Research Review By Dr. Demetry Assimakopoulos©

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Date Posted:

February 2014

Study Title:

Sports and exercise-related tendinopathies: a review of selected topical issues by participants of the second International Scientific Tendinopathy Symposium (ISTS) Vancouver 2012

Authors:

Scott A, Docking S, Vicenzino B et al.

Author's Affiliations:

Department of Physical Therapy, UBC, Vancouver, British Columbia; School of Physiotherapy, Monash University, Melbourne, Victoria, Australia; Division of Physiotherapy, Brisbane, Queensland, Australia; Department of Surgical and Perioperative Sciences, Sports Medicine, Umea University, Umea, Sweeden; University of Groningen, University Medical Center Groningen, Center for Sports Medicine, Groningen, The Netherlands; Department of Orthopedics, Lovisenberg Deaconal Hospital, Oslo Sports Trauma Research Centre, Oslo, Norway (and various others).

Publication Information:

British Journal of Sports Medicine 2013; 47: 536-544.

Background Information:

Tendons located in different regions of the body often feature distinct functional loading and structural properties. For instance, tendons located in the lower extremity, such as the Achilles tendon, store and release substantial amounts of tensile energy, while tendons in the wrist are designed to glide and have adapted to resist frictional loading as they pass alongside retinaculae or synovial sheaths. All told, tendons are distinct in their quality, based on their requirement to absorb load through the body.

Tendons are dynamic structures, insomuch as they have the ability to shift their anabolic/catabolic balance according to their mechanical load history. This adaptability is mediated by their expression of the scleraxis gene, which is up-regulated in a dose-response manner with increasing strain or repetition of movement. The structural and functional cells of the tendon (tenocytes) are known to release neuromodulators, otherwise known as neuropeptides, and are involved in the regulation of tissue remodeling and in nociception. Tendons are also densely innervated by mechanoreceptors, including Ruffini fibers, Pacinian corpuscles and free nerve endings; it is theorized that these receptors participate in proprioception and nociception. The autonomic system also contributes to the function of tendons, as they are likely involved in regulating blood flow, local tenocyte metabolism and pain signaling.

Summary:

Pain and Pathogenesis:

Contrary to the popular belief of various manual therapists and medical professionals, research in into the pathophysiology of tendinosis over the last decade actually shows an absence or minimal presence of inflammatory cells during acute flare ups. This is a profound finding, as many believe this condition to be inflammatory in nature. Repetitive mechanical loading of tendons has been shown to produce nociceptive and inflammatory substances (namely neuropeptides, described above). It is uncertain as to whether or not these substances are associated with the perception of pain. However, nerve fascicles containing sensory afferents are present in peritendinous tissue, which express receptors for the nociceptive substances which could sensitize the nerve endings, augmenting pain signaling.

The pathogenesis of chronic tendinopathy can be different at various anatomic locations:
  • Achilles: research out of Sweden highlights the possible role of the central nervous system in generating tendon pain, tissue pathology and abnormal patterns of movement. Through the application of scraping techniques such as Graston or Gua Sha on one side of a case involving bilateral Achilles tendinopathy, a reduction or resolution of symptoms can occur bilaterally (1). The question remains, is it the CNS that is mediating this response, or could be that when one tendon is treated, both tendons undergo a period of relative rest, leading to bilateral improvement?
  • Patellar: one study showed a reduced mechanical pain threshold and pinprick allodynia in patellar tendinopathy patients. The researchers believe that central sensitization of sensory input via the A-delta fibers could be responsible for this (2). Another study showed that Victorian Institute of Sport Assessment-Patellar questionnaire score correlates inversely with the presence of sulfated glycosaminoglycans. This demonstrates that tissue pathology is also related to pain and functional deficits in tendinopathy, in spite of the fact that the nervous system might be playing a neuromodulatory role.
  • Rotator Cuff: One recent paper identified and described degenerative mechanisms, including classic inflammatory pathways (ILK-1, Substance P), altered loading conditions (i.e. impingement) and systematic influences (such as aging), to name a few, which participate in the pathogenesis of rotator cuff injury. The researchers also noted a discrepancy between the amount of degenerative change and the extent of symptoms (3).
  • Elbow: The CNS has also been implicated in the pathogenesis of lateral epicondylalgia (LE). An integrated model has been proposed where local tissue pathology interacts with the nervous system to create a widespread mechanical hyperalgesia and motor control deficits. It is hoped that this model can assist in the identification of individuals who may have more substantial motor system deficits and substantial pain, as they may be a subset of patients who might respond differently to clinical interventions (4).
Diagnosis and Imaging:

