Physical Therapy in Sport
Volume 13, Issue 1 , Pages 3-10, February 2012

Tendinopathy in athletes

  • Mark Reinking

      Affiliations

    • Corresponding Author InformationTel.: +1 314 977 8531; fax: +1 314 977 8513.

Saint Louis University, Department of Physical Therapy and Athletic Training, Doisy College of Health Sciences, 3437 Caroline Mall, Saint Louis, MO 63104, United States

Received 23 September 2010; received in revised form 11 June 2011; accepted 17 June 2011. published online 05 August 2011.

Article Outline

Abstract 

Overuse related tendon pain is a significant problem in sport and can interfere with and, in some instances, end an athletic career. This article includes a consideration of the biology of tendon pain including a review of tendon anatomy and histopathology, risk factors for tendon pain, semantics of tendon pathology, and the pathogenesis of tendon pain. Evidence is presented to guide the physical therapist in clinical decision-making regarding the examination of and intervention strategies for athletes with tendon pain.

Keywords: Tendinopathy, Tendinitis, Tendinosis, Overuse injury

 

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1. Introduction 

Overuse related tendon pain is a very common condition in sport. Kannus (1997, p. 53) wrote that tendon pain is a “source of major concern in recreational and competitive athletes”. Overuse injuries are more common than macrotraumatic injuries in athletics (Brukner & Bennell, 1997), and much of overuse injury is tendon related. Tendon pain is frequently reported in sports including volleyball, basketball, long distance running, and jumping events in track and field (Ferretti et al., 1985, Jarvinen et al., 2005, Kujala et al., 2005, Lian et al., 2005, Taunton et al., 2002). The tendons most commonly susceptible to overuse injuries are the patellar, Achilles, posterior tibialis, rotator cuff, long head of the biceps brachii, and the wrist extensors (Maffulli, Wong et al., 2003, Rees et al., 2006).

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2. Tendon histology 

The function of a tendon is to attach muscle to bone, thereby transferring force of the contracting muscle to bone and either inducing or controlling movement. The efficiency of this force transfer is maximized by minimal elasticity of the tendon. When muscular contraction occurs, the tendon is subjected to tensile loading. This results in the storage of elastic energy within the tendon. As human tendons demonstrate minimal hysteresis, most of the elastic energy stored in the tendon is released when the tensile load is removed (Maffulli, Renström, & Leadbetter, 2005). During the stretch-shortening cycle when an eccentric contraction is immediately followed by a concentric contraction, this stored energy is thought to contribute to the force generation and mechanical efficiency of the movement (Lieber, 2002, p. 168). This phenomenon has been supported is research in vivo on human Achilles tendons (Kubo, Kanehisa, & Fukunaga, 2005).

Each tendon has two junctional regions; the myotendinous junction (MTJ) at the muscle end of the tendon and the osseotendinous junction (OTJ) at the bone end. At the OTJ, or enthesis, there is a gradual transition of tissue from tendon to fibrocartilage to bone. Some tendons like the Achilles and the wrist extensors have the muscle insertion along the same line as the muscle belly and are referred to as traction tendons. In other tendons, like the posterior tibialis and the quadriceps, the tendon direction is not along the same line as the muscle belly, and these are referred to as gliding tendons. As gliding tendons encounter compressive and shear forces as they course around bony landmarks, the etiology of tendon pain in these tendons is likely different than that in traction tendons (Pufe, Petersen, Mentlein, & Tillmann, 2005).

The microanatomy of the tendon includes an extracellular matrix containing water, proteoglycans, glycoproteins, collagen, and elastin. The collagen is predominantly Type I in a normal tendon and the collagen fibers are arranged in a parallel fashion. The orientation of the fibers and the biomechanical properties of Type I collagen are designed for the force transmission from muscle to bone. The cells of the tendon tissue are tenoblasts and tenocytes, which are fibroblastic cells and active in the production and secretion of proteins (Maffulli et al., 2005). Tendon loading stimulates an acute increase in collagen synthesis, which peaks around 24 h after exercise and remains elevated for up to 72 h (Magnusson, Langberg, & Kjaer, 2010). However, the degradation of collagen is also increased after exercise, likely at a greater level than the increase in synthesis. Consequently, for the first 36 h after exercise, the collagen metabolic system is in a negative balance with degradation greater than synthesis (Fig. 1). This may explain that repeated exercise without sufficient rest can leave an athlete in a state of repeated collagen breakdown, and the development of overuse injury (Magnusson et al., 2010).

The collagen fibers are arranged into bundles, or fascicles, which are surrounded by the endotenon. The fascicles are bundled together by the outer epitenon layer which is intimately attached to the tendon. In some tendons, there is a layer external to the epitenon, the paratenon, which is lined with synovial cells and provides a resistance to friction over bony surfaces (Fig. 2). A painful tendon may have histopathological changes in the collagenaceous matrix or in the sheath, or both (Abate et al., 2009).

The vascular supply for most tendons comes from the OTJ and the MTJ, leaving a potential vascular compromise in the mid region between the OTJ and MTJ. Small vessels extend through the mesotenon, connecting the paratenon and the epitenon. In painful tendons, neovascularization occurs in which small, thin walled blood vessels proliferate, causing an increase in tendon blood flow (Alfredson and Ohberg, 2005, Alfredson et al., 2003, Cook, Malliaras et al., 2005, Ohberg et al., 2001, Pufe et al., 2005). The stimulation for this angiogenesis is upregulation of vascular endothelial growth factor (VEGF) in pathic tendons (Pufe et al., 2005, Scott et al., 2008). Not only does VEGF stimulate the formation of the neovessels, but it also stimulates production of metalloproteinase enzymes, lytic to collagen, and downregulates the inhibitors of such enzymes (Pufe et al., 2005). The consequence of the VEGF action is decreased collagen strength and predisposition to additional microtears. VEGF and angiogenesis has been associated with painful tendons in several studies (Alfredson and Ohberg, 2005, Cook, Malliaras et al., 2005, Ohberg et al., 2001, Pufe et al., 2005).

Nerve supply to and from tendons comes from surrounding muscle and vary by tendon and by regions of the tendon (Abate et al., 2009). For example, tendons of the finger flexors have greater innervation than the Achilles, and innervation tends to be greater toward the MTJ and the OTJ. The nerve endings in tendons include Ruffini corpuscle and Golgi tendon organ mechanoreceptors as well as free nerve endings that serve a nociceptive function. In a painful tendon, there is a marked increase in the ingrowth of these free nerve endings (Magnusson et al., 2010, Sanchis-Alfonso et al., 2001), and there is also evidence of higher concentrations of excitatory neurotransmitters in painful tendons (Alfredson, 2005, Andersson et al., 2007, Bjur et al., 2005, Lian et al., 2006, Schubert et al., 2005).

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3. Risk factors for tendon pain 

There is evidence that some individuals may be more at risk for developing tendon pain than others. These risk factors are classified as intrinsic (within the body) or extrinsic (outside the body) and modifiable or non-modifiable. Intrinsic non-modifiable risk factors include increasing age (Astrom, 1998, Birch et al., 2001, Riley et al., 2001, Sargon et al., 2005, Tuite et al., 1997), gender (Ashford et al., 2002, Astrom, 1998, Astrom and Rausing, 1995, Holmes and Lin, 2006, Knobloch et al., 2008, Lian et al., 2005, Ramos et al., 2009, Riley et al., 2001), and an individual’s genetic makeup. Josza et al. (1989) described an increased frequency of tendon injury in persons with blood type O, and this was confirmed by Kujala et al. (1992). However, other studies have not found this same association between blood group and tendon pain (Leppilahti et al., 1996, Maffulli et al., 2000). New evidence suggests that one or more genes proximal to the ABO gene on chromosome 9 may be a causal factor in the development of tendon pain (Magra and Maffulli, 2007, Mokone et al., 2005, Mokone et al., 2006).

