Calcific Tendinopathy

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Written by: Dr Jeremy Steinberg โ€“ created: 1 March 2022; last modified: 15 April 2022

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Supraspinatus calcific tendinopathy.jpg
Right supraspinatus calcific tendinopathy
Calcific Tendinopathy
Pathophysiology Calcification between healthy collagen fibrils in a 'critical zone' 1-2cm from the tendon insertion due to high shear and stress forces.
Classification Formative, resting, and resorptive stages.
Clinical Features Spectrum of no symptoms to debilitating pain most commonly affecting the supraspinatus, but other tendons can be involved.
Treatment Corticosteroid injection, barbotage, extracorporeal shockwave, surgical debridement

Calcific tendinopathy is most commonly seen in the shoulder (but also in other tendons) and is characterised by the deposition of calcium hydroxyapatite crystals within a healthy tendon.


The calcification is different to that seen in degenerative tendinopathy. In degenerative tendinopathy there is a heterogenous mixture of calcium salts that are diffusely scattered throughout the tendon in an area of collagen degeneration or tearing.

In calcific tendinopathy on the other hand, the calcification forms focally in a 'critical zone' which is 1-2cm from the tendon insertion. This critical zone is thought to have high shear and stress forces that promote the development of a focal calcium deposit between healthy collagen fibrils.

It is thought that these deposits occur due to the "failed cell-mediated healing theory." Here excessive loading and repetitive microtrauma results in an aberrant healing response and focal calcification. That may be why more commonly loaded tendons such as supraspinatus are more vulnerable.

The following stages of the disease can be seen to occur:

  • Precalcific stage: fibrocartilaginous metaplasia of tenocytes into chondrocytes which creates an environment where calcification can occur
  • Calcific stages
    • Formative stage: calcium crystals are formed and coalesce into large foci of calcification, typically with a chalk-like appearance
    • Resting stage: stable presence of mature calcifications surrounded by a fibrocartilaginous tissue border or 'cap'
    • Resorptive stage: inflammatory reaction towards the calcific deposits with development of vascularised tissue at the periphery of the calcification or cap. Resorption is mediated through macrophages and multi-nuclear gian cells and these phagocytose calcific deposits. The calcification is toothpaste like in consistency during this stage. It can leak into nearby bursae, bone, or muscle, which can cause severe pain
  • Post-calcific / Reparative stage: Fibroblasts remodel the space previously occupied by calcium with type III collagen. Type III collagen is then replaced by type I collagen for complete healing.


Calcific tendinopathy is most commonly seen in the supraspinatus tendon. Other tendons of the shoulder are less commonly affected.

It can also be seen in multiple other different tendons in the body including supraspinatus, infraspinatus, subscapularis, long head biceps, rectus femoris, gluteus medius, gluteus minimus, proximal hamstring, common extensor and flexor tendons of the elbow, quadriceps tendon, patellar tendon, Achilles tendon.


Usually seen in patients in their 30s to 50s, and women are more commonly affected than men. This is in contrast to degenerative tendinopathy where patients are in their 50s to 60s.

It is associated with diabetes, hypothyroidism, and hyperlipidaemia.

Clinical Features

Many patients are asymptomatic, and so the spectrum of clinical features ranges from no symptoms to debilitating pain. Symptoms can relate to the stage of the disease. Patients may start with diffuse pain which progresses to severe focal pain and finally resolution.

Patients in the formative stage may describe a poorly localised, subacute, low grade pain that may be more pronounced at night. On exam there may be vague pain provoked by shoulder movements but no localisable or specific findings. A small minority of patients remain in the formative phase for months or years without progressing.

However most patients progress from the formative to the resting stage in 3-6 months. Symptoms become more mechanical in nature and patients may complain of clicking, snapping, or catching with joint motion. They may have impingement pain such as rotator cuff impingement signs for supraspinatus involvement.

Often the pain isn't bad enough in the above phases to seek medical care. Typically patients present in the resorptive stage which is the most painful stage of calcific tendinopathy. Sometimes patients may not have had any symptoms from the previous stages at all. In the resorptive stage patients have acute severe pain and there is a restricted range of motion. The symptoms and signs may mimic a septic arthritis with erythema and swelling.

When patients transition from resorptive to reparative there is a gradual reduction in symptoms and signs.

Differential Diagnosis

For shoulder calcific tendinopathy the main mimics are adhesive capsulitis, long head biceps tendinopathy, degenerative tendinopathy, acute synovitis or septic arthritis, and tendon injury.

Adhesive capsulitis: In calcific tendinopathy the passive range of motion should be normal but limited in adhesive capsulitis. However it can be tricky to differentiate from adhesive capsulitis in the resorptive phase.


Plain radiographs: in most cases plain films can show calcific tendinopathy.

The Gartner and Heyer classification system can be used which can correlate to the pathophysiology but may not correlate with patient symptoms.

  1. Well circumscribed and dense (resting phase);
  2. Well circumscribed with an inhomogeneous structure or poorly circumscribed with a homogeneous structure (formative)
  3. Poorly circumscribed and translucent (resorptive phase)

Ultrasound: there is a hyperechoic focus with posterior acoustic shadowing. Appearances can correlate with the pathological stage.

  1. Hyperechoic arc-shaped deposits (resting phase)
  2. Non-arc shaped, fragmented, or nodular calcifications with increased colour Doppler signal (resorptive phase).

Some findings correlate with symptomatic calcific tendinopathy: fragmentation, power Doppler signal, and distention or extrusion of calcium into the surrounding bursal structures. Findings may not correlate with the degree of symptoms however.

MRI: this modality is traditionally less helpful with false-negatives from missed deposits and false-positives of normal hypointense healthy tendons. MRI can be helpful however in excluding other pathologies such as tendon tears, osteoarthritis, chondral injury, and labral injury. Also newer sequences have improved the accuracy (susceptibility weighted imaging).


Treatment options include analgesia, corticosteroid injection, extracorporeal shockwave therapy, ultrasound guided percutaneous barbotage, and surgical debridement. Ultrasound appearances can help guide treatment recommendations by determining the pathological stage.

Resting stage: Often more aggressive treatments are needed such as barbotage or shockwave.

Resorptive stage: Often patients can be managed with NSAIDs and physiotherapy. There are no proven physiotherapy programmes. If pain is severe then consider an isolated bursal or peritendinous corticosteroid injection. There is no reduction in the ability of the body to resorb the calcific deposits with corticosteroid.[1]

See Also

See open access review by Catapano an colleagues.[1]


  1. โ†‘ 1.0 1.1 Catapano M, Robinson DM, Schowalter S, McInnis KC. Clinical evaluation and management of calcific tendinopathy: an evidence-based review. J Osteopath Med. 2022 Feb 4;122(3):141-151. doi: 10.1515/jom-2021-0213. PMID: 35119231.

Literature Review