MSc Physiotherapy Tendon_Nov_ 2023 - Tagged.pdf

MSc Physiotherapy PP6007 MSK1 Lower Quadrant - Tendon Declan O’ Sullivan Tendon - Lecture Goals 1. 2. 3. 4. Understand the gross and micro structure of tendon Understand the viscoelastic properties of tendon To be able to identify tendon pathology To understand the pathomechanisms of tendon injury t...

MSc Physiotherapy PP6007 MSK1 Lower Quadrant - Tendon Declan O’ Sullivan Tendon - Lecture Goals 1. 2. 3. 4. Understand the gross and micro structure of tendon Understand the viscoelastic properties of tendon To be able to identify tendon pathology To understand the pathomechanisms of tendon injury to permit optimal management planning Tendons – Where are they? Gross Tendon Structure highly ordered hierarchical structure Tendon- Microscopic Structure Tendons are Type 1, dense, regular connective tissue (Collagen) structures in the body and are defined by their anatomical position connecting muscle to bone Normal tendon is a well-organized network of parallel collagen fibrils with a sparse amount of tendon cells, tightly packed between the collagen bundles Tendon collagen fibres are discontinuous structures which slide past each other during elongation (load) Average collagen fibril elongation is only a fraction of macroscale tissue elongation Crimp Crimp Crimp morphology is grossly disturbed in tendon tissue that has been injured, and is associated with sub-optimal response to mechanical loading (Jarvinen et al. 2004) Therefore the proposal that cells actively pull on their immediate matrix (tenocyte cell contractility) has direct relevance to crimp formation and the restoration of mechanical function after injury. The observation that crimp formation requires forces generated by cells and is sensitive to the relative mechanical properties of the fibrils and inter-fibrillar material, has implications for tissue healing and regeneration (Herchenen et al 2012) – Rehab implications?? Crimp and Ageing A reduction in the crimp angle occurs with aging, with a differentially greater reduction in the central fibres (Patterson-Kane 1997) (animal study) Could be proposed that the changing crimp morphology with age is merely a function of a changed cell-to-matrix ratio caused by increased collagen content and cross-linking (Diamant et al 1972) As a tendon undergoes deformation, the central fibres straighten first and therefore receive differentially greater load than the peripheral fibers, which may explain the site of common pathological damage (Non insertional Achilles tendinopathy – central tendon unit) (Herchenan et al 2012) (horse tendon studies) Tropocollagen – Triple Helix Molecules Glycine Proline Hydroxyproline 02/04/2024 Declan O'Sullivan 9 Interfibrillar Collagen Sliding Collagen fibrils are discontinuous and that relative sliding between fibrils accounts for the difference between the tissue and fibril strain Therefore, Load must be transferred between fibrils, possibly via shear forces produced during their relative sliding and modulated by the viscosity of the ECM (Szczesny et al 2014) and rate of loading (Hijazi et al 2019) Slow heavy movements creates Shear forces which creates sliding of collagen and cross link tearing Fast movements force the tendon to ack like a sheet so there is no interfibrillar collagen sliding, therefore the tendon becomes stiff and increasing its modulus Collagen fibrils, if not strongly crosslinked, may slide between one another and effectively elongate the contour length of the fiber. The interfibrillar sliding will decrease the effective modulus of a collagen fiber. Cross linkage Function & Effects of Disease Modulate structure, stability and mechanical properties of the ECM 2 types of cross linkages 1. Glycated lysine (normal, increases with maturation) 2. Sugar mediated AGEs (Advanced Glycation End products) (abnormal - diabetes AGEs crosslinks impair the flexibility and permeability of the tissues affecting cell growth, motility, and differentiation through integrin signaling Bo Sun 2021 Tendon Insertion - Enthesis 1 2 3 4 Muscle Tendon Junction Tidball et al 1984 Interface consists of tendon like finger projections into muscle tissue that increase contact surface area Two distinct morphological