Origins of Tendopathy: Where is the Evidence?
A significant portion of my caseload consists of helping patients recover from tendon disorders. Rotator cuff pathology seems to comprise the greatest percentage of these conditions at our clinic, but there have been no shortages of patellar tendopathy, Achilles tendopathy, and the ubiquitous (read: worn out) diagnosis previously known as tennis elbow.
I was first exposed to the clinical management of tendon disorders while working as a PT technician back in the mid-1990’s. At that time, pretty much everyone walked in with an “-itis” attached to the end of their anatomical diagnosis. predictably, these supposed inflammatory conditions were all managed according to the standards of care at that time. Orthopedists injected and provided oral NSAIDs. PTs provided ice, pulsed ultrasound, and activity modification. Progressive exercise to the extremity was initiated with emphasis on exercises such as the empty can and stretching the posterior capsule. Some elements of this treatment paradigm remain, but the key is that the entire treatment algorithm back in the 90’s was based on the assumption that the problem was grounded in the inflammatory process.
What’s In a Name?
The treatment of tendopathy has undergone a dramatic transformation over the last fifteen years. A subtle but significant advance has come in modifying our taxonomy of tendon disorders. Specifically, we have stopped referring to all musculotendinous disorders as “tendonitis”. Mercifully we’ve also stopped diagnosing people who have never picked up a racket with “tennis elbow” and chronically sedentary patients with anterior knee pain as having “jumper’s knee.” Simply changing what we called a condition has led to some pretty innovative treatments and paving the way for revolutionizing how we help our patients recover.
Degenerative vs Inflammatory Origins
Degeneration, not inflammation, appears to be the primary pathophysiology of most tendon disorders seen in clinical settings. While it is reasonable to suggest acute inflammation plays a role at the earliest stages of the disease, this process is rapidly replaced by tissue degeneration. Although the timeline for the transition from inflammatory to degenerative is somewhat unclear, it could occur as early as two weeks and has been consistently demonstrated at four months after initial injury.
Theoretical Models of Tendon Pathology
Our evolution of understanding brings us to examine three etiological models of tendon pathology: mechanical, vascular, and neural.
The Mechanical Model
The mechanical model of tendon overload is consistent with commonly held notions of an “overuse” injury. The essential premise is that healthy tissue is subjected to supraphysiologic loads. The result is a mechanical failure of the tendon substance. A similar situation would exist if so-called unhealthy tissue were subjected to normal loads. Mechanistic models of tendon dysfunction make sense and are consistent with empirical histological observations of degeneration, spontaneous disruption of unhealthy tendons, and fits well within the scope of biomechanics.
Although the mechanical model seems to be a plausible link to the degeneration associated with tendopathy, there are some important features of tendopathy forcing us to look in other areas. Firstly mechanistic models do not explain why treatments such as eccentric exercise have recently been shown to be very beneficial for Achilles and supraspinatus tendopathy. Secondly, a mechanical model doesn’t account for tendon failure at specific points within the substance of the tendon. Achilles tendon and supraspinatus tendon failure often occurs at predictable sites, which eludes a purely mechanical rationale. Lastly, mechanistic models simply cannot explain the pain associated with chronic degeneration.
The Vascular Model
The role of vascularity in tendon dysfunction fills in some of the gaps left by the mechanical model. Tendons, oft perceived as passive structures, are metabolically active tissues capable of adapting to loading (and unloading). The metabolic activity within a tendon is chiefly derived from its vascularity. A vascular model of tendon pathology has been bolstered by observations that Achilles, supraspinatus, and posterior tibial tendons frequently fail within zones of hypovascularity.
The vascular model shows promise but, like the mechanical model, fails to account for some important observations about tendon pathology. Some researchers have shown that tendon vascularity is more uniform than initially theorized. Secondly, the vascular model does not explain why young healthy athletes would be susceptible to vascular compromise. Lastly, a firm link between vascularity and the positive effects of eccentric exercise has yet to be made.
The Neural Model
The neural model of tendon dysfunction has gained significant momentum in recent years. The first, and rather obvious premise of this model is that tendons are often well innervated. consequently, these tissues are capable of generating mechanical or chemical nociceptive drive to the central nervous system. Histopathological investigation of tendons have discovered Substance P and calcitonin gene related peptide (CGRP) which further increase the sensitivity of nociceptive drive, making such tendons more sensitive to deformation. There is even recent evidence suggesting individuals with radiculopathy may be more susceptible to ipsilateral Achilles tendopathy.
The most significant limitation of the neural model is that we don’t fully understand it yet. It is simply too early to speculate how these discoveries will be useful in the diagnosis and treatment of tendopathy.
The Next Evolution: An Integrated Model
I’m certainly not the first person to offer this as a suggestion, but answers to the riddles presented by chronic tendopathy are likely present within a much more complex system analysis. In other words, simply viewing tendopathy as mechanistic, vascular, or neural is likely lead to inaccurate or at least incomplete information. In my opinion, the most clinically useful management model of tendopathy has been proposed by Coombes et al in a 2008 article in the British Journal of Sports Medicine. This model accounts for local tendon pathology, changes in the patient’s pain system, and sensorimotor dysfunction as interactive components of the patient’s presentation. I believe this integrated model offers tremendous upside in the assessment and management of tendon pathology and avoids much of the inadequacies of more reductive linear models.
There is clearly more to learn with respect to how we help patients manage the rather complex nature of tendon pathology. I am looking forward to a further refinement of our assessment and treatment models in 2010! I wish you all a Happy and Prosperous New Year.
Rees, J. (2006). Current concepts in the management of tendon disorders Rheumatology, 45 (5), 508-521 DOI: 10.1093/rheumatology/kel046
Coombes, B., Bisset, L., & Vicenzino, B. (2009). A new integrative model of lateral epicondylalgia British Journal of Sports Medicine, 43 (4), 252-258 DOI: 10.1136/bjsm.2008.052738