Week 7 Lecture

• 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

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

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

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)

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

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

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.

• 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

• 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

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

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

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

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.

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)

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

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

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

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,

Increase load without increasing symptoms Regular increase in weight 10% Address muscle strength/ endurance- high reps low loads Increase speed of excercises

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

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)

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)

• 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

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