Achilles Tendonitis vs Tendinopathy 2026 | DPM

Feature	Achilles Tendinitis (Reactive)	Achilles Tendinopathy (Degenerative)	Insertional vs. Mid-Portion
Pathology	Acute inflammatory response; edema; cytokine cascade	Failed healing response; collagen disorganization; neovascularization; no true inflammation	Insertional: at calcaneal attachment (2–3 cm); Mid-portion: 2–7 cm above insertion
Duration	Acute (days to 6 weeks)	Chronic (more than 6 weeks; often months to years)	Both locations can be either acute or chronic
MRI Finding	Peritendinous edema; tendon signal intact or mildly increased	Intratendinous signal change; thickening; mucoid degeneration	Insertional: calcification on X-ray; Haglund deformity; retrocalcaneal bursitis
NSAIDs / Anti-Inflammatory	Helpful — addresses true inflammation	Limited benefit — no inflammation to reduce	Insertional: avoid cortisone (tendon rupture risk at insertion)
Cortisone Injection	Reasonable for peritendinitis; avoid intratendinous	Avoid — accelerates tendon degeneration; rupture risk	NEVER inject at Achilles insertion; acceptable in retrocalcaneal bursa only

Treatment	Mid-Portion Tendinopathy	Insertional Tendinopathy	Evidence / Success Rate
Eccentric Loading (Alfredson Protocol)	First-line — 3 sets of 15 eccentric heel drops, 2x/day, 12 weeks; on step	Modified protocol on flat surface (not over edge — loads insertion)	Level I; 60–80% improvement at 12 weeks for mid-portion
Heavy Slow Resistance (HSR)	3 sets of 15 bilateral heel raises; increase weight progressively	Flat surface bilateral heel raises; avoid excessive dorsiflexion	Comparable to eccentric; better compliance; preferred by many
ESWT (Shockwave)	3 sessions; excellent evidence	3–5 sessions; especially effective when calcification present	Level I for mid-portion; Level II for insertional; 65–80% improvement
PRP Injection	1–2 injections; superior to cortisone at 6 months	1–2 injections; safer than cortisone at insertion	Level II; 65–75% improvement; preferred in high-demand athletes
Heel Lift	8–12 mm heel lift reduces Achilles tension	Critical — reduces impingement of Haglund against shoe	Immediate pain reduction; adjunct to all protocols
Surgical (Gastrocnemius Recession / Debridement)	FHL transfer + tendon debridement for large intratendinous tears	Haglund resection + insertional debridement + FHL transfer	80–90% success in carefully selected patients failing 6 months conservative

https://www.youtube.com/watch?v=iyhRz44SA6Y

Why the Terminology Matters

For decades, pain and dysfunction in the Achilles tendon was called “tendonitis” — implying inflammation as the primary driver. Histological studies have since shown that chronic Achilles conditions often show minimal inflammatory cells but significant disorganized collagen, neovascularization, and degenerative changes. This condition is better described as tendinopathy or tendinosis.

The distinction has real treatment implications. Anti-inflammatory medications (NSAIDs, cortisone) are appropriate for acute inflammatory tendonitis but have limited benefit — and cortisone may even be harmful — in chronic degenerative tendinopathy.

Acute Achilles Tendonitis

Acute tendonitis presents with rapid-onset pain, warmth, swelling, and tenderness in the tendon, usually following a sudden increase in activity, a new shoe, or a training change. The tendon may be visibly thickened and hot to touch. This presentation truly involves inflammatory mediators and responds to rest, ice, NSAIDs, and temporary activity modification.

The goal in acute tendonitis is preventing progression to chronic tendinopathy through prompt, appropriate management. This means not pushing through pain and not immediately injecting cortisone into the tendon substance.

Chronic Achilles Tendinopathy

Chronic tendinopathy is characterized by morning stiffness that warms up with activity, thickening of the tendon (especially the mid-portion, 2-6 cm above the insertion), and pain that correlates with activity load rather than appearing acutely. Histologically, the tendon shows angiofibroblastic changes without significant inflammation.

The key distinction: insertional vs. non-insertional tendinopathy. Insertional tendinopathy involves the attachment site at the heel bone, often with Haglund’s deformity (bony prominence) and is more complex to treat. Non-insertional (mid-substance) tendinopathy has the best evidence base for eccentric exercise protocols.

Treatment Approach

Eccentric loading exercises — specifically the Alfredson protocol of eccentric heel drops off a step — have the strongest evidence for mid-substance tendinopathy. The mechanism involves progressive mechanical loading that stimulates tendon remodeling. This program typically takes 12 weeks to show significant results and requires consistency.

ESWT (extracorporeal shockwave therapy) is an effective adjunct, particularly for cases that haven’t responded to eccentric exercise alone. Multiple sessions stimulate a controlled healing response in the tendon.

PRP (platelet-rich plasma) injections deliver concentrated growth factors directly into the tendinopathic tissue to stimulate repair. Evidence is supportive, particularly when combined with structured rehabilitation.

Heel lifts and orthotics reduce the stretch placed on the Achilles during gait, providing symptomatic relief and reducing provocative loading.

Surgery is reserved for recalcitrant cases after 6+ months of conservative care — tendon debridement for mid-substance disease, or Haglund’s resection and insertional repair for insertional disease.

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