Modifiable intrinsic risk factors for tendon pain that have been reported include abnormal kinematics (Abate et al., 2009, Azevedo et al., 2009, Grau et al., 2008, Richards et al., 2002, Richards et al., 1996, Ryan et al., 2009, Souza et al., 2010), muscle inflexibility (Cook et al., 2004, Witvrouw et al., 2001), obesity (Frey and Zamora, 2007, Holmes and Lin, 2006), and decreased eccentric muscle strength (Gaida et al., 2004, Grau et al., 2008). Modifiable extrinsic risk factors include sport (Ferretti, 1986, Kujala et al., 2005, Lian et al., 2005, Maffulli, Sharma et al., 2004, Maffulli, Wong et al., 2003, Sein, 2006) and training volume and surface (Ferretti, 1986).

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4. Semantics of tendon pathology 

One of the issues that have contributed to confusion in understanding tendon pain is the multiple terms associated with tendon pain. Bernstein (2006) wrote in an editorial on linguistic determinism in medicine that “the names of the diseases, one might argue, set the bounds on our thought, possibly to the detriment of patients.” One example he used in that editorial was the rather indiscriminate use of the term “tendinitis” for all tendon pain. Tendinitis describes a specific histopathological entity in which a predominant characteristic of the condition is inflammatory. In fact, multiple studies have suggested that a painful tendon may not have the presence of inflammatory cells or mediators (Abate et al., 2009, Hashimoto et al., 2003, Khan et al., 1999, Maffulli, Testa et al., 2004, Movin et al., 1997, Potter et al., 1995, Uhthoff and Sano, 1997). Bernstein (2006) argued that naming all tendon pathology “tendinitis” may lead a practitioner to an incorrect line of reasoning in designing a plan of care.

Tendinosis is used to describe a chronic degenerative state of a tendon where there is a conspicuous lack of inflammatory cells, disorganization and separation of the collagen bundles, increased proteoglycans in the extracellular matrix, hypercellularity, and neovascularization (Khan et al., 1999, Khan et al., 2002, Maffulli, Wong et al., 2003). Paratenonitis, also known as tenosynovitis, is an inflammatory condition of the paratenon and is characterized by the presence of inflammatory cells, hypervascularity of the sheath, and development of a fibrinous exudate in the sheath space causing tendon crepitation.

The terms tendinitis, tendinosis, and paratenonitis are all reserved for specific histopathologic conditions of the tendon, which, in fact, may not be known by the treating clinician. Several authors have suggested that tendinopathy is a better term for clinicians to use in describing tendon pain as it is histopathologic neutral (Cook, Khan, Kiss et al., 2000, Jarvinen et al., 2005, Khan et al., 2002, Khan et al., 2000, Maffulli et al., 1998, Stasinopoulos and Johnson, 2006).

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5. Pathogenesis of tendinopathy 

The controversy pertaining to the pathogenesis of tendinopathy and the inflammatory pathway is one that has persisted. Fredberg and Stengaard-Pedersen (2008) challenged the tendinitis myth with recent evidence that pro-inflammatory agents are present in chronic tendinopathies, and the rapid response to corticosteroid intervention. These authors described a “tendinopathic iceberg” (Fig. 3) with a long period of time of asymptomatic changes in tendon with the exposed tip of the iceberg being a painful tendon. In a review paper, Abate et al. (2009) supported this iceberg theory and proposed a pathway of the pathogenesis of tendinopathy beginning with overuse leading to microdamage of the tendon, followed by inadequate tendon healing, a pathologic cascade of events including neovascularization, nerve ingrowth, tendon degeneration, and, ultimately, a painful tendon at the tip of the iceberg. In their conclusion, Abate et al. (2009) wrote that “it is conceivable that inflammation and degeneration are not mutually exclusive, but work together in the pathogenic cascade of tendinopathy.”

Cook and Purdam (2009) have described a pathological model of the tendinopathy continuum with three stages: reactive tendinopathy, tendon disrepair, and degenerative tendinopathy (Fig. 4). The purpose of this model is to assist the clinician in determining appropriate intervention for the tendinopathy based on the pathology stage. These authors provide pharmacological and physical management guidelines based on whether the athlete is in the reactive tendinopathy/early tendon disrepair, or the late tendon disrepair/degeneration stage.

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6. Clinical examination of the athlete with a painful tendon 

In the clinical examination of an athlete with a painful tendon, taking a thorough history is crucial. Leadbetter (1992) emphasized the significance of the “principle of transitions” for athletes with overuse injury. This principle states that injury is most likely when an athlete has made some kind of training change including training routine (intensity, frequency, duration), training surface, equipment, or technique. Accordingly, taking the history must include questions that provide the examiner with information about potential transitions that may have led to the development of tendon pain. The typical presentation of tendinopathy is gradual onset of load-related tendon pain which, depending on the chronicity of the problem, may interfere with athletic performance or, in late stages, with activities of daily living. Staging of the overuse tendon condition is recommended using a grading system like that of Blazina, Kerlan, Jobe, Carter, and Carlson (1973) or Nirschl (1992) in order for the examiner to understand the level of restrictions of activities and sport performance resulting from the painful tendon. Additionally, there are tendon-specific outcomes assessment tools including the VISA scale for patellar (Visentini et al., 1998) or Achilles tendon pain (Robinson et al., 2001) which provide information on the effect of tendon pain on life activities.

Clinical examination of an athlete with tendon pain includes careful observation of skeletal alignment, muscle bulk, tendon size, and swelling. Joint mobility and muscle length are assessed with notation of joint end feels. Standard muscle performance testing is completed which involves loading of the involved tendon, and the examiner should record the presence and location of pain and/or weakness. In some cases, specific tendon loading tests are advocated for testing of the painful tendon such as the decline squat for patellar tendinopathy (Purdam, Cook, Hopper, & Khan, 2003), or the heel raises for Achilles tendinopathy (Alfredson and Cook, 2007, Silbernagel et al., 2006).

Based on the evidence that abnormal kinematics may be risk factors for the development of tendon pain (Abate et al., 2009, Azevedo et al., 2009, Grau et al., 2008, Richards et al., 2002, Richards et al., 1996, Ryan et al., 2009, Souza et al., 2010, Van Ginckel et al., 2009), movement analysis is a critical part of the clinical examination of an athlete with tendon pain. Examples of abnormal kinematic risk factors include excessive foot pronation for patellar (Grau et al., 2008) and Achilles (Donoghue et al., 2008, McCrory et al., 1999, Ryan et al., 2009) tendinopathy and abnormal scapular position and movement for rotator cuff tendinopathy (Ludewig & Reynolds, 2009). Souza et al. (2010) reported that significant differences existed in hopping kinematics between a group of athletes with patellar tendinopathy and a control group with the tendinopathy group showing decreased demand on the knee joint. What is unknown from these data, however, is whether the kinematic differences led to the patellar tendon pain, or were a result of the patellar tendon pain.

