Clinical synthesis based on the most recent meta-analyses and international consensus statements: EFORT Open Reviews network meta-analysis 2025, Guido 2025 scoping review, Ricci Diagnostics 2022, Brindisino 2024 ESWT SR/MA, the KALK trial (BMJ 2023), JOSPT CPG 2025, Dutch update 2026, Louwerens JSES 2014, epidemiological data 2018-2025.

Rotator cuff calcific tendinopathy (RCCT) is a clinical condition of active cellular origin and not passive degenerative origin. Described as early as 1907 by Painter and then revisited by Codman, it was Uhthoff & Loehr in 1997 who proposed the current consensus pathophysiological model: fibrocartilaginous metaplasia of the tenocytes precedes the formation of crystalline deposits of calcium hydroxyapatite within the tendon, mainly in the critical hypovascular zone of the supraspinatus.¹ This nuance is crucial: we do not treat a "wear" that we would wait out passively, we support a dynamic biological process whose resorption phase is paradoxically the most painful but also the signal of a spontaneous return to normal. 🦴

How is this condition defined, who does it affect and what are the risk factors?

The narrative review by Sansone & colleagues 2018, published in Orthopedic Research and Reviews, and the scoping review by Guido 2025 (50 studies included, Shoulder & Elbow) converge on the definition: RCCT is characterised by deposits of calcium phosphate crystals (essentially hydroxyapatite Ca₁₀(PO₄)₆(OH)₂) within the tendons of the rotator cuff.²,³ It is neither a chronic inflammatory process nor simple wear: it is an ectopic chondrogenesis mediated by tendon cells, whose exact trigger remains partly unclear (ischaemic hypothesis, metabolic hypothesis, repeated mechanical hypothesis).¹,² On the epidemiological level, recent data consolidate several findings:

• Prevalence in the general population of between 2.7% and 22% depending on the populations and the imaging methods used; a substantial proportion is entirely asymptomatic and discovered incidentally.²,³
• Peak incidence between 40 and 60 years, with marked sexual dimorphism: female predominance (ratio about 2:1).²,³,⁴
• More common in sedentary workers than in manual workers, a strong argument against the hypothesis of simple repeated mechanical overload as the sole cause.²,⁵
• The supraspinatus tendon is by far the most involved (≈ 80% of cases), followed by the infraspinatus (15%) and the subscapularis (5%).³

The metabolic risk factors are now the best documented:

• The presence of diabetes significantly increases the risk: the matched cohort of Su 2021 using the Taiwanese national database (42,915 patients with diabetes vs 171,660 controls) finds an adjusted HR = 1.27 (95% CI 1.18-1.38) at 8 years for developing RCCT.⁵
• The thyroid disorders (mainly hypothyroidism) have a well-established association dating from Harvie 2007, confirmed in several more recent cohorts.²,⁶
• The metabolic syndrome as a whole (obesity + hypertension + dyslipidaemia + insulin resistance) is correlated with RCCT and with its more prolonged course (Bechay 2020 Phys Sportsmed).⁶

What happens in the tendon and how does the condition naturally progress?

The reference pathophysiological model remains the one proposed by Uhthoff & Loehr in 1997 in the Journal of the American Academy of Orthopaedic Surgeons, refined since by the work of Sansone, Oliva, and the dynamic imaging of Sconfienza-Serafini.¹,²,⁷ It describes a cycle in three distinct phases :

1. Pre-calcification phase (silent): fibrocartilaginous metaplasia of the tenocytes, with no deposit yet visible and no notable symptoms.¹
2. Calcific phase divided into:
   • Formation : calcium accumulates in a dense, chalky form, a well-demarcated deposit, with a clear acoustic shadow on ultrasound. The patient is often only mildly symptomatic or has chronic mechanical discomfort.¹,⁸
   • Rest : a stable phase, with a possible plateau lasting several months.
   • Resorption ⚠️: the deposit becomes pasty ("toothpaste"), loses its outline and recruits an intense inflammatory reaction mediated by phagocytes (macrophages, neutrophils). It is the most painful phase (acute, sleep-disturbing, throbbing pain) but paradoxically the signal of an imminent self-resolution.¹,⁷,⁹
3. Post-calcification phase : tendon remodelling, healing, return to homeostasis. Often painless but may leave partial tendon sequelae.¹,⁷

