Revisiting The Continuum Model of Tendon Pathology: What Is Its Merit in Clinical Practice and Research?
Revisiting The Continuum Model of Tendon Pathology: What Is Its Merit in Clinical Practice and Research?
Revisiting The Continuum Model of Tendon Pathology: What Is Its Merit in Clinical Practice and Research?
Figure 2 Schematic representation of ‘reactive-on-degenerative’ tendinopathy. A representation an example of the presentation on (ultrasound
tissue characterisation is presented by Rudavsky and Cook.45
as a potential driver of nociception51 These substances may Loading a painful tendon perpetuates nociceptive stimuli, and
sensitise peripheral mechanoreceptors near or in the periten- it is plausible that secondary hyperalgesia in tendinopathy is a
don52 stimulating the peripheral nerve and be interpreted as response to ongoing nociception. Hyperalgesia by itself does
pain. This may explain why pathology can occur deeper in not define tendinopathy as a pathophysiological pain state or
tendons without tendon pain as this region is remote to the centrally driven phenomenon.51 Several clinical features support
nerve supply. Theoretically, a painful reactive or reactive- this concept; tendon pain remains localised and temporally
on-degenerative tendon may increase expression of nociceptive linked to tissue loading,54 with little evidence of spontaneous
substances and their receptors, stimulating the peripheral nerve tendon pain (stimulus-independent pain) that is a feature of
and be interpreted as pain. Diffuse reactive pathology may also other pathophysiological pain states.
irritate the peritendon due to an increase in tendon size. Some consider tendinopathy to be centrally driven, while also
The pain-free tendon may contain substantial matrix and cell questioning the relevance of local changes in tendon structure.
abnormalities, but limited nociceptive substance production, sig- While there is evidence of contralateral sensory perception
nalling ability or receptor activation, which is in summary an changes in people with tendinopathy,55 this can equally reflect
insufficient nociceptive stimulus. The role of the central nervous persistent nociceptive drive from the local tissue. Acute pain
system in the modulation of nociception and output of pain is conditions, such as acute inversion ankle sprain, also caused sec-
acknowledged and well described by others;8 53 however, it is ondary hyperalgesia;56 however, this can be reversed instantan-
beyond the scope of this paper. eously with an anaesthetic. This suggests that the nociceptive
Figure 4 Schematic representation of how we may phenotype patients with tendinopathy in relation to the continuum and target treatments. The
aim of treatment is to push the tendon into the green section with relatively little pain and good function. Tendon structure can be normalised in
the early stages of the continuum where rehabilitation can push the tendon ‘up the continuum’. In the latter stages of the continuum, ‘moving up
the continuum’ may not be possible, so interventions should be focused in ‘moving the tendon sideways’. It is important to note that interventions
directed solely at pain will not drive the tendon to a positive outcome as they do not address dysfunction, such as motor inhibition, strength and
power deficits, or tendon load capacity. Interventions that target structure may improve tendon structure and direct the tendon ‘upwards along the
continuum’; however, it will not address functional deficits (effect on pain is inconclusive) or load capacity and may leave the tendon vulnerable to
reinjury.
input from the periphery maintains sensitisation.57 Unilateral preseason; this supports the adaptive pathway suggested within
isometric exercises in patellar tendinopathy have no effect on the continuum.70 However, in this same cohort, 3 out of the 18
contralateral pain,58 suggesting that local factors or pathways participants progressed to a reactive pathology, that is, structure
are critical in pain production. In summary, we acknowledge deteriorated and pain developed. This highlights that the effect
that there is good evidence for adaptations (both motor and of load on tendon structure may vary depending on intrinsic
sensory) in tendinopathy, yet we cannot dismiss the role of local risk factors (genetics, adiposity, age, etc) and other features
nociceptively driven pain. within loading history.71 Load magnitude and recovery time, as
well as numerous other factors (type and consistency of load
stimulus), may influence tendon response and the progression
IS A RESPONSE TO LOAD PART OF AN ADAPTIVE OR
along the continuum.35 Furthermore, it also highlights the diffi-
PATHOLOGICAL PROCESS?