Palpation of the involved tendon is routinely done to assess pain, tissue quality, and the presence of crepitation. Studies pertaining to the clinical utility of palpation suggest that moderate tenderness of a tendon is a normal finding in athletes and does not predict pathologic changes within the tendon (Cook, Khan, Kiss, Purdam et al., 2001, Maffulli, Kenward et al., 2003, Ramos et al., 2009).

Imaging of the tendon may provide additional information regarding intra-tendinous changes. Generally, plain-film radiography is of little diagnostic value unless there is calcification within the tendon. Both gray-scale ultrasonography and magnetic resonance imaging can reveal structural changes in tendon including tendon swelling and collagen disorganization. However, such structural changes are not well correlated to symptoms as athletes can have painful tendons without structural change and structural change without pain (Cook, Khan, Kiss, Coleman et al., 2001, Cook, Khan, Kiss, Purdam et al., 2001, Cook, Khan, Kiss et al., 2000, Gold et al., 1993, Khan et al., 1997). Color Doppler sonography allows for quantification of tendon neovascularity in a painful tendon (Cook, Ptazsnik et al., 2005, Gisslen and Alfredson, 2005).

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7. Intervention for the painful tendon 

The intervention plan for an athlete with tendon pain should be based on an integration of the clinician’s clinical judgment, the patient’s values, and the best available evidence (Sackett, 2000). Although tendinopathy is a common condition in athletes, there are few randomized controlled trials that have investigated the interventions recommended for athletes with tendon pain. Consequently, clinical reasoning is crucial in linking restrictions in daily and sport activities with impairments in body structure and function. The focus of this section of the paper is on those interventions typically used by physical therapists.

In the model described by Cook and Purdam (2009), an athlete with reactive tendinopathy/early tendon disrepair should have an imposed period of relative rest in which tendon load is reduced to minimize progression of pathology. This period should not be complete cessation of the offending activity, but a decrease in the overall training volume of the activity. Complete rest through immobilization of a joint has a negative effect on tendon strength and should not be practiced (Kannus, Jozsa, Natri, & Jarvinen, 1997). The training volume parameters – intensity, frequency, or duration – are evaluated and adjusted based on the individual athlete and the circumstances of the case. To maintain cardiovascular and pulmonary fitness, cross training activities with reduced tendon loads are appropriate.

Although physical agents including cryotherapy, ultrasound (US), phonophoresis, and iontophoresis are commonly employed clinically in the treatment of athletes with tendinopathy, there is a paucity of evidence to support their use. Cryotherapy is often used to decrease painful tendinopathic symptoms; Rivenburgh (1992) described the tissue effects of cold including decreasing the movement of protein from capillaries and may decrease blood flow. However, there is no higher level evidence that supports or refutes the use of cold for tendon pain.

Therapeutic US is also a commonly utilized clinical modality for tendon pain. Like cryotherapy, there is no compelling evidence to support or refute its use in patellar tendon pain. Therapeutic US has been shown to have positive effects on collagen production in vitro (Ramirez, Schwane, McFarland, & Starcher, 1997). It has also been shown to have a significant thermal effect when using a 3 MHz treatment at 1.0 W/cm2 (Chan, Myrer, Measom, & Draper, 1998), but whether this is desirable for healing of tendon pain is not known. One study on the effect of low-intensity pulsed ultrasound (LIPUS) on patellar tendinopathy (Warden et al., 2008) concluded that this modality had no additional benefit when compared to placebo ultrasound on patellar tendon symptoms.

Phonophoresis is a technique in which US is used to drive a pharmaceutical agent through the skin into a painful region. Klaiman et al. (1998) compared the effect of US and phonophoresis using fluocinonide on various musculoskeletal conditions including tendon pain. They found that US alone decreased pain and increased pressure tolerance, but the addition of fluocinonide did not augment the effect. Penderghest, Kimura, and Gulick (1998) examined the effect of the addition of phonophoresis to a stretching and strengthening program for patients with tendon pain. Their results were consistent with those of Klaiman et al. (1998). These studies do not support the use of phonophoresis for patients with tendon pain.

Iontophoresis is another modality used to treat tendon pain with a similar rationale as phonophoresis in driving a pharmaceutical across the skin. There is animal research evidence that iontophoresis is effective in driving dexamethasone into patellar tendon tissue (Nowicki, Hummer, Heidt, & Colosimo, 2002). Pellechia, Hamel, and Behnke (1994) showed that iontophoresis with dexamethasone and lidocaine was more effective than modalities combined with transverse friction massage (TFM) for decreasing pain and increasing function in patients with patellar tendon pain. However, the clinical decision to use iontophoresis or phonophoresis with an anti-inflammatory pharmaceutical for tendon pain may be flawed as it presupposes that an inflammatory process is the primary pain generator in tendon pain (Abate et al., 2009, Andres and Murrell, 2008, Cook, Khan, Maffulli et al., 2000, Cook and Purdam, 2009, Khan et al., 2002, Khan et al., 2000).

Another intervention that has been used to treat tendon pain is low-lever laser therapy (LLLT). This modality is relatively new to the United States but has been used in Europe and Canada for many years. A systematic review with meta-analysis on the use of LLLT for tendinopathy was conducted, and 25 controlled clinical trials met the standards to be included in the review (Tumilty et al., 2010). The finding of the review were mixed, with 12 studies supporting the use of LLLT and 13 studies were either not conclusive or did not demonstrate an effect. However, the authors identified that one finding of their review was that the 12 positive studies shared the use of dosages consistent with current dosage recommendations for the treatment of tendon pain (Tumilty et al., 2010).

Transverse friction massage, advocated by Cyriax and Coldham (1984) for tendon pain, is purported to reduce adhesions within the tendon and encourage normal realignment of collagen fibers. There is basic science evidence from animal studies that soft tissue mobilization can increase fibroblastic activity (Davidson et al., 1997, Gehlsen et al., 1999) but there are no studies of the tissue effect of TFM on tendinopathy in humans. The aforecited work by Pellecchia, Hamel, and Behnke (1994) showed a positive effect of the combined TFM/modality intervention, but whether the effect was from the TFM, modalities, or combination is unknown. In a recent systematic review on the use of TFM for treatment of tendonitis, the authors concluded that there was no evidence to support the use of deep TFM (Brosseau et al., 2002).

A common intervention used for patients with tendon pain is counterforce bracing. These braces are applied in circumferential manner to impose a compressive force on a tendon, with the intent of “unloading” the tensile force at the tendon insertion to bone. Studies on the use of counterforce bracing for wrist extensor tendinopathy have shown no change in the force production of the muscle but an increase in the patients’ pain threshold to muscle stretch (Chan and Ng, 2003, Ng and Chan, 2004). In spite of the very common use of this intervention for patients with tendinopathy, evidence to support its use for patellar or Achilles tendon pain is lacking.

As tendon pathology has been historically associated with tendinitis, it is not surprising that anti-inflammatory pharmaceuticals are suggested for patients with tendon pain. Although the prescription of pharmaceuticals is the purview of the physicians, patients seen by rehabilitation professionals may be using over-the-counter non-steroidal anti-inflammatory drugs (NSAIDs) by their own choice. In a systematic review of the literature on treatment of tendinitis, Almekinders and Temple (1998) reported that the use of oral NSAIDs may result in pain relief but the long term effect on the tendon is not known. Similarly, the use of injected corticosteroids may result in pain relief, but there is concern regarding the effect of corticosteroid on tendon strength (Paavola et al., 2002; Shrier, Matheson, & Kohl, 1996). In a randomized, double-blind, placebo-controlled study (Fredberg et al., 2004) of steroid injection in patients with patellar and Achilles tendinopathy, a significant reduction in pain and tendon thickness was observed in the steroid groups for both Achilles and patellar tendon pain. Fredberg et al. (2004) argued that the results of this study suggest that the tendinitis–tendinosis question remains unresolved.

