Tendinopathy: Clinical Update

Author: Michael Braccio, DC/Wednesday, January 06, 2016/Categories: January/February 2016

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By Michael Braccio, DC

TENDINOPATHY IS A CONDITION commonly seen in the chiropractic clinic. While any tendon can become problematic with sufficient overload, the Achilles, patella and supraspinatus are some of the most commonly injured tendons. The diagnosis of tendinopathy is made with a thorough history and physical assessment. The history will typically include an insidious onset of pain after a sudden bout of activity. The physical assessment usually reveals pain that increases with load and decreases with rest. 

The understanding of tendinopathy has changed over the previous few decades. Tendinopathy was initially thought to be caused by inflammation, hence the term tendinitis. This led to anti-inflammatory treatment strategies such as NSAIDs and corticosteroid injections. Further research into tendon pain revealed degeneration of the tendon without inflammation. This was called tendinosis. The treatment strategies shifted from anti-inflammatory in nature to regenerative options such as platelet-rich plasma and sclerosing injections. The current theory for tendinopathy is the continuum model, as presented by Cook and Purdam.1 The continuum model suggests that tendinopathy is a spectrum from normal tendon to pathologic tendon. The three stages included in the continuum model are (1) reactive tendinopathy, (2) tendon dysrepair and (3) degenerative tendinopathy.

Reactive tendinopathy occurs in response to acute tensile or compressive overload. In this stage, there is a non-inflammatory proliferative cell response in the cell and tendon matrix. The increase in the cell and tendon matrix increases the cross-sectional area of the tendon, which decreases the stress on the tendon in the short term. The changes at this stage to the tendon are reversible with reduced loading or sufficient rest.

The tendon dysrepair stage is a failed attempt at tendon healing. With chronic overloading of the tendon, there is continued production in the cells and tendon, which results in an accumulation of fluid in the extracellular matrix. This leads to the separation of collagen and disorganization in the extracellular matrix. Some of the changes in this stage are reversible.

The final stage is degenerative tendinopathy, which is characterized by cell apoptosis and extensive matrix disorganization due to chronic overloading. There is also neovascularization in the degenerated tendon. The changes at this stage have little capacity to revert to normal tendon. While pain can occur at any stage of tendinopathy, it is not associated with structural changes in the tendon.2,3 Therefore, pain management is possible at each stage of tendinopathy.

Clinical Treatment


The stages of tendinopathy for clinical treatment purposes can be divided into two groups: reactive tendinopathy/early tendon dysrepair and late tendon dysrepair/degenerative tendinopathy. The primary treatment approach during reactive/early tendon dysrepair tendinopathy is load management.1,2,4 Appropriate load management will allow the tendon to adapt to the acute stresses and limit the progression to tendon dysrepair and subsequent degeneration.

Adjunct therapies for this stage may include NSAIDs, corticosteroid injections, manual therapy and instrument-assisted soft-tissue mobilization (IASTM). NSAIDs and corticosteroid injections may be beneficial to the reactive/early dysrepair tendon because of their ability to limit cell activity.1,4,5 However, prolonged use of these modalities can have negative effects on tendon integrity5 and have not been shown to stimulate tendon remodeling.6 Manual therapy and IASTM are both common treatments for tendinopathy. It was once thought that these therapies were used to break up scar tissue formation in the tissues, however, further research has suggested that the amount of force needed to deform the tissues may not be possible.7,8 Manual therapy instead has been suggested to stimulate mechanoreceptors, notably ruffini and interstitial receptors, which can modulate pain and alter tissue tone.8

In late dysrepair/degenerative tendinopathy, the focus of treatment should be on stimulating tendon repair through exercise and manual therapy. Manual therapy and IASTM are proposed to be used during this stage of tendinopathy because of their ability to stimulate cell production for healing and decreasing collagen disorganization.1,6,9,10 Manual therapy and IASTM may also help in delivering nutrients to the tendon by increasing vasodilation through the activation of interstitial mechanoreceptors.11 

The use of exercise for stimulating healing is based on mechanotherapy, which is defined as “the process whereby cells convert physiological mechanical stimuli into biochemical responses.”12 Mechanotherapy is divided into three phases: (1) mechanocoupling, (2) cell-cell communication and (3) effector cell response. The mechanocoupling phase refers to the transformation of mechanical forces into chemical signals in the cell. The chemical signals can then be dispersed to neighboring cells, which is the cellcell communication phase. The final phase is the effector response of the cell, which can be an increase in protein synthesis, resulting in increased collagen formation with the appropriate stimulus. Since tendons are dynamic, mechanosensitive tissues, the modification of mechanical stimulus will have a direct result on the tendon.

Introduction Of Loading

The introduction of loading in the treatment of tendinopathy is a difficult clinical decision. Insufficient loading causes stress-shielding, whereas overloading will cause cell apoptosis. In both scenarios, the tendon goes through cell and matrix changes and will have decreased mechanical integrity.1 There are four loading programs (See chart) that have been described in the literature: Alfredson; Stanish and Curwin; Silbernagel; and heavy-slow resistance.