culty in attempting to dichotomise the tendon’s response as
Normal tendon tissue responds to load with both synthesis and
being pathological or adaptive, as these changes are likely to fall
degradation of the matrix; however, turnover rates vary depend-
within a greater continuum.
ing on the protein.59–61 Collagen turnover is minimal after skel-
etal maturity,11 12 whereas non-collagenous substances, such as
proteoglycans, are synthesised and degraded much more quickly HOW WOULD THE PRACTITIONER CHOOSE A TREATMENT
(days), suggesting that they may be a critical component in early BASED ON THE CONTINUUM?
pathological or adaptive changes.12 The continuum model suggested that management may be opti-
We proposed that reactive pathology (as defined in the mised by tailoring interventions to the stage of pathology and tar-
model) results in an increase in large proteoglycans but further geting the primary driver (cell activation) and inter-related
consideration and recent studies suggest that there must be an alterations in matrix integrity. While exercise and load management
earlier phase that is less intense and potentially transient. The are fundamental to management, a plethora of intratendinous and
Achilles tendon62 and superficial digital flexor tendon in the peritendinous interventions exist to ‘treat’ tendinopathy—this
horse63 undergo a definite but subtle structural response on increases the complexity of the clinical decision-making process.
imaging 2 days after high loads that returned to normal by day Tendinopathy is a heterogeneous clinical presentation due to
4. The time course of these changes in imaging appearance the variable change in matrix structure, pain and dysfunction.9
(ultrasound tissue characterisation (UTC) echopattern) is similar Phenotyping of patients based on structure, pain, dysfunction
to that of the 2–3 days it takes to express and break down large and load capacity may allow the clinician to direct appropriate
proteoglycans such as aggrecan.64–67 A similar response is seen treatments at the critical limiting factors (figure 4).
using MRI—this suggests an increase in large proteoglycans and
associated bound water in response to high load exercise.68 It is Interventions targeting pain
unclear whether these changes are adaptive or pathological and Patients with tendinopathy present clinically primarily due to
whether they have a lasting effect on the health of the tendon pain, with available interventions directed at the painful tendon
(in reference to pain). including non-steroidal anti-inflammatory drugs, corticosteroid
The normal Achilles tendon improves in structure as seen injections,72 extracorporeal shockwave therapy,73 extratendinous
using UTC69 over the course of an elite Australian football high volume injection74 and surgical scraping.75 While the
4 of 7 Cook JL, et al. Br J Sports Med 2016;50:1187–1191. doi:10.1136/bjsports-2015-095422
Review
majority of these treatments reduce pain in the short to medium build load capacity in the aligned fibrillar matrix portion of the
term, the longer term efficacy of some has been questioned.72 tendon rather than attempting to stimulate healing in the degen-
Addressing pain is critical; however, interventions directed erative portion.
solely at pain have a minimal effect on the associated kinetic While the continuum classifies tendons based on the extent/
chain deficits or tissue capacity and may result in the recurrence presence of structural disorganisation, targeting treatments at
of pain (figure 4).55 regenerating the area of disorganisation may be futile as the
Interestingly, isometric quadriceps muscle contractions in tendon may have already compensated, or be in the process of
patellar tendinopathy induce immediate analgesia and reduce doing so. This conceptual shift may be explained by the meta-
cortical inhibition of the muscle, which in turn improves phor, treat the doughnut (area of aligned fibrillar structure), not
strength.58 Intervening with a loading programme also has the the hole (area of disorganisation). However, sufficient aligned
advantage of benefiting the tendon,76 the muscle,77 as well as tissue of itself will not protect from further episodes of reactive
the cortical control of that muscle, which may lead to improve- pathology; to achieve this, management must progress to
ments in function and a positive clinical outcome. An incremen- improving the load capacity of the ‘doughnut’ through a pro-
tal load-based rehabilitation programme is capable of modifying gressive loading rehabilitation.
