Study Title: Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy
Study Title: Is tendon pathology a continuum? A pathology model to explain the clinical presentation of load-induced tendinopathy
Author(s): Cook JL, Purdam CR
Publication Information: British Journal of Sports Medicine 2009; 43: 409-416.
Tendon injuries are extremely common and encounteredfrequently in all manual medicine settings, including chiropracticoffices. The majority of tendon injuriesoccur subsequent to overuse, essentially meaning that the imposed demands onthe tendon have exceeded its load-bearing capacity, resulting in molecular andstructural changes to the tendon that reduce its ability to sustain subsequentloads.
Many years ago, the pain in chronic tendon overuse injuries was believedto be the direct result of a chronic inflammatory process, but becauseinflammatory cells could be consistently demonstrated in damaged tendons, theopinion changed from inflammation (implied by the older term ‘‘tendinitis’’) todegeneration (represented by the newer terms ‘‘tendinosis’’ or “tendinopathy”).To date, a large amount of scientific data has not shown any direct evidence ofinflammation in chronic tendinopathy. In fact, leading researchers and contemporaryclinicians have suggested abandoning the term “tendonitis” altogether1,2There is controversy however – although mosthistologic findings in tendinopathy represent chronic degeneration,regeneration, and microtears of the tendinous tissue, newer studies usingimmunohistochemistry and flow cytometry have shown inflammatory cells 8.
Clinically, tendinopathies in both the upper andlower extremity can lead to pain, reduced exercise tolerance, impaired functionor performance and even disability or lost playing time. These injuries can be challenging to manage,and presentation is extremely variable.
Continuing progressive research in molecular biology and biomechanicshas provided valuable new information and has given rise to new hypotheses inchronic tendinopathy. This condition hasbeen described as degenerative and failed healing, yet neither fully explainsthe observed variability. The goal ofthis review paper was to discuss these findings in the framework of a newcontinuum pathology model for load-induced tendinopathies.
Tendinopathy Concepts & Research
In general, tendon injuries can occur in themid-tendon or at the attachment of the tendon to the bone, also called theenthesis. Although the mid-portion andinsertion site of tendons are structurally different when normal, the onset ofpathology creates cell and matrix alterations that are virtuallyindistinguishable. That being said, thereader should be reminded that in some regions (specifically the Achilles) – insertional and mid-portion tendinopathiesrespond differently to the same treatment intervention.
TheRole of Load in Tendon Pathology:
Despite the obvious importance of load in tendoninjuries, it is rarely considered when implementing treatment – the authorspropose that their model will take this into account and assist the clinicianto tailor treatment to the pathology:
- load has been shown to be both anabolic and catabolic in tendons
- repetitive energy storage and release and compression are thought to be important contributing factors
- the amount of load necessary to being a pathological process or cause injury is unknown
- however, allowing sufficient time intervals between loading sessions seems to be important
- the role of load in injury genesis is modulated by intrinsic factors such as gender, age, genetics, local cytokine production, biomechanics and body composition
- it should also be remembered that tendon injury has been induced in the absence of load (also referred to as a stress-shielded condition – unloading a tendon can cause similar changes to those seen in an overload state)
- since the demise of the inflammatory model (although as mentioned, controversy still exists), tendinopathy has been considered as a degenerative condition – spawning various pathological terms such as hypoxic degeneration, hyaline degeneration or mucoid degeneration – all suggest a non-reparative, final-stage pathology
- others have suggested that injured tendons are in a healing flux, with active protein production but disorganized cell structure in the matrix and neovascularization – this has been termed “failed healing” or “angiofibroblastc hyperplasia” 3
A NewModel of Tendon Pathology:
The authors propose the following pathologicalcontinuum model that has three phases (each discussed below):
2) TendonDysrepair (failed healing)
- this is a non-inflammatory proliferative response in the cells and matrix occurring after acute or repetitive tensile or compressive load
- the result is a short-term adaptive and homogenous thickening of a section of the tendon (increased cross-sectional area) that is thought to be an adaptation to deal with compression
- the initial changes in ground substance and matrix can occur quickly due to the rapid upregulation of larger proteoglycans (aggrecan and versican) and some glycoproteins (hyaluronan) which can occur in minutes up to a few days (note the upregulation times in normal tendons are approximately 20 days)4
- clinically, this will normally result from: 1) acute bursts of unaccustomed physical activity in younger patients; 2) in tendons chronically exposed to low loads that are exposed to a moderate load increase; 3) direct trauma
- imaging may reveal fusiform swelling (increased diameter) on MRI or diagnostic ultrasound (US)
- is an attempt at tendon healing, similar to reactive tendinopathy but with an increased matrix breakdown
- overall cell number increases – mainly chondrocytes and myofibroblasts – leading to disorganization of the matrix
- there may be an increase in vascularity and/or associated neural ingrowth
- imaging will reveal increased collagen disorganization and discontinuity (on US will represent small focal hypoechoic areas)
- clinically this may appear across a variety of loading patterns and age groups – overall this may be hard to distinguish
- is well documented in the literature – involving progression in both cell and matrix changes
- within the tendon, areas of cell death or tenocyte exhaustion are apparent, as large areas of matrix become disordered and filled with vessels, products of matrix breakdown etc.
