Calcific Tendinopathy of the Shoulder

Original Editors Mary Harris, Tom Lawlor, Patrick Bales, Misty Hillin, Rick Wetherald as part of the Texas Evidence Based Practice Project.

Top Contributors - Mary Harris, Thomas Lawlor, Karina Leahy, Rick Wetherald and Patrick Bales



Calcific tendinopathy, or "calcium hydroxyapatite crystal deposition disease”[1], refers to the deposition of calcium—predominantly hydroxyapatite—in a tendon, most often in those of the rotator cuff. It may be secondary to a local decrease in oxygen tension resulting in fibrocartilaginous metaplasia and resulting calcification.[2]

Shldr2.jpg[3] Siegal D, Wu J, Newman J, Del Cura J, Hochman M. Calcific tendinitis: a pictorial review. Canadian Association Of Radiologists Journal [serial online]. December 2009;60(5):263-272.[4]


Etiology is still unclear.

Possible Causes[1][5]:

  • Hypovascularization, but has been removed from both poorly and well-vascularized tissues.
  • Compression 
  • Metabolic factors
  • Mesodermal defects   
  • Local degenerative and proliferative changes

Unlikely Causes[1]:

  • Infection and trauma
  • Blood or urine chemistry

Calcific tendinopathy occurs in 2.5%–7.5% of healthy shoulders in adults[2], and 39-62% of those being seen in medical centers for shoulder pain[1]. It's more commonly seen in women (70% of cases) and most frequently during the 5th decade of life, but has been seen in a 3 year-old and a 72 year-old.[2][1]. Right shoulder is more frequently affected but there is no evidence to support predisposing factors.[1]

Common locations[2]

  • Supraspinatus tendon (80% of cases): critical zone - Most Common
  • Infraspinatus tendon (15% of cases): lower 1/3
  • Subscapularis tendon (5%of cases): pre-insertional fibers

The consistency of the calcium deposit (seen via imaging) seems to be correlated with pain severity, not the size. [1] 

  • Asymptomatic: appear granular or cheesy, and have sharply defined borders.
  • Symptomatic: enlarge, liquify, and have less well-defined borders.
            "dry powder", "chalk-like", "semi-liquid toothpaste", "milky" and "creamy"

Characteristics/Clinical Presentation

Clinical presentation varies.[5]

Calcific tendinopathy is a self-limiting condition.[2] Symptoms may last several days or become chronic; there is no clear prediction of disease course. Time required for symptoms to disappear is typically too long for patient’s QoL.[5]

The typical clinical manifestation is a sub-acute, low-grade shoulder pain that increases at night (50% of patients), with restricted range-of-motion.[2]

Stage Name Presentation
 Chronic (Silent)
  • Presence of the calcific deposit 
    is asymptomatic and may be so for years.

Acute Painful Phase

  • Severe pain, disability, and
    frequently nocturnal discomfort.

Mechanical Phase 

  • Tendon impingement being a prominent finding
  • Pain of less severe nature than the acute phase

Differential Diagnosis

 Pathologies which present similiar to Calcific Tendinopathy of the Shoulder:

Outcome Measures

Outcome measures to track treatment efficacy:


Images: [3]


As Calcific tendinopathy is a soft tissue injury that can only be conclusively diagnosed via imaging, it is important to rule out other shoulder pathologies. It is recommended that the initial images include the anteroposterior view in neutral, internal, and external rotation[7]. Imaging will provide definitive proof of calcific build-up through what appear to be “bone spurs”.  An ultrasound image of the area is also advised, as this will rule out or rule in any differential diagnosis of soft tissue injuries such as a rotator cuff tear [9].  20-46.4 % of all cases are bilateral in nature, so all images and examinations should be conducted in a bilateral fashion [10][7]. Only 35% of cases are symptomatic, so bilateral imaging and examination can detect calcified deposits in an asymptomatic shoulder, if one side is already experiencing calcific tendinitis. This can help to guide treatment and decrease possible patient expenses and future visits.