Exercise intervention for tendon pain is common, and decision-making regarding exercise selection should be based on the impairments identified in the examination. Muscle tightness has been proposed as a risk factor for patellar tendon pain (Cook et al., 2004, Witvrouw et al., 2001) and Achilles tendon pain (Kaufman, Brodine, Shaffer, Johnson, & Cullison, 1999). In one study, 46 patients with Achilles tendon pain were randomly assigned to a 12-week eccentric Achilles training program or a calf-stretching program (Norregaard, Larsen, Bieler, & Langberg, 2007). Patients were reevaluated at 3, 6, 9, 12, and 52 weeks for tendon pain, tendon thickness measure by ultrasonography, and the patients’ self-reported outcome. Both groups showed improvement but there was no significant difference between groups (Norregaard et al., 2007). No other study was identified that studied the effect of stretching only on tendon pain.

One area of emerging evidence for the treatment of tendon pain is eccentric exercise. The seminal work on the use of eccentric exercise in tendon pain was done by Curwin and Stanish (1984). They advocated eccentric exercise for patellar tendinopathy to maximally stress the tendon to increase tendon strength. Their program involved six weeks of drop squat training (3 × 10 repetitions/day), progressing in the first week from a slow speed to faster speeds, and then adding resistance in weeks two through six. In a retrospective review of 66 patients treated with the eccentric program for patellar tendon pain, the authors reported complete relief of pain in 20 patients, marked decrease in symptoms in 42 patients, and four patients reported worsening of symptoms (Stanish, Curwin, & Mandel, 2000).

High-load eccentric training has been used successfully to treat non-insertional Achilles tendinopathy (Alfredson, Pietila, Jonsson, & Lorentzon, 1998). One feature of this eccentric training is the significance of pain during the eccentric exercise. Alfredson et al. (1998) proposed that the eccentric exercise should be dosed at 3 × 15 repetitions twice daily, seven days/week for 12 weeks and should be painful to perform. These authors recommended that when a patient reaches the point that the exercise is no longer painful; the load should be increased to the point that it becomes painful again. A systematic review on the appropriate dosage for eccentric exercise in non-insertional Achilles tendinopathy concluded that there is insufficient evidence at this time to establish a set dosage, but the effect of eccentric exercise on Achilles tendon pain was positive (Meyer, Tumilty, & Baxter, 2009).

Eccentric exercise has been used successfully to treat patellar tendon pain (Bahr et al., 2006, Cannell et al., 2001, Frohm et al., 2007, Jonsson and Alfredson, 2005, Purdam et al., 2004, Stasinopoulos and Stasinopoulos, 2004, Young et al., 2005), supraspinatus tendinopathy (Eriksson, 2006, Jonsson et al., 2006), wrist extensor tendinopathy (Croisier et al., 2007, Martinez-Silvestrini et al., 2005, Svernlov and Adolfsson, 2001), and posterior tibialis tendinopathy (Kulig, Lederhaus, Reischl, Arya, & Bashford, 2009). Rees, Wolman, and Wilson (2009) summarized the existing evidence on the effect of eccentric exercise on tendinopathy and identified emerging evidence including increase collagen synthesis, decrease in neovascularization, and a pattern of oscillatory loading not present in concentric exercise.

There is evidence, however, that eccentric exercise may not always be successful in the treatment of tendinopathy. Visnes, Hoksrud, Cook, and Bahr (2005) found that a group of volleyball athletes with patellar tendinopathy did not respond to 12 weeks of eccentric training during the competitive season. As the athletes continued to participate in volleyball training and competition during the eccentric training period, it is not known whether the athletes would have responded to the eccentric training if they were not participating in volleyball activities. Sayana and Maffulli (2007) studied the use of eccentric exercise in a group of 34 sedentary, non-athletic patients. They found that only 56% of patients responded favorably to the eccentric training program, with the other 44% requiring tendon injection or surgery, A follow-up study using high-load eccentric training for Achilles tendinopathy in athletic patients found a similar percent of patients (60%) responded to the eccentric exercise treatment as in the study of non-athletic patients (Maffulli, Walley, Sayana, Longo, & Denaro, 2008).

As described earlier, there is evidence that the development of tendon pain may be related to abnormal kinematics during functional activities. These findings would suggest that a potential intervention for tendinopathy would be interventions to address these abnormal movement patterns. For Achilles tendon pain, a recent published clinical guideline (Carcia, Martin, Houck, & Wukich, 2010) indicated that there was C level evidence (weak) to support the use of foot orthotics to “reduce pain and alter ankle and foot kinematics while running”. Otherwise, evidence is lacking to support interventions designed to address abnormal kinematics in athletes with tendinopathy.

Davenport, Kulig, Matharu, and Blanco (2005) have proposed a non-surgical treatment model for tendinopathy that they referred to as the EdUReP model (Fig. 5). In this model, the approach to tendon pain is educational intervention (Ed), unloading of the tendon (U), gradual reloading of the tendon (Re), and prevention of tendon pain recurrence (P). Although the authors did not subject this model to testing, they proposed it as “an evidence-based treatment construct that aims to reduce functional limitation and disability through amelioration of tissue pathology.”

Other interventions for tendon pain include those that are physician driven including extracorporeal shock wave therapy, nitric acid patches, injections with substances such as normal saline, anesthetics, corticosteroids, polidocanol, aprotinin, or platelet rich plasma, and surgery. Review of these interventions are outside the scope of this paper, but several excellent evidence-based expert reviews of such interventions have been published (Maffulli et al., 2010, Rees, Maffulli et al., 2009, Rees et al., 2006, Riley, 2008).

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8. Conclusion 

Tendon pain is a common condition seen by sports medicine health care professionals. At this time, the evidence suggests that while tendon pain may have an early inflammatory stage, much of what is seen is not a primary inflammatory problem but one characterized by tendon disrepair and degeneration. The treatment of tendon pain is multifactorial and thereby challenging and requires careful consideration of the chronicity of the problem and the athlete-specific impairments associated with the tendon pain. At present, most evidence supports an approach to tendon pain using eccentric exercise, but non-responders must be identified and considered for treatment with other interventions as directed by a physician. There is a pressing need for ongoing research to better identify risk factors and appropriate prevention and intervention strategies for tendon pain.

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Conflict of interest 

There are no conflicts of interest for the author of this manuscript.

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Funding 

No external funding was used in this research.