the balance of excitability and inhibition in muscle control,78 In this context, it is difficult to find relevance for treatments
thus altering the loads transmitted by the tendon. directed at repairing tendons and normalising structure through
the addition of growth stimulants (eg, platelet-rich plasma),81
Interventions addressing function and load capacity which do not appear appropriate for the pathological process at
There are few papers that investigate dysfunction in tendinopa- any of the continuum stages. It should also be recognised that
thy because pain and structure have been deemed to be more there is a hyperactive tendon cell response, as well as an increase
important. It is also difficult in the clinic to quantify function in tendon cell numbers, in all stages of tendinopathy, even in
and the tendon’s load capacity, where pure measures of strength the degenerative stage.64 The addition of additional cells (stem
may not reflect the whole picture (see separate paper on or tenocytes) into a hypercellular environment would appear
‘Capacity’ in BJSM79). There can be alterations to the graded counter-intuitive, as the ability to recreate a viable cell–matrix
recruitment of muscles associated with tendinopathy leading to relationship is limited in a frankly degenerative region of the
changes in function.58 Return to sport is potentially a measure tendon that is unable to transmit tension.
of function and load capacity, though most research has been
conducted outside of the competitive season. While addressing
pain may remove a barrier for improving function, dysfunction DISCUSSION AND FUTURE DIRECTIONS
including persistent deficits in muscle performance or the Regardless of the initiating event (overstimulation of resident
kinetic chain, as well as insufficient tendon load capacity, may tenocyte, collagen disruption/tearing, inflammation), tendon
well predispose the tendon to reinjury (figure 4). Further pathology is characterised by a significant cell response to
research is needed to better characterise the functional deficits injury.7 82 It is unlikely that any one model fully explains all
associated with tendinopathy and develop useful tools for the aspects of the pathoaetiology of tendon pathology and its links
clinician. to pain and function, as these processes and relationships are
complex.
Interventions targeting structure Equivocal clinical intervention outcomes from research that
The continuum model1 provided a framework to understand may well be due to heterogeneity in the research cohorts.
the potential of the tendon to regain normal structure. This par- Subgrouping by tendon pathology for clinical trials may give
ticularly applies to the reactive stage (figure 4) of the model clearer outcomes and better clinical guidance.
where it remains possible for the tendon to regain its normal The capacity to test the continuum in humans is limited in
structure with optimal management.16 Treatments that may part by the capacity of present imaging modalities to detect
dampen tendon cell response at this stage (unloading, medica- pathological and structural changes, along with the need for a
tion directed at inhibiting the cell and resultant matrix changes) deeper understanding and greater precision in the measurement
may also reduce pain, although this is yet to be substantiated. of the various aspects of pain and associated dysfunction in ten-
Notably, heavy load eccentric exercises or intratendinous injec- dinopathy. The requirement to better comprehend these inter-
tions may be highly provocative and deleterious within this relationships in time should guide effective management
reactive stage. through considered interventions across the spectrum of presen-
In degenerative tendinopathy, interventions influencing tations. The history of biomedical research would remind us
tendon structure are less critical, as the pathology appears to that this paper, as with many of our colleagues, are just a part of
have limited reversibility. Although the original continuum the very long and complex journey in the better understanding
paper suggested that treatments should focus on stimulating the of this challenging condition.
cell to produce collagen (in the degenerative region) and restruc-
ture the matrix, it has since been demonstrated that interven- Twitter Follow Ebonie Rio at @tendonpain, Sean Docking at @SIDocking and Jill
Cook at notifications@ProfJillCook
tions designed to change structure do not necessarily result in
these improvements.17 Competing interests None declared.
Furthermore, the pathological tendon appears to effectively Provenance and peer review Not commissioned; externally peer reviewed.
compensate for areas of disorganisation by increasing in cross-
sectional dimension to maintain sufficient volumes of aligned
fibrillar structure.80 Since the degenerative tendon has sufficient REFERENCES
levels of load-bearing tissue, and given the limited ability of the 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
tendon to reverse the pathology, treatment strategies should be 2009;43:409–16.
directed at optimising adaptation of the tendon as a whole 2 Lewis JS. Rotator cuff tendinopathy: a model for the continuum of pathology and
(figure 4). Specifically, treatment at this stage should aim to related management. Br J Sports Med 2010;44:918–23.