Since imaging is the only way to diagnose calcific tendinopathy, physical examinations will seek to rule out a condition rathar than to rule in a condition.  Several systemic diseases are associated with an increased risk of calcification, such as gout, hypercalcemia of any cause, and various rheumatic diseases[11][7].

The chief patient complaints to expect in calcific tendinopathy are:
1.) Night pain, causing loss of sleep.[11][7][12][1].
2.) Constant dull ache[1].
3.) Pain increases considerably with AROM[1].
4.) Decrease in ROM, or complaint of stiffness [10][12][1].
5.) Radiating pain up into the suboccipital region, or down into the fingers[11][7][1].

• Observation-check bilaterally for swelling, atrophy or scapular movement that will indicate compensation for decreased humeral movement.

• Palpation-attention to any swelling, temperature difference, point tenderness. Most specifically, the supraspinatus tendon, as it is the most commonly affected[7]. The infraspinatus, teres minor, subscapularis, and biceps tendons are also involved and follow in incidence in the afore-mentioned order[1].

• Neuro and cervical screen may be indicated as N&T, or radiating pain may be present.

• AROM and PROM-pain and decreased ranges may be present in any, or all planes (depending on tendon(s) involved).  Observe end feel, may be empty 2˚ to pain.

• MMT’s-may demonstrate decrease from contralateral side or be limited by pain.

Medical Management

Most current medical treatment approaches for calcifying tendinopathy involve removal or downsizing of the calcium deposit(s). This is usually accomplished by excision or surgery, or by attempting to activate the body’s natural calcium resorption processes. First line treatments, especially in primary care offices, are most often non-steroidal anti-inflammatory drugs, or possibly local steroid injections. These treatments are done with the goal of decreasing pain and inflammation, but there is little evidence that they promote resorption of the calcium deposits. In fact, some researchers believe steroid drugs may actually inhibit the resorption process [13].

Needle aspiration of medium to large (>1.5cm) calcium deposits is easily administered in the outpatient setting, and has evidence showing positive outcomes up to 2 years post treatment. The procedure is done under local anesthesia, with ultrasound guidance. Two needles pierce the deposit; one to evacuate the toothpaste-like calcium, and one to flush the shell with saline. Evidence shows that this process is most effective when the disease is in the acute phase, and the calcium within the deposit is viscous enough to be aspirated by a large bore needle. Once progressed to the chronic stage, the calcium in the deposit is too solid in consistency to be aspirated, thereby limiting the effectiveness of the treatment. [3]

Arthroscopic excision of the deposit is argued by some to be the best treatment option for patients in the chronic stage of calcific tendinopathy. This procedure has an advantage over needle aspiration in that it can remove hardened deposits that can’t be drawn through a needle bore. Performing any surgical procedure local to the affected tendon, like any acute injury, will stimulate the body’s calcium resorption system, which will help rid the tendon of any further deposits left behind after surgery. There is currently debate among surgeons concerning acromioplasty during procedures for deposit excision. Some believe that symptoms caused by calcific tendinopathy is independent from rotator cuff impingement, and therefore the procedure doesn’t need to be performed if a type III acromion is not observed.[14] [13]  Others have demonstrated that even with small diffuse deposits, pain is not relieved from excision alone, and relief only comes after subsequent acromioplasty. [15]

Physical Therapy Management

There is evidence supporting the use of extracorporeal shock wave therapy (ESWT) as a potentially effective treatment of calcific tendinopathy. The modality administers high frequency sound waves to the affected area with the intent of breaking up the calcification. Researchers claim that this will cause the body to activate or increase the body’s calcium resorption system, removing the deposit. Depending on the frequency used, the treatment can be painful, but research shows the modality to be most effective at the highest frequency the patient can tolerate.ESWT is a potential alternative to surgery with good mid-term effectiveness and minimal side effects. [16] But ECSW is not free from complications, that included transient bone marrow edema and even reported cases of humeral head necrosis.[17][18]

Most authors report short term symptomatic improvement[19], but long term positive outcomes (past one year) have not been definitively demonstrated in research. [20]

Radial shock wave therapy (RSWT) is another modality that has been used in the treatment of calcific tendinopathy. RSWT is similar to ESWT in that it does not require puncture of the skin for treatment application. While RSWT has been shown to decrease pain and demonstrated at least partial deposit resorption in all subjects, long term positive outcomes (past 6 months) have not been demonstrated. [5]

Shock wave therapy increases shoulder function, reduces pain, and is effective in dissolving calcifications.[21] These results were maintained over the following 6 months.