interlocking interfaces which undergo shear forces when loaded Muscle Tendon Junction At the end of all skeletal muscle fibers, the collagenous fibrils of the tendons penetrate into the deep finger-shaped indentations of the sarcolemma (cell membrane of a muscle fiber). Tendons are fixed to skeletal muscle fibers by adhesion molecules such as fibronectin The dynamic function of the MTJ Folding structure increases the angle of force transmission, and consequently a high proportion of force is transmitted through shear stress (sliding of collagen filaments) MTJ response to movement is dependent on the Rate of tissue loading Slow heavy Shear forces creates sliding of collagen and cross link tearing (making muscle tissue junction interface more compliant and less stiff) Fast movements force the tendon to ack like a sheet there are no collagen fibre cross link tearing therefore so the tendon is stiff. Changes in MTJ with Atrophy Decrease in complexity and density of tendon finger like projections into muscle with muscle atrophy Ultrastructural findings indicate that mechanical failure of the junction occurs just external to the junctional plasma membrane in atrophied cells. Healthy cells do not exhibit mechanical failure at the junction. These findings suggest that increased stress at the junction is associated with muscle atrophy and may cause failure at the myotendinous junction (Tidball 1984, Tidball 1990) Classification of Tendons -Shape -Whether they have a tendon sheath -Whether they are positional tendons or elastic storage tendons Classification of Tendons- Synovial Sheath The tendon sheath directs the path of the tendon and produces a synovial fluid, which allows tendon gliding and contributes to tendon nutrition Classification of Tendons Paratenon usually surrounds tendons without a true synovial tendon sheath. Composed of loose fibrillar tissue Functions as an elastic sleeve and permits free movement of the tendon against the surrounding tissue, although it is not as efficient as a true tendon sheath. Peritendinitis- inflammation of the paratenon only and not the true tendon. Characterised by crepitus. Crepitus is a palpable or audible grating or crunching sensation produced by motion. This sensation may or may not be accompanied by discomfort. Crepitus may be articular or tendinous or bursal Classification of Tendons Elastic Storage or Positional tendons Bimodal vs Unimodal Fibril density Bimodal and unimodal refers to the percentage of large and small fibrils present within the tendon. Mature tendons tend to have both large and small fibrils present (bimodal) where as young tendons tend to have only large fibrils present (unimodal) Thorpe et al (2013) What do they do? Function dictated by morphology: Long & thin tendons are elastic in nature and good energy storers Short & thick tendons are good force transducers e.g. RC Large Cross section area tendons reduce the quantity of internal stress experienced by the tendon Vasculature of Tendons Mature tendons are poorly vascularised Tendon nutrition is more reliant on synovial fluid diffusion than vascular perfusion The vascular supply from three distinct areas: 1. Musculotendinous junction; 2. Osseotendinous junction 3. Vessels from various surrounding connective tissue such as the paratenon, mesotenon and vincula which are folds in the synovial membrane that carry blood vessels to the body and insertion of the tendon Vasculature of Tendons Achilles tendon has a poor blood supply throughout its length, as determined by the small number of blood vessels per cross-sectional area, which do not in general vary significantly along its length (Ahmed et al 1998) The middle-third Patellar Tendon has a richer intrinsic vascularity, which may enhance its ingrowth as a graft, and supports its conventional use in cruciate ligament reconstruction (Pang et al 2009) Tibialis Anterior - an avascular zone between 45 and 67 mm in length. The location of the avascular zone correlates well with the location of the most frequent site of spontaneous rupture of the tibialis anterior tendon reported in the literature (Peterson & Tillman 1999) Tendon Injuries – Risk Factors As with all injuries, Injury to tendons is often multifactorial, with