Calcific tendinitis is a common pathology characterized by calcium hydroxyapatite crystal deposition in rotator cuff tendons (most commonly supraspinatus — 80%). Prevalence is 3-7% and more common in women aged 30-50. Disease stages: pre-calcific (tendon degeneration), calcific (calcium deposition — formative and resorptive phases), and post-calcific (healing). In resorptive phase, calcium crystal leakage into subacromial bursa causes severe acute pain ('calcific crisis'). Calcification deposit near tendon insertion on radiograph is the most fundamental diagnostic finding. On MRI, it appears as focal low-signal lesion on all sequences — surrounding reactive edema and bursal fluid may accompany. On US, it appears as hyperechoic focus (may or may not create shadow). Treatment may be conservative (NSAIDs, steroid injection), US-guided barbotage (percutaneous aspiration), or arthroscopic resection.
Age Range
30-60
Peak Age
40
Gender
Female predominant
Prevalence
Common
Calcific tendinitis is a self-limiting disease characterized by calcium hydroxyapatite (Ca₁₀(PO₄)₆(OH)₂) crystal deposition in rotator cuff tendon matrix. Pathophysiology progresses in three stages: (1) Pre-calcific stage — fibrocartilage metaplasia and chondrocytic transformation develops in tendon matrix; vascularity decreases in this area creating a hypoxic environment. (2) Calcific stage — consists of two phases: formative phase (calcium crystals accumulate around chondrocyte-like cells, smooth-bordered calcified mass forms within tendon) and resorptive phase (phagocytic activity of macrophages and giant cells begins calcium resorption — this phase is characterized by severe inflammatory response and clinically creates 'calcific crisis'). In resorptive phase, calcium deposit softens, surrounding tissue edema increases, and calcium particles can leak into subacromial bursa — triggering acute chemical bursitis. (3) Post-calcific stage — calcium is completely resorbed and tendon regeneration begins; granulation tissue and neovascularization are seen. The physics basis of calcification appearing bright on radiograph is calcium (Z=20) absorbing X-rays at high rate — photoelectric effect stems from calcium's high atomic number. On MRI, the reason calcification shows low signal on all sequences is the solid crystal structure containing no mobile protons — without protons no MR signal can be generated and it disrupts field homogeneity causing T2* shortening (susceptibility effect). On US, the hyperechoic appearance results from calcium crystals having very different acoustic impedance from soft tissue, strongly reflecting sound waves.
On MRI, focal lesion within supraspinatus tendon showing homogeneous low signal on all sequences T1, T2, PD. This appearance results from solid calcium crystals containing no mobile protons and is characteristic of calcific tendinitis. Diagnosis is confirmed with radiograph or US correlation.
On radiograph or CT, high-density calcification deposit near supraspinatus tendon insertion (at greater tuberosity level) is seen. In formative phase, deposit is homogeneous, smooth-bordered, and dense. In resorptive phase, deposit is heterogeneous, ill-defined, and fragmented. Deposit size is generally 5-25 mm. Multiple tendon involvement is rare but possible.
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A calcified deposit measuring approximately ___ mm near supraspinatus tendon insertion at greater tuberosity level is seen, consistent with calcific tendinitis.
On MRI, focal low-signal lesion within supraspinatus tendon is seen on all sequences (T1, T2, PD) — calcification deposit. In resorptive phase, T2 hyperintense reactive edema area surrounding deposit and fluid accumulation in subacromial bursa is seen. Susceptibility artifact (blooming) on T2*-GRE sequences is prominent causing calcification to appear larger than actual size. Surrounding edema is minimal in formative phase.
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A focal low-signal lesion on all sequences within supraspinatus tendon is seen with surrounding reactive edema and bursal fluid; consistent with calcific tendinitis in resorptive phase.
On US, a hyperechoic focus within supraspinatus tendon is seen. Appearance varies by calcification phase: in formative phase smooth-bordered, homogeneous hyperechoic focus with prominent posterior acoustic shadow (hard, organized calcium); in resorptive phase irregular, heterogeneous echoes with weak or no shadow (soft, fragmented calcium). US-guided barbotage (percutaneous needle calcium aspiration) is an effective treatment method especially in resorptive phase.
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A hyperechoic calcification deposit measuring approximately ___ mm within supraspinatus tendon is seen on US, consistent with calcific tendinitis.
On T2*-GRE (gradient echo) sequences, calcification deposit shows prominent blooming artifact — lesion appears larger than actual size as ill-defined low signal area. This susceptibility artifact results from paramagnetic properties of calcium. GRE sequences are more sensitive than spin-echo sequences for detecting calcification.
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A susceptibility focus showing blooming artifact within supraspinatus tendon is seen on T2*-GRE sequences, consistent with calcification deposit.
On power Doppler in resorptive phase, increased vascularity (hyperemia) around calcification deposit is seen — this is a finding of active inflammatory resorption process. Perilesional vascularity is minimal in formative phase. Resorptive phase clinically correlates with acute pain and is optimal time for US-guided barbotage.
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Increased perilesional vascularity around calcification deposit is seen on power Doppler, consistent with active resorptive phase.
Criteria
Homogeneous, smooth-bordered calcification, no/minimal surrounding edema
Distinct Features
Usually asymptomatic or mild pain, conservative treatment, spontaneous resolution may be expected
Criteria
Irregular, ill-defined calcification, prominent surrounding edema and bursal fluid
Distinct Features
Severe acute pain, most symptomatic phase, optimal time for barbotage, NSAIDs + steroid injection effective
Distinguishing Feature
In rotator cuff tear tendon gap and fluid signal; in calcific tendinitis focal low-signal lesion — but calcification may coexist with rotator cuff tear
Distinguishing Feature
In isolated bursitis no intratendinous calcification; in calcific tendinitis bursal fluid develops reactively in resorptive phase of calcification
Distinguishing Feature
In tendinopathy intermediate signal increase, no calcification; in calcific tendinitis focal low-signal lesion on all sequences + radiograph correlation
Urgency
routineManagement
conservativeBiopsy
Not NeededFollow-up
3-monthCalcific tendinitis is generally a self-limiting disease managed with conservative treatment (NSAIDs, physiotherapy) in formative phase. In resorptive phase (calcific crisis), subacromial corticosteroid injection is effective for acute pain management. US-guided barbotage (percutaneous needle calcium aspiration + lavage) is the most effective minimally invasive treatment in resorptive phase (60-90% success rate). ESWT (extracorporeal shock wave therapy) can be used to fragment deposit in formative phase. Arthroscopic calcification resection is performed in resistant cases not responding to conservative treatment in 3-6 months. 90% of patients are relieved of symptoms within 3 years (including spontaneous resolution).
The formative phase is asymptomatic and does not require treatment. The acute resorptive (migration) phase causes severe pain and is treated with NSAIDs, subacromial corticosteroid injection, or US-guided barbotage (calcium aspiration). Refractory cases may undergo arthroscopic calcium excision. Calcific tendinitis is a self-limiting process and shows spontaneous resolution in most cases.