APTA CSM Combined handouts Final - Orthopaedic Section · • Recognize the findings from current...

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Current evidence for the management of lower

extremity tendinopathies

American Physical Therapy Association Combined Sections Meeting 2015

Indianapolis, Indiana February 4-7, 2015

Disclosure

•  The authors/presenters of this session declare that no relevant financial relationship exists

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Course Objectives •  Upon the completion of this session, the participant will be able to: •  Identify current research explaining the pathophysiology for tendinopathy

development. •  Recognize the findings from current research explaining the physiological

processes for tendon remodeling. •  Describe various risk factors for the development of posterior tibialis tendinopathy. •  Identify the best practices for examining a patient with posterior tibialis

tendinopathy. •  Describe the findings from current literature regarding the management of

posterior tibialis tendinopathy. •  Describe various risk factors for the development of triceps surae tendinopathy. •  Identify the best practices for examining a patient with triceps surae tendinopathy. •  Describe the findings from current literature regarding the management of triceps

surae tendinopathy. •  Describe various risk factors for the development of patellar tendinopathy. •  Identify the best practices for examining a patient with patellar tendinopathy. •  Describe the findings from current literature regarding the management of patellar

tendinopathy. 3

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Tendon: homeostasis, Degradation and remodeling

Craig R. Denegar, PT, PhD, ATC, FNATA University of Connecticut

Storrs, Connecticut

Purpose – review the role of mechanical signaling on tendon

homeostasis and the paradox of exercise as an effective

treatment for overuse disease •  Tendon structure & homeostasis •  Basics of mechanobiology •  Tendon disease: etiology, progression and

histology •  Repair mechanisms: Role of the tenocyte and

tendon progenitor cell 5

What maintains homeostasis and tendon health?

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TENDON 7

Gap junctions are the specialized regions where cells connect via chemical / electrical signals

Cell to Cell interaction

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Tenocyte

Compression Shear Tension

Mechanotransduction

Gene / Protein Expression Growth Factors

ECM Protein production

Matrix Remodeling Enzymes (MMPs)

remodeling / repair

Tendon Homeostasis

Healthy Tendon 9

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Mechanobiology •  Mechanically mediated signal transduction

(mechanotransduction) is involved in a myriad of physiologic processes such as: –  touch and pain sensation, – hearing and vestibular function – blood pressure control – cell volume regulation –  tissue growth and adaptation.

•  Involves cellular / extracellular interaction

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Mechanobiology

Mechanical Load

gene expression, protein translation, and

posttranslational modification

protein synthesis in the

ECM

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ECM Production ECM Remodeling

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What goes wrong? •  Overload or Underload?

•  Damage to extracellular collagen framework due to overload (and thus loss of signaling to the tenocyte), or fragility of the collagen composition or lack of activity induced mechanical stimulation lead to TENDINOPATHY!!

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Tenocyte

Compression Shear Tension

Mechanotransduction

Gene / Protein Expression Growth Factors

Inadequate ECM protein production

Matrix Remodeling Enzymes (MMPs)

Pro-inflammatory Cytokines (IL-1, IL-6)

Tendinopathy

ECM protein degeneration

Overuse Catabolic Cascade

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GFs: ECM Production

MMPs: ECM Remodeling

Relative Imbalance

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Understanding tendon pathology & nomenclature

Tendonitis: inflammation, pain and swelling

Tendinopathy: description of clinical presentation

of tendon overuse

Tendinosis: degeneration of ECM in the absence of

active inflammatory cells.

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Tendinopathy – a progressive disorder

•  Reactive tendinopathy •  Tendon disrepair (failed healing) •  Degenerative tendinopathy

Cook JL, Purdam CR. Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy. Br J Sports Med. 2009; 43:409-16.

