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Kvist, M. Annals Chirurgie Gynecologie 80, 88— Lysholm, J. American Journal of Sports Medicine 15, — Maffulli, N. Arthroscopy 14, — Springer, London. Knee Surgery, Sports Traumatology, Arthroscopy 9, 42— Magnusson, S. European Journal of Applied Physiology 90, — Milgrom, C. Movin, T. Karolinska Institutet, Stockholm, Sweden. Niesen-Vertommen, S. Clinical Journal of Sports Medicine 2, — Nigg, B. Clinical Journal of Sport Medicine 11, 2—9. Paavola, M. Journal Bone and Joint Surgery.
American volume, 84, — Peacock, E. Annals of Surgery. Peers, K. International Orthopaedics 27, — Puddu, G. American Journal of Sports Medicine 4, — Robinson, J. British Journal of Sports Medicine 35, — Rompe, J. Archives of Orthopedic Trauma and Surgery , 75— Silbernagel, K. BMC Musculoskeletal Disorder 6, Stanish, W.
Clinical Orthopaedics , 65— Tallon, C. Medicine and Science in Sports and Exercise 33, — Teitz, C. Jr, Miniaci, A. American volume 79, — Tuite, D. Scandinavian Journal of Medicine and Science in Sports 7, 72— Pain 81, — Sports Medicine 19, — Williams, J. Achilles tendon lesions in sport. Sports Medicine 3, — Winge, S. International Journal of Sports Medicine 10, — Woo, S. Quasistatic and nonlinear viscoelastic properties. Biorheology 19, — KHAN Understanding the etiology of tendinopathy is a critical aspect of improving knowledge in this area, as it would allow active intervention in athletes prior to the onset of debilitating symptoms or tendon rupture.
The investigation of tendinopathy is hindered by experimental and ethical factors, such as the lack of a suitable animal model, the onset of pathology in humans before pain and the limitations of investigating cellular processes without an intact matrix. Currently, very little is understood about the cause of tendinopathy, mechanical load is implicated in the etiology of both pain and pathology; however, the type and magnitude of load is not known.
As the tensile model of overload does not explain many aspects of tendinopathy, a primary shift is occurring from a tensile cause to the addition of compression and stress-shielding as a load factor in tendon disease. The processes of tendinopathy at a cellular level is also under review. Each athlete may have a preset load tolerance, over which they develop tendinopathy. Understanding this individual variation will allow better management of athletes in the future. Introduction Tendinopathy primarily affects active people; the more active they are, the greater chance of developing tendon pathology and pain.
The recreational athlete has some risk of developing tendinopathy, but the elite athlete has the greatest prospect of tendon pain and pathology. Tendinopathy can curtail or even end an athletic career and, as treatment options are limited, understanding the etiology of tendinopathy and identifying risk factors for tendinopathy may allow for the implementation of preventative strategies. Currently, the cause of tendinopathy is unknown. Experimental and clinical research is clarifying aspects of the etiology of pain and pathology but the relationship between them is unclear.
Elucidating reasons for the onset of pain has clinical utility; however, acute tendon pain may not equal acute tendon pathology. Pathology is likely to have temporally preceded symptoms and symptoms may be the consequence of the combination of pathology and load. The etiology of pain in tendinopathy is often examined at an organism level; in humans the athlete is the ideal subject.
Tendon pain is correlated with performance, capacity, or function of the athlete. The etiology of pathology is examined by necessity etiology of tendinopathy in vitro or in animal models. Understanding the relationship and interaction between factors examined microscopically and those examined in the athlete is problematic, and this remains one of the key challenges in tendon research. Some factors, such as tendon load and vascular changes, are implicated in the etiology of both pathology and pain and, as such, these must be a priority to investigate.
However, both tendon load and vascularity may be factors that are responsible for, and affected by, a cascade of smaller changes. Only investigation of factors on both a small and large scale will allow the etiology of tendinopathy to be fully understood. Consequently, a chapter on the etiology must examine both the etiology of tendon pathology and the etiology of tendon pain. This chapter also examines the risk factors associated with tendon pathology and pain. Risk factors have clinical relevance and may help the clinician treat athletes, but may also aid researchers understand the etiology of tendinopathy.
Does pathology precede pain?
