Tendinopathy: The New Science of Pain and Repair

This summary is based on the Nature Reviews Disease Primers article “Tendinopathy” by Neal L. Millar et al. (published in 2021). It outlines the current scientific understanding of the condition’s pathology, diagnosis, and management.

Overview

Tendinopathy is a complex, multifaceted clinical syndrome characterised by persistent pain, localised swelling, and impaired performance. It is a spectrum of changes that occur when a tendon fails to heal correctly following injury or repetitive strain. While often referred to in the past as “tendinitis” (implying inflammation) or “tendinosis” (implying degeneration), the term tendinopathy is now preferred to encompass the diverse histological and molecular changes involved.

1. Epidemiology and Risk Factors

The condition is highly prevalent, accounting for up to 30% of musculoskeletal consultations.

• Common Sites: The most frequently affected areas are the Achilles tendon, patellar tendon (jumper’s knee), rotator cuff, and the medial/lateral epicondyles (golfer’s/tennis elbow).
• Demographics: Prevalence increases with age. In sports, it affects up to 50% of elite runners (Achilles) and 40% of volleyball players (patellar).
• Risk Factors: These are divided into extrinsic (e.g. training errors, poor equipment, occupational repetitive loading) and intrinsic (e.g. age, genetics, obesity, metabolic conditions like diabetes and high cholesterol certain medications such as fluoroquinolones and excessive corticosteroid use).

2. Pathophysiology

Healthy tendons are composed of highly organised Type I collagen fibres. In tendinopathy, this structure undergoes significant “disrepair”:

• Matrix Disorganisation: Collagen fibres become fragmented and haphazard. There is a shift from Type I collagen to the weaker, less organised Type III collagen.
• Cellular Changes: Resident cells (tenocytes) change shape, and there is an increase in programmed cell death (apoptosis).
• Neovascularisation and Innervation: There is an abnormal “sprouting” of new blood vessels and sensory nerves into the tendon tissue. These new nerves are thought to be a primary source of the chronic pain experienced by patients.
• Inflammatory Role: While not a classic inflammatory disease (like rheumatoid arthritis), the Primer highlights that inflammatory mediators (cytokines and prostaglandins) play a critical role in the early and chronic stages of the disease.

3. Diagnosis

Diagnosis remains predominantly clinical, based on patient history and physical examination.

• Symptoms: Pain that is usually “load-dependent” (worsens with activity) and localized tenderness.
• Imaging: Ultrasound and MRI are frequently used to confirm the diagnosis and assess the extent of structural damage. However, the article notes a “clinico-radiological paradox”: many people have structural changes on scans but no pain, while others have severe pain with relatively “normal” looking tendons.

4. Management Strategies

Management is often challenging, with no “one-size-fits-all” cure. The primary goal is to increase the tendon’s load-bearing capacity.

• Exercise-Based Rehabilitation: This is the gold-standard treatment. Progressive loading (including isometric, isotonic, and heavy slow resistance training) is essential to stimulate tendon remodelling.
• Pharmacotherapy: NSAIDs may provide short-term pain relief but do not address the underlying pathology. Corticosteroid injections are common but are now used with caution due to the risk of long-term tendon weakening.
• Adjunct Therapies: Treatments like shockwave therapy (ESWT) and Platelet-Rich Plasma (PRP) injections show varied results and lack consistent high-level evidence.
• Surgery: Generally considered a last resort when 6–12 months of conservative management has failed.

5. Future Outlook

The Primer concludes that future research must move beyond viewing tendinopathy as simple “overuse”. There is a need for:

• Precision Medicine: Tailoring treatments based on an individual’s genetic and metabolic profile.
• Biological Therapies: Developing drugs that can specifically target the molecular pathways causing matrix degradation.
• Refined Rehabilitation: Better understanding of how much “load” is optimal for different stages of the disease to prevent the “cycle of disrepair.”