🔄 The natural history of this condition is a cardinal parameter in guiding management. RCCT is frequently self-resolving, but the time to resolution is highly variable. The study by Cho 2010 (Journal of Shoulder and Elbow Surgery, 87 consecutive patients / 92 shoulders, conservative treatment, mean follow-up) documented a clinical improvement in the majority of patients, with a Constant score rising from 76.17 at inclusion to 83.64 at last follow-up (p < 0.001).⁸ Cho also stresses an essential point: the initial radiological appearance of the deposit does not influence the final clinical result. In other words, one can be asymptomatic with a calcification that persists on imaging. This dissociation between imaging and symptoms is confirmed by Drummond 2021 (JSES International, 239 patients), which nevertheless shows that a calcification > 1 cm is a predictor of failure of conservative treatment (OR 2.86, 95% CI 1.25-6.29; p < 0.05).⁷

Diagnosis of rotator cuff calcific tendinopathy rests on a structured approach in three stages: targeted history, clinical examination (of low specificity but useful for the differential) and confirmation by imaging. As the condition is common and sometimes asymptomatic, the challenge is not only to detect it but above all to determine whether it is indeed the current source of the symptoms of the patient, which can be difficult because of the frequent dissociation between imaging and symptoms.¹,²

Which questions should you ask to understand the patient and their history?

History-taking is the most discriminating step. 🤔 It should explore:

• Patient profile : woman aged between 40 and 60, occupation (sedentary vs manual), metabolic comorbidities (diabetes, thyroid dysfunction), personal or family history of RCCT.²,³
• Pain characteristics : distinguish two distinct presentations:
  1. Chronic form : dull mechanical pain, discomfort on elevation, painful side-lying, progressing over several months. Often corresponds to a formation or rest phase.²
  2. Acute hyperalgesic form : pain of sudden onset, throbbing, sleep-disturbing, sometimes described as "one of the worst pains ever experienced". Patient in a sling, near-total functional loss. Corresponds to the inflammatory resorption phase.²,⁴
• Cyclical history : previous episodes of pain, periods of spontaneous remission, previous traumatic episodes.²,⁵
• Aggravating/relieving factors : triggering movements (elevation above 60-120°), night positions, specific ADLs.²

The distinction chronic versus acute hyperalgesic form is not merely academic: it shapes the immediate therapeutic decision (analgesia in the acute phase, possibly by subacromial infiltration; progressive rehabilitation in the chronic phase; lavage comes into play only after failure of the initial treatment).

Which clinical tests should you perform and which other conditions need to be ruled out?

🩺 The clinical examination is of low specificity for RCCT itself. The reference meta-analysis by Hegedus 2012 (British Journal of Sports Medicine) showed that the classic subacromial impingement tests (Neer, Hawkins-Kennedy, painful arc) have modest sensitivity and specificity and do not on their own allow a pathognomonic diagnosis.⁶ Three practical consequences:

• Impingement tests are frequently positive in RCCT through the mass effect of the deposit, but a positive result is not specific.²,⁶
• Muscle tests of the cuff (Jobe, lift-off, belly-press) can be painful without an associated tear: do not draw conclusions too early.⁶
• The most clinically useful sign is an exquisite, highly focal pain on palpation at the greater tuberosity or at the insertion of the supraspinatus.⁶

Imaging settles the diagnosis. The recommended hierarchy is:

• Standard radiograph as first line: AP views in neutral, internal and external rotation + Lamy Y view. Visualisation of the deposit, localisation, measurement of its size.²,⁷
• Ultrasound as the reference for characterisation: excellent sensitivity, non-irradiating, allows dynamic assessment, precise measurement, analysis of morphology (arciform, fragmented, nodular), assessment of the power Doppler around the deposit: the presence of peri-calcific hyperaemia is strongly associated with the resorption phase (Ricci 2022, Chiou 2010).⁷,⁸
• MRI only as second line if an associated tear is suspected or for pre-surgical work-up.²

Should patients be classified, and what are the benefits?

