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Tendinopathy Management

Tendinopathy or Tendonitis? Pathophysiology and Management

Definition: The evolution from tendonitis to tendinopathy

The understanding and management of tendinopathy have evolved considerably. The term “tendinitis”, which implied an inflammatory reaction as the main mechanism, has now been replaced by “tendinopathy”. Current theories suggest that chronic overload or acute stress are responsible for structural changes. These changes may be reversible, or progress to flawed healing and tendon degeneration. 

Tendinopathies generally manifest as a symptomatic triad: pain on stretching, pain on isometric contractions and pain on palpation.

Since 2009, the “continuum of tendinopathy” model has become a reference in the literature, dividing the pathology into three successive evolutionary stages: Reactive tendinopathy, tendon remodeling and degenerative tendinopathy.

Tendinopathie, traitement, ostéopathe Paris 16
  • Reactive Tendinopathy

Reactive tendinopathy is the first stage of the continuum. It occurs in response to a sudden increase in load on the tendon, due for example to a rapid intensification of training, unusual activity in a sedentary person or direct trauma. The cellular reaction is mainly non-inflammatory, but leads to increased production of proteoglycans, which retain water and produce a characteristic ultrasound image of tendon thickening. This stage is completely reversible, allowing rapid adaptation to loads.

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  • Tendon Dysrepair

The second stage involves deeper structural changes, where prolonged overload leads to matrix disorganization and cell proliferation. This results in localized, heterogeneous thickening visible on ultrasound, with increased vascularization. Early load management and an appropriate rehabilitation program can help reverse these changes.

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  • Degenerative Tendinopathy

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The third stage, or degenerative tendinopathy, results from chronic overload, leading to cell apoptosis and significant matrix breakdown. The tendon then becomes fragile, at risk of rupture, and displays significant vascular and neuronal proliferation. At this stage, the tendon is more vulnerable to recurrence and may require complementary biological treatments such as shock waves or platelet-rich plasma injections to optimize regeneration.

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Recently, Cook and Purdam have adjusted their model, showing that tendon lesions are more complex, and that the same tendon can present both reactionary and degenerative zones simultaneously. This finding enables a personalized therapeutic approach, aimed first at relieving pain, then at strengthening the tendon structure through appropriate physical rehabilitation.

In conclusion, recent discoveries have made it possible to develop advanced therapeutic strategies, combining analgesia and structural regeneration to limit recurrence and restore optimal tendon functionality. 

modéle du mécanisme des tendinites, Charbel Kortbawi, ostéopathe Paris 16

Pain management and tendinopathies treatment

Medicinal Treatments

  • Analgesic and anti-inflammatory treatments

Analgesic treatments often bring clinical improvement in the short and medium term. However, when administered in isolation, they show little long-term benefit, as the altered tendon structure persists, leading to a high prevalence of recurrence.

The first line of treatment is to remove the cause of the injury by resting the tendon and adopting a wait-and-see approach. For top-level athletes, it is possible to reduce training intensity without exceeding the pain threshold, thus allowing relative rest. A balance is needed between sufficient rest and prolonged immobilization: adequate rest promotes clinical healing, whereas excessive immobilization weakens the tendon due to lack of stimulation.

 

Non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen, are the treatment of first choice in the acute phase. In addition to their analgesic effects, they reduce the cellular response and synthesis of proteoglycans responsible for intratendinous edema. However, prolonged use is not recommended, due to the risk of gastrointestinal complications, hypertension and renal disturbances.

In the chronic phase, NSAIDs are less effective, as inflammatory cells become rarer.

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  • Corticosteroid injections

Although commonly used, corticosteroid infiltration has limited long-term efficacy. The review by Coombs et al. shows that, for epicondylitis, corticosteroids offer inferior results in terms of pain reduction and improved functionality after 26 weeks, compared with wait-and-see treatments, NSAIDs, manual therapy or PRP. Repeated injections (3-4 over 6 to 18 months) appear to be less effective than a single injection.

Corticosteroids also carry side-effect risks, such as subcutaneous tissue atrophy (9%), residual pain (8%), local depigmentation (<1%) and, rarely, tendon rupture. They are also less effective on degenerative tendons, due to the low inflammatory component. A controlled trial on patellar tendinopathies observed similar improvement at 12 weeks between three groups (corticosteroid injection, eccentric program and heavy-load program), but the effects of corticosteroids diminished after 6 months. Furthermore, corticosteroids reduce collagen concentration, disrupt tendon homeostasis and slow healing, which explains their high rate of recurrence.

Osteopathic treatment and rehabilitation exercises

  • Sustained isometric contraction

Sustained isometric contraction is effective for pain management. The Rio et al. study in athletes showed that isometric contraction of the quadriceps (5 repetitions of 45 seconds with knee flexion at 60°) immediately reduced pain and cortical motor inhibition, increasing strength and function. Cook and Purdam also support this approach for athletes, as it provides a prolonged analgesic effect, enabling training to be maintained. In the case of hyperalgesic tendinopathy, exercise can be adapted using a bipodal position with a reduction in contraction time and repetitions.

 

  • Eccentric contraction

Eccentric contraction is particularly effective in the treatment of tendonitis, especially in the chronic stages or when the tendinopathy has been present for some time. It is used to promote tendon rehabilitation and regeneration. Eccentric contraction is often introduced after the acute phase, when inflammation is under control and the tendon is ready for more intensive exercise. Eccentric contraction helps to strengthen the tendon, improve its load-bearing capacity and reduce pain. It stimulates collagen production in the tendon and helps restore muscle and tendon function.

 

  • Manual therapy and osteopathy

 

Manual therapy and osteopathy play an important role in the management of tendinitis, and their effectiveness varies according to the stage of tendinopathy.

- Acute stage of tendonitis: Osteopathy can include muscle release and joint mobilization techniques to improve local blood circulation and fluidity of movement. This can also help reduce swelling and prevent stiffness in the affected area. 

-Chronic stage: Manual techniques such as manipulation, muscle stretching and myofascial techniques are commonly used to help restore tendon function and mobility.

Contraction exceentrique, tendinopathie traitement

Conclusion

Tendinopathies must be approached holistically, taking into account biomechanical and environmental factors (body axes, stiffness, unsuitable sports equipment). Patient involvement is crucial, not only to promote healing, but also to ensure the duration of treatment. Eccentric exercises, in particular, require multi-day commitment. Prior isometric contraction can help improve patient tolerance and adherence to the exercises.

The main aim of treatment remains pain reduction and functional recovery. Radiological normalization is not a priority, as the correlation between imaging and clinical findings is limited.

Finally, although ultrasound abnormalities are a risk factor for symptomatic tendinopathies, preventive screening remains controversial. In athletes, many abnormalities may appear on imaging without translating into symptoms, and there is no consensus on the degree of ultrasonographic change that warrants prophylactic treatment.

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