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References 

  1. Abate M, Gravare Silbernagel K, Siljeholm C, Di Iorio A, De Amicis D, Salini V, et al. Pathogenesis of tendinopathies: inflammation or degeneration?. Arthritis Research and Therapy. 2009;11(3):235
  2. Alfredson H. The chronic painful Achilles and patellar tendon: research on basic biology and treatment. Scandinavian Journal of Medicine & Science in Sports. 2005;15(4):252–259
  3. Alfredson H, Cook J. A treatment algorithm for managing Achilles tendinopathy: new treatment options. British Journal of Sports Medicine. 2007;41(4):211–216
  4. Alfredson H, Ohberg L. Neovascularisation in chronic painful patellar tendinosis-promising results after sclerosing neovessels outside the tendon challenge the need for surgery. Knee Surgery, Sports Traumatology, Arthroscopy. 2005;13(2):74–80
  5. Alfredson H, Ohberg L, Forsgren S. Is vasculo-neural ingrowth the cause of pain in chronic Achilles tendinosis? An investigation using ultrasonography and colour Doppler, immunohistochemistry, and diagnostic injections. Knee Surgery, Sports Traumatology, Arthroscopy. 2003;11(5):334–338
  6. Alfredson H, Pietila T, Jonsson P, Lorentzon R. Heavy-load eccentric calf muscle training for the treatment of chronic Achilles tendinosis. The American Journal of Sports Medicine. 1998;26(3):360–366
  7. Almekinders LC, Temple JD. Etiology, diagnosis, and treatment of tendonitis: an analysis of the literature. Medicine & Science in Sports & Exercise. 1998;30(8):1183–1190
  8. Andersson G, Danielson P, Alfredson H, Forsgren S. Nerve-related characteristics of ventral paratendinous tissue in chronic Achilles tendinosis. Knee Surgery, Sports Traumatology, Arthroscopy. 2007;15(10):1272–1279
  9. Andres BM, Murrell GA. Treatment of tendinopathy: what works, what does not, and what is on the horizon. Clinical Orthopaedics and Related Research. 2008;466(7):1539–1554
  10. Ashford RL, Cassella JP, McNamara S, Stevens RM, Turner P. A retrospective magnetic resonance image study of patellar tendinosis. Physical Therapy in Sport. 2002;3(3):134–142
  11. Astrom M. Partial rupture in chronic Achilles tendinopathy. A retrospective analysis of 342 cases. Acta Orthopaedica Scandinavica. 1998;69(4):404–407
  12. Astrom M, Rausing A. Chronic Achilles tendinopathy. A survey of surgical and histopathologic findings. Clinical Orthopaedics and Related Research. 1995;316:151–164
  13. Azevedo LB, Lambert MI, Vaughan CL, O’Connor CM, Schwellnus MP. Biomechanical variables associated with Achilles tendinopathy in runners. British Journal of Sports Medicine. 2009;43(4):288–292
  14. Bahr R, Fossan B, Loken S, Engebretsen L. Surgical treatment compared with eccentric training for patellar tendinopathy (Jumper’s Knee). A randomized, controlled trial. Journal of Bone and Joint Surgery. 2006;88(8):1689–1698
  15. Bernstein J. In the beginning was the word. Journal of Bone and Joint Surgery. 2006;88(2):442–445
  16. Birch H, Smith T, Tasker T, Goodship A. Age-related changes to mechanical and matrix properties in human Achilles tendon. 2001;San Francisco, CA
  17. Bjur D, Alfredson H, Forsgren S. The innervation pattern of the human Achilles tendon: studies of the normal and tendinosis tendon with markers for general and sensory innervation. Cell Tissue Research. 2005;320(1):201–206
  18. Blazina ME, Kerlan RK, Jobe FW, Carter VS, Carlson GJ. Jumper’s knee. Orthopedic Clinics of North America. 1973;4(3):665–678
  19. Brosseau L, Casimiro L, Milne S, Robinson V, Shea B, Tugwell P, et al. Deep transverse friction massage for treating tendinitis. Cochrane Database of Systematic Reviews. 2002;(4):CD003528
  20. Brukner P, Bennell K. Overuse injuries: where to now?. British Journal of Sports Medicine. 1997;31(1):2
  21. Cannell LJ, Taunton JE, Clement DB, Smith C, Khan KM. A randomised clinical trial of the efficacy of drop squats or leg extension/leg curl exercises to treat clinically diagnosed jumper’s knee in athletes: pilot study. British Journal of Sports Medicine. 2001;35(1):60–64
  22. Carcia CR, Martin RL, Houck J, Wukich DK. Achilles pain, stiffness, and muscle power deficits: Achilles tendinitis. Journal of Orthopaedic & Sports Physical Therapy. 2010;40(9):A1–26
  23. Chan AK, Myrer JW, Measom GJ, Draper DO. Temperature changes in human patellar tendon in response to therapeutic ultrasound. Journal of Athletic Training. 1998;33(2):130–135
  24. Chan HL, Ng GY. Effect of counterforce forearm bracing on wrist extensor muscles performance. American Journal of Physical Medicine & Rehabilitation. 2003;82(4):290–295
  25. Cook JL, Khan KM, Kiss ZS, Coleman BD, Griffiths L. Asymptomatic hypoechoic regions on patellar tendon ultrasound: a 4-year clinical and ultrasound followup of 46 tendons. Scandinavian Journal of Medicine & Science in Sports. 2001;11(6):321–327
  26. Cook JL, Khan KM, Kiss ZS, Purdam CR, Griffiths L. Prospective imaging study of asymptomatic patellar tendinopathy in elite junior basketball players. Journal of Ultrasound in Medicine. 2000;19(7):473–479
  27. Cook JL, Khan KM, Kiss ZS, Purdam CR, Griffiths L. Reproducibility and clinical utility of tendon palpation to detect patellar tendinopathy in young basketball players. Victorian Institute of Sport tendon study group. British Journal of Sports Medicine. 2001;35(1):65–69
  28. Cook JL, Khan KM, Maffulli N, Purdam CR. Overuse tendinosus, not tendinitis. Part 2: applying the new approach to patellar tendinopathy. The Physician and Sports Medicine. 2000;28(6):1–46
  29. Cook JL, Kiss ZS, Khan KM, Purdam CR, Webster KE. Anthropometry, physical performance, and ultrasound patellar tendon abnormality in elite junior basketball players: a cross-sectional study. British Journal of Sports Medicine. 2004;38(2):206–209
  30. Cook JL, Malliaras P, De Luca J, Ptasznik R, Morris M. Vascularity and pain in the patellar tendon of adult jumping athletes: a 5 month longitudinal study. British Journal of Sports Medicine. 2005;39(7):458–461discussion 458–461
  31. Cook JL, Ptazsnik R, Kiss ZS, Malliaras P, Morris ME, De Luca J. High reproducibility of patellar tendon vascularity assessed by colour Doppler ultrasonography: a reliable measurement tool for quantifying tendon pathology. British Journal of Sports Medicine. 2005;39(10):700–703
  32. Cook JL, Purdam CR. Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy. British Journal of Sports Medicine. 2009;43(6):409–416
  33. Croisier JL, Foidart-Dessalle M, Tinant F, Crielaard JM, Forthomme B. An isokinetic eccentric programme for the management of chronic lateral epicondylar tendinopathy. British Journal of Sports Medicine. 2007;41(4):269–275
  34. Curwin S, Stanish WD. Tendonitis: Its etiology and treatment. Lexington, MA: DC Heath & Co; 1984;
