Calcific tendinitis

Last revised by Craig Hacking on 21 Apr 2024

Calcific tendinitis, also known as calcific tendinopathy or tendonitis, is a self-limiting condition due to the deposition of calcium hydroxyapatite within tendons, usually of the rotator cuff. It is a common presentation of hydroxyapatite crystal deposition disease (HADD)

Typically this condition affects middle-aged patients between the ages of 30 and 60, with a slight predilection for women 2.

The condition passes through four stages 2 (Uhthoff cycle):

  1. precalcific

    • asymptomatic

    • fibrocartilaginous metaplasia (see below)

  2. calcific or formative

    • symptoms are variable from none to pain on movement

  3. resorptive

    • most symptomatic

    • pain due to extravasation of calcium hydroxyapatite into adjacent tissues, especially subacromial bursa, causing calcific bursitis

    • pain typically lasts two weeks

  4. postcalcific

    • variable symptomatology

    • some restriction of movement is common

    • may last months

Calcific tendinitis results from the deposition of calcium hydroxyapatite within the substance of a tendon and is thought to be due to decreased oxygen tension, leading to fibrocartilaginous metaplasia and secondary mineralization 1.

This condition most frequently affects the rotator cuff of the shoulder 1.

However, the condition may occur anywhere in the body with the hip and knee joints being the 2nd and 3rd most common locations respectively 10,11.

Calcific deposits are usually visualized as homogeneous hyperdensity with variable morphology, but typically globular/amorphous with smooth or ill-defined margins.

Features of calcific tendinitis on ultrasound may include 7:

  • a curvilinear/ovoid calcification with acoustic shadowing

  • capsular soft tissue swelling

  • T1

    • hypointense homogeneous signal

    • the adjacent tendon may be thickened

    • some enhancement surrounding the deposit may be seen

  • T2

    • hypointense calcium deposits

    • hyperintense signal may be present peripherally due to edema

    • hyperintense subacromial-subdeltoid bursal fluid

  • T2*: calcifications may bloom

The treatment is controversial and its efficacy is difficult to assess due to the inherent variability of the symptoms and the self-limiting nature of the disease. Potential treatments include 2:

  • oral analgesic/anti-inflammatory medication

  • subacromial local anesthetic/steroid injection

  • barbotage

  • extracorporeal shock wave therapy

  • arthroscopy

  • migration of calcium deposits from tendons into the subacromial-subdeltoid bursa or into the humeral greater tuberosity 15.

In the shoulder consider:

  • incidental calcification: seen in 2.5-20% of "normal" healthy shoulders 1,2

  • degenerative calcification

    • seen in previously torn tendons

    • generally smaller

    • slightly older individuals

  • loose bodies

    • associated chondral defect

    • associated secondary osteoarthritis

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