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Fiber disorganization and increased proteoglycan content in degenerated

tendon

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Tendon: “Challenged Healing” •  Tendon is characterized as having

limited vascularity

•  Greater autocrine / paracrine influence

on homeostasis and thus repair

•  Cellular crisis

– Tenocyte & tendon progenitor cells 19

A Note on Epidemiology – loading is not the only factor

•  Tendinopathy is associated with activity and overuse

• Obesity however increases risk of lower AND upper extremity tendinopathy

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Link with obesity and insulin insensitivity

•  Prevalence of tendinopathy and low grade systemic inflammation in obese patients with decreased insulin sensitivity –  Systemic low grade inflammatory state due to

release of adipokines TNF-α, IL-6.

•  Macrophages and other inflammatory cells surround fat cells. Free glucose molecules attach to collagen, impair crosslinking.

•  Less mechanical signal transduction 21

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Tendon repair – more than up-regulating tenocytes

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If the tenocyte dies, what happens? Tendon Stem / Progenitor Cells (TSPCs)

•  Recently Identified (2007) •  Promote repair through:

•  cellular proliferation → tenocyte differentiation → repair

•  Promote Tendinopathy through: •  Differentiation into fat, cartilage and bone cells

(adipocytes, chondrocytes, osteocytes) → failed repair → common histologic changes

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Tendon stem cell niche

•  Just as mature tenocyte relies on attachment

and surrounding extracellular matrix, the tendon

progenitor cell relies on it’s environment for

survival and activation / differentiation

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Evidence suggests mechanical loading regulates stem cell proliferation &

differentiation •  Tendon Stem / progenitor Cells (TSPCs) were

isolated from the patellar and Achilles tendons of 15 New Zealand white rabbits (female, 4–6 months, 3–4 kg).

•  Cell culture dish containing microgrooves and coated with ProNectin-F (promotes cell attachment)

•  4% & 8% stretch vs control (no stretch) at 0.5Hz for 12h

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Evidence suggests mechanical loading regulates stem cell proliferation & differentiation

Cell proliferation measured 3days post

↑ 18% ↑ 36% ↑ 77% ↑ 193%

Patella Tendon (PTSC)

Achilles Tendon (ATSC)

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The collagen production decision

•  Specific markers for gene expression measured immediately post-stretching qRT-PCR (collagen type I, collagen type II, PPARg (Transcription factor, adipocyte differentiation ) Sox9 (Transcription factor, chondrocyte differentiation ) Runx2 (Transcription factor osteoblast differentiation)

•  Application of 4% stretching to PTSCs and ATSCs significantly increased cellular expression of collagen type I gene, but not PPARg (a marker for adipocytes), collagen type II and Sox9 (markers for chondrocytes), and Runx2 (marker for osteocytes)

•  Application of 8% stretching to the cells significantly increased expression of all these genes, albeit at different levels

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Cell differentiation with 4% and 8%

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Considerations •  Data from animal modeling

•  Stretching loads do not equate to human in-vivo

loading

•  Data suggest the different tendons may have

unique responses

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But clinical evidence for effective treatment through exercise

exists

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Before closing – a note on phoresis

•  Does the phoresis (phono or ionto) effect treatment outcome?

•  Research offer a mixed message •  Study at the cell level tells an important

story

•  The effects of dexamethasone on human patellar tendon stem cells: implications for dexamethasone treatment of tendon injury. Zhang J, Keenan C, Wang JH, J Orthop Res. 2013;31:105-10.

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Effect of Dexamethasone on Tendon Progenitor Cells

Collagen I

Adipogenesis

Chondrogenesis 32

Summary •  Mechanical load stimulates tendon cells through

integrin receptors and is essential to tendon health and tendon repair

•  Tendinopathy is characterized by disorganized collagen, increased proteoglycan and often fat and bony accumulation

•  Progenitor cell differentiation is an important consideration in understanding repair (not just a function of fibroblasts)

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Posterior Tibialis Tendinopathy

Gary Wilkerson, EdD, ATC University of Tennessee at Chattanooga

Combined Sections Meeting 2015

Indianapolis, IN February 4-7, 2015

Disclosures

•  No relevant financial relationship exists that could be viewed as a conflict of interest

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Learning Objectives

•  Upon the completion of this session, the participant will be able to: 1. Describe various risk factors for the development

of posterior tibialis tendinopathy. 2. Identify the best practices for examining a patient

with posterior tibialis tendinopathy. 3. Describe the findings from current literature

regarding the management of posterior tibialis tendinopathy.