Both ultrasound and pulsed electromagnetic field therapy resulted in improvement compared to placebo in pain in calcific tendinitis. [22]

Patients presenting with previously diagnosed calcific tendinopathy may have had medical treatment prior to PT. Limited research exists showing good short and long-term outcomes using an impairment based approach following medical treatment (aspiration or excision). These PT treatments were similar to treatment for adhesive capsulitis or rotator cuff impingment, including PROM/AAROM/AROM, capsule stretching and isometric activation of the affected rotator cuff musculature. Grade II-IV glenohumeral anterior-posterior and caudal glides should also be used when applicable restrictions are found.[1]

Key Research

Lam et al 2006 is a concise evidence summary encompassing most of the research surrounding diagnosis and medical management of calcific tendinopathy. The article outlines indications and contraindications of popular treatment approaches, and gives a thorough explanation of each procedure. There are also helpful radiographs of different types and stages of the pathology.[3]

Wainner & Hasz 1998 is a case study that provides a concise explanation of the pathology as it applies to physical therapy practice. It outlines classification of stages of calcific tendinopathy based on pain and physical exam findings, and also highlights how the combination of orthopaedic and physical therapy management can expedite the healing process.[1]

Clinical Bottom Line

Calcific tendinopathy is a comparatively common disease with an incidence between 2.7 and 7.5% and minority of cases are symptomatic3. Its unknown etiology and impact on quality of life and function are just two reasons it requires further research. A thorough physical examination and patient history review can only help to distinguish it from other pathologies  with a similar presentation as imaging is the only definitive diagnosis. Since the condition will often present as a number of other pathologies, treating calcific tendinopathy with traditional therapy, based on a wrongly hypothisized pathology may result on little to no improvement of symptoms. If this situation presents in the clinic, imaging must be ordered to rule out calcific tendinopathy. Current best evidence suggests that shockwave therapy has benefits to reabsorption of the calcific deposit. Impairment based therapy is still believed to be of greatest benefit through increasing blood flow to allow the bodys natural reabsorptive processes to work.


