Week 7 Lecture Flashcards
• Describe the composition and structure of normal tendon
- Tenocytes(fibroblasts) (<1%of wet mass) synthesise:
Collagen
Ground substance components - Parallel arrays of collagen fibres (~86% of dry mass)
– Bundled as fibrils , closely packed
– Type I (>97%)
– Held together by proteoglycan components and GAG’s - Extracellular matrix (ECM)
– Groundsubstance (Proteoglycans etc)
– Water(70% of wet mass)
4. Epitenon, endotenon, peritendon – Surrounds tendon and tertiary fibre bundles – Contains capillaries, lymphaLcs nerve – Synovial cell lining • Tendon is hypovascular
• Discuss briefly how tendon morphology reflects function
Tendon functions:
Tendon functions:
1. Force transfer (Muscle to bone)Short thick
2. Energy storage and release (via SSC) Long thin
energy conservation
– 90% stored elastic energy can be returned
– Interaction between collagen fibres & the ECM provides tendon with its viscoelastic mechanical
Properties
– Tendons from different sites are different in structure, composition, cell phenotypes, and metabolism
• Larger tendon cross sectional area reduces internal stress
• Describe the intrinsic and extrinsic factors influencing tendinopathy developmen
Intrinsic risk factors: Biological age, weight(sedentary/obese), male sex, tendon temp, Blood supply, systemic disease,Muscle strength, flexibility, previous injury.
Extrinsic factors: Environmental conditions, shoes, equipment, surfaces, occupation, Physical activity, sport, training errors, nutrition, smoking, medications
Age
Young, high load athletes @ in tensile loaded tendons
Older, low load post menopausal women
Young:Compressed tendons under some load are vulnerable eg Glut med, Rotator cuff
Old: Loss of proteoglycans & water, tendons become stiffer, programmed cell sensence
Body composition- obesity Visceral fat>proinflamm adipokines(cytokines)
Lipid deposition in arteries>artherosclerosis (vascular compromise to tendons)
BMI over 35= increased risk of shoulder tendon surgery by more than 3 times.
Gender- Female hormones protective of tendons: non load related tendinopathy in post menapausal women more common.
Non insulin Dependent Diabetes Mellitus(NIDDM)
Increased TNF
Increased Interleukin -1 beta
Increased vascular endothelial growth factor( neovascularisation)
Risk of different tendinopathies b/n different genders
Females: Gluteal tendinopathy & achilles tendinopathy
Males: Adductor tendinopathy & mid portion achilles tendinopathy
• Describe the aetio-pathogenesis of tendinopathy•
Different tendons have different functions so have significant anatomical regional differences(histologically, mechanically )
Tenocytes exposed to prolonged and excessive stress or strain > cell death
Triggers: Oxidative stress, chemical stress, radiation, metabolic stress, mechanical stress.
SIPS (stress induced premature tenocyte senescence) leads to an increase of tenocytes expressing SASP
( Senesence- associated secretory phenotype).
SASP leads to increased expression of proinflammatory cytokines and proteases(MMPS)
• Discuss how tendinopathy may become painful
A perfect storm of factors cumulating at one time. Pain is the catalyst.
Nocioceptiive (cell driven/biochemical) hypothesis
– Biochemical substances stimulated by overload
-Tenocytes produce catecholamines, acetylcholine, glutamate
– Hallmark of reactive/early tendon disrepair phase but low correlation between these and irritability
• Neovascular hypothesis
– Altered ECM matrix turnover with MMP synthesis
– Leads to neoinnervation
• Neurogenic (inflammamation) hypothesis – Evidence of high levels of sP in pathological tendon – A response to tendon hypoxia? • Iceberg hypothesis – Pain is the “iceberg Lp
Tendon pain does not necessarily mean that significant pathology is present
the presence of significant pathology does not necessarily mean there will be pain
• Describe the tendinopathy continuum
REVIEW THIS
REACTIVE/PROLIFERATIVE (Thickened tendon( fusiform), Increased stiffness & reduced internal stress
TENDON DYSREPAIR (tendon breakdown and attempted repair)
DEGENERATIVE TENDINOPATHY (failed repair & Progressive cell & matrix injury with little/reduced potential for regeneration)
According to sdgjsg just 2 stages
Different parts of tendon may be in different stages of continuum at any one point in time
Can be reactive on degenerative
Tendinopathic iceburg: Can’t change degenerative section but can treat the areas around it.
Good photos in notes pg 28
Describe the pathology of
REACTIVE/PROLIFERATIVE TENDON
Clinical features
PATHOLOGY- reactive proliferative
-changes to ground substance
-slight tenocyte proliferation
- Increased protein synthesis (proteoglycans, collagen, GAG)
t/f thickened tendon (fusiform), Increased stiffness & reduced internal stress
Clinical features
Younger athletes, Hx acute overload, mod- severe severity
Ultrasound: Fusiform swelling, Diffuse hyperechoic
MRI: Fusiform swelling.