4. Relate the possible role of posterior tibialis dysfunction in the development of chronic ankle instability

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Role of Posterior Tibialis Muscle

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1

2

Up to 10X BW

37 Property of G. Wilkerson, not to be distributed without permission 2/7/2015

Posterior Tibialis Tendon •  Primary insertion on navicular tuberosity •  Dynamic stabilizer of medial longitudinal arch

–  Subjected to great mechanical stress •  Eccentric action: Heel strike to mid-stance

– Deceleration of pronation •  Concentric action: Mid-stance to push-off

– Supination of foot (increased rigidity)

•  Pathology –  Tenosynovitis –  Longitudinal tears –  Complete rupture


Posterior Tibialis Tendon Dysfunction

•  Early identification and treatment of PTTD critical

•  4 distinct stages of –

– Progressive weakening

– Tissue degeneration

– Structural deformity


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Posterior Tibialis Tendon Dysfunction •  Stage 1:

– PT weakness without rearfoot or forefoot deformity –  Loss of strength may be progressive or sudden – Aching discomfort on medial aspect of ankle and

foot •  Exacerbated by activity and relieved by rest

•  Stage 2: – Some degree of rearfoot valgus and forefoot

abduction •  Accentuated by increased axial loading •  Manual repositioning into normal alignment possible

– Persistent discomfort; medial swelling may be evident


Posterior Tibialis Heel Elevation Test 41

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NORMAL Property of G. Wilkerson, not to be distributed without permission 2/7/2015

Posterior Tibialis Tendon Dysfunction

•  Stage 3: – Rigidity of both the rearfoot and forefoot – Osteoarthritic degeneration of subtalar joint – Development of lateral aching (bony impingement)

•  Contact of calcaneus with fibular malleolus

•  Stage 4: – Elongation of the deltoid ligament – Valgus displacement of talus within tibiofibular

mortise

42 Myerson, 1996

Property of G. Wilkerson, not to be distributed without permission 2/7/2015

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Posterior Tibialis Tendinosis

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Distraction of Joint Surfaces

(Tension)

SUBTALAR EVERSION


Effect of Achilles Tendon Tightness

44 Biga ,2009

• Achilles Tendon tightness restricts tibia rotation over talus (reduced range of dorsiflexion)

• Anterior margin of tibia exerts downward force on talus that depresses MLA

• Tibia rotates over talus (dorsiflexion of talocrural joint) as body mass moves from posterior to anterior position during the stance phase of gait


Medial vs. Lateral Pathology?

•  Impaired ability to effectively control foot and ankle displacements: 1. Posterior tibialis tendon dysfunction

•  Excessive Eversion (Pronation) 2. Lateral ankle sprain

•  Excessive Inversion (Supination)

•  Intricate “gear” and “strap” mechanisms transfer torque from the to the leg, and vice versa


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Subtalar Inversion + External Leg Rotation

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Axis for Frontal Plane Tilt of the Talus

Axis for Transverse Plane Internal Rotation of Talus

Functional Axis for Subtalar Joint Inversion


Posterior Tibialis Muscle Weakness

•  May be a consequence of arthogenic inhibition

–  Wilkerson et al, 1997 –  Munn et al, 2003

•  May be a predisposing factor for LAS –  Baumhauer et al, 1995 –  Willems et al, 2005


Evertor/Invertor (E/I) Strength Ratio

Baumhauer JF, et al: A prospective study of ankle injury risk factors. Am J Sports Med. 1995;23(5):564-570. •  145 college-aged athletes tested at 30°/s

•  15 athletes subsequently sustained LAS

•  Mean E/I peak torque ratio for uninjured = .80

•  67% of injured had E/I peak torque ratio >1.00

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Evertor/Invertor (E/I) Strength Ratio

Wilkerson GB, Pinerola JJ, Caturano RW: Invertor vs. evertor peak torque and power deficiencies associated with lateral ankle ligament injury. J Orthop Sports Phys Ther. 1997;26(2):78-86.