  1. 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 1.11 1.12 1.13 1.14 1.15 1.16 Wainner R, Hasz M. Management of acute calcific tendinitis of the shoulder. Journal Of Orthopaedic & Sports Physical Therapy [serial online]. March 1998;27(3):231-237. ( LOE 4 )
  2. 2.0 2.1 2.2 2.3 2.4 2.5 Serafini G, Sconfienza L, Lacelli F, Silvestri E, Aliprandi A, Sardanelli F. Rotator cuff calcific tendonitis: short-term and 10-year outcomes after two-needle us-guided percutaneous treatment--nonrandomized controlled trial. Radiology [serial online]. July 2009;252(1):157-164. Available from: CINAHL Plus with Full Text, Ipswich, MA. Accessed September 20, 2011.
  3. 3.0 3.1 3.2 3.3 Lam, F, Bhatia, D, K, J.F. de Beer. Modern management of calcifying tendonitis of the shoulder. Current Orthopaedics; 2006, 20, 446–452.
  4. Siegal D, Wu J, Newman J, Del Cura J, Hochman M. Calcific tendinitis: a pictorial review. Canadian Association Of Radiologists Journal [serial online]. December 2009;60(5):263-272.
  5. 5.0 5.1 5.2 5.3 5.4 5.5 Cacchio A, Paoloni M, Spacca G, et al. Effectiveness of radial shock-wave therapy for calcific tendinitis of the shoulder: single-blind, randomized clinical study. Physical Therapy [serial online]. May 2006;86(5):672-682.( LOE 1b )
  6. 6.0 6.1 Loew M, Sabo D, Wehrle M, Mau H. Relationship between calcifying tendinitis and subacromial impingement: a prospective radiography and magnetic resonance imaging study. Journal Of Shoulder And Elbow Surgery / American Shoulder And Elbow Surgeons ... [Et Al.] [serial online]. July 1996;5(4):314-319.
  7. 7.0 7.1 7.2 7.3 7.4 7.5 7.6 Gimblett P, Saville J, Ebrall P. A conservative management protocol for calcific tendinitis of the shoulder. Journal Of Manipulative And Physiological Therapeutics [serial online]. November 1999;22(9):622-627.
  8. Takahashi M, Ogawa K. Calcific tendinitis of the rotator cuff showing a contracted state of abduction: a report of four cases. Journal Of Shoulder And Elbow Surgery / American Shoulder And Elbow Surgeons. January 1997;6(1):72-76.
  9. Rapp S M. With few advances in calcific tendinitis treatment, diagnosing it becomes critical. Orthopedics Today. 2008; 70.
  10. 10.0 10.1 Fusaro I, et. al. Functional results in calcific tendinitis of the shoulder treated with rehabilitation after ultrasonic-guided approach. Musculoskeletal Surgery. 2011 (95): S31–S36.
  11. 11.0 11.1 11.2 Ebenbichler G R. et. al. Ultrasound therapy for calcific tendinitis of the shoulder. New England Journal of Medicine. 1999; Vol 340 (20): 1533-1538.
  12. 12.0 12.1 Alexander L D., et. al. Exposure to Low Amounts of Ultrasound Energy Does Not Improve Soft Tissue Shoulder Pathology: A Systematic Review. Physical Therapy. 2010; vol 90 (1): 14-25.
  13. 13.0 13.1 Uhthoff HK, Sarkar K. Calcifying tendinitis. Rockwood Jr CR,fckLRMatsen III FA, editors. The shoulder, vol. 2. Philadelphia: WBfckLRSaunders; 1990, 774–90.
  14. Neer CS. Anterior acromioplasty for the chronic impingementfckLRsyndrome of the shoulder. J Bone Joint Surg (Am) 1972;54A:fckLR41–50.
  15. Resch H, Povacz P, Seykora P. Excision of calcium deposit andfckLRacromioplasty? In: Gazielly DF, Gleyze PTT, editors. The cuff.fckLRParis: Elsevier; 1997. p. 169–71.
  16. Lee SY1, Cheng B, Grimmer-Somers K. The midterm effectiveness of extracorporeal shockwave therapy in the management of chronic calcific shoulder tendinitis. ( LOE 2a )
  17. Humeral head osteonecrosis after extracorporeal shock-wave treatment for rotator cuff tendinopathy. A case report. Liu HM, Chao CM, Hsieh JY, Jiang CC J Bone Joint Surg Am. 2006 Jun; 88(6):1353-6. ( LOE 4 )
  18. Osteonecrosis of the humeral head after extracorporeal shock-wave lithotripsy. Durst HB, Blatter G, Kuster MS J Bone Joint Surg Br. 2002 Jul; 84(5):744-6. ( LOE 4 )
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  20. Harniman, E, Carette, S, Kennedy, C, Beaton, D. Extracorporeal shock wave therapy for calcific and non-calcific tendonitis of the rotator cuff: a systematic review. Journal of Hand Therapy, April 2004; 17(2), 132-151. ( LOE 1a )
  21. Ioppolo F, Tattoli M, Di Sante L, Venditto T, Tognolo L, Delicata M, Rizzo RS, Di Tanna G, Santilli V. Clinical improvement and resorption of calcifications in calcific tendinitis of the shoulder after shock wave therapy at 6 months' follow-up: a systematic review and meta-analysis. ( LOE 1a )
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