Basic calcium phosphate disease

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Basic calcium phosphate is a family of calcium-containing microcrystals, most importantly carbonated hydroxyapatite. The label describes several clinical phenotypes rather than one uniform arthritis. Calcific tendinopathy most often affects supraspinatus near its insertion, acute calcific periarthritis results when deposit resorption inflames adjacent tissues, and Milwaukee shoulder combines massive cuff failure, a large usually non-inflammatory or haemorrhagic effusion and rapidly destructive glenohumeral change.

A radiographic deposit is evidence of deposition, not proof that it causes current pain. Diagnostic reasoning therefore matches the site and phase of the deposit to focal tenderness, movement pattern, ultrasound findings and competing diagnoses. Unlike monosodium urate or calcium pyrophosphate, the tiny non-birefringent particles evade routine compensated polarised microscopy; aspiration remains valuable principally to exclude infection and identify other crystals.

Key points

Basic calcium phosphate includes hydroxyapatite and produces calcific tendinopathy, acute calcific periarthritis, destructive Milwaukee shoulder and crystal-associated osteoarthritis.
The usual presentation is severe focal shoulder pain from a resorbing rotator-cuff deposit, but deposits can be asymptomatic and may occur around other joints.
Routine polarised microscopy does not visualise basic calcium phosphate crystals; a negative crystal report therefore does not exclude the disorder.
Initial imaging for suspected calcific tendinopathy usually includes a plain radiograph; ultrasound localises the deposit, evaluates the cuff and guides aspiration, injection or lavage.
First-line care is explanation, short relative rest during extreme pain, early range restoration, graded tendon loading and topical or brief oral analgesia matched to risk.
For one inflamed bursa or joint, ultrasound-guided aspiration and corticosteroid injection is considered only after infection has been excluded and the tendon itself is avoided.
Persistent symptomatic focal deposits may be considered for ultrasound-guided needling and lavage; extracorporeal shockwave therapy should be used only in research under current NICE guidance.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Idiopathic tendon deposition

Most calcific tendinopathy reflects locally formed basic calcium phosphate, usually carbonated hydroxyapatite, within a viable rotator-cuff tendon; a systemic calcium excess is usually absent.

Age and tissue environment

Disease is most common in middle age, and local hypoxia, fibrocartilaginous metaplasia, mechanical loading and altered mineral regulation are proposed contributors rather than a single proven cause.

Degenerative destructive phenotype

In Milwaukee shoulder, cuff failure and basic calcium phosphate deposition accompany a rapidly destructive glenohumeral arthropathy, usually in an older person with a large effusion.

Associated systemic settings

Basic calcium phosphate deposition can accompany advanced osteoarthritis, chronic kidney disease or disordered mineral metabolism, although a focal rotator-cuff deposit usually remains idiopathic.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Formative phase
Calcium-containing crystals accumulate in a tendon focus after local cell transformation; a deposit may remain quiescent and appear as a dense, sharply defined radiographic opacity.
2
Resorptive inflammatory phase
Macrophage-driven dissolution can release crystals into nearby bursa or soft tissue, generating abrupt severe pain, warmth, restricted movement and a fluffy or poorly defined deposit.
3
Crystal-mediated inflammation
Basic calcium phosphate crystals activate innate inflammatory pathways and tissue-degrading enzymes, but they are too small and non-birefringent to identify by routine polarised-light microscopy.
4
Cuff and cartilage destruction
In Milwaukee shoulder, cuff incompetence, abnormal mechanics, crystal-induced protease activity and cartilage loss reinforce one another, producing superior migration, bone remodelling and rapid functional decline.
5
Repair and recurrence
After resorption, tendon structure may heal and symptoms settle, but residual weakness, subacromial pain or recurrent deposition can maintain disability independently of active crystal inflammation.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Acute calcific periarthritis

Hours-to-days onset of intense focal pain, warmth and guarding near a tendon insertion or bursa, often without preceding trauma; the resorptive deposit may look fluffy on radiography.

Rotator-cuff calcific tendinopathy

Lateral upper-arm pain, painful arc, sleep disturbance and pain-limited abduction occur with a deposit in supraspinatus or another cuff tendon; passive movement is relatively preserved outside severe flares.