Ultrasound (US) and MRI are often used clinically to confirm the presence and location of tendon thickening or other structural changes. Various studies have been performed evaluating the accuracy and sensitivity of US and MRI: values range from 0.63-0.83 and 0.68-0.87 for US, respectively, and 0.68-0.70 and 0.50-0.57 for MRI, respectively. Overall, US has been shown to be more diagnostically accurate than MRI, in trained hands. US imaging has the added value of anatomic precision, as it has shown a great ability to pinpoint patellar tendinopathy to the superior aspect of the tendon (~70% of cases). This is of value to practitioners who perform precise tendon-directed treatments such as injections or exercise. However, these findings can be a red-herring, as studies have shown that 22% of elite athletes demonstrate pathological lesions within the patellar tendon, in spite of the absence of symptoms (5). As always, we must treat the patient, not necessarily their pictures!

Despite their accuracy, both imaging modalities are subject to artifact and have poor inter- and intra-observer reliability. Additionally, using imaging to assess the effectiveness of treatments as a primary outcome measure for tendinopathy is not recommended. Often, there is a lack of imaging improvement, in spite of clinical improvement or even resolution. However, at longer time points, imaging may be used as a secondary outcome measure, as US has been shown to find improvement in fibrillar architecture in chronic Achilles tendinopathy (average follow up 3.8 years) subsequent to an eccentric loading program.

Rehabilitation:

The various components of a rehabilitation program targeted to tendons, most especially loading, must be manipulated according to the natural speed and magnitude of the forces applied to the muscle/tendon/bone unit. Understanding this will help the manual therapist to achieve their management goals without causing exacerbation. Rehabilitation can help to accomplish many helpful biological processes, such as matrix reorganization, collagen synthesis, a reduction in tenocyte activity, improved tendon compliance and analgesia.

It is important to note that a measureable change in collagen integrity and matrix reorganization, indicating an improvement in one’s condition, does not necessarily correlate with the patient’s perception of recovery. It is thus believed that exercise prescription may exert its positive therapeutic effect through other mechanisms, such as an improvement in functional strength, tendon compliance, innervation, vascularity and the perception of pain.

Recently, evidence has surfaced supporting the theory of an increased spinal hyperexcitability in patients with painful tendinopathies, and even some evidence strengthening the argument for central involvement in the etiology of tendinopathy. Because of this, it is important for clinicians to assess the potential contribution of spinal function and central sensitization. This can be achieved through a targeted intervention to the contralateral limb, as it may have the dual benefit of limiting the progression of the tendinopathy to the non-affected side through spinal means, while at the same time affecting the symptomatic side via the crossover effect.

Clinicians should consider the re-education of muscle function, as opposed to simply targeting the tendon in isolation when planning a rehabilitative strategy. Early on, it may be important to focus on isometric muscular activation, which may include muscle stimulation, followed by progression to higher loads, guided by symptomatology. It is also apparent that tendinopathies present with concomitant muscle atrophy, requiring a prolonged stimulus at moderate loads (3-4 sessions/week) to induce muscle hypertrophy.

Programming beyond the point of hypertrophy and strength requires the clinician to consider functional strengthening of the muscle/tendon unit and gradually increasing load on the tendon through more explosive concentric work, which prepares the tissue for beginning eccentric work later on (such as landing and other sport-specific challenges).

