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Is compressive load a factor in the development of tendinopathy?

Cook, J.L. and Purdam, C., 2012. Is compressive load a factor in the development of tendinopathy?. British journal of sports medicine, 46(3), pp.163-168.

In today’s letter

• Overview of how compression may affect the development of tendinopathy

• 4 clinical tips

• Audio version of the newsletter

• As always, a fun infographic for you to save and use in the future

• Rapid Results = Excessive load without adequate rest changes the extra cellular matrix properties near the bony attachments of the tendon which make them more susceptible to compression based forces at end ranges

• Professional takeaway = Avoid end ranges in early tendinopathy rehab to allow tendons to rebuild and recover (Except if you’re dealing with mid-tendon achilles tendinpathy)

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Aim of the study

This paper investigated how compressive loads may contribute to the onset and persistence of tendinopathy, reviewing anatomical, epidemiological, and clinical evidence supporting this idea

Did you know?

• Excessive training volume or overuse of tendon elasticity are key factors in tendon overload, leading to tendinopathy.

• Tendons primarily transmit tensile loads due to their fibrous structure, so traditionally, tendon overload was considered purely tensile.

• Recent studies show evidence of compressive loads at or near regions where tendinopathy occurs.

• Almekinders et al. were the first to propose that compression or varying tensile loads could overload tendons, suggesting that the Achilles tendon insertion experiences different types of strains with potential compressive loads at the heel attachment

  

   

What is the evidence that compression affects tendons?

• Collagen-based connective tissues adapt to various loads by modifying their structure.

• Compression induces changes in tendon matrix composition, as demonstrated by Milz et al.

• Using 3-D reconstruction of the Achilles tendon, fibrocartilage was observed near the Achilles insertion, indicating the influence of compressive forces.

• Tenocytes respond to cyclic compression by adopting a chondrocytic phenotype (specialised cells responsible for cartilage formation and maintenance) and producing large proteoglycans like aggrecan (maintains the structure and function of cartilage tissue, providing resilience and resistance to compression)

• Increased deposition of aggrecan and type II collagen occurs in compressed tendon areas, especially near bony prominences.

• Biomechanical modeling and cell culture studies suggest that hydrostatic pressure stimulates these adaptive responses.

What is the relationship between tissue adaptation, compression & tendinopathy?

• Normal tendon have Fibrous tissue with highly structured type I collagen-based extracellular matrix, few cells, and nerve endings

• Altered tendons (tendinoapthy) have more cellular tissue with substantial matrix changes including increased large aggregating proteoglycans, type III collagen, disorganisation of fibres, and neurovascular ingrowth (leading to increased sensitivity/discomfort/pain)

• Tissue/cell responses to load suggests compressive forces lead to fibrocartilage formation in tendons.

Fibrocartilage = Has strong and resilient properties, making it suitable for locations in the body subjected to high levels of mechanical stress

• This suggest that compressive loads induce tendon pathology.

• Study by Soslowsky et al: looked at different loads on rat supraspinatus tendon – compressive, tensile, and combination.

• They found that the only the combination of compressive and tensile loads were particularly damaging to tendons, leading to increased cross-sectional are and decreased resilience

  

Are there compressive loads where tendon pathology occurs?

• Normal tendon attachment transitions from tendon —> through fibrocartilage —> to mineralised fibrocartilage —> to bone over a short distance (<2 mm).

• However, additional structures close to insertion have an active role in force transmission from tendon to bone.

• Benjamin et al. coined the term 'enthesis organ' for both the insertion and additional structures around tendon attachments.

  Enthesis organ = the area of where tendon inserts into bone. Theres often a bursa between the tendon and bone & fibrocartilage on bone

• Enthesis organ reduces the tensile load on insertion

• Examination of loads on enthesis organ, especially close to the insertion, shows areas to both tensile and compressive loads, potentially affecting tendinopthy development

• Clinical tendinopathy presentations often occur at area of compression close or adjacent to tendon insertion, rather than at actual insertion.

• Some tendons have fixed bony prominence, others have prominence modified by movement, while others have movement-modified prominence external to bone-tendon continuum.

• Some tendons lack bony prominence, which indicate that compression is unlikely to play significant role in tendinopathy onset (e.g., flexor tendons of forearm and patellar tendon insertion into patella)

How does this relate to tendinopathy?

• Wren et al. used a model to suggest that compression zones with low-fluid permeability, due to aggrecan's water binding properties, protect cells and collagen.

• Conversely, tensile regions with higher fluid permeability are less suitable for high cyclic compression loads.

• Transition zone between compressive (adjacent to bone) and tensile (removed from bone) zones of tendon show features of both

• Excessive loading may partially deplete bound water in tensile and transitional zones, as suggested by Grigg et al.

• Loss of water may expose tenocytes to greater cyclic compressive load, encouraging creation of large water binding proteoglycans, a process seen in tendinopathy.

• Reduced permeability in this region protects against further insult but further loading may perpetuate response, hindering equilibrium attainment.

How does this concept help clinically?

• Common aggravating activities for insertional tendinopathy align with this concept.