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This study demonstrated that tendon pathology is not always painful. This has been further examined in several longitudinal imaging studies of tendon pathology in athletes. These studies have demonstrated that pathology not only preceded symptoms in both the Achilles and patellar tendons, but abnormal tendons could remain pain free for years despite continued athletic activity Khan et al.
In this series of imaging studies a consistent pattern of outcomes was demonstrated; approximately one-third of pathologic tendons resolved on imaging, of the remaining two-thirds, only one-third of these became symptomatic. The remaining pathologic tendons stayed both abnormal and asymptomatic. Where does tendon pathology occur in athletes? Although tendon pathology is considered primarily to occur in the tendon, most problematic tendon injuries occur at the bone—tendon junction enthesis.
While most tendon disease in athletes occurs at the enthesis, the majority of research has been directed at the tendon. It is unclear if results from research directed at a pure tendinopathy are applicable to pathology and processes at the bone— tendon junction. The enthesis is clearly structurally and histologically different from the tendon proper. Entheseal layering increases the capacity of the enthesis to bear all types of load, and the stress levels at the enthesis may be four times that of the tendon midsubstance Woo et al.
However, the enthesis is strong enough to withstand high forces, and disruption occurs most commonly in the underlying bone. The bone of the enthesis may become reactive to high load, and osteitis and positive bone imaging have 12 c ha p t e r 2 been demonstrated in disease Woo et al. Fibrocartilage and its associated proteoglycans aggrecan and possibly versican; Thomopoulos et al. Why does the Achilles tendon suffer midtendon pathology more often than bone—tendon pathology? Smith et al. Long tendons appear more at risk of midtendon tendinopathy and fatigue rupture than shorter, broader tendons Ker Ker hypothesizes that tendons have a structural unit of a designated length, and fatigue and consequent pathology may occur if the tendon is longer than the structural unit.
Although the enthesis is affected by pathology more commonly than the tendon itself, by necessity we will examine the etiology of tendon pathology, and assume that factors that affect the tendon also impact on the enthesis. Etiology of tendon pathology Mechanical load Overloading at the organism level and at the tendon level are often hypothesized to be the reason for the onset of pain and pathology, respectively. However, the nature and the timing of the stimuli needed to cause tendon pathology are unknown. Alternately, the type of tendon pathology may be determined by factors that occur subsequent to the onset of a primary pathologic state.
Overload must vary from tendon to tendon and between athletes. In addition, overload can not be the sole reason for tendon pathology, and tendon pathology may be caused by many factors that are either working alone, in cooperation or as a cascade. Traditionally, pathology is reported to be caused by repeated strain that is less than the force necessary to rupture. Collagen tearing caused by tensile load has long been considered to be the primary event in tendinopathy. Although logical, this hypothesis lacks evidence, and the response of tendon cells to load must be considered.
Mechanical load at physiologic levels has been shown to deform tendon cells in situ Arnoczky et al. The presence of load is then communicated to adjacent cells through gap junctions Banes et al. This normal cellular response to mechanical load may be supplemented when larger or repetitive loads etiology of tendinopathy are applied. Similarly, exercise has been demonstrated to increase levels of PGE2 in the Achilles peritendinous space Langberg et al. A reaction to excessive tendon strain may result in tendon pathology, as a response to low level tendon strain may implement tendon repair.
The capacity of the tendon to recover after load centers on the ability of the tendon cells to manufacture extracellular components of the tendon, and to organize these proteins into a structured extracellular matrix. They hypothesize that this incapacity for adaptation is brought about by a lack of cellular communication and the loss of growth factors to stimulate the cells to manufacture matrix components. Growth factors with load stimulated mitogenesis in tendon cells Banes et al.
However, continued load without growth factors may induce cell death and matrix degradation. Conversely, Ker suggests that tendon load during life must create tendon damage and tendon repair must be occurring constantly. Similarly, collagen showed continued remodeling when collagen cross-links were investigated in human rotator cuff tendon, indicating regular, and continued matrix replacement Banks et al. In addition to remodeling, repair must also encompass adaptation to repeated overload. The response of tendons to exercise is ambiguous 13 because of the range of tendon tissue examined age, species, and tendon and variation in exercise loads.