• Describe the pathology and clinical features of TENDON DISREPAIR including the typical features seen on imaging (US/MRI)
- Increased tenocyte production
- Increased protein synthesis
- Separation and disorganisation of collagen(MRI)
- Focal disorganisation of ECM
- Appearance of neovascular changes(US)
Clinical features
Spectrum of ages, Hx chronic overload, thickened tendon with focal structural changes
MRI: Fusiform swelling, increased disorganised collagen
DOPPLER US:Increased vascularity
• Describe the pathology and clinical features of degenerative tendinopathy including the typical
features seen on imaging (US/MRI)
PATHOLOGY
- Progression of cell and matrix changes
- Apoptosis
- Highly disorderd ECM with: (US)
- blood vessels (doppler US)
- Matrix breakdown products
CLINICAL FEATURES
Older, HX chronic overload & repeated tendon pain, one or more focal nodular areas w or w out general thickening.(MRI)
US: Hypoechoic regions coz matrix changes
(dark tissue=collagen & matrix breakdown)
DOPPLER US: Numerous large vessels
MRI: Thickened tendon with focal nodular changes
• Outline the common locations for tendinopathy to occur
LL & UL
Lower limb tendinopathies – Common • Achilles • Plantar fascia – Histologically not dissimilar to tendon • Patella • Proximal hamstring • Gluteal insertion (GTPS)
– Less common
• Adductor origin
• Tibialis posterior
Upper limb tendinopathies
– Common
• Rotator cuff insertion
• Common flexor and extensor origins
– Less common • Biceps origin • ECRL • EPB • EPL
• Outline the clinical (behavioural) classification of tendinopathy
Sx behaviour
– Pain is typically load dependent
• With mild moderate cases reports of classic warm up pain that eases followed by post activity pain
– Morning stiffness pain especially
• In more severe and/or highly irritable cases can get pain through activity that (again) feels even worse further post activity
– Pain often worst 1-2 days after
• Reflects slow tenocyte activity cycle
• Describe common loading tests for various regional tendinopathies
Low load testing Achilles - SL heel raise Patella - SL decline squat Prox hamstring - SL bent knee raise Gluteal tendon- SL stance
High load testing Achilles -Hop Patella - SL jump/drop landing Prox hamstring - SL deadlift Gluteal tendon- Hop
Resisted tests – Reproduce pain on tendon loading/resisted movement
• Discuss the limitations associated with imaging tendinopathies
Poor correlation between symptoms and evidence of pathology on imaging.
Can have + imaging but no symptoms and vice versa.
Can have responded well to rehab but pathological changes still evident well after.
Potential reasons: Tendons metabolically really slow t/f will take very long to change or tissue state will not change at all.
• Evaluate where in the continuum of tendinopathy a patient presents
According to the tendinopathic iceburg model
Patient will only be clinically symptomatic (painful tendon) after they have exceeded:
Normal physiological adaptations to healthy excercise
Relative overload (> microruptures)
Neo-angiogenesis & nerve proliferation
(> neurogenic inflammation)
Will be reactive or reactive on degenerative (pain with loss of function)
Can be just reactive
Could also be normal painful tendon(unlikely)
Describe and implement treatment and management interventions for tendons in the tendinopathy
reactive/early disrepair phase
Goal: Unload/ relative rest
Decrease symptoms
- Isometric mid-inner range exercises( eg heel raise)
- NSAID
Load modification
-Short period of unloading ( no more than 2 weeks)
(Allows tendon/matrix to revert back to normal state)
-Lower and slower impulse loading in reactive phase
(Less likely to up-regulate tenocytes or matrix)
-Antipronation taping may reduce pain is excessive pronation occurs during funtional tasks
Facilitate remodeling and load-tolerance via progressive excercise loading programme
-Slow moderate- heavy loads introduces ASAP after symptom settling.
(avoiding compression e.g. EROM dorsiflexion)
Isometric holds
Load management.
Reduction in frequency ±
intensity of tendon load
Describe and implement treatment and management interventions for tendons in the tendinopathy
late disrepair/degenerative phase
Goal: Stimulate a repair/healing response
Mechanical loading can accelerate tenocyte metabolism and repair.
-Graduated tendon loading, 3 day cycles (high, lo, med)
High load eccentric programmes indicated
mild pain w exercise ok, 2-3/10 as long as it reduces
-Address contractile defecits ( muscle bulk) ^ general strength
-Address kinetic chain deficits
(lumbopelvic hip control, generating power & absorbing forces)
-Improve coordination strength & endurance
-Address LL mobility issues
(muscle length, ankle & foot mobility)
-Training and technique causing factors
6 month loading programme optimal , followed by maintenance
3 months min, more likely 6-9 month RTS
• Prescribe an exercise program for an athlete with achilles and patellar tendinopathy
and rationalise your approach to loading at different stages in the tendinopathy continuum.
