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COLUMNS: Medical Report

Tendinopathy Not Tendonitis

Now Is the Time for a Change

Trojian, Thomas M.D., M.M.B., FACSM; Amoako, Adae M.D.

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doi: 10.1249/FIT.0000000000000159
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INTRODUCTION

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Tendon is a very organized fibrous connective tissue structure joining muscle to bone (9). The regular densely arranged collagenous tissue is made up of collagen fibers, sparse cells of various shapes, and ground substance (Figure 1). This arrangement of collagen fibers makes it capable of resisting high tensile forces while transmitting forces from muscle to bone. Nearly 85% of the dry weight of tendon is made up of collagen and mostly type I collagen. The mechanical and physiological characteristics of collagen dictate the qualities of tendon. Tendon also shows a degree of extensibility. The tendon has a crimped pattern like a mild zigzag. There is a flattening of the tendon crimped pattern during the first stage of tendon stretching and with increasing stretch, other mechanisms such as an interfibrillar gliding may be involved. The strain used to stretch a tendon is partially regained on return to normal architecture of the tendon, then a beneficial elastic effect would be achieved. In the example of the Achilles tendon, which can take loads of 12 times the body’s weight, it is stretched late in the stance phase as the soleus and gastrocnemius muscles contract and the ankle dorsiflexes. Before plantar flexion occurring, muscle activation ceases and stored energy helps to initiate planter flexion (9).

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Figure 1:
Histological stain of normal densely arranged collagen tissue showing fibers, sparse cells of various shapes, and ground substance.

When tendons are injured, it is often called tendonitis (or tendinitis). This tendonitis, which literally means inflammation of the tendon, is labeled incorrectly. Inflammation is not seen histologically when the tendon is examined under the microscope. Tendinitis oftentimes has been used interchangeably with tendinopathy. To treat tendon injuries properly, one must understand the pathology that is occurring; therefore, it is inherent that these two terms are differentiated from each other. The term “tendinitis” has been used in sports medicine for many years to describe the cycle of damage, improper healing patterns, and the subsequent reinjuries of tendons. This cycle of tendon disordered degeneration secondary to abnormal, haphazard, and poor healing response is actually a tendinopathy (Figure 2) and not an inflammatory tendinitis. Authors have been calling for an end to the term tendinitis for more than a decade. The term “tendonitis” has been so commonly used in the medical vernacular that it is often still used in the medical literature, even as recent as 2014. Now, it is the time to stop using “tendinitis” and start using the correct term “tendinopathy.”

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Figure 2:
Histological stain of tendinopathy showing discontinuous and disorganized collagen fibers.

The normal process for tendon healing involves three different but overlapping phases (Figure 3) (13). There is an initial inflammatory phase that lasts only 24 to 48 hours. At this phase, erythrocytes, platelets, and inflammatory cells (e.g., neutrophils, monocytes, and macrophages) migrate to the site of damage and clean the site of dead materials. Cells also release factors that recruit tendon fibroblast to begin collagen synthesis and deposition. This phase is relatively short compared with the other two phases; it fades quickly and is replaced by the proliferative phase. The inflammation stops at this time, and after 48 hours, inflammatory cells are replaced quickly. This second phase usually takes place for the next 6 to 12 weeks. During this phase, the body produces a different form of collagen, called type III, which is not the normal tendon collagen, which is type I collagen. The type III collagen is used to protect the tendon by developing a scar patch. New blood vessels (neovessels) and nerve endings are brought in to help supply the repair. This leads to the third phase (remodeling) where the type III collagen and the new blood vessels and nerves are removed and the normal type I collagen replaces the type III collagen to form normal tendon (13). The disruption of this normal process causes the tendon to develop an abnormal thickened tendon (Figure 4), leading to pain and a weakened tendon, hence tendinopathy.

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Figure 3:
The normal process of tendon healing, which involves the overlapping phases of inflammation, repairing, and remodeling.
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Figure 4:
Sonogrpahic findings of normal tendon (left) showing homogeneous, linear, and fibrillar pattern compared to tendinopathy (right) showing thickened area with loss of fibrillar pattern represented by hypoechoic regions on ultrasound.