Energy storage tendons, those that develop tendinopathy in athletes, are reported to be incapable of adapting to repeated load with tendon hypertrophy Woo et al. Buchanan and Marsh report increase in tensile strength and stiffness apparently resultant from collagen cross-link changes. This minimal response to exercise in experimental studies supports the concept of minimal tendon adaptation to load proposed by Smith et al.
However, in pathologic tissue, it may perpetuate the tendinopathy cycle Pufe et al. Impingement in the Achilles tendon, rotator cuff, and the patellar tendon have been reported to cause tendinopathy. The shape of the calcaneus appears to affect the morphology of the Achilles insertion Rufai et al. Johnson et al. A dynamic magnetic resonance study that investigated this hypothesis Schmid et al. The angle of the tendon to the patella either with or without quadriceps contraction was similar in both these groups.
Clinical testing of patellar tendinopathy 14 c ha p t e r 2 suggests that pain can occur at or near full extension in both the loaded and unloaded knee. In the rotator cuff tendons, arguments to counter impingement come from Uhthoff and Matsumoto who suggest that if impingement was the cause of rotator cuff disease, then the pathology should be consistently on the bursal side of the tendon. Yet, rotator cuff pathology is in fact nearly always on the articular side of the tendon. Compressive or stress-shielding as an etiological cause of tendon pain have recently been proposed by several authors Almekinders et al.
The compression hypothesized is not mechanical impingement in nature, but more intrinsic to the tendon. These theories need investigation as it is clear that critical etiologic questions such as the nature of tendon load must be answered quickly, as it is the essence of adequate management. Tendon load can take many forms, tensile, compressive or shearing.
Tendon load may be directly responsible for tendon pathology, and induce many changes in the tendon. However, tendon load may also provoke other reactions in the tendon as a response to load. These tendon reactions may initiate or accelerate tendon pathology, alone or in conjunction with other tendon reponses, and are considered in the following sections. Thermal The storage and release of elastic energy in tendons discharge intratendinous heat.
Cell loss affects the tendons ability to respond to stress and remodel the matrix. This particular model of etiology of tendon pathology explains central core tendinopathies very well. Good vascularity may allow for adequate cooling of the tendon. However, the relationship between the increase in vascularity seen in tendinopathy and thermal model of pathology has not been established. There is a similar species of nitrogen based molecules, and a combined nitrogen and oxygen species may also be formed. Although these species are formed during normal cell function, strong stimuli such as exercise may enhance their formation.
During exercise, bouts of ischemia and reperfusion may stimulate formation of reactive oxygen species Kannus Cell death may be a consequence of reactive species, and has been shown to be increased by greater amounts and longer exposure to hydrogen peroxide Yuan et al. Similarly, nitrous oxide has been extensively investigated as a messenger molecule that responds to shear stress in cells van Griensven et al. Measured nitrous oxide levels were increased with cyclic strain and these increased levels were hypothesized to positively modulate cellular function Murrell et al. Recent research indicates that the treatment of tendinopathy may be enhanced by the addition of nitrous oxide Paoloni et al.
Tendons may adapt to the presence of reactive species when exposed continually to them, as in etiology of tendinopathy regular and similar exercise routines, by increasing antioxidant defense mechanisms. Endstage disease in humans have shown no physiologic increase in PGE2 in tendinopathic tissue at several different sites when compared with normal tendon tissue Alfredson et al. PGE2 has been shown to increase in the peritendinous space after exercise Langberg et al.
As mechanical load can increase the tendinous Almekinders et al. Autocrine and paracrine substances Cells in or near to the tendon produce many substances cytokines and enzymes that act on tendon tissue. The cytokines produced by the tendon and peritendon cells act in many different ways including as growth factors Molloy et al.
The peritenon cells appear to be more active than, and respond differently to, the 15 tendon cells themselves Banes et al. Very small amounts of cytokines are needed to affect tissue changes, and more of these substance does not necessarily increase its effectiveness Evans Cytokines interact with other cytokines and substances, so investigation of single cytokines may not be relevant to in vivo tendon pathophysiology.
Consideration of all substances is beyond the scope of this chapter. The role of matrix metalloproteinases MMP and other substances that have been investigated including stress-activated protein kinases can be found in other chapters in this book. Theoretically, cell disablement or death should be the main effect of hypoxia, with a consequent decrease or abolition of the capacity of the tendon to produce tendon matrix components and repair. Importantly, these changes were seen in cells from samples taken after tendon rupture, which does not delineate cause and effect.
