Tendinopathy vs Tendonitis

The two words encode different claims about the same clinical picture. Tendonitis asserts inflammation. Surgical specimens from chronically painful Achilles, patellar and elbow tendons instead show degeneration: disorganised, separated collagen, increased ground substance, rounded tenocytes replacing spindle-shaped ones, and neovascularisation with ingrowing nerve fibres, the classical inflammatory infiltrate largely absent. Tendinosis names that histology; tendinopathy is the agnostic clinical umbrella covering pain, swelling and impaired load tolerance.

The change in name changed treatment. If the problem is degenerative matrix failure rather than inflammation, an anti-inflammatory strategy targets the wrong thing, and the trial data broadly agree. In lateral epicondylalgia, corticosteroid injection beats placebo for pain at around six weeks and gives worse outcomes at one year, including higher recurrence. Progressive loading, eccentric or heavy slow resistance, has the most supportive controlled evidence, working over months rather than weeks.

What this lets you conclude is limited but real: a treatment justified on anti-inflammatory grounds needs separate justification in a tendon that is not inflamed. What it does not license is the strong version. More recent immunohistochemistry has found macrophages, mast cells and inflammatory mediators in tendinopathic tissue, so inflammation is better described as present and low-grade than as absent.

Two errors recur. Marketing still says tendonitis, then offers an anti-inflammatory mechanism as the rationale for a degenerative condition. And imaging is over-read: tendon thickening, hypoechoic change and Doppler neovascularity are common in asymptomatic athletes, so an ultrasound abnormality does not by itself explain pain or prove a treatment worked.