–  15 acute & 15 chronic injured subjects –  30°/s Evertor to Invertor Peak Torque Ratio

–  “Optimal” E/I @ 30°/s = .75 to .85

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Test 1 Test 2 ACUTE 1.18 .81 CHRONIC .96 .83

* Test 1 to Test 2: 25 ±8 days


Supination at Heel-Lift/Push-Off

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Internal Inversion Moment

External Inversion Moment

RIGHT FOOT


Effect of Weightbearing on Injured Ankle Following Inversion Sprain?

•  With chronic lateral ankle instability, progressive application of body weight to involved extremity: – Pronation of foot (medial longitudinal arch

depression)

–  Internal rotation and anterior translation of talus •  Caputo et al, 2009 •  Omori et al, 2004 •  Tochigi, 2003


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Optimal Stimulus for Adaptation?

•  Some combination of strain magnitude, frequency, rate, and duration appears to set lower and upper limits for catabolic and anabolic tenocyte functions –  < 3% insufficient to induce tendon adaptation –  > 8% likely to cause microscopic tendon degeneration

•  55% MVC 2.5-3% strain •  90% MVC 4.5-5% strain

•  Major disadvantage of elastic band resistance: –  Lack of a means to accurately quantify resistance


Posterior Tibialis Muscle Strengthening •  ER of foot with heel elevated

– Elastic cord resistance – Evertor/Invertor co-contraction

•  3 X per week for 3 weeks; n=19 •  ~ 40% isometric peak force increase

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ROTEX Simply Stable


Posterior Tibialis Muscle Strengthening

54 54 Property of G. Wilkerson, not to be distributed without permission 2/7/2015

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Posterior Tibialis Muscle Weakness

•  Prolonged duration of stance phase pronation •  Talus will remain in an internally rotated position

–  Heel begins to rise –  Forefoot rapidly supinates –  Leg externally rotates

•  Tibia excursion over talus within transverse plane –  Subluxation during every repetition of gait cycle –  Intra-articular shear loading

•  Hashimoto & Inokuchi, 1997


Tibia-Talus-Calcaneus Alignment


Dynamic Control of Rotary Displacements Within the Transverse Plane

•  Strategies: 1. Eccentric strengthening of Post. Tibialis

2. Support for Medial Longitudinal Arch

3. Taping for subtalar joint stabilization

4. Core stabilization training


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Medial Longitudinal Arch – Pronation –  Chippaux-Smirak Foot Width Index (FWI)

•  FWI = Line B / Line A – Line A: Widest portion of anterior 1/3 of foot – Line B: Most narrow portion of middle 1/3 parallel to Line A

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Low Medial Longitudinal Arch Arch Height FWI

High ≤ .29 Normal .30 - .39

Low ≥ .40

Mei-Dan et al, 2005 Property of G. Wilkerson, not to be distributed without permission 2/7/2015

Arthrogenic Muscle Inhibition

)


Summary •  Early identification and treatment of PTTD is

critical to prevent progressive degeneration

•  Tendinosis may result from a combination of diminished muscle strength and joint instability

•  The ankle is far more susceptible to arthritic degeneration than generally recognized

•  Somewhat paradoxical concepts appear to provide a plausible explanation for the exceedingly high rate of chronic ankle instability

60 [email protected]