ETIOLOGY

Tendon injuries can be caused by both intrinsic and extrinsic risk factors. Intrinsic risk factors include age, genes, diabetes, thyroid disease, and elevated cholesterol. Extrinsic factors include training errors, biomechanics, and medications such as fluoroquinolones, statins, and corticosteroids. Age of participant and training errors seem to be the two most influential factors that predispose active individuals to tendinopathy. Although tendinopathy affects individuals regardless of age, older individuals are more susceptible than younger individuals and these older athletes are likely to have severe forms of tendinopathy. The loading of specific tendons will often vary by the nature of the sport played. For example, running sports load the Achilles tendon and jumping sports load the patellar tendons. Tendons with different genetic alterations to the collagen molecules that make up tendon or the supporting extracellular molecules have been shown to be more common in tendinopathy compared with the normal tendons. Studies on training errors point to increased landing frequency and substandard quadriceps extensibility as risk factors for developing tendinopathy.

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When training clients with certain medical conditions, be mindful that some may be more prone to tendinopathy. The prevalence of tendinopathy is increased in patients with diabetes mellitus. The abnormal tendon structure occurs because of abnormal healing and the development of disorganized fibril structure. Elevated cholesterol has been associated with tendinopathy, and some have recommended measuring cholesterol levels in tendinopathy patients. The statins used to treat hypercholesterolemia have been associated with tendinopathy, but whether this is caused by treatment of the hypercholesterolemia or the medication itself is unknown. For clients taking a fluoroquinolone-type medication, used for treating many infections, the risk of Achilles tendon rupture is tripled; however, the overall incidence among users is low (∼18 per 100,000 users within 30 days of medication).

Just like most injuries, tendinopathy starts with an insult to the normal anatomy. This frequently follows a normal reparative process to return the tendon to normal structure. But on occasion, the normal healing pattern is disrupted and tendinopathy occurs after a cascade of events. Three theories have attempted to explain how tendinopathy comes about. In the mechanical theory, it is thought that mechanical overload to the tendons causes damages to collagen and other matrix components which, across time, can accumulate during repeated stretch cycles to the tendon (Figure 5). Tendons frequently have an area that is fed poorly with blood supply. This area of the tendon is called the watershed area. The vascular theory proposes that these watershed areas of the tendons are prone to vascular insufficiency and therefore heal poorly because the neovascularization is unable to occur normally. An alteration to the homeostasis of tendon innervations is thought to be responsible for tendinopathy according to the neural theory. This is supported by the finding of increased Achilles tendon injuries in patients with sciatica. The nerve supply of tendons includes many autonomic fibers, which are involved in regulating tendon blood flow as well as local tendon cell metabolism, collagen production, and pain signaling. This would allow for abnormal healing and dysfunction of the tendon.

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Figure 5:
In the mechanical theory of tendinopathy, tendons do not undergo adequate repair leading to tenocyte disruption, which predisposes tendons to repeated injuries after the initial increase demands on the tendon.
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Three Theories of Tendinopathy

DIAGNOSIS

The diagnosis of tendinopathy is based on clinical examination assisted by imaging. The key feature in tendinopathy is tenderness with activity. This is essential when it comes to diagnosis because abnormal image findings can exist without symptoms (7). Direct palpations of the suspected injured tendon will elicit the pain. However, this may not necessarily indicate that tendinopathy is the source of the pain (5). The positive predictive value of tendon palpation tenderness being tendinopathy is 68% for the patella tendon (5). Those patients tender to palpation and with activity-related symptomatic tendons are more likely to have ultrasound abnormality than those tender to palpation alone. The level of tenderness is more predictive of tendinopathy, as moderate and severe tenderness is more predictive than mild or no tenderness (5).