  35. Cyriax JH, Coldham M. Treatment by manipulation, massage and injection. 11th ed.. London; Philadelphia: Bailliáere Tindall; 1984;
  36. Davenport TE, Kulig K, Matharu Y, Blanco CE. The EdUReP model for nonsurgical management of tendinopathy. Physical Therapy. 2005;85(10):1093–1103
  37. Davidson CJ, Ganion LR, Gehlsen GM, Verhoestra B, Roepke JE, Sevier TL. Rat tendon morphologic and functional changes resulting from soft tissue mobilization. Medicine & Science in Sports & Exercise. 1997;29(3):313–319
  38. Donoghue OA, Harrison AJ, Laxton P, Jones RK. Lower limb kinematics of subjects with chronic Achilles tendon injury during running. Research in Sports Medicine. 2008;16(1):23–38
  39. Eriksson E. Eccentric training of painful supraspinatus tendinosis. Knee Surgery, Sports Traumatology, Arthroscopy. 2006;14(1):1
  40. Ferretti A. Epidemiology of jumper’s knee. Sports Medicine. 1986;3(4):289–295
  41. Ferretti A, Puddu G, Mariani PP, Neri M. The natural history of jumper’s knee. Patellar or quadriceps tendonitis. International Orthopaedics. 1985;8(4):239–242
  42. Fredberg U, Bolvig L, Pfeiffer-Jensen M, Clemmensen D, Jakobsen BW, Stengaard-Pedersen K. Ultrasonography as a tool for diagnosis, guidance of local steroid injection and, together with pressure algometry, monitoring of the treatment of athletes with chronic jumper’s knee and Achilles tendinitis: a randomized, double-blind, placebo-controlled study. Scandinavian Journal of Rheumatology. 2004;33(2):94–101
  43. Fredberg U, Stengaard-Pedersen K. Chronic tendinopathy tissue pathology, pain mechanisms, and etiology with a special focus on inflammation. Scandinavian Journal of Medicine & Science in Sports. 2008;18(1):3–15
  44. Frey C, Zamora J. The effects of obesity on orthopaedic foot and ankle pathology. Foot & Ankle International. 2007;28(9):996–999
  45. Frohm A, Saartok T, Halvorsen K, Renstrom P. Eccentric treatment for patellar tendinopathy: a prospective randomised short-term pilot study of two rehabilitation protocols. British Journal of Sports Medicine. 2007;41(7):e7
  46. Gaida JE, Cook JL, Bass SL, Austen S, Kiss ZS. Are unilateral and bilateral patellar tendinopathy distinguished by differences in anthropometry, body composition, or muscle strength in elite female basketball players?. British Journal of Sports Medicine. 2004;38(5):581–585
  47. Gehlsen GM, Ganion LR, Helfst R. Fibroblast responses to variation in soft tissue mobilization pressure. Medicine & Science in Sports & Exercise. 1999;31(4):531–535
  48. Gisslen K, Alfredson H. Neovascularisation and pain in jumper’s knee: a prospective clinical and sonographic study in elite junior volleyball players. British Journal of Sports Medicine. 2005;39(7):423–428discussion 423–428
  49. Gold RH, Seeger LL, Yao L. Imaging shoulder impingement. Skeletal Radiology. 1993;22(8):555–561
  50. Grau S, Maiwald C, Krauss I, Axmann D, Janssen P, Horstmann T. What are causes and treatment strategies for patellar-tendinopathy in female runners?. Journal of Biomechanics. 2008;41(9):2042–2046
  51. Hashimoto T, Nobuhara K, Hamada T. Pathologic evidence of degeneration as a primary cause of rotator cuff tear. Clinical Orthopaedics and Related Research. 2003;415:111–120
  52. Holmes GB, Lin J. Etiologic factors associated with symptomatic achilles tendinopathy. Foot & Ankle International. 2006;27(11):952–959
  53. Jarvinen TA, Kannus P, Maffulli N, Khan KM. Achilles tendon disorders: etiology and epidemiology. Foot and Ankle Clinics. 2005;10(2):255–266
  54. Jonsson P, Alfredson H. Superior results with eccentric compared to concentric quadriceps training in patients with jumper’s knee: a prospective randomised study. British Journal of Sports Medicine. 2005;39(11):847–850
  55. Jonsson P, Wahlstrom P, Ohberg L, Alfredson H. Eccentric training in chronic painful impingement syndrome of the shoulder: results of a pilot study. Knee Surgery, Sports Traumatology, Arthroscopy. 2006;14(1):76–81
  56. Jozsa L, Balint JB, Kannus P, Reffy A, Barzo M. Distribution of blood groups in patients with tendon rupture. An analysis of 832 cases. Journal of Bone and Joint Surgery. 1989;71(2):272–274
  57. Kannus P. Tendons–a source of major concern in competitive and recreational athletes. Scandinavian Journal of Medicine & Science in Sports. 1997;7(2):53–54
  58. Kannus P, Jozsa L, Natri A, Jarvinen M. Effects of training, immobilization and remobilization on tendons. Scandinavian Journal of Medicine & Science in Sports. 1997;7(2):67–71
  59. Kaufman KR, Brodine SK, Shaffer RA, Johnson CW, Cullison TR. The effect of foot structure and range of motion on musculoskeletal overuse injuries. The American Journal of Sports Medicine. 1999;27(5):585–593
  60. Khan KM, Cook JL, Bonar F, Harcourt P, Astrom M. Histopathology of common tendinopathies. Update and implications for clinical management. Sports Medicine. 1999;27(6):393–408
  61. Khan KM, Cook JL, Kannus P, Maffulli N, Bonar SF. Time to abandon the "tendinitis" myth. British Medical Journal. 2002;324(7338):626–627
  62. Khan KM, Cook JL, Kiss ZS, Visentini PJ, Fehrmann MW, Harcourt PR, et al. Patellar tendon ultrasonography and jumper’s knee in female basketball players: a longitudinal study. Clinical Journal of Sport Medicine. 1997;7(3):199–206
  63. Khan KM, Cook JL, Taunton JE, Bonar F. Overuse tendinosus, not tendinitis. The Physician and Sportsmedicine. 2000;28(5):38–47
  64. Kirkendall DT, Garrett WE. Function and biomechanics of tendons. Scandinavian Journal of Medicine & Science in Sports. 1997;7(2):62–66
  65. Klaiman MD, Shrader JA, Danoff JV, Hicks JE, Pesce WJ, Ferland J. Phonophoresis versus ultrasound in the treatment of common musculoskeletal conditions. Medicine & Science in Sports & Exercise. 1998;30(9):1349–1355
  66. Knobloch K, Schreibmueller L, Meller R, Busch KH, Spies M, Vogt PM. Superior Achilles tendon microcirculation in tendinopathy among symptomatic female versus male patients. The American Journal of Sports Medicine. 2008;36(3):509–514
  67. Kubo K, Kanehisa H, Fukunaga T. Effects of viscoelastic properties of tendon structures on stretch – shortening cycle exercise in vivo. Journal of Sports Science and Medicine. 2005;23(8):851–860
  68. Kujala UM, Jarvinen M, Natri A, Lehto M, Nelimarkka O, Hurme M, et al. ABO blood groups and musculoskeletal injuries. Injury. 1992;23(2):131–133
  69. Kujala UM, Sarna S, Kaprio J. Cumulative incidence of achilles tendon rupture and tendinopathy in male former elite athletes. Clinical Journal of Sport Medicine. 2005;15(3):133–135
  70. Kulig K, Lederhaus ES, Reischl S, Arya S, Bashford G. Effect of eccentric exercise program for early tibialis posterior tendinopathy. Foot & Ankle International. 2009;30(9):877–885