Incidental deposition

A dense deposit on imaging without concordant focal symptoms, examination or inflammatory change is common enough that another source of pain must be sought.

Milwaukee shoulderRed flag

An older person, often a woman, develops major painless or painful swelling, recurrent large haemorrhagic effusions, crepitus, instability and profound active-movement loss from cuff failure and rapid destruction.

Non-shoulder disease

Acute periarthritis can occur at the wrist, elbow, hip, knee, ankle or foot and may mimic cellulitis, gout or infection when calcium extrudes into adjacent soft tissue.

Red flags requiring action

Fever, rigors, hypotension, an acutely hot effusion or severe pain on passive movement requires urgent septic-arthritis assessment even when calcification is visible.
Recent trauma with inability to abduct, contour change, bony tenderness or neurovascular deficit raises fracture, dislocation or acute rotator-cuff tear rather than uncomplicated calcific tendinopathy.
Rapid joint destruction, a large recurrent haemorrhagic effusion and profound cuff weakness in an older adult suggests Milwaukee shoulder and warrants specialist imaging and aspiration.
A calcified periarticular mass that is enlarging, unusually located or associated with hypercalcaemia, renal failure or skin breakdown needs investigation for tumour, tumoral calcinosis or metastatic calcification.
Night pain, weight loss, previous cancer or a destructive bone lesion is not explained by an incidental tendon deposit and needs an urgent malignancy pathway.
Progressive objective weakness, cervical neurological signs or a persistently pseudoparalytic shoulder requires assessment for full-thickness cuff failure or neurological disease.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Initial plain radiographFirst step
Why
Confirm a peri-tendinous calcium deposit and assess bone, alignment and destructive change.
Interpretation and limitations
Obtain appropriate orthogonal views. A sharply defined homogeneous opacity suggests a resting deposit, while ill-defined fluffy change may accompany resorption; location and symptom concordance matter more than presence alone.
02
Musculoskeletal ultrasound
Why
Localise the deposit, evaluate bursa and cuff and guide a procedure.
Interpretation and limitations
Echogenic foci with variable acoustic shadowing support calcific tendinopathy; Doppler hyperaemia and bursal fluid suggest active inflammation, while tendon discontinuity or muscle atrophy changes the pathway.
03
Diagnostic aspiration
Why
Exclude infection and identify a coexisting visible crystal when an effusion or bursa is accessible.
Interpretation and limitations
Send cell count, Gram stain and culture, and polarised microscopy. Routine microscopy can miss basic calcium phosphate because particles are submicroscopic and non-birefringent; low cellularity can occur in Milwaukee shoulder.
04
Alizarin red S stain
Why
Demonstrate calcium-containing material when specialist microscopy is available.
Interpretation and limitations
A positive stain supports calcium but is not specific for basic calcium phosphate and can be affected by technique; it cannot replace culture or clinical correlation.
05
MRI shoulder
Why
Define an uncertain full-thickness cuff tear, muscle quality, occult bone disease or surgical anatomy.
Interpretation and limitations
MRI is not the first test for confirming a calcium deposit and can make surrounding oedema conspicuous while the small calcification itself is less well characterised than on radiograph or ultrasound.
06
Focused blood tests
Why
Assess infection or an atypical systemic mineral context rather than diagnose routine local deposition.
Interpretation and limitations
Use FBC and CRP for a hot systemic presentation and renal function, calcium, phosphate, ALP and PTH when disease is widespread or renal/metabolic features exist; normal results do not exclude focal disease.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Septic arthritis or bursitis

Fever, systemic illness and marked passive restriction demand aspiration and culture; neither a calcium deposit nor a low peripheral inflammatory response safely excludes infection.

Rotator-cuff tear or impingement

Painful arc and weakness overlap, but ultrasound or MRI can demonstrate tendon discontinuity, atrophy and retraction and clarify whether calcification is incidental.

CPP or urate crystal arthritis

An intra-articular effusion may contain positively birefringent CPP or negatively birefringent urate crystals; either can coexist with calcium seen on plain imaging.

Adhesive capsulitis

Global restriction of active and passive movement, especially external rotation, without a dominant acute inflammatory episode favours capsular contracture rather than focal deposit resorption.