The hypoxic changes may have occurred during the process of tendon pathology, during tendon rupture or after rupture prior to sampling. The presence of hypoxia in tendon pathology prior to rupture is supported by reports of increased lactate levels in Achilles tendinopathy Alfredson et al. Increased lactate suggests anaerobic metabolism, used by tendon cells with a limited supply of oxygen. This study did not report if the pathologic tendons demonstrated increased vascularity on imaging, a common occurrence in tendon pathology that should preclude hypoxia.
Cells exposed to decreased oxygen tension still exhibited cell proliferation but 16 c ha p t e r 2 demonstrated decreases in collagen production Mehm et al. Similar to Mehm et al. These two studies suggest that hypoxia may affect the extracellular structure of tendon, rather than the cellular components.
Tendinopathy in athletes - Ghent University Library
This is consistent with what is seen histopathologically in tendon pathology, where cellular presence is maintained in most situations, but the extracellular structure is disrupted. The link between hypoxia and changes in vascularity in tendon pathology is unclear. Hypoxia is a powerful stimulant to angiogenesis. Alternatively, impaired vascularity may lead to hypoxia. Angiogenesis is controlled by a variety of mitogenic, chemotactic, or inhibitory peptide and lipid factors Pufe et al. Vascular endothelial growth factor is absent in adult tissue Pufe et al. Some pathologic tendons do not demonstrate increased vascularity on imaging Zanetti et al.
It is unknown why some tendons react by markedly increasing vascularity visible on imaging and others do not. In vivo, Biberthaler et al. Lower vascularity may be associated with areas of decreased oxygen levels. Other authors do not support this, Uhthoff and Matsumoto consider that the area of hypovascularity is not related to the etiology of tendinopathy, and that the pathology process starts at the insertion. Neural The body of a tendon is poorly innervated. The myotendinous and osseotendinous junctions and the peritendon are well innervated, but the tendon proper does not have a good neural supply.
Although sparse in sections, the nerve supply of the tendon may have important roles in the onset of pathology, pain production, and tendon repair. Substance P can induce mast cells to release other substances that affect tendon tissue Hart et al. The role of neural substances in tendon repair has also been reported. Increases in heat and mechanical sensitivity were associated with these changes. Apoptosis Cell death apoptosis is a physiologic event that maintains, protects, and develops the body, and may be programmed or occur in response to trauma.
Pathologically, apoptosis is associated with neural and joint disease, with impaired apoptosis being associated with cancer Yuan et al. Apoptosis is closely associated with the levels and actions of reactive nitrogen and oxygen species. Investigations of apoptosis in tendinopathy have increased dramatically in the last few years. Although apoptosis has been demonstrated in pathologic tissue, it is not yet been shown if apoptosis is a cause or a consequence of tendon pathology. Only mechanically induced apoptosis is likely to be a direct cause of tendinopathy, whereas in the remaining circumstances other events must precede apoptosis Scott et al.
Pathologic tissue has been examined in the ruptured rotator cuff, and the amount of apoptosis in the tendon cells was greater than normal tendon Yuan et al. It is unclear from this data whether apoptosis is a cause or effect of the tendon rupture; if a ruptured tendon is not under tension, it may well change its nature and content. The authors suggest that the apoptosis could be secondary to ischaemia, hypoxia, free radical generation, and nutritional imbalances. This same study also demonstrated that increasing age and pathology in 17 associated tendons might increase the amount of apoptosis in normal tissue.
Ground substance Tendon remodeling and response to load may be implicated in tendon pathology. An investigation of the patellar tendons in a cohort of young active individuals suggests that there may be a sequence of pathologic changes in tendon Cook et al. In this study, activation of tenocytes occurred in isolation in some tendons while increased ground substance only existed in conjunction with activated tenocytes. Tendons with collagen separation were associated with both increased ground substance and tenocyte activation.
Neovascularization was not evident in this cohort of asymtomatic tendons that were mostly normal on imaging, suggesting that changes in vascularity may be associated with both pain and imaging changes. Although the study was cross-sectional in nature, it is tempting to speculate that a temporal sequence of events occurs in tendon exposed to load. Ground substance increases underpin many of the changes seen in tendinopathy, and may be responsible for some or all of the collagen changes seen.