In assessing tendinopathy, two useful clinical tools have been developed. The Victorian Institute of Sports Assessment-Achilles (VISA-A) (Table 1) and the Victorian Institute of Sports Assessment-Patella (VISA-P) have been validated as measures of Achilles and patella pathology. VISA-A is a summed score with a maximum of 100 points if asymptomatic. The effect-size thresholds are 5 points for a small effect and 15 points for a moderate effect. The VISA-P is scored similarly. These can be found with any Web search. It is helpful to assess client’s tendon health.

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TABLE 1:
VISA-A Components

The imaging of choice for viewing of tendons is either ultrasonography or magnetic resonance imaging (MRI). Ultrasonography has been shown for multiple different tendons to be more accurate in the diagnosis of tendinopathy than MRI (12, 15). It is the initial diagnostic tool of choice because of its relative low cost, easy accessibility of equipment, accuracy of the test, and safety compared with MRI. It is important to remember that tendon abnormalities without symptoms do not predict future tendinopathy because many of these tendon abnormalities will resolve without treatment.

TREATMENT

In the past, tendon injuries have been treated as an inflammatory process. Therefore, nonsteroidal anti-inflammatory drugs like naproxen or ibuprofen were prescribed or an anti-inflammatory medication like corticosteroid was injected (10). However, it is now known that these medications do not help the healing process, and studies point to them having a negative effect long-term, although they help reduce short-term discomfort. The main goal of treatment of tendinopathies should be alteration of the abnormal healing pattern so that the body can use its natural healing process to start healing again (14).

Treatment of tendinopathy should start with mechanotherapy (mechanical therapy). Mechanotherapy (e.g., eccentric exercises or heavy slow resistance exercises) is the employment of mechanotransduction for the stimulation of tissue repair and remodeling (8). These therapeutic exercises prescribed to promote the repair or remodeling of injured tissue should be done for at least 6 weeks, along with a relative reduction in training load. Eccentric exercises should be done multiple times a day but take a shorter time to complete than heavy slow resistant training exercises. These exercises stimulate the tendon repair by increasing collagen synthesis rate to restore the tendon structure. The heavy slow resistance exercises are recommended to be done three times a week with multiple sets during each session. The load is then increased weekly using the maximum lift for the squat, hack squat, and leg press (4). The heavy weight and slow repetitions load the tendon, triggering signaling to produce observable structural change in the tendon. Both eccentric exercises and heavy slow resistance training produce good results for Achilles tendinopathy, but heavy slow resistance has a slightly higher compliance rate and patient satisfaction rate (4).

Stretching has been discussed across the years to prevent hamstring injuries and other tendon injuries. Despite the change in the stiffness feeling after a good massage and stretch, the studies on the effects of stretches and prevention of injuries to tendons are not favorable. One review of the literature stated “No evidence was found for a positive effect of stretching exercises” (11). People like the feeling after a good stretch and massage, but it is not going to protect against tendon injury.

Despite the effectiveness of mechanotherapy, not everyone’s response to the modality is positive and further treatment is needed. It is important as a fitness professional to be aware of these further treatment options to help guide clients and not cause further injury. Treatments can be divided intratendonous and extratendonous. Procedures into the tendon can cause weakening, and tendon rupture has been reported with intratendonous procedures in the first 6 weeks postprocedure. Table 2 shows many of the current procedures and treatments with comments about their effectiveness and current research. This information can be useful when planning programs for your clients.

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TABLE 2:
Postmechanotherapy Treatments and Procedures

In summary, “tendinitis” is not an appropriate term to describe the degenerative chronic injuries to tendons. “Tendinopathy” is disruption of the normal healing process developing an abnormal thickened tendon. Treatments are geared at restarting the normal healing process. Many treatments for tendinopathy have been recently developed geared at restarting the healing process. We reviewed mechanotherapy, platelet-rich plasma, tenotomy, sclerotherapy, shock wave, and topical glycerol trinitrate. It is not known which treatment is better, but mechanotherapy is the recommended starting point for the first 6 weeks, but these tendinopathy treatments normally take 12 weeks for full recovery.

References

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© 2015 American College of Sports Medicine.