Radiographic and ultrasound classifications help to correlate the morphological appearance with the clinical stage of evolution and to guide treatment. 🔬 Two are in common use:

• Gartner classification (1995, Orthopade), based on radiography:⁹
  • Type I : dense, homogeneous deposit with sharp outlines and a clear acoustic shadow on ultrasound. Corresponds to the formation/rest phase. Often only mildly symptomatic or with chronic pain. Slower spontaneous prognosis; best target for mechanical thermolysis (UGN, focused ESWT).
  • Type II : dense deposit with less sharp outlines, fragmented or polylobed. Transition phase.
  • Type III : flocculent, translucent, poorly defined deposit. Corresponds to the resorption phase. Very painful but excellent spontaneous prognosis.
• Molini / Sconfienza ultrasound classification : precise morphology (arciform, fragmented, nodular, cystic) correlated with the Gartner types.⁷

Criticism and controversy

The correlation between the size or type of the calcification and the intensity of symptoms is notoriously weak.⁵,⁸ Large Type I calcifications can be asymptomatic, whereas small Type III deposits can trigger disabling pain. The transition from one type to another is not linear and its timing is unpredictable. The clinician must therefore reason on the pairing of morphology and clinical picture, not on imaging alone. Moreover, the frequent positivity of impingement tests (Neer, Hawkins, painful arc) in RCCT has historically led to excessive indications for surgical acromioplasty, a procedure whose efficacy is strongly called into question for this indication by recent trials (Beard 2018 CSAW, Paavola 2018 FIMPACT) and meta-analyses.⁶,¹⁰

Two recent guidelines cover the calcific form: the JOSPT 2025 CPG, which addresses rotator cuff tendinopathy with or without calcifications,¹⁴ and the 2026 update of the Dutch guideline.¹³

Management of RCCT forms part of a progressive continuum, always starting with conservative interventions before considering more invasive techniques. This progressive approach is justified by the often self-resolving nature of the condition: intervening too early and aggressively would risk attributing to the treatment a benefit that would have emerged spontaneously. The updated hierarchy is based on the EFORT Open Reviews 2025 network meta-analysis by Yao (33 RCTs, 26 treatments compared), published in July 2025, the broadest synthesis to date.¹

Where do you start? What is the recommended hierarchy of interventions?

🎯 The evidence-based therapeutic hierarchy in 2026 is:

1. First line: education + exercise + occasional NSAIDs : information about the self-resolving nature of the condition, temporary activity modification, personalised exercise programme (cuff strengthening + scapular stabilisers).¹,²
2. Second line (after 3-6 months of failed conservative treatment) :
   • High-energy ESWT (focused) : Brindisino 2024 (Physiother Res Int, RCCT-specific SR/MA, 21 trials) finds, against sham, a clinically significant effect on pain and function at 24 weeks, and high energy superior to low energy, with very low certainty; focused and radial appear equivalent.³
   • Ultrasound-guided lavage (UGN, barbotage, US-PICT) : Brindisino 2024 (SR/MA), Yao 2025 (NMA); the EFORT NMA could not rank resorption for lack of poolable data and describes UGN + subacromial injection as promising on this outcome; Brindisino finds lavage superior to shock waves for pain, at under 24 weeks and under 48 weeks, comparisons of low to very low certainty.¹,³,¹² The only trial against a sham procedure (KALK, 220 patients, symptoms for at least 3 months, exercises for all) finds no benefit of lavage with corticosteroid at 4 and 24 months.¹¹ The 2026 Dutch update, which discusses this trial, proposes considering barbotage, preferably with an infiltration, in patients with a large calcification not relieved by an infiltration, specifying that its additional benefit over infiltration alone is limited.¹³
3. Third line (after failure of the previous modalities) : arthroscopy with removal of the deposit + cuff repair if an associated tear is present. Routine acromioplasty is no longer recommended (Beard 2018 CSAW).⁵

Corticosteroids by injection deserve specific comment. The meta-analysis by Mohamadi 2017 (Clinical Orthopaedics and Related Research, 11 studies included) showed that corticosteroid injections provide at best minimal and transient relief in cuff tendinosis, without altering the natural course of the disease.⁶ In the acute hyperalgesic resorptive phase, a subacromial injection may be indicated for analgesic purposes. The KALK trial, conducted in patients with pain for at least 3 months and outside the acute resorptive phase, finds infiltration better than sham at 2 and 6 weeks (secondary outcomes), with no effect at 4 months; its authors judge it useful when the aim is temporary relief, but report a possible rebound effect, the infiltration-alone arm doing worse than sham at 24 months.¹¹

Conventional therapeutic ultrasound (continuous or pulsed US) is not recommended as the main treatment: the Cochrane review by Page 2016 (CD012225) concluded that there is little or no evidence supporting its efficacy for cuff tendinosis in terms of pain, function or resorption.⁸ This finding is essential because it paradoxically continues to be prescribed.