This study suggests that activated tenocytes preferentially manufacture ground substance, rather than collagen. Pharmacology There are medications that are known to directly and adversely affect tendon tissue. The Achilles tendon is most affected and rupture occurs in approximately one-third of affected patients Movin et al.
Symptoms in those that do not rupture settle in several months. Corticosteroids are unique in that they are used to treat tendon pain, but at the same time are reported to potentially have adverse effects on tendon tissue. Although clinically and anecdotally it has been associated with rupture, and most clinicians are hesitant to use corticosteroids to treat tendon pain, there is little evidence to suggest that it has any impact on tendon tissue. It could be hypothesized that rupture after corticosteroid injection occurs because the pain is removed, and the athlete places increased load on the tendon.
Until there is a clearer understanding of the role of corticosteroids in tendon pathology and repair, their clinical use should be minimal. In vitro, corticosteroids have been shown to affect tendon cell migration. The authors hypothesize that this may be a factor in the relationship between corticosteroid and tendon pathology Tsai et al. Etiology of tendon pain Clinically, tendon pain is considered to be the onset of tendinopathy.
Acknowledging that there is likely to be a pre-existing pathology challenges both clinical acumen and treatment options. The source of pain in tendinopathy is obscure. Although biochemical substances have been proposed Ljung et al. Vascular and neural mechanisms have also been investigated Ohberg et al.
An unknown pain pathway compromises our understanding of the etiology of symptoms, as both the stimulus for pain and its perpetuation are unknown. It is then certain that the treatment for tendon pain must also be obscure. Although the imaging is normal, the tendon may not be. Tendon imaging is a wonderful clinical tool, but it does not show low levels of tendon disease. Several studies have shown pathology in imaging normal areas of tendon Movin et al. Tendon pain may exist in imaging normal tendons, but low levels of pathology may still exist for tendon pain.
Most importantly, the clinician must be an accurate diagnostician as many tendons are surrounded by complex anatomic areas, and non tendinous structures may be the source of pain. The load reported by the athlete is nearly always associated with a change in training type, volume, intensity, or frequency. The quantity and quality of overload needed to exacerbate symptoms may vary between individuals and depend on physical capacity, tendon capacity, tendon pathology, or individual characteristics such as biomechanical alignment.
The type of muscle contraction, the frequency, speed, and amount of tendon load may have independent or cumulative effects on tendon pain. However, clinically it is clear that eccentric load is implicated in the onset of tendon pain. Rotator cuff pathology and pain is common in swimmers; however, this tendon condition is complicated by the anatomic, biomechanical, and functional complexity of the shoulder in swimming. Eccentric exercise offers its best outcomes in tendon pain in the midtendon, and is less effective in insertional tendinopathy Fahlstrom An increase or sudden change in load has been associated with an onset of pain in several tendons.
Increasing training times has been linked to the onset of pain in the patellar tendon Ferretti , Achilles tendon Clement et al. Recent research has reported that female athletes with patellar tendon pathology not necessarily pain trained on average 2. More weight training has been linked to symptoms in the patellar tendon Lian et al. The association between pain and neovascularization is not absolute, as some studies demonstrate that tendons with neovascularization may not be painful Khan et al.
Conversely, pathologic tendons without neovascularization may also be painful. However, there is evidence that there is more pain in pathologic tendons with neovascularization compared with pathologic tendons without neovascularization Cook et al. Neuropeptides Neuropeptides transmit nociceptive information to the central nervous system, as well as have a local effect on tendon tissue.
Their effect on regional tissue and the possible role in tendon pathology has been considered in this chapter, and their nociceptive role may be implicated in tendon pain. Neuropeptide substance P and the associated sensory nerves have been demonstrated in elbow tendinopathy Ljung et al. As these peptides increase with chronic pain they may be implicated in tendon pain. Risk factors for tendinopathy Many characteristics have been hypothesized to be risk factors for the development of tendon pathology and pain.
These factors must be considered by clinicians when assessing an athlete with tendinopathy; however, little evidence underpins their role in tendon pain and pathology. Demonstrated risk factors for tendinopathy are sparse in the literature as most studies of risk factors investigate all injuries. In addition, most risk factors have been investigated for the onset of symptoms as this has clinical importance. Few studies have reported risk factors for pathology, and as many pathologic tendons do not go on to cause symptoms or rupture, identifying risk factors for both symptoms and pathology has value.