The effectiveness of each program may depend on which tendon is pathological. A review of loading programs for the Achilles and patellar tendinopathies determined that eccentric-concentric loading may be as effective or more effective for the treatment of tendinopathy and the return to sport compared with eccentric exercises alone.10 Therefore, there seems to be no rationale to avoiding concentric exercises. The review also suggested that heavy load training or maximal eccentric loading may be better suited to achieve tendon adaptation needed for degenerative tendinopathy.10,13 With all of the loading programs studied, pain was an acceptable component, although to different degrees, which demonstrates that pain does not necessarily correlate to tissue damage and can be included in the healing process.14

It is important for the loading program to match the tendon tissue capacity. In the beginning of a loading program, isometric exercises can be used to decrease the pain until loading becomes more tolerable.6,19 The loading program can then progress to eccentric/ eccentric-concentric and heavy-slow resistance exercises to further increase the strength of the tendon. The final stage of a loading program can include stretch shortening cycle exercises, which will further stimulate tendon healing and better prepare an individual for return to play.20 While the loading program may focus on a specific region, the full kinetic chain should also be assessed since pain has been shown to alter movement patterns even after the resolution of pain.4,10,13,21

The treatment of tendinopathies can be difficult. Being able to determine where the patient is in the continuum of tendinopathy will provide direction as to which treatments should be used. The recognition of the stage of tendinopathy will also allow clinicians to appropriately manage a loading program for the patient. With a better understanding of the pathology, clinicians can be better equipped to create a comprehensive treatment approach for tendinopathies.

References


1 Cook JL, Purdam CR. Is Tendon Pathology a Continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy. Br J Sports Med 2009; 43:409-41.

2 Glasgow P, Phillips N, Bleakley C. Optimal Loading: key variables and mechanisms. Br J Sports Med 2015; 0:1-2.

3 Rio E, Moseley L, Purdam C, Samiric T, Kidgell D, Pearce AJ, Jaberzadeh S, Cook J. The Pain of Tendinopathy: Physiological or Pathophysiological. Sports Med 2014. 44:9-23.

4 Scott A, Docking S, Vicenzino B, et al. Sports and Exercise-Related Tendinopathies; a review of selected topical issues by participants of the second International Scientific Tendinopathy Symposium (ISTS) Vancouver 2012. Br J Sports Med 2013. 47:536-544.

5 Rees JD, Stride M, Scott A. Tendons – time to revisit inflammation. Br J Sports Med 2013. 0:1-7.

6 Cook JL, Purdah CR. The Challenge of Managing Tendinopathy in Competing Athletes. Br J Sports Med 2014. 48:506-509.

7 Chaundhry H, Schleip R, Ji Z, Bukiet B, Maney M, Findley T. Three-dimensional mathematical model for deformation of human fasciae in manual therapy. J Am Osteopath Assoc 2008. 108(8): 379-390.

8 Schleip R. Fascial plasticity – a new neurobiological explanation: Part 1. J Body Mov Ther 2003. 7(1): 11-19.

9 Davidson CJ, Ganion LR, Gehlsen GM, Verhoestra B, Roepke JE, Sevier TL. Rat tendon morphologic and functional changes resulting from soft tissue mobilization. Med Sci Sports Exerc 1997. 29(3): 313-319.

10 Malliaras P, Barton CJ, Reeves ND, Langberg H. Achilles and Patellar Tendinopathy Loading Programmes. A systemic review comparing clinical outcomes and identifying potential mechanics for effectiveness. Sports Med 2013; 43:267-286.

11 Schleip R. Fascial plasticity – a new neurobiological explanation - Part 2. J Body Mov Ther 2003. 7(2): 104-116.

12 Khan KM, Scott A. Mechanotherapy: how physical therapists’ prescription of exercise promotes tissue repair. Br J Sports Med 2009; 43:247-252.

13 Rudavsky A, Cook J. Physiotherapy management of patellar tendinopathy (jumper’s knee). J Physiother 2014. 60: 122-129.

14 Rio E, Moseley L, Purdam C, Samiric T, Kidgell D, Pearce AJ, Jaberzadeh S, Cook J. The Pain of Tendinopathy: Physiological or Pathophysiological. Sports Med 2014. 44:9-23.

15 Alfredson H, Pietiliä T, Jonsson P, Lorentzon. Heavy-load eccentric calf muscle training for the treatment of chronic achilles tendinosis. Am J Sports Med. 1998 26(3): 360-366.

16 Stanish WD, Rubinovich RM, Curwin S. Eccentric exercise in chronic tendinitis. Clin Orthop Relat Res 1986. 208: 65-68.

17 Sibernagel KG, Thomeé R, Eriksson BI, Karlsson J. Continued sports activity, using a painmonitoring model, during rehabilitation in patients with achilles tendinopathy: a randomized controlled study. Am J Sports Med. 2007. 35(6): 897-906.

18 Kongsgaard M, Kovanen V, Aagaard P, Doessing S, Hansen P, Laursen AH, Kaldau NC, Kjaer M, Magnusson SP. Corticosteroid injections, eccentric decline squat training and heavy slow resistance training in patellar tendinopathy. Stand J Med Sci Sports 2009. 19: 790-802.

19 Rio E, Kidgell D, Purdam C, Gaida J, Moseley L, Pearce A, Cook J. Isometric exercise induces analgesia and reduces inhibition in patellar tendinopathy. Br J Sports Med 2015. 49(19): 1277-83.

20 Allison GT, Purdam C. Eccentric Loading for Achilles Tendinopathy – strengthening or stretching? Br J Sports Med 2009; 43:276-279.

21 Hodges PW, Tucker K. Moving Differently in Pain: A new theory to explain the adaptation to pain. Pain 2011; 152:S90-S98.

Dr. Michael Braccio is a graduate of Palmer West Chiropractic College. He has a diplomate in chiropractic rehabilitation, and he is certified in RockTape, FMS, and SFMA. He currently practices in Seattle. 
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