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Achilles Tendinopathy

R. Barry Dale, PT, PhD, OCS, SCS, ATC, CSCS Associate Professor

University of South Alabama Mobile, AL

Triceps Surae Anatomy

•  Gastrocnemius – Medial head – Lateral head

•  Soleus •  Plantaris

–  InserBon •  Achilles tendon

– Mostly equal contribuBons from gastrocnemius and soleus

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Achilles Tendon Anatomy

•  Thickest and strongest in the body – Average length 15 cm (11-‐26 cm range) – Average width is 6.8 cm at origin, 1.8 cm at midsecBon

– Rounded width of 3.4 cm at inserBon

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Achilles Tendon Anatomy

•  Three main vascular areas – Proximal (posterior Bbial artery) – MidsecBon (peroneal artery) – Distal (posterior Bbial artery) – Mid-substance of tendon

•  Poor blood supply •  Increased injury incidence?

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Achilles Tendon Disorders

•  Mid-‐porBon tendinopathy •  Paratendinopathy •  InserBonal tendinopathy •  Rupture

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•  Prevalence of Tendinopathy – AthleBc vs. non-‐AthleBc populaBon

•  ~30% do not engage in phys. act. (Ames et al. 2008)

– Adolescent populaBon •  1.8% for Achilles; 5.8% for patellar (Cassel et al. 2014) •  12-‐18% for gymnasts (Emerson et al. 2010)

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•  Prevalence of Tendinopathy – Adult populaBon

•  Age •  AcJvity level

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•  Risk Factors (Magnan et al. 2014) –  Intrinsic

•  Age, gender, body mass, tendon temperature, systemic diseases, muscle properJes (strength, flexibility, history, & anamoly), geneJc predisposiJon, blood supply

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•  Risk Factors (Magnan et al. 2014) –  Extrinsic

•  MedicaJons •  Overuse

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•  Risk Factors – Body Mass Index (BMI) (Klein et al. 2013)

•  Overweight: 2.6 Jmes more likely than normal BMI •  Obese paJents: 6.6 Jmes more likely

•  Pathogenesis algorithm (Magnan et al. 2014)

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Continuum

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ExaminaBon of Achilles Tendon

•  Imaging – ~ One-‐third of symptomaBc tendons

•  show histopathological changes (van Sterkenburg and van Dijk, 2011)

•  Subclinical progresses into clinical – DiagnosBc Ultrasound Imaging – Shear-‐wave Elastography

•  Highly specific, low sensiJvity (Aubry et al. 2014)

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Achilles Imaging

•  DiagnosBc Ultrasound •  Normal

– Hyperechoic(genecity) •  Abnormal

– Hypoechoic – NeovascularizaBon

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Achilles Imaging •  VascularizaBon Grading System (Del Buono et al. 2012) •  Grade I

–  One vessel into the tendon •  Grade II

–  Two vessels into the tendon •  Grade III

–  Neovascularisation involving less than 50 % of tendon thickness •  Grade IV

–  Neovascularisation involving from 50 % to 90 % of tendon thickness

•  Grade V –  Neovascularisation involving more than 90 % of tendon

thickness

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ExaminaBon of Achilles Tendinopathy

•  Importance of proper examinaBon – One cannot assume that all Achilles-‐related pain is tendinopathy

– DifferenBaBon is important •  IntervenJonal success depends upon proper subgrouping

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•  Clinical Exam (Rieman et al. 2014) – Morning sBffness – PalpaBon for crepitus – Arc sign – Royal London Hospital test – Tendon loading test

•  Passive dorsiflexion •  Single-‐leg raise •  Hop test

–  The Sargeant Hop Test

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•  Clinical Exam –  SubjecBve

•  c/o pain with iniJal loading and eases with sustained acJvity

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•  Victorian Institute of Sport Assessment-Achilles (VISA-A) scores

•  The American Orthopedic Foot and Ankle Society hindfoot scale (AOFAS)

•  Functional Index of the Leg and Lower Limb (FILLA)