Risk factors such as tendon load and pharmacology considered in other sections are not reviewed here. Mokone et al. Both these genes are found near to the locus for the ABO blood group. Wide variation in tendon strength and size between individual horses has been reported Smith et al. If humans have various tendon sizes, and these tendons have limited capacity to adapt their matrix when under increased load Smith et al. The ABO antigens of blood groups are found in other tissues including tendon, and may affect tendon tissue directly or through its genetic location on chromosome 9 Maffulli et al.
In the Achilles tendon, studies have shown both a positive association Kujala et al. Ethnic group differences in the subjects of these studies may have impacted on the results. Gender Female gender is reported to increase the risk of tendinopathy Kannus due to strength, body composition, and biomechanical differences in women compared with men. Despite these reports, women are much less likely than men to present etiology of tendinopathy for either conservative or surgical treatment for tendon injury.
This suggests that women suffer less tendinopathy than men. However, reporting prevalence of a disease based only on those presenting with symptoms may not give a clear picture of the true gender distribution of tendinopathy. Large cohort studies of patellar tendinopathy support a decreased risk for females to develop lower limb tendinopathy. In a large series of adolescent and adult patellar tendons, there was a greater ratio of tendon pathology not symptoms in males compared to females 2 : 1 Cook et al. Similar ratios are demonstrated in the Achilles tendon Maffulli et al.
Several studies report that the risk of tendinopathy for females compared with males increases with age. Biomechanically it has been reported that older female tendons were stiffer than male tendon, which may predispose to tendon pathology Hart et al. Both these factors may increase the risk of tendon disease in older females Maffulli et al.
This may explain the greater prevalence of repetitive motion disorders often peritendon pathology in females. Peritendon disorders are reported to be more common in women than men and hand and wrist disorders have a ratio of at least 4 : 1 women to men Ta et al. A proposed subset of sufferers of repetitive motion disorders has multiple sites of tendon disorders mesenchymal syndrome. This is commonly seen in women over 30 years and is reported to be associated with diminished estrogen levels and premature menopause Nirschl The syndrome has been reported in men.
Ligament injury has been linked to the phases of the menstrual cycle Karageanes et al. Ligament tissue and tendon tissue are similar and it could be suggested that a similar situation existed in tendons. Both ligaments 21 and tendons have estrogen receptors Hart et al. It has also been shown that estrogen affects tissue repair Liu et al. In this study, athletes with unilateral tendinopathy could be discriminated from normal subjects by a greater tibial length, a smaller waist : hip ratio and eccentric strength of the affected leg. Subjects with bilateral tendinopathy did not vary from normal subjects.
This is consistent with research that suggested that the prevalence of bilateral tendinopathy may be different from that of unilateral tendinopathy Cook et al. In this study, women had 1 : 1 ratio of bilateral tendinopathy with men. Unilateral tendinopathy has a 2 : 1 ratio. Both these studies suggest that the cause of bilateral tendinopathy may be different than unilateral tendinopathy. Hypothetically, those athletes without a genetic predisposition to tendinopathy would sustain pathology in the tendon subject to a causative factor, such as load.
Those predisposed to tendinopathy when exposed to a causative factor develop pathology in both knees. Therefore, redevelopment of symptoms in tendons may not be associated with injury to scar tissue from previous injury as seen in other types of injury such as musculotendinous sprain Orchard Clinically, previous injury appears to affect muscle strength, which appears to place the tendon under increased potential to develop symptoms.
Although quadriceps strength has been shown to be 22 c ha p t e r 2 lower in affected patellar tendons Gaida et al. Several other systemic and genetic diseases predispose the tendon to symptoms. Systemic lupus erythematosus Prasad et al. Psoriasis has also been associated with tendon rupture Aydingoz and Aydingoz Lipid metabolism Increased levels of blood lipids may directly affect the tendon or tendon vascularity, both of which may lead to pathology and pain.
Increased serum lipids levels have been associated with Achilles tendon rupture in several studies. Only one study has compared results with a control group and they reported serum cholesterol levels to be higher in subjects with tendinopathy than the control group Ozgurtas et al. Other studies of subjects with Zehntner et al. This suggests that old age for tendon pathology may in fact be earlier than middle age, as pathology precedes rupture. In isolation, ageing does not mean that a tendon must be degenerate or have pathology.