To ensure compliance, it is necessary for the clinician to explain the nature of the pathology, including the slow nature of tendon healing. It is also important to manage the expectations of the athlete and warn them that it is unlikely they will participate in training and competition until the tissues can sustain load effectively (especially early on).

It is important to manage tendon injuries in the off-season to prevent further issues. The athlete’s propensity for tendinopathy should be communicated to coaches and athletes, and off season training should include a continued tendon loading program to prevent a reduction in tendon integrity and stiffness. Failure to do this will increase the athlete’s predisposition to re-injury. Attention should also be paid to the tendon with its kinetic chain. Joint range of motion and muscular function of related structures which function to absorb load should be considered.

Injection:

Injection of tendons and their related structures (bursae) have become an attractive therapeutic opportunity. Glucocorticoids are the most widely used substance. Often, they are administered with an anesthetic, however other treatments including prolotherapy, sclerotherapy, protease inhibitor injections, biologics and platelet rich plasma (PRP) have been developed as injectable medical treatments. Typically, injections are guided by ultrasound, to improve precision.

Glucocorticoid injections are believed to operate via a reduction of extrinsic or intrinsic inflammation, reduction of tenocyte proliferation (cellular activity), anti-angiogenic activity, limitation of the development of scarred tissue/adhesion, or a combination therein. Studies have shown that the majority of patients may experience short-term improvement in pain and function, but experience a high risk of relapse in the medium-to-long-term.

Prolotherapy was originally developed to promote a local inflammation-repair response. One systematic review (6) concluded that that US guided injection of lauromacrogol and prolotherapy injection of hypertonic glucose plus a local anesthetic are potential good quality therapeutic techniques, based on moderate evidence of improvement in the intermediate term.

While their exact mechanism of action is unclear, other injectable agents such as sodium hyaluronate, botox and protease inhibitor solutions have recently been used. However, these agents have not been studied exhaustively and have not shown much efficacy for reducing pain or restoring function. Protease inhibitor agents have actually been shown to have a high rate of systemic allergic reaction, especially when aprotinin agent is used.

Autologous whole blood platelet rich plasma (PRP) and other biological therapies have garnered recent popularity for the treatment of tendinopathy. The mechanism of action is said to be from the delivery of bioactive substances to the site of pathology, thereby stimulating a healing response through normal physiological pathways, as opposed to an inflammatory response to a noxious substance. In spite of their popularity, especially PRP, evidence for their use for specific tendinopathies are limited. Still, some favorable results have been found with its use for patellar and Achilles tendinopathy. However, these results must be tempered by other high quality studies suggesting that PRP offers no benefit in the treatment of Achilles and rotator cuff tendinopathy.

Surgery:

Few studies with great scientific design have been performed assessing the efficacy of surgery for the chronically painful, but not ruptured tendinopathic tendon. Few studies measuring mid- or long-term follow-up efficacy have been performed.

Outcome Measures:

Few outcome measures exist that are specifically designed for tendinopathies, and those that do exist have not reached widespread implementation. The VISA-P (VISA = Victorian Institute of Sport Assessment) was originally developed in the 1990’s for patellar tendinopathy, and was later modified for use in other regions (the VISA-A is used for Achilles tendinopathy, for instance). This questionnaire incorporates elements of symptom ratings in various loaded states, amount of activity possible and ratings of participation. The general consensus of this group is that the questionnaire is an appropriate outcome measure specific for tendinopathy (reviewer’s note: this is true provided that the questionnaire exists. A questionnaire has not been developed for every type of tendinopathy). However, the group also states that more outcome measures need to be developed for the different types of tendinopathy.

Prevention of Tendinopathy:

The sports injury prevention research model developed in 1992 based on Machelen et al.’s work (7) could be used as a framework for this.