  71. Leadbetter WB. Cell-matrix response in tendon injury. Clinics in Sports Medicine. 1992;11(3):533–578
  72. Leppilahti J, Puranen J, Orava S. ABO blood group and Achilles tendon rupture. Annales Chirurgiae et Gynaecologiae. 1996;85(4):369–371
  73. Lian O, Dahl J, Ackermann PW, Frihagen F, Engebretsen L, Bahr R. Pronociceptive and antinociceptive neuromediators in patellar tendinopathy. The American Journal of Sports Medicine. 2006;34(11):1801–1808
  74. Lian OB, Engebretsen L, Bahr R. Prevalence of jumper’s knee among elite athletes from different sports: a cross-sectional study. The American Journal of Sports Medicine. 2005;33(4):561–567
  75. Lieber RL. Skeletal muscle structure, function & plasticity: the physiological basis of rehabilitation. 2nd ed.. Philadelphia: Lippincott Williams & Wilkins; 2002;
  76. Ludewig PM, Reynolds JF. The association of scapular kinematics and glenohumeral joint pathologies. Journal of Orthopaedic & Sports Physical Therapy. 2009;39(2):90–104
  77. Maffulli N, Kenward MG, Testa V, Capasso G, Regine R, King JB. Clinical diagnosis of Achilles tendinopathy with tendinosis. Clinical Journal of Sport Medicine. 2003;13(1):11–15
  78. Maffulli N, Khan KM, Puddu G. Overuse tendon conditions: time to change a confusing terminology. Arthroscopy. 1998;14(8):840–843
  79. Maffulli N, Longo UG, Denaro V. Novel approaches for the management of tendinopathy. Journal of Bone and Joint Surgery. 2010;92(15):2604–2613
  80. Maffulli N, Reaper JA, Waterston SW, Ahya T. ABO blood groups and achilles tendon rupture in the Grampian Region of Scotland. Clinical Journal of Sport Medicine. 2000;10(4):269–271
  81. Maffulli N, Renström P, Leadbetter WB. Tendon injuries: Basic science and clinical medicine. London: Springer; 2005;
  82. Maffulli N, Sharma P, Luscombe KL. Achilles tendinopathy: aetiology and management. Journal of the Royal Society of Medicine. 2004;97(10):472–476
  83. Maffulli N, Testa V, Capasso G, Ewen SW, Sullo A, Benazzo F, et al. Similar histopathological picture in males with Achilles and patellar tendinopathy. Medicine & Science in Sports & Exercise. 2004;36(9):1470–1475
  84. Maffulli N, Walley G, Sayana MK, Longo UG, Denaro V. Eccentric calf muscle training in athletic patients with Achilles tendinopathy. Disability and Rehabilitation. 2008;30(20–22):1677–1684
  85. Maffulli N, Wong J, Almekinders LC. Types and epidemiology of tendinopathy. Clinical Journal of Sport Medicine. 2003;22(4):675–692
  86. Magnusson SP, Langberg H, Kjaer M. The pathogenesis of tendinopathy: balancing the response to loading. Nature Reviews Rheumatology. 2010;6(5):262–268
  87. Magra M, Maffulli N. Genetics: does it play a role in tendinopathy?. Clinical Journal of Sport Medicine. 2007;17(4):231–233
  88. Martinez-Silvestrini JA, Newcomer KL, Gay RE, Schaefer MP, Kortebein P, Arendt KW. Chronic lateral epicondylitis: comparative effectiveness of a home exercise program including stretching alone versus stretching supplemented with eccentric or concentric strengthening. Journal of Hand Therapy. 2005;18(4):411–419quiz 420
  89. McCrory JL, Martin DF, Lowery RB, Cannon DW, Curl WW, Read HM, et al. Etiologic factors associated with Achilles tendinitis in runners. Medicine & Science in Sports & Exercise. 1999;31(10):1374–1381
  90. Meyer A, Tumilty S, Baxter GD. Eccentric exercise protocols for chronic non-insertional Achilles tendinopathy: how much is enough?. Scandinavian Journal of Medicine & Science in Sports. 2009;19(5):609–615
  91. Mokone GG, Gajjar M, September AV, Schwellnus MP, Greenberg J, Noakes TD, et al. The guanine-thymine dinucleotide repeat polymorphism within the tenascin-C gene is associated with Achilles tendon injuries. The American Journal of Sports Medicine. 2005;33(7):1016–1021
  92. Mokone GG, Schwellnus MP, Noakes TD, Collins M. The COL5A1 gene and Achilles tendon pathology. Scandinavian Journal of Medicine & Science in Sports. 2006;16(1):19–26
  93. Movin T, Gad A, Reinholt FP, Rolf C. Tendon pathology in long-standing achillodynia. Biopsy findings in 40 patients. Acta Orthopaedica Scandinavica. 1997;68(2):170–175
  94. Ng GY, Chan HL. The immediate effects of tension of counterforce forearm brace on neuromuscular performance of wrist extensor muscles in subjects with lateral humeral epicondylosis. Journal of Orthopaedic & Sports Physical Therapy. 2004;34(2):72–78
  95. Nirschl RP. Elbow tendinosis/tennis elbow. Clinical Journal of Sport Medicine. 1992;11(4):851–870
  96. Norregaard J, Larsen CC, Bieler T, Langberg H. Eccentric exercise in treatment of Achilles tendinopathy. Scandinavian Journal of Medicine & Science in Sports. 2007;17(2):133–138
  97. Nowicki KD, Hummer CD, Heidt RS, Colosimo AJ. Effects of iontophoretic versus injection administration of dexamethasone. Medicine & Science in Sports & Exercise. 2002;34(8):1294–1301
  98. Ohberg L, Lorentzon R, Alfredson H. Neovascularisation in Achilles tendons with painful tendinosis but not in normal tendons: an ultrasonographic investigation. Knee Surgery, Sports Traumatology, Arthroscopy. 2001;9(4):233–238
  99. Paavola M, Kannus P, Jarvinen TA, Jarvinen TL, Jozsa L, Jarvinen M. Treatment of tendon disorders. Is there a role for corticosteroid injection?. Foot And Ankle Clinics. 2002;7(3):501–513
  100. Pellecchia GL, Hamel H, Behnke P. Treatment of infrapatellar tendonitis: a combination of modalities and transverse friction massage versus iontophoresis. Journal of Sport Rehabilitation. 1994;3(2):135–145
  101. Penderghest CE, Kimura IF, Gulick DT. Double-blind clinical efficacy study of pulsed phonophoresis on perceived pain associated with symptomatic tendinitis. Journal of Sport Rehabilitation. 1998;7(1):9–19
  102. Potter HG, Hannafin JA, Morwessel RM, DiCarlo EF, O’Brien SJ, Altchek DW. Lateral epicondylitis: correlation of MR imaging, surgical, and histopathologic findings. Radiology. 1995;196(1):43–46
  103. Pufe T, Petersen WJ, Mentlein R, Tillmann BN. The role of vasculature and angiogenesis for the pathogenesis of degenerative tendons disease. Scandinavian Journal of Medicine & Science in Sports. 2005;15(4):211–222
  104. Purdam CR, Cook JL, Hopper DM, Khan KM. Discriminative ability of functional loading tests for adolescent jumper’s knee. Physical Therapy in Sport. 2003;4(1):3–9
  105. Purdam CR, Jonsson P, Alfredson H, Lorentzon R, Cook JL, Khan KM. A pilot study of the eccentric decline squat in the management of painful chronic patellar tendinopathy. British Journal of Sports Medicine. 2004;38(4):395–397
  106. Ramirez A, Schwane JA, McFarland C, Starcher B. The effect of ultrasound on collagen synthesis and fibroblast proliferation in vitro. Medicine & Science in Sports & Exercise. 1997;29(3):326–332