Maffulli et al. Major changes associated with aging include a decrease in ultimate strain and load, tensile strength, and an increase in stiffness. It is clear that these many changes must compromise the capacity of the tendon to absorb and respond to load. These changes in function are a result in structural change.
For example, a decrease in cartilage oligomeric matrix protein whose function is to align collagen molecules Smith et al. Changes in collagen cross-links in aging tendon are also important in changing the mechanical properties of tendon Banks et al. This may be because of the capacity of the original tissue as well as a decline in the ability of older tendons to repair.
Young age Tendons of younger athletes may be structurally and functionally adaptable, but this does not protect them from tendon pathology and symptoms. As young tendons are smaller and can take less stress than mature tendons Ker , overload at this age may easily stimulate tendinopathy Smith et al. Young partially disrupted ligament tissue repairs more quickly than older tissue and this may be analogous to tendon Provenzano et al. Tendinopathy has been shown to exist and to change in the patellar tendons of young athletes.
More importantly, when followed over time, these young athletes were at a greater risk of developing symptoms than the adult athletes Cook et al. Witvrouw et al. Kaufmann et al. Clinically, assessing and treating foot mechanics remains an important part of a management plan. Gaida et al. Lian et al. The difference in athlete gender, experimental method, and diagnostic criteria may explain the difference in the outcomes of these studies.
Very little research has been conducted that investigates strength in other tendons, except when the athlete presents for treatment of symptoms with conservative or surgical management. Recent success with heavy load eccentric exercise in the treatment of tendinopathy Alfredson et al. Extrinsic risk factors It is clinically accepted that a change in load, training errors linked to a change in load , changes in the environment, and change or faults with 24 c ha p t e r 2 equipment such as racquets can result in an onset in tendon symptoms Kannus Other extrinsic factors have little evidence to support them and further research is required.
Conclusions This chapter has highlighted the challenges that face researchers and clinicians in understanding and treating tendinopathy. As pathology and pain may have different etiologies, and clinicians and researchers have different priorities, amalgamating knowledge in a form that will deliver better outcomes for athletes will be a long-term prospect. Eccentric load that occurs in many athletic activities is associated with the onset of tendinopathy, as those sports without large eccentric loads cycling, rowing do not have athletes with tendinopathy.
However, reducing eccentric load in an athletic training program remains almost impossible. Tendon matrix response to load seems to be slow several days see Chapter 5 , and this suggests that high tendon load activity should not be undertaken daily. Contrary to this, each individual may have the potential to respond differently to tendon load, and simple load management may not be applicable to every athlete. Gender, age, and disease are all known to directly affect tendons; however, these are not under the control of either the coach or the athlete.
Future directions The direction of future research must focus on factors both within the tendon and within the athlete as well as extrinsic factors and preventative strategies. Tendon factors that require investigation include the stimulants to repair, understanding the source of pain, the relationship between pain and pathology, and the stimuli that set an athlete on the pathways to pathology and to pain. In vitro models of tendinopathy are improving but remain independent of so many factors intrinsic to an athlete. In vivo examination of tendon response is the future for this research.
Identifying athletes at risk may allow the athlete strategies to avoid tendon pain and pathology. A step by step research program with multicenter collaborations will be the best approach to future tendinopathy research in all these areas. Journal of Orthopaedic Research 21, — Knee Surgery Sports Traumatology Arthroscopy 11, — An investigation using microdialysis technique.
Journal of Orthopaedic Research 20, — Journal of Orthopaedic Research 19, — Acta Orthopaedica Scandinavica 71, — As of , all the articles are published in English, Catalan and Spanish. All of which undergo an anonymous external peer review process. CiteScore measures average citations received per document published.
Read more. SRJ is a prestige metric based on the idea that not all citations are the same. SJR uses a similar algorithm as the Google page rank; it provides a quantitative and qualitative measure of the journal's impact. SNIP measures contextual citation impact by wighting citations based on the total number of citations in a subject field.