both intrinsic and extrinsic forces recognized Intrinsic Factors such as increasing age, male, and obesity have been shown to have positive correlation with Achilles tendon pathology Extrinsic Factors such as the use of fluoroquinolones and corticosteroids (both oral and intrasubstance) have also been shown to lead to weakening of the Achilles, with associated tendon weakness and an increased risk of rupture Tendon injuries range from: Tendinopathies- Insertional/Non insertional Strains Ruptures Common areas of tendinopathy Millar et al 2021 Age Related Tendon Injuries- Apophysitis Sever’s Calcaneal Apophysitis 6-15% of overuse injuries Osgood-SchlattersTibial Apophysitis representing 10% of all sports-related injury Sinding Larsonn Johanson Apophysitis- Inferior Pole of Patella Age Related Tendon Injuries- Rupture The incidence of Achilles tendon ruptures in men is about 1.7 to 7 times greater than in women The first peak in incidence of Achilles tendon rupture is between 30 and 40 years of age, then 50-60years Möller et al, 2001) reported that ball games covered about 90% of all sports-related Achilles ruptures Upper & Lower Limb Risk Factors-Overuse Tendinopathy - Definition “Persistent tendon pain and loss of function related to mechanical loading” “Diagnosis is based on clinical symptoms and patient history of activity-provoked localized tendon pain and stiffness” (Scott, A. et al. ICON 2019: International Scientific Tendinopathy Symposium consensus: clinical terminology. Br. J. Sports Med. 54, 260–262 (2020)) Many terms described historically: Tendinosus, paratendinitis, tendinitis Tendinopathy Is heterogeneous in prevalence, mode of onset and presentation Susceptible to many intrinsic and extrinsic risk factors Presents in: Young high load experiencing athletes Middle aged moderate load athletes Mature low load menopausal females Sedentary individuals with recent uptake of activity (poor load management) Obesity Tendinopathy Substance P / Glutamate Tendinopathy Tendinopathies- Risk Factors Tendinopathies Risk Factor Weak Evidence 02/04/2024 Declan O Sullivan 38 Tendinopathy – Theories Tendinopathy is an area rich in good quality research. As such this has led to many theories proposed for the development of a tendinopathy 1. 2. 3. 4. Mechanical theory Inflammation theory Apoptosis theory Vascular or neurogenic theory Theoretical Pathogenesis of Tendinopathy Mechanical theory: First theories proposed in 1978 this theory led to the classic definition of ‘tendinosis’ and suggested that impaired healing of tendon lesions leads to degenerative changes It resulted from increased demand on the tendons with inadequate repair and progressive cell death. Trigger of tenocytes, induces tendon degenerative changes. (Millar et al, 2021) Theoretical Pathogenesis of Tendinopathy Inflammation theory: Pathological changes in the tendon arise from inflammatory processes and chemical cascades. Results of some studies have led to this hypothesis being disputed but current studies have confirmed the presence of inflammatory mediators, So inflammation and overuse are not mutually exclusive (Millar et al, 2021) Theoretical Pathogenesis of Tendinopathy Apoptosis theory: Links high doses of cyclic strain (repetitive load) with oxidative stress causing over activation of extracellular matrix metalloproteinases (MMP) (enzymatic collagen moderator) with the development of degenerative injuries. Vascular or neurogenic theory: Increased vascular ingrowth into tendons may cause tendon weakening and rupture. Additionally, neurogenic inflammation has also been suggested to mediate adaptive responses of tendons to mechanical overload (Millar et al 2021) Conclusion “Any one model is unlikely to fully explain the aetiology of tendon pathology and the complex interaction between pain and function, which lead to the development of the disease” (Millar et al, 2021) “It is conceivable that inflammation and tissue degeneration are not mutually exclusive but work together in the pathogenic cascade of Tendinopathy” (Abate et al,2009) Theoretical Pathogenesis of Tendinopathy Continuum model: The continuum model of tendon pathology was conceptualized to integrate clinical symptoms and laboratory-based research