Calcific Tendonitis

“All At Once it Was Gone” – Explaining Extreme Shoulder Pain Related to Calcific Tendonitis
Calcific tendonitis is a common shoulder disorder in which multifocal, cell-mediated calcification is deposited within or around the rotator cuff tendons. Interestingly, this is usually followed by a spontaneous phagocytic resorption and tendon restoration. Little is known about the cause and it remains controversial but tissue hypoxia and localized tissue pressure related to increased cellularity often found in a “reactive tendinopathy” are thought to be triggers for the formation of calcium.

AP Xray View of Calcific Deposit

It was originally thought that calcific tendonitis was related to aging, wear and tear and tendon degeneration but recent studies have rejected this model and proposed “reactive cell mediated calcification” as the mechanism and excessive or prolonged tendon loading as the driver (see Rotator Cuff Tendinopathy).


This reactive process has three stages:

Pre-calcific stage – is characterized by tendon cells (tenocytes) turning into calcium cells (chondrocytes).

Calcific stage – has 3 phases which sees calcium being laid down to form large foci of calcification, a resting phase where deposition and inflammation cease and a resorptive phase which sees a process where by calcium is resorbed.

Post-Calcific Stage – the final stage see tendon re-modelling and subsequent fiber realignment.

Mild or moderate pain can be present but not always during the the formative phase when calcium is being laid down. The acute, resorptive phase may be accompanied by severe pain that limits function. For reasons unknown during the resorptive phase those with the worst pain and symptoms usually have the best prognosis. Pain is usually caused by inflammation around the calcium deposits and as a result of subacromial impingement, bursal irritation or prominent deposit size. It is also not unusual for some people to develop a contracted “frozen” shoulder secondary as a result of calcific tendonitis.

Women, mostly between 30 and 50 years of age are affected. As many as 10% of people will have bilateral deposits. More than 30% of insulin dependent diabetics develop tendon calcification although with the tendency to be more asymptomatic than others. Tears of the rotator cuff are not unusual and coexist in 25% of cases. The supraspinatus tendon is by far the most common rotator cuff tendon affected with deposits usually 1.5 – 2cm from its humeral insertion.

Calcific tendonitis is usually diagnosed after a thorough shoulder examination and assessment of plain X-rays. AP, internal and external rotation, Lateral Y views and axillary views are best to determine deposit location. MRI investigation could also be important if a rotator cuff tear is suspected as the treatment of the cuff tear is inherently different.

There is a strong tendency towards natural healing by spontaneous resorption of the deposits within 2-3 weeks of pain onset with or without intervention. Unfortunately, this is not always the case and symptomatic deposits and a disrupted quality of life can be long lasting.

The focus and the mainstays of treatment are pain reduction, decreasing intra-tendinous pressure, maintaining range of motion, muscle activation and the uptake of the calcific deposits. Non-surgical treatments include non-steroidal anti-inflammatory drugs e.g. Ibuprofen, subacromial hydrocortisone injections, needle lavage and extracorpeal shockwave therapy (ESWT). There is no evidence for Glucosamine. Open or arthroscopic surgery is reserved for those 10% who are unsuccessful with conservative interventions.

That means 90% of people get better with conservative treatment.


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Uhthoff HK, Loehr JW: Calcific tendinopathy of the rotator cuff: Pathogenesis, diagnosis and managemenet. J Am Acad Orthop Surg 1997; 5: 183-191

Hurt G, Baker CL Jr: Calcific tendinitis of the shoulder. Orthop Clin North Am 2003; 34: 567-575

Galatz, LM (Ed): Orthopaedic Knowledge Update 3rd Edition, Shoulder and Elbow: AAOS 2008.