limited evidence, thus rarely covered
by health insurance
Platelet Rich Plasma (PRP)
 Peerbooms, et al. Am J Sports Med,
2010
 DBRCT 100 patients lateral
epicondylitis
 Eccentric exercise with PRP or
Corticosteroid
 73% vs 51% improved at 1 year
PRP Lateral Epicondylitis
 Hechtman, et al. Orthopedics, 2011
 30 patients, Symptoms >6mos,
unresponsive to conservative therapy
(inc steroid injection)
 1 PRP injection
 Overall success 90% = 25%
reduction in pain scores at 1 year
followup
PRP for Achilles?
 DeVos, et al. JAMA 2010.
 DBRCT 54 patients
 Eccentric exercise with PRP or Saline
injection
 No statistical difference in outcomes
Why the difference?
Castillo, et al. AJSM, 2011.
 >16 different platelet separation
systems = different platelet-rich
concentrates
 Varying amount of starting blood
volume, spin times
 Varying WBC concentrations (↑ or ↓)
 Thus varying growth factor
concentrations
 Needs more study!
Prolotherapy
 Sclerosing therapy
 Reduces neovascularization but not
tendon thickness
 Ohberg, Alfredson, Br J Sports Med, 2002.
 Review article suggests promise and
evidence of effectiveness in
tendonopathy
 Distel, Best, PMR, 2011.
Extracorporeal Shockwave Therapy
(ESWT)
 Approved for multiple locations
 Review article (patellar tendon)
 Van Leeuwen, et al. Br J Sports Med,
2009.
 Variable treatment protocols
 Positive outcomes – safe, effective
 Uncertain mechanism
 Availability?
Minimally Invasive Release
 Dry needling, Needle tenotomy
 Saline barbotage for calcifications
 Percutaneous longitudinal tenotomy
 Maffuli, Am J Sports Med, 1999; Wilder, Clin Sports
Med, 2004.