- at this stage, it is thought that there is little chance for reversal
- there are “islands of degenerative pathology interspersed between other stages of pathology and normal tendon”
- imaging will reveal: hypoechoic areas with few collagen reflections on US, with numerous and larger vessels visible on Doppler US; MRI shows focally increased tendon size and intratendious signal
- clinically, the classic presentation is a middle-aged recreational athlete with one or more focal nodular areas with or without tendon thickening, preceded by a history of recurrent tendon pain
- these cases are typically older patients, but can also be seen in a younger patient with a chronically overloaded tendon
- most tendons that rupture are likely in this stage
Commentsand Supporting Literature for this Model
- It is very difficult to longitudinally study degenerative changes in human tendons, so this model is derived from the integration of cross-sectional studies with animal evidence.
- Longitudinal imaging studies have provided evidence that up to 30 per cent of tendons that show reactive change can change back to normal, supporting the idea that the first phase of the model is reversible5
- At this time, there is no convincing evidence of transition back to normal from tendon disrepair.
- The authors note than some tendons can contain discrete areas that are in different stages of this model at the same time.
- The authors note that some athletes appear to be completely resistant to tendinopathy despite high loads; conversely, others seem highly susceptible
The pain associated with load-induced tendinopathynormally has two distinct characteristics:
1) adose-dependent relationship related to a singular or repeated load
2) localizedto the tendon or enthesis
In order to decide which treatment is appropriate,the authors suggest two clear groupsbased on their model:
1.Reactive/Early Tendon Disrepair – normally a younger athletewith acute overload and fusiform swelling about the tendon:
- load management (reduction) is paramount to allow cells to become less reactive
- this could be as simple as allowing one to two days between higher loading sessions
- activities that do not involve tendon energy storage/release can be used – examples include cycling and strength-based weight training
- eccentric and high load activities should be avoided
- NSAIDs may reduce pain, but have a deleterious effect on tendon healing6
2. LateDisrepair/Degenerative – normally an older athlete with athickened, nodular tendon:
- treatments should stimulate cell activity, increase protein production and restructure the matrix
- friction interventions have been shown to increase protein production in animals, but human evidence is lacking and existing results are variable
- Extracorporeal Shock Wave Therapy (ESWT) has been shown to reduce pain levels, but has not proven its superiority to placebo treatments in existing trials
- increasing attention is being paid to injection therapies (blood, medications etc.) – specifically, blood injection has been suggested to increase cell proliferation and production of vascular endothelial growth factor – it has also demonstrated reduced vascularity and tendon diameter on US7
- injection itself, regardless of associated substance, has shown promise for improving tendon structure (RRS note: this may beg the question about the potential benefits of acupuncture?)
- eccentric exercise has been shown to have beneficial effects on both tendon structure, collagen production and pain in abnormal tendons – other reviews will deal with this topic in more detail
It should be noted that pain can occur at any stage in this model, which supports thewell-established dissociation between pain and tendon damage. To illustrate, up to 2/3 of tendons thatrupture have been reported as painless prior to the rupture, despite a highprevalence of degenerative changes.
This paper presented a pathology model forload-induced tendinopathy. The authorsadequately reviewed existing literature and appropriately addressed potentialshortcomings of their model.
CONCLUSIONS AND PRACTICAL APPLICATIONS
The authors of this paper have presented a simple and succinct model for load-induced tendinopathy that appropriately includes contemporary, multidisciplinary literature on this topic.
The authors wisely reiterate that this is merely a model of pathology, and that clinicians should remember that load tolerance and soft tissue healing are individual factors with wide variability. That being said, they have provided an excellent and simple framework for us to work with.
They also emphasize the need for more research on early-stage tendon pathology, the area that is currently most lacking.
1) Khan KM, Cook JL,Bonar F, Harcourt PAM. Histopathology of common tendinopathies. Update andimplications for clinical management. Sports Med 1999: 27: 393–408.
2) Khan KM, Cook JL,Kannus P, Maffulli N, Bondesteam S. Time to abandon the ‘‘tendinitis’’ myth(editorial). BMJ 2002: 324: 626–627.
3) Kraushaar B, Nirishi R. Tendinosis of the elbow (tennis elbow).Clinical features and findings of histological, immunohistochemical, andelectron microscopic studies. J Bone Joint Surg Am 1999; 81-A: 259-278.
4) Samiric T, Llic ZM, Handley CJ. Characterization of proteoglycansand their catabolic products in tendons and explants cultures of tendon. MatrixBiol 2004; 23: 127-140.
5) Fredberg U, Bolvig L. Significance of ultrasonography detectedasymptomatic tendinosis in the patellar and Achilles tendons of elite soccerplayers: a longitudinal study. Am J Sports Med 2002; 30: 488-491.
6) Ferry ST et al. The effects of common anti-inflammatory drugs onthe healing rat patellar tendon. Am J Sports Med 2007; 35: 1326-1333.
7) Anitua E et al. Autologous preparations rich in growth factorspromote proliferation and induce VEGF and HGF production in human tendon cellsin culture. J Orthop Res 2005; 23: 281-286.
8) Fredberg U, Stengaard-Pedersen K. Chronic tendinopathy tissuepathology, pain mechanisms, and etiology with a special focus on inflammation.Scand J Med Sci Sports 2008: 18: 3–15.
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Shawn Thistle, BKin (Hons), DC, CSCS – Dr. Shawn Thistle is the founder and president of Research Review
Service Inc., an online, subscription-based service designed to help busy practitioners to integrate current, relevant scientific evidence into their practice. Shawn graduated from CMCC and holds an Honours Degree in Kinesiology from McMaster University. He also holds a certificate in Contemporary Medical Acupuncture from McMaster University, and is a Certified Active Release Techniques (ART®) Provider. For more information about the Research Review Service, visit www.researchreviewservice.com.
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