• For instance, dorsiflexion load like walking barefoot or on sand aggravates Achilles tendon insertion issues.

• Patients with Achilles insertional tendinopathy may experience pain during ankle dorsiflexion load (e.g., push-off) but not when hopping on toes.

• Load on gluteal tendon during hip adduction, as seen in walking with poor lumbopelvic stability, induces compressive load and provokes pain.

• Although Soslowsky reported minimal impact from solely compressive loads, sustained compressed positions often cause discomfort

• For example, sleep disruption from lying on the affected side is common in gluteal tendinopathy, as is sitting for hamstring tendinopathy.

• Stretching may provoke pain in insertional tendinopathies with muscle tension, such as stretching the Achilles

• Compression at bony prominence proximal to insertion helps explain gender differences of pelvic tendinopathies.

• Women are more likely to get gluteal tendinopathy, men are over-represented in adductor tendinopathy.

• Application of enthesis organ and compression model suggests increased neck of femur angles may increase tendon compression against greater tuberosity more in women than in men; whilst men are more prone to adductor tendinopathy due to lesser abduction/extension before compression of tendon complex against pubic ramus

What about true enthesopathies?

Enthesopthy = Condition characterised by inflammation, degeneration, or structural abnormalities at the sites where tendons or ligaments attach to bones (known as entheses)

• Some tendons lack bony prominence, and pathology occurs solely at bone-tendon junction, like medial elbow and patellar tendon.

• These tendons primarily endure tensile load, yet pathology mirrors other insertional tendinopathies.

• Lateral elbow primarily suffers from true enthesopathy, but its enthesis organ is more complex.

• Enthesis has variable bony prominence in radial head, acting as prominence in forearm pronation and mid-prone, not in supination.

• Maximal extensor muscle loads occur in pronated position, compressing tendon against radial head to reduce insertion load.

• Heavy use of screwdriver or wringing out clothes may lead to lateral elbow tendinopathy after repeated pronation and supination, placing direct load on enthesis.

What about achilles the mid-tendon?

• Mid-substance of Achilles tendon primarily endures high tensile and elastic loads.

• Achilles tendinopathy common among badminton players, sprinters, and distance runners

• Sedentary people are also susceptible to mid-Achilles tendinopathy despite lack of tensile overload.

• Theres a potential for compressive loads even in mid-tendon.

• Internal tendon shear force may result from gastrocnemius and soleus fibers' contribution to Achilles tendon.

• Plantaris tendon may apply compressive force in some athletes, contributing to Achilles tendinopathy.

• Invaginated plantaris tendon, stiffer than Achilles, creates shearing or compressive load, especially in dorsiflexion/ eversion.

• Raised heel height in shoe may alleviate mid-Achilles pain for those with invaginated plantaris tendon, but not necessarily for those with solely mid-Achilles tendinopathy.

• Role of posterior retinaculum may also contribute to purely compressive load, similar to retinacular metaplasia in de Quervain’s tendinopathy and trigger finger.

• Achilles tendon bowstrings over retinaculum during plantarflexion, potentially contributing to tendinopathy even in inactive individuals or those with minimal elastic and tensile loads

How does this concept help clinical understanding?

• Tendon insertion and enthesis organ adept at absorbing functional loads, but slow to adapt and resolve after.

• Load management in tendinopathy focuses on reducing training load volume/intensity and correcting biomechanical issues.

• Reducing compressive loads in insertional tendinopathies is crucial for further unloading.

• Complete rest from tensile loads is not advisible, as it weakens tendon and may induce tendinopathic changes.

• Applying moderate tensile, isometric loads while protecting against compression may aid recovery.

• Jonsson et al. demonstrated improvement by applying tensile load through limited joint range, reducing compression on tendon in dorsiflexion.

• Full range ankle movement in eccentric exercise successful in 30% with insertional Achilles tendinopathy; limiting dorsiflexion to plantargrade improved 70%

Clinical implications

1. Recommending shoes with a heel raise or placing heel wedges can be beneficial for decreasing pain in the Achilles insertion. This modification can help decrease tension on the tendon during activities and reduce discomfort.

2. In cases of tendinopathy with a compressive element, focusing on managing muscle compliance and length through massage techniques may be more effective than stretching. Massage can help address muscle tightness and improve tissue flexibility without exacerbating compression on the tendon.

3. To reduce compressive loads, consider adjusting training strategies. This could involve reducing stretching that may exacerbate compression and implementing high intensity isometrics to help tendon adapt in a safe environment

4. Patients experiencing minimal pain can gradually resume training with the implementation of strategies mentioned above. You can also consider, adjusting training volume and intensity, and monitoring pain levels

Top 3 resources

To further your knowledge about compression and tendons

1. Tendinopathy & running

   https://www.running-physio.com/tendon-staging/ 

2. Exercises for progressing achilles & patellar tendinopathy

   https://ars.els-cdn.com/content/image/1-s2.0-S1886658117300580-mmc1.pdf 

3. FANTASTIC video explaining tendon compression

   https://www.youtube.com/watch?v=Xbsc5aJ47iQ

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