Tendinopathy has a multifactorial etiology that is not well understood. Risk factors are often separated into extrinsic those acting on the body and intrinsic groups those acting from within the body. In this narrative review, we will separate potential risk factors into 1 load-related extrinsic ; 2 biomechanical factors intrinsic ; and 3 other individual factors such as systemic factors intrinsic.
Too much load is clearly linked to tendinopathy, but there appears to be large variation in how much load individuals can endure before developing tendinopathy. Less active people also suffer tendinopathy, suggesting that the effect of load is likely to be moderated by intrinsic factors. These individual intrinsic factors are likely to reduce tolerance or capacity to withstand load.
This narrative review will provide a brief overview of key potential risk factors and mechanisms, as well as limitations in the current literature.. In the lower limb, repetitive stretch-shortening cycles SSC of the muscle-tendon unit e. During SSC there is energy storage through elastic lengthening of the tendon and subsequent release of some of the stored energy to reduce the energy cost of locomotion. The magnitude of tendon load can be quite high during SSC activities. For example, Achilles tendon load is reported to be times bodyweight in running 5,6 and as high as times bodyweight in submaximal hopping.
Even during a maximal isometric planterflexion contraction load is about of a third to half 3. Patellar tendon load during loaded squatting 4. The tendon strain rate may explain why tendinopathy is associated with repetitive SSC rather than slow and heavy loads. Compression has been suggested to play a part in most insertional tendinopathies, or enthesopathies. A bony prominence, and at some sites bursa adjacent to the enthesis, have a role in absorbing and dispersing enthesis loads thereby limiting stress concentration at the tendon-bone junction.
Tendons adapt to the increased compressive loads at the enthesis with increased fibrocartilage, larger water-binding proteoglycans and type II collagen.
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Their conclusions were that a compressive load alone did not lead to reduced mechanical properties, but a combination of compressive and tensile load was more damaging than tensile load alone. For insertional tendinopathies reducing enthesis compression is suggested to be an important aspect of prevention and management. Tensile stress may not be uniform throughout a tendon. Studies investigating cadavers, 16 optic fibers in vivo 17 and mathematical modeling 18 have found greater tensile strain in the posterior compared with the anterior side of the patellar tendon.
This contrasts to Almekinders et al. This is an ambiguous term, but is normally considered to encompass any alterations in physical load on the tendon. Returning to training after a short break, e. The break in exercise is thought to lead to deconditioning, resulting in tendinopathy on a return to normal load. This is often evidenced in patients who misguidedly go through periods of rest to settle the tendon and then return to normal loading immediately, inevitably re-triggering symptoms.. Load management has recently been extensively investigated by Gabbett and colleagues.
Training hours per week is associated with patellar tendon pain e. McCrory et al. Repeating loading too often frequency may also be important. Four or more volleyball sessions per week was associated with a doubling of the prevalence of patellar tendon pain. It should be made clear, however, that factors such as training hours per week and sessions per week are not consistently associated with tendinopathy in the literature. This may be explained by confounders, including change in load..
How does load lead to pathology? How energy storage and compressive loads may lead to tendon pathology is largely unknown. The current body of evidence suggests the pathogenesis of tendinopathy involves a change in tissue homeostasis. Homeostasis is normally maintained by the tendon cells tenocytes , which control tendon protein synthesis through various chemical messengers.
Tendon matrix is directly influenced by the activity of tenocytes. In a normal Achilles tendon we expect to find a change in the collagen structure to fibro-cartilage at zones that undergo high compressive loads, this is an example of the capacity of tenocytes to respond to different loads. Individual biomechanics, including movement kinetics and kinematics, foot posture, flexibility, neuromuscular capacity and structural anatomy may influence tendinopathy risk. Given patellar tendon forces were similar between the groups, the authors suggest that the landing strategy of the pathology group may involve greater patellar tendon shear forces.
Azevedo et al. It is possible that this kinematic pattern is a protective compensation to reduce Achilles tendon load. This example highlights the limitations of cross sectional research design where associated factors may develop secondary to pain.. Foot posture and function dynamic pronation has been proposed as a risk factor for lower limb tendinopathy, 27 although there is conflicting literature. There is also limited or conflicting evidence linking plantar heel pain with static and dynamic foot posture.
Murley et al. Muscle flexibility e.
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Unfortunately, the results are often conflicting, which leaves the clinician with a dilemma in attempting to manage and prevent injury.