•  Roles and Maudsley Score

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IntervenBons for Achilles Tendon

•  Footwear modificaBons – Lies – Rocker shoes

•  Microtenotomy •  Soe-‐Bssue mobilizaBon

–  Instrumented – Manual

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•  Whole-‐body vibraBon •  Extracorporeal shockwave therapy •  Cryo-ultrasound •  Laser

– Cold Air and High Energy Laser Therapy (CHELT) – Low-‐level laser

•  Human Tecar

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•  TherapeuBc Exercise – Strengthening

•  Classic eccentric studies –  Stanish and Curwin –  Alfredson – Meta-‐Analyses

http://app.isai.co.uk/app_helper/app_web_mobile/23/Custom_82159.html 81

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•  TherapeuBc Exercise – Evidence for strengthening – Mid-‐porBon tendinopathy (Zwiers et al. 2014, Rowe et al. 2012)

•  Eccentric loading, 12-‐week program –  Strong evidence

• Mixed-‐modal strengthening

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•  TherapeuBc Exercise – Stretching

• Mechanical sJmulus vs. intervenJon for inflexibility •  Controversy with range of moJon and inflexibility with Achilles tendinopathy (Mahieu et al. 2006)

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Summary

•  Achilles tendinopathy is a common disorder that has a variable presentation

•  Clinical differentiation is important during the clinical examination – mid-portion vs. insertional

•  Evidence is strong for exercise interventions for mid-portion tendinopathy

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Contact Information R. Barry Dale, PhD, PT, ATC 5721 USA Drive North Room 2011 Mobile, AL 36688 [email protected]

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Patellar Tendinopathy (aka Jumper’s Knee)

Jeremiah Tate, PT, PhD Assistant Professor

Department of Physical Therapy University of Tennessee at Chattanooga

Patellar Tendinopathy (Warden and Brukner, 2003)

•  Activity related anterior knee pain

•  Focal tenderness at inferior patella pole/proximal tendon

•  Abnormal tendon tissue

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Prevalence •  Elite athletes (Lian et al, 2005)

–  45% and 32% prevalence in volleyball and basketball players, respectively.

•  Recreational athletes (Zwerver et al, 2011) – Overall prevalence of 8.5% – Highest prevalence in volleyball players (14.5%)

and lowest amongst soccer players (2.5% –  2x as common in males – Risk factors: loading characteristics, younger

age, taller body stature, and higher body weight

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Risk Factors (van der Worp et al, 2011)

•  No strong or moderate evidence for any risk factor associated with patellar tendinopathy

•  Limited evidence related to: – Weight, body mass index, waist-to-hip ratio,

limb length inequality, arch height, quadriceps and hamstring flexibility, quadriceps strength, and vertical jump performance

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Sports Specialization •  Hall et al (2014) analyzed

relative risks of knee pain in adolescent females who specialized in 1 sport vs. playing multiple sports

•  Findings demonstrated a 4-fold increase in developing Sinding-Larsen-Johansson, patellar tendinopathy and Osgood- Schlatter’s Disease in those who specialized.

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Continuum Model (Cook and Purdam, 2009)

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Pathophysiology

•  Morphology –  Individuals with patellar tendinopathy demonstrated

larger tendons compared to non-involved side and controls (Cook, 2000; Zhang et al, 2014)

•  Elasticity –  Individuals with patellar tendinopathy demonstrated

increased proximal tendon stiffness compared to non-involved side and controls (Zhang et al, 2014)

•  Stiffness was associated with pain and dysfunction

–  Others have demonstrated similar stiffness throughout the entire tendon (Kongsgaard, 2010)

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Clinical Exam

•  History of exercise-associated knee pain at the inferior pole of the patella

•  Focal tenderness at the inferior pole of the patella

•  Differential Diagnosis – Patellofemoral pain syndrome – Osgood-Schlatter’s Disease – Sinding-Larsen-Johansson

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Imaging (Peers and Lysens, 2005)