Tumoral or metastatic calcification

Large lobulated periarticular masses, renal failure, hyperphosphataemia or hypercalcaemia suggest systemic mineral deposition rather than ordinary calcific tendinopathy.

Additional chapter-specific clues

Mechanical versus inflammatory limitation

Painful active movement with better passive range favours cuff or bursal disease; severe restriction of both directions raises joint sepsis, acute synovitis or adhesive capsulitis.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01First diagnostic stepMatch radiograph to phenotypeFirst stepFocal atraumatic shoulder or periarticular pain suggests calcific disease without systemic instability.

1Examine active and passive movement, cuff strength, focal tendon and bursal tenderness, neck and neurovascular status and sepsis or trauma features.
2Request plain radiographs first and use ultrasound when the deposit, bursa or tendon must be localised or a tear or guided procedure is being considered.
3Treat the opacity as causal only when its site, inflammatory phase and clinical pattern agree; pursue adhesive capsulitis, cuff tear, referred pain or OA otherwise.

02Urgent hot-joint pathwayAspirate before injectingFever, major effusion, severe passive restriction, immunosuppression or rapid destruction makes infection or another crystal arthritis plausible.

1Arrange urgent aspiration for cell count, Gram stain, culture and visible crystal analysis and take blood cultures before antibiotics when febrile and safe.
2Remember that basic calcium phosphate is usually invisible on routine microscopy and that visible CPP or urate crystals do not exclude concurrent infection.
3Withhold corticosteroid injection and manage suspected sepsis immediately until clinical and microbiological assessment makes infection sufficiently unlikely.

03First-line symptomatic careProtect briefly, then reloadFirst lineA symptomatic deposit has no red flag or major tear and function can be managed conservatively.

1Explain the often self-limiting resorptive phase, use ice or heat by preference and allow only short relative rest during intolerable pain.
2Start comfortable range-of-motion work early, then progressive cuff and scapular loading with physiotherapy and work or sleep modification.
3Offer topical NSAID first where suitable; use a brief oral NSAID or paracetamol only after individual renal, gut, cardiovascular, bleeding and pregnancy assessment.

04Image-guided escalationTreat a persistent concordant lesionEscalationPain and disability remain important after an adequate rehabilitation and analgesic trial.

1Reconfirm symptom-deposit concordance by examination and ultrasound and exclude substantial cuff tear, adhesive capsulitis, infection and competing referred pain.
2Consider ultrasound-guided bursal aspiration and corticosteroid injection for prominent bursitis, or specialist needling and lavage for a suitable focal calcific deposit.
3Do not offer extracorporeal shockwave therapy as routine NHS care: NICE permits use only in research because efficacy evidence is inadequate.

05Destructive diseaseSeparate pain control from reconstructionMilwaukee shoulder or major cuff-tear arthropathy causes recurrent effusion, instability and profound disability.

1Aspirate new or changing effusions to exclude infection and other crystals and define cuff integrity and bone stock with radiography plus ultrasound or MRI.
2Use aids, adapted activity, targeted rehabilitation and carefully selected analgesia; repeated injection should not substitute for functional planning.
3Refer shoulder specialists for reconstruction or arthroplasty assessment when symptoms, anatomy, frailty and patient goals justify operative risk.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

First-line pharmacological treatment for local shoulder or periarticular pain when an NSAID is appropriate, with lower systemic exposure than oral treatment.

Diclofenac 1.16% gel

Apply 2 to 4 g to the painful area three or four times daily, gently rubbing it in; use the smallest area and shortest duration needed and wash the hands afterwards unless they are treated.

Avoid broken skin, NSAID hypersensitivity and use with another NSAID without review. Systemic renal, gastrointestinal and cardiovascular effects remain possible with extensive or prolonged use. Avoid in the third trimester of pregnancy and seek medicine-specific advice earlier in pregnancy or while breastfeeding.

Short systemic anti-inflammatory treatment when topical care and protected movement are insufficient and there is no safer local option.

Naproxen

For a severe inflammatory episode, a common off-label short course is 250 to 500 mg orally twice daily with food for 3 to 5 days, at the lowest effective dose; add a proton-pump inhibitor when gastrointestinal risk warrants it.

