Tendinopathy Terminology for Clinicians: Why We Stopped Saying 'Tendonitis' (And What to Use Instead)

If you trained more than a decade ago, you were almost certainly taught to call it tendonitis. The suffix "-itis" implies inflammation, and inflammation was the dominant model for explaining tendon pain. You treated accordingly: relative rest, ice, NSAIDs, maybe a cortisone injection, and a gradual return to activity.

The problem is that the histological research doesn't support this model for chronic tendon pain — and the terminology shift from tendonitis to tendinopathy isn't just semantic housekeeping. It reflects a genuinely different understanding of what's happening in the tissue, and it has direct implications for treatment.

This post is for clinicians who want to get current on the terminology and the rationale behind it. I'll also cover the clinical subtypes that are worth distinguishing in practice.

What the histology actually shows

The foundational work here comes from Nirschl and Pettrone in the 1970s and was significantly advanced by Khan, Maffulli, Cook, and others from the late 1990s through the 2000s. When researchers examined tendon tissue from patients with chronic tendon pain — using biopsy and later imaging — they consistently found the same picture: collagen disorganisation, increased ground substance, neovascularisation, and the presence of tenocytes showing degenerative changes.

What they did not find, consistently, was the cellular infiltrate of an acute inflammatory response. There were few or no inflammatory cells — no neutrophils, limited macrophage activity — in the tissue of people with chronic tendon pain.

This finding has been replicated across multiple tendon sites. The tissue in chronic tendon pain doesn't look like inflamed tissue. It looks like tissue that has failed to remodel appropriately after repeated stress — a failed healing response rather than an active inflammatory one.

"Calling chronic tendon pain 'tendonitis' isn't just inaccurate — it actively misdirects treatment toward anti-inflammatory strategies that don't address the pathology."

The tendinopathy continuum model

Cook and Purdam's continuum model (2009, updated 2016) is the most clinically useful framework for understanding tendon pathology and remains highly relevant in practice. It describes three stages:

Reactive tendinopathy. An acute response to unaccustomed load — tendon swelling without significant structural disruption. This is the stage where anti-inflammatory approaches are most relevant. The tissue hasn't yet undergone significant pathological change and can recover well with load management.

Tendon dysrepair. An attempt at intratendinous healing that has become disorganised. Matrix breakdown, increased ground substance, and beginning of neovascularisation. The structural changes are more significant but not permanent.

Degenerative tendinopathy. Established pathological changes — cell death, extensive matrix disruption, disorganised collagen. This is what's present in most chronic cases seen in clinical practice. The likelihood of full histological normalisation decreases at this stage, but clinical outcomes (pain and function) can still be excellent with appropriate loading.

The continuum model is most useful for load management decisions. Reactive presentations need load reduction and monitoring. Dysrepair and degenerative presentations need progressive loading to drive remodelling — rest is counterproductive beyond the short term.

Current terminology: what to use

Tendinopathy is the preferred umbrella term for clinical tendon pain syndromes, regardless of presumed pathological stage. It makes no assumption about mechanism and is appropriate when you haven't performed diagnostic imaging.

Tendinosis is sometimes used to describe histologically confirmed degenerative change without inflammation — useful in research and imaging contexts, less so in routine clinical communication.

Paratenonitis (formerly peritendinitis) — inflammation of the paratenon or tendon sheath rather than the tendon itself. Relevant for tendons with sheaths (e.g. tibialis posterior, finger flexors). This IS an inflammatory condition and responds differently to treatment.

Insertional vs. mid-portion tendinopathy is a clinically important distinction that affects exercise prescription. Insertional tendinopathy (at the bone-tendon junction) involves the enthesis and is more mechanically sensitive to compression. Mid-portion tendinopathy is more amenable to full-range loading including eccentric work.

Tendon tear / rupture — when the structural integrity of the tendon is compromised. A distinct entity, requires different management, and should be excluded when the presentation warrants it (imaging indicated).

Why this matters for treatment

The terminology shift matters because it changes the treatment logic. If you believe the problem is inflammation, the treatment is to reduce inflammation. If you correctly understand the problem as a failed remodelling response, the treatment is to provide the appropriate mechanical stimulus to drive that remodelling.

That mechanical stimulus is progressive loading — specifically, heavy slow resistance training during the dysrepair and degenerative phases, with isometric loading as an initial option for pain management and as a starting point for highly irritable presentations.

This shift also changes how we frame prognosis and patient education. "You have inflammation that needs to settle" sets a different expectation than "your tendon hasn't been adequately loaded to stimulate remodelling — that's what we're going to address." The second framing is more accurate, more empowering, and sets a more realistic timeline.

A note on imaging

Ultrasound and MRI findings should be interpreted with caution. Structural changes on imaging — hypoechoic regions, increased tendon thickness, neovascularisation — correlate poorly with symptoms. Asymptomatic tendons frequently show pathological changes on imaging, and pathological-looking tendons can be completely pain-free.

Imaging is most useful for ruling in or out specific differentials (partial or full-thickness tear, calcification, paratenonitis), not for confirming tendinopathy or directing loading parameters. A clinical diagnosis based on symptom location, provocation testing, and loading history is usually sufficient for initiating treatment.

Resources worth knowing

For clinicians looking to go deeper: Cook and Purdam's continuum model papers are essential reading (British Journal of Sports Medicine, 2009 and 2016). Jill Cook's work on the insertional vs. mid-portion distinction is equally practical. Seth O'Neill has produced useful clinical resources on hamstring and Achilles tendinopathy specifically.

I'll be publishing more clinician-focused content here on assessment approaches, loading program design, and the evidence on adjunct therapies including shockwave and laser. If you work with tendon pain regularly and want to stay current, the newsletter is the best way to stay across new content as it comes out.