to guide treatment choices for the clinical presentations of tendinopathy. The model consists of three stages — 1. Reactive tendinopathy, 2. Tendon disrepair (failed tendon healing) 3. Degenerative tendinopathy Tendon Collagen Turnover Kjaer 2004 Pathogensis of Tendinopathy is a continuum from physiology to overt clinical presentation If an elastic tendon has been overloaded (elastic region) repeatedly the cumulative micro trauma is thought to weaken the non-collagenous matrix in a process known as: Tissue denaturation breaking of many of the weak cross linkages within a protein molecule Two phases of tendon change are described; the Asymptomatic and Symptomatic phases. Asymptomatic Phase – “Calm before the storm” Tendon is submitted to strenuous exercise, very high temperatures develop inside. Failure to control exercise-induced hyperthermia can result in tendon cell apoptosis. Peaks of 43 to 45°C can be reached inside the tendon and experimental studies show that temperatures above 42.5°C result in fibroblast death. This might predispose the collagen tissue to degeneration mainly when, in hypovascular areas, its capability to regulate its inner temperature is hampered. Therefore, there is the possibility that exercise-induced localized hyperthermia may be detrimental to tendon cell survival rather than vascular compromise itself 02/04/2024 Declan O Sullivan 48 Damage and Repair Mechanisms Inflammatory cytokines are predominantly produced by macrophages and involved in the upregulation of inflammatory reactions Induce Neoangiogenesis Matrix metalloproteinases degrade both collagen matrix and noncollagen matrix proteins Asymptomatic here – No Pain Yet! 02/04/2024 Declan O Sullivan 49 Symptomatic Phase When the overload overcomes the thresholds of repair (tendon capacity) or the tendon is submitted to further loads without adequate recovery time, the healing process fails and the pathogenetic cascade leading to tendinopathy occurs. The transition to the symptomatic phase is usually marked by the presence of pain through Neurogenic inflammation (glutamate and Sub P) 02/04/2024 Declan O Sullivan 50 Iceberg Theory of Tendinopathy Ice Berg Theory if the recovery time is too short and blood flow is inadequate, the repetitive strain will lead to microdamage inside the tendon Symptom If the tendon is given adequate time to recover, in good local conditions of blood flow and nutrition, the healing machinery will prevail with complete repair The base of the ‘iceberg’ represents what happens under normal physiological conditions Fredberg et al 2008 02/04/2024 Declan O Sullivan 52 Failed healing theory for the pathogenesis of tendinopathy (Fu et al, 2010) Repair processes are very slow (months) – Low tenocyte metabolic rate – 13%oxygen uptake compared to contractile tissue – 50-100 days to synthesise new collagen – Maturation of new collagen takes months Failed Healing – Fu et al (2010) Pathogenesis of Tendinopathies“Under-stimulation” Vs Over-Stimulation Hypothesis: Under-stimulation resulting from altered tenocyte cell-matrix interaction and not a repetitive over-stimulation of tendon cells is the potential aetiopathogenic stimulus for the degenerative cascade which may eventually lead to tendinopathy Painful Tendon Han et al 2017 Millar et al 2021 Tang et al 2018 Painful Tendon Presence of Pain with palpation in the tendon is a reliable indicator of the presence of tendinopathy but not a marker of severity, prognosis or improvement (Ramos et al 2009) Tendinopathy Locations Classification of Tendinopathy Fu et al 2010 Failed Healing Tendinopathy- Effects on Collagen Warming effectTendon will imbibe interstitial fluid in order to increase its cross sectional area thereby improving the tendon capacity Pathophysiology – Finley & Rodgers 2004 Crucial decision making period Cook & Purdam 2009 Loss of elasticity / loss of potential energy production / decreased power Tendinopathy - Diagnosis Tendinopathy- Diagnosis 02/04/2024 Declan O Sullivan 71 02/04/2024 Declan O Sullivan 72 02/04/2024 Declan O Sullivan 73 02/04/2024 Declan O Sullivan 74 02/04/2024 Declan O Sullivan 75 02/04/2024 Declan O Sullivan 76 02/04/2024 Declan O Sullivan 77 02/04/2024 Declan O Sullivan 78 Treatment Efficacy