  107. Ramos LA, de Carvalho RT, Garms E, Navarro MS, Abdalla RJ, Cohen M. Prevalence of pain on palpation of the inferior pole of the patella among patients with complaints of knee pain. Clinics (Sao Paulo). 2009;64(3):199–202
  108. Rees JD, Maffulli N, Cook J. Management of tendinopathy. The American Journal of Sports Medicine. 2009;37(9):1855–1867
  109. Rees JD, Wilson AM, Wolman RL. Current concepts in the management of tendon disorders. Rheumatology (Oxford). 2006;
  110. Rees JD, Wolman RL, Wilson A. Eccentric exercises; why do they work, what are the problems and how can we improve them?. British Journal of Sports Medicine. 2009;43(4):242–246
  111. Richards DP, Ajemian SV, Wiley JP, Brunet JA, Zernicke RF. Relation between ankle joint dynamics and patellar tendinopathy in elite volleyball players. Clinical Journal of Sport Medicine. 2002;12(5):266–272
  112. Richards DP, Ajemian SV, Wiley JP, Zernicke RF. Knee joint dynamics predict patellar tendinitis in elite volleyball players. The American Journal of Sports Medicine. 1996;24(5):676–683
  113. Riley G. Tendinopathy – from basic science to treatment. Nature Clinical Practice Rheumatology. 2008;4(2):82–89
  114. Riley GP, Goddard MJ, Hazleman BL. Histopathological assessment and pathological significance of matrix degeneration in supraspinatus tendons. Rheumatology (Oxford). 2001;40(2):229–230
  115. Rivenburgh DW. Physical modalities in the treatment of tendon injuries. Clinics in Sports Medicine. 1992;11(3):645–659
  116. Robinson JM, Cook JL, Purdam C, Visentini PJ, Ross J, Maffulli N, et al. The VISA-A questionnaire: a valid and reliable index of the clinical severity of Achilles tendinopathy. British Journal of Sports Medicine. 2001;35(5):335–341
  117. Ryan M, Grau S, Krauss I, Maiwald C, Taunton J, Horstmann T. Kinematic analysis of runners with achilles mid-portion tendinopathy. Foot & Ankle International. 2009;30(12):1190–1195
  118. Sackett DL. Evidence based medicine: How to practice and teach EBM. 2nd ed.. Edinburgh; New York: Churchill Livingstone; 2000;
  119. Sanchis-Alfonso V, Rosello-Sastre E, Subias-Lopez A. Neuroanatomic basis for pain in patellar tendinosis ("jumper’s knee"): a neuroimmunohistochemical study. American Journal of Knee Surgery. 2001;14(3):174–177
  120. Sargon MF, Ozlu K, Oken F. Age-related changes in human tendo calcaneus collagen fibrils. Saudi Medical Journal. 2005;26(3):425–428
  121. Sayana MK, Maffulli N. Eccentric calf muscle training in non-athletic patients with Achilles tendinopathy. Journal of Sports Science and Medicine. 2007;10(1):52–58
  122. Schubert TE, Weidler C, Lerch K, Hofstadter F, Straub RH. Achilles tendinosis is associated with sprouting of substance P positive nerve fibres. Annals of the Rheumatic Diseases. 2005;64(7):1083–1086
  123. Scott A, Lian O, Bahr R, Hart DA, Duronio V. VEGF expression in patellar tendinopathy: a preliminary study. Clinical Orthopaedics and Related Research. 2008;466(7):1598–1604
  124. Sein ML. Shoulder pain in elite swimmers. Sydney, Australia: University of South Wales; 2006;
  125. Shrier I, Matheson GO, Kohl HW. Achilles tendonitis: are corticosteroid injections useful or harmful?. Clinical Journal of Sport Medicine. 1996;6(4):245–250
  126. Silbernagel KG, Gustavsson A, Thomee R, Karlsson J. Evaluation of lower leg function in patients with Achilles tendinopathy. Knee Surgery, Sports Traumatology, Arthroscopy. 2006;14(11):1207–1217
  127. Souza RB, Arya S, Pollard CD, Salem G, Kulig K. Patellar tendinopathy alters the distribution of lower extremity net joint moments during hopping. Journal of Applied Biomechanics. 2010;26(3):249–255
  128. Stanish WD, Curwin S, Mandel S. Tendinitis: Its etiology and treatment. Oxford; New York: Oxford University Press; 2000;
  129. Stasinopoulos D, Johnson MI. ‘Lateral elbow tendinopathy’ is the most appropriate diagnostic term for the condition commonly referred-to as lateral epicondylitis. Medical Hypotheses. 2006;67(6):1400–1402
  130. Stasinopoulos D, Stasinopoulos I. Comparison of effects of exercise programme, pulsed ultrasound and transverse friction in the treatment of chronic patellar tendinopathy. Clinical Rehabilitation. 2004;18(4):347–352
  131. Svernlov B, Adolfsson L. Non-operative treatment regime including eccentric training for lateral humeral epicondylalgia. Scandinavian Journal of Medicine & Science in Sports. 2001;11(6):328–334
  132. Taunton JE, Ryan MB, Clement DB, McKenzie DC, Lloyd-Smith DR, Zumbo BD. A retrospective case-control analysis of 2002 running injuries. British Journal of Sports Medicine. 2002;36(2):95–101
  133. Tuite DJ, Renstrom PA, O’Brien M. The aging tendon. Scandinavian Journal of Medicine & Science in Sports. 1997;7(2):72–77
  134. Tumilty S, Munn J, McDonough S, Hurley DA, Basford JR, Baxter GD. Low level laser treatment of tendinopathy: a systematic review with meta-analysis. Photomedicine and Laser Surgery. 2010;28(1):3–16
  135. Uhthoff HK, Sano H. Pathology of failure of the rotator cuff tendon. Orthopedic Clinics of North America. 1997;28(1):31–41
  136. Van Ginckel A, Thijs Y, Hesar NG, Mahieu N, De Clercq D, Roosen P, et al. Intrinsic gait-related risk factors for Achilles tendinopathy in novice runners: a prospective study. Gait Posture. 2009;29(3):387–391
  137. Visentini PJ, Khan KM, Cook JL, Kiss ZS, Harcourt PR, Wark JD. The VISA score: an index of severity of symptoms in patients with jumper’s knee (patellar tendinosis). Victorian Institute of Sport Tendon Study Group. Journal of Sports Science and Medicine. 1998;1(1):22–28
  138. Visnes H, Hoksrud A, Cook J, Bahr R. No effect of eccentric training on jumper’s knee in volleyball players during the competitive season: a randomized clinical trial. Clinical Journal of Sport Medicine. 2005;15(4):227–234
  139. Warden SJ, Metcalf BR, Kiss ZS, Cook JL, Purdam CR, Bennell KL, et al. Low-intensity pulsed ultrasound for chronic patellar tendinopathy: a randomized, double-blind, placebo-controlled trial. Rheumatology (Oxford). 2008;47(4):467–471
  140. Witvrouw E, Bellemans J, Lysens R, Danneels L, Cambier D. Intrinsic risk factors for the development of patellar tendinitis in an athletic population. A two-year prospective study. American Journal of Sports Medicine. 2001;29(2):190–195
  141. Young MA, Cook JL, Purdam CR, Kiss ZS, Alfredson H. Eccentric decline squat protocol offers superior results at 12 months compared with traditional eccentric protocol for patellar tendinopathy in volleyball players. British Journal of Sports Medicine. 2005;39(2):102–105

PII: S1466-853X(11)00046-0

doi:10.1016/j.ptsp.2011.06.004

Physical Therapy in Sport
Volume 13, Issue 1 , Pages 3-10, February 2012

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