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