Step 1 – Magnitude of the Problem:
  • It has been recommended in the past that quantification of overuse injuries use prevalence, and not incidence, in prospective studies, in addition to using continuous or serial measurements of symptoms.
  • Sensitive and valid scoring instruments that measure pain and functional level should be used. Examples of this include the VISA-A and the VISA-P.
Step 2 – Establishing Etiology and Mechanisms of Injury:
  • Intrinsic and extrinsic factors for tendinopathy have been described in the literature. However, often these factors are inconsistent.
  • The most important risk factor in the etiology of sport related and exercise related tendinopathy is load; in spite of it being pervasive, it is likely preventable.
  • Load is a difficult risk factor to report and track, as variables such as number of jumps per hour, hours of training and distance running, to name a few, can be inaccurate and difficult to reflect.
  • Truthfully, the only recourse clinicians have is to attempt to engage in a discussion with our patients regarding how much load an individual patient can safely sustain, and to caution against sudden changes in tendon loading patterns and training schedules.
Steps 3 & 4 – Developing, Introducing and Evaluating a Training Program:
  • Training programs geared towards teaching coaches and athletes how to load tendons in the most appropriate way, and how to change their relative flexibility, proprioception and strength is the most efficient way of preventing and reducing the risk of developing tendinopathy.
  • For instance, prospective studies have shown a targeted prevention program such as soccer-specific balance training can reduce the incidence of patellar and Achilles tendinopathy. In this study, a dose-effect relationship was found between the duration of balance training and injury incidence.

Clinical Application & Conclusions:

The researchers conclude by stating that the integration of the evidence presented in this document is pertinent in the practice of manual therapists, physicians, athletic trainers, coaches and strength/conditioning managers involved in the care of patients suffering from tendinopathy. Understanding the anatomy/biology of tendinopathy, and the pathogenesis of the disorder are important factors in the management of tendinopathy. Various treatments exist that are evidence-based; some stronger, some weaker. It is thus up to the clinician to sift through the research and apply what he/she believes to be within their level of comfort. While integration of research into practice is important and takes effort, it is only part of the puzzle. Keep in mind that one needs to also utilize their clinical insights as well as the treatment preferences of the patient to optimize patient care.

Study Methods:

This was consensus piece put together by a number of researchers in a round-table format. No statistical analysis was performed, nor a detailed description of their methods to come to consensus.

Study Strengths / Weaknesses

Weaknesses:
  • No description of their search process was performed.
  • No statistical analysis was done.
  • No part of this document dedicated a specific part to the weaknesses of any tendinopathy. Are there any contraindications to care? Is there a linearity for the loading pattern for rehabilitation (isometric  concentric  eccentric)? How does one make a decision on how much load to use and when?
Strengths:
  • Very comprehensive in its inclusion of the different methods of treatment.
  • Numerous references were included for continued learning.

Additional References:

  1. Alfredson H, Spang C, Forsgren S. Unilateral surgical treatment for patients with midportion Achilles tendinopathy may result in bilateral recovery. Br J Sports Med 2012; [EPub ahead of print].
  2. Van Wilgen CP, Konopka KH, Keizer D, et al. Do patients with chronic patellar tendinopathy have an altered somatosensory profile?—A Quantitative Sensory Testing (QST) study. Scand J Med Sci Sports 2013; 23: 149–55.
  3. Dean BJF, Franklin SL, Carr AJ. A systematic review of the histological and molecular changes in rotator cuff disease. Bone Joint Res 2012; 1: 158–66.
  4. Coombes BK, Bisset L, Vicenzino B. A new integrative model of lateral epicondylalgia. Br J Sports Med 2009; 43: 252–8.
  5. Cook J, Khan K, Harcourt P, et al. Patellar tendon ultrasonography in asymptomatic active athletes reveals hypoechoic regions: a study of 320 tendons. Victorian Institute of Sport Tendon Study Group. Clin J Sport Med 1998; 8: 73–7.
  6. Coombes BK, Bisset L, Vicenzino B. Efficacy and safety of corticosteroid injections and other injections for management of tendinopathy: a systematic review of randomised controlled trials. Lancet 2010; 376: 1751–67.
  7. Van Mechelen W, Hlobil H, Kemper HC. Incidence, severity, aetiology and prevention of sports injuries. A review of concepts. Sports Med 1992; 14: 82–99.