•  Radiographs –  May identify bony abnormalities (eg, Osgood-

Schlatter’s or Sinding-Larsen-Johansson)

•  Ultrasonography –  Disruption of collagen fibers and areas of focal

hypoechogenicity

•  MRI –  Focal thickening of tendon (increased signal

intensity); tendon tears in proximal tendon in areas of tendinosis

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Radiographs

Osgood-Schlatter’s Sinding-Larsen-Johansson

http://www.ultrasoundcases.info/Slide-View.aspx?cat=509&case=3976

http://radiopaedia.org/articles/osgood-schlatter-disease

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Diagnostic Ultrasound (Hoksrud et al, 2006)

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Diagnostic Ultrasound (Hoksrud et al, 2006)

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MRI (Warden et al, 2007)

Normal Abnormal

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Outcome Measures

•  Numeric pain rating scale

•  Victorian Institute of Sport Assessment Patella (VISA-P) Questionnaire

•  Vertical jump performance (height & power)

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VISA-P Questionnaire (Visentini et al, 1998)

•  0 to 100 points – 100 points = no pain and normal function

•  Questions – Pain with sitting, walking downstairs, active

knee extension, full lunge, squatting, during or after 10 single leg hops, current sports/physical activity participation, and irritability

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Conservative Management (Peers and Lysens, 2005)

•  Training & risk factor modifications •  Symptomatic approach

– Relative rest – NSAIDS/ice – Modalities (electrotherapy, US, laser)

•  Loading Program •  Peritendinous injections •  Extracorporeal Shock Wave Therapy

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Loading Programs (Pearson and Hussain, 2014)

•  Both the Alfredson Protocol using a decline squat and heavy-slow resistance training have been demonstrated to be effective in treatment of patellar tendinopathy.

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Alfredson Protocol (Zwerver et al, 2007)

•  Squats on decline board (25°)

•  Contraction type –  Eccentric

•  3 sets of 15 performed twice daily for 12 weeks

•  Progressed by increasing load via backpack

•  Pain up to moderate levels (ie, 3/10 VAS)

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Biomechanics of Single-Leg Decline Squat

(Zwerver et al, 2007)

•  Single leg squat on decline boards (ranging between 15-30° resulted in increased knee extensor moment and reduced hip extensor and ankle plantar flexion moments

•  Recommended to limit knee flexion to 60° due to steeper increase in patellofemoral joint reaction forces

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Heavy Slow Resistance (Kongsgaard, 2010)

•  3 main exercises – Squat, leg press, and hack squat

•  Performed 3x/week

•  4 sets of each exercise – Week 1 - 15 repetition maximum (RM) – Weeks 2-3 – 12 RM – Weeks 4-5 – 10 RM – Weeks 6-8 – 8 RM – Weeks 9-12 – 6 RM

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Peritendinous Injections (van Ark et al, 2011)

•  Dry needling –  Stimulate inflammatory

response

•  Platelet-rich plasma (PRP)/Autologous blood –  “cocktail” of growth factors

•  Sclerosis/high-volume –  Reduce/eliminate

neovacularization and accompanying nerve fibers

•  Aprotinin –  Collagenase inhibitor

(Hoksrud, AJSM, 2006) 106

Extracorporeal Shock Wave Therapy (ESWT)

•  ESWT has been demonstrated as superior to other conservative treatments and equal to long-term surgical outcomes. (Mani-Babu et al, 2014)

http://www.physio-chelsea.co.uk/shockwave.html

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Surgical Managment •  Longitudinal tenotomy (Bahr et al, 2006)

– Removal of abnormal tendon tissue – Similar results compared to eccentric exercise

group – Recommended only after failure of conservative

treatment

•  Arthroscopic shaving (Willberg, 2011) – Targets tissue with high blood flow and nerves on

dorsal aspect of tendon – Fast recovery (6-8 weeks) with good results

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Thank You!

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