Avoid active ulcer, severe renal, hepatic or heart failure, NSAID hypersensitivity, concurrent NSAIDs and major bleeding risk. Review anticoagulants, ACE inhibitor or ARB plus diuretic exposure. Avoid from 20 weeks of pregnancy unless essential and do not use in the final trimester.

An adjunct for marked concordant subacromial bursitis when pain prevents rehabilitation; injection does not reliably remove the calcium deposit.

Subacromial triamcinolone acetonide

After infection exclusion, a specialist may inject 10 to 40 mg from the 40 mg/mL suspension into the affected bursa using image guidance and strict asepsis; use the lowest dose appropriate to the site and do not inject the tendon deposit itself.

Calcific tendinopathy is not a named licensed indication. Do not inject through infection, into tendon substance or repeatedly without reassessment. Warn about post-injection flare, infection, skin or fat atrophy, transient hyperglycaemia and possible tendon harm; pregnancy and poorly controlled diabetes require individual review.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Persistent pain and stiffness

Prolonged guarding, bursitis and altered mechanics can leave restricted movement, sleep disturbance and work limitation after the acute inflammatory phase resolves.

Tendon damage

Large or recurrent deposits and needling may coexist with tendon degeneration or tear, causing weakness that requires rehabilitation and occasionally repair.

Rapid destructive arthropathy

Milwaukee shoulder can cause major glenohumeral bone loss, recurrent large effusions, instability and profound loss of upper-limb function.

Treatment-related harm

NSAID renal, gastrointestinal and cardiovascular toxicity, post-injection infection, hyperglycaemia and inadvertent intratendinous steroid injury can exceed the harm from the deposit.

Unnecessary procedures

Treating an incidental opacity without linking it to symptoms exposes patients to lavage, shockwave or surgery while the true diagnosis remains untreated.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

Review severe acute pain within days to confirm improvement and reconsider infection, fracture, full-thickness tear or another crystal arthritis if the trajectory is wrong.
Record active and passive range, cuff strength, sleep, work and a patient-selected activity before treatment and after six to twelve weeks of rehabilitation.
After injection or lavage, provide same-day contact instructions for fever, increasing warmth, swelling, weakness or uncontrolled pain and recheck function rather than imaging alone.
Monitor renal function, pressure, oedema, gastrointestinal bleeding and interacting medicines when oral NSAID exposure extends beyond a very brief course.
Do not serially image an improving asymptomatic deposit; repeat imaging when persistent disability, new weakness, destructive change or procedure planning will alter management.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Microscopy has a blind spot

Basic calcium phosphate particles are generally smaller than the resolving power of routine light microscopy and show no diagnostic birefringence, unlike CPP and urate.

Resorption can hurt most

The dramatic painful phase may occur while the deposit is fragmenting and shrinking, so severe symptoms do not necessarily mean progressive structural damage.

Radiograph before MRI

Plain radiography depicts calcium more directly, whereas MRI is reserved for unresolved cuff, muscle, bone or surgical questions.

Aspiration still matters

Failure to see a crystal does not make aspiration futile: culture can identify infection and microscopy may reveal coexisting CPP or urate.

Milwaukee fluid can look deceptively quiet

A large haemorrhagic effusion may have a relatively low leukocyte count despite rapid destruction, making imaging, cuff assessment and exclusion of infection essential.

Shockwave evidence is restricted

Current NICE guidance finds no major short-term safety concern but inadequate efficacy evidence, so extracorporeal shockwave treatment should occur only in research.

11Common pitfallsFrequent interpretation and management errors.

01
Calling every shoulder opacity symptomatic without matching it to examination, ultrasound and the pain site.
02
Reporting a negative polarised crystal examination as excluding basic calcium phosphate deposition.
03
Injecting a hot swollen joint or bursa before septic arthritis has been adequately considered and sampled.
04
Putting corticosteroid into tendon substance or repeating injections while progressive weakness suggests a tear.
05
Ordering MRI as the first test and overlooking a deposit that plain radiography or ultrasound demonstrates more clearly.
06
Offering routine shockwave therapy despite NICE restricting it to research because efficacy evidence is inadequate.