Understanding Chronic Tendon Pain


Tendinopathy accounts for up to half of all sporting injuries and around one-third of musculoskeletal pain consultations. Traditionally described as a degenerative or inflammatory disorder of the collagen matrix, new evidence challenges this view. Current research points to neurogenic inflammation and pathologic nerve ingrowth as key drivers of chronic tendon pain.

The New Biology of Tendon Pain

In healthy tendons, nerve fibers primarily exist in the outer layers—the paratenon, epitenon, and endotenon. The dense tendon core (tendon proper) is mostly aneural. Pain-free function depends on this arrangement, with few sensory inputs in the fibrous core.

However, in chronic tendinopathy, this architecture changes. Studies show abnormal nerve sprouting from the surrounding tendon envelope into the tendon proper. This process brings with it the growth of small, unmyelinated sensory fibers and an influx of pain mediators such as substance P, CGRP, and glutamate. These neurochemicals activate mast cells, tenocytes, and nerve endings, amplifying a feedback loop of pain and inflammation. The result is not simply a “degenerating tendon,” but one with active neuro-immune signaling.

The Tendon Envelope: A Key Pain Regulator

Histological findings emphasize the paratenon and its associated nerve plexus as the “control hub” for tendon nociception. Chronic irritation or microtrauma in this region may trigger persistent pain even when the tendon appears structurally intact on imaging. Understanding this anatomy provides therapists with a new framework: tendon pain is as much a neural disorder as a structural one.

Implications for Therapy

If chronic tendon pain arises from aberrant nerve growth and neuroinflammation, then treatments that target these nerve pathways could offer relief. Traditional therapies—eccentric loading, manual release, or dry needling—may work partly by modulating local neural signaling rather than collagen remodeling alone.

Emerging interventional techniques support this perspective. Percutaneous Ultrasound-Guided Tenotomy (PUT), such as the TENEX® procedure, uses high-frequency ultrasound energy to fenestrate the paratenon. This technique appears to separate the pain-generating envelope from the tendon core, potentially denervating the area. Patients often report rapid pain relief, suggesting mechanisms beyond gradual tissue regeneration.

Other approaches, such as controlled denervation or neuroablative procedures, are being explored. The challenge is achieving pain modulation without compromising tendon integrity.

Takeaway for Clinicians and Therapists

  • Chronic tendon pain reflects neurogenic and immune mechanisms, not just tissue degeneration.
  • The tendon envelope (paratenon and epitenon) plays a central role in regulating pain signaling.
  • Manual therapy, dry needling, or ultrasound-guided techniques may help by modulating pathological nerve activity.
  • Understanding tendon innervation supports a more integrated, fascia- and neurobiology-informed model of pain management.

This evolving view encourages therapists to consider tendinopathy as a neurosomatic disorder—a condition where structure, inflammation, and nerve signaling intersect. Future therapies may focus less on “repairing” the tendon and more on retraining its sensory environment.

Palee , et al. “Is chronic tendon pain caused by neuropathy? Exciting breakthroughs may direct potential treatment.” Current Pain and Headache Reports 28.12 (2024): 1235-1239.