Achilles tendinopathy exercise programme
Early reactive
- Heel raise, antipronation taping
3x 15 reps 2x daily Achilles (bent and straight knee) Alfredson programme
Progress loading by approx. 10% every 3-4 days
Slow eccentric excercise
Increase weight with load not speed
• Discuss how management may vary in a mid-substance achilles tendinopathy versus insertional
Insertional Achilles tendinopathy does NOT respond well to eccentric exercises. Enthuses acts as an anchor to bone- the role, structure and pathology of the enthuses are different to the main tendon body.
Cant take them to EOR,
Adapting tendon to increased loads
REVEIW THIS
Increase load without increasing symptoms
Regular increase in weight 10%
Address muscle strength/ endurance- high reps low loads
Increase speed of excercises
Isometric loading exercises:
Reactive tendinopathies & Irritable cusp
Benefits
Parameters
For irritable & non irratable cuff
BENEFITS
Pain relief for reactive tendons
Minimises compression & loading related pain.
Minimises strain with longer contractions
Minimises DOMS
Low risk of injury
Parameters 2-4x a week
Irritable:
Mid ROM – heel just off ground
Low load (PWB) pain free
Stable/low irritability:
Mid-Inner range(Heel off step)
FWB + external load Pain free
Concentric- eccentric loading
Benefits
Benefits
Reverses ‘concentric performance deficit’
Specificity of muscle response
Still has an eccentric component
Parameters
Care with loading at EROM
3 sessions per week ( 2x high load , 1x endurance)
Eccentric only loading (high load demands in sport)
Benefits
Indications
Parameters
Benefits
Rightward shift in the length-tension curve.
Potent way to introduce high load tendon strain
Indications
Where high load demands in sport
A need to optimise length tension for functional demands eg need to be loaded at length such as dance, gymnasts, sprinting.
Parameters
Through full ROM, careful at EROM
3 sessions a week (2x high load , 1x endurance)
Stretch shortening elastic storage training. SSC (Stretch shortening cycle)
Define
What are the 2 components that make it up?
- An eccentric (lengthening) muscle action
w elastic energy storage of muscle and tendons. - Concentric (shortening) muscular contraction coupled with release of elastic energy
* refer to image in slide very helpful
SSC capacity is critical in sprinting, jumping ect. The very activities that are associated with tendinopathy
Training MUST address this part of return to sport preparation.
Need to establish: Adequate tendon stiffness& concentric strength
Running itself does not do this as there is INSUFFICIENT STRAIN.
Helps address ‘’yellow flag’’ fear avoidance issues
Criteria to commence SCC training
Late stage rehab progression
Tolerating high intensity tendon loading.
Low irritability including low levels of latency (stiffness pain)
Pain free walking
*can potentially begin some form of early gentle ASAP if degenerative stable and non irritable
Stretch shortening parameters 2-3 days recovery Control volume carefully, graduations 2-5 mins in early sessions 5 sets 3-4 reps w minimal form fatigue, build to 5-10 sets of 6-10 reps
Isometric
Parameters
Achilles
Patella
Inner range(Irritable) Mid- Inner( low irritability)
Hold time 10-20 secs then 30 to 60-120 secs
6 reps, 3 sets , 3 times a week
Achilles
- DL/SL Inner range heel raise
- DL/SL Inner range leg press
Patella
Inner range leg extension (machine)
DL/SL Inner range leg press (machine)
Hamstring
– Standingpush back
– DL→SL deadlift
Concentric- Eccentric loading
Achilles
Patella
(building to FROM)
2x high load sessions
6-10 reps 3-4 sets (1-2 x body weight)
1x endurance session
2 sets to failure
Achilles
Bent knee heel raise (soleus)
Straight knee heel raise (Gastroc)
Heel raise with toes in extension (Loads the plantar fascia)
(Heel hanging off step, towel under toes so start in extension)
Patella Leg press Knee extension Squat DL/SL Upper Hamstring tendinopathy Single leg bridge Mid to inner range Resisted deadlift, DL,SL
Eccentric only
Parameters
Excercises:
Achilles
Patella
-2x high load sessions
6-8 reps 3-4 sets Long and slow
(1-2x body weight)
-1x endurance session
2x sets to failure
Achilles
Heel raises
Patella tendinopathy
Decline heel raises
Inner range Knee extension(machine)
Upper hamstring tendionopathy
Nordic lowers * refer to pics
Stretch shortening
Excercises
Parameters
DL, SL trampette, skipping DL bunny hops,DL jumps, DL box jumps SL hop, SL box hop, SL forwards hop Tripple extensions (Hip knee ankle) Locomotor training( Walk, jog ,run)
Parameters Once or twice a week 2-3 days recovery Control volume carefully, graduations 2-5 mins in early sessions 5 sets 3-4 reps w minimal form fatigue, build to 5-10 sets of 6-10 reps
Discuss how you could monitor treatment response in tendinopathy
Monitor response to load over 24 hours: During activity After exercise Morning stiffness Functional tasks (24 hours later) Small increase in VAS over 24 hours is acceptable if it resolves within 24 hours
Monitor pain response 24 hours post provocative activities. Pain needs to be stable
VISA-A for achilllies tendionopathy
VISA-P for patella tendinopathy