What is the place of exercise, and is there a superior approach?

💪 Therapeutic exercise is a non-negotiable pillar of management, not because it dissolves the deposit but because it treats the subacromial pain component (SAPS) that almost systematically accompanies RCCT and restores optimal shoulder function.²,⁹ The reference systematic review by Pieters & Lewis 2020 (JOSPT 50(3):131-141) synthesised 16 earlier systematic reviews on subacromial pain and issued a strong recommendation for therapeutic exercise as first-line treatment.² The programme targets:

• Strengthening of the rotator cuff, particularly infraspinatus (external rotation) and subscapularis (internal rotation) for humeral centring.²,⁹
• Strengthening of the scapular stabilisers : lower trapezius, serratus anterior, rhomboids, to optimise scapulothoracic rhythm.⁹
• Glenohumeral and scapulothoracic mobility.
• Education in progressive load management.

Key point: no specific exercise protocol is required (eccentric, concentric, isometric) according to recent reviews; what matters most is individualisation, progressiveness and the patient's adherence.²,⁹

Shock waves, ultrasound-guided lavage, manual therapies: how effective are they really?

Extracorporeal shock wave therapy (ESWT). The recent RCCT-specific SR/MA by Brindisino 2024 (Physiotherapy Research International) finds, against sham, an effect of ESWT on pain and function at 24 weeks, with very low certainty; high energy does better than low energy, including on resorption of the deposit at 12 weeks. Radial ESWT is a more accessible alternative: focused and radial appear equivalent.³

Ultrasound-guided lavage (UGN, barbotage, US-PICT). This minimally invasive technique consists of fragmenting and aspirating the calcification using saline under constant ultrasound guidance. The EFORT 2025 NMA by Yao (33 RCTs, 26 modalities) could not meta-analyse resorption, as the statistical methods diverged and the data were lacking for pooling, and describes the UGN + subacromial injection as promising on this outcome. The Brindisino 2024 SR/MA, for its part, finds ultrasound-guided lavage superior to shock waves for pain, at under 24 weeks and under 48 weeks.¹,³ But the only trial against a sham procedure (KALK, Moosmayer 2023: 220 patients, symptoms for at least 3 months, four home exercises for all) finds no benefit of lavage with corticosteroid at 4 and 24 months; the benefit of lavage itself remains uncertain, and the patient must be informed of this.¹¹

Manual therapy. Joint mobilisations (glenohumeral, scapulothoracic, upper thoracic segment) can be integrated as a complement to exercise: improved mobility, pain modulation. Evidence for a direct effect on the calcific deposit is non-existent ; mobilisations remain a behavioural and functional adjunct.²

Beyond the physical: how do you educate the patient and address psychological factors?

🧠 The psychosocial dimension is decisive. Therapeutic education is the first step: explaining the self-resolving nature of the condition reduces anxiety and catastrophising, which are established predictors of pain persistence in musculoskeletal disorders.² Distinguishing between pain and tissue damage makes it possible to encourage the maintenance of an adapted activity and to avoid deconditioning through kinesiophobia. The biopsychosocial approach must incorporate:

• Identification of mistaken beliefs (e.g. "I am going to have to have surgery", "calcium means irreversible wear").
• Setting realistic functional goals (resumption of sleep, return to ADLs, gradual return to sport).
• Self-management strategies and recognition of the signs of overload.
• Assessment of moderating factors: stress, sleep quality, metabolic health.

Criticism and controversy

Three grey areas persist. First, the phenotyping of patients remains a challenge: why do some respond brilliantly to a simple exercise programme while others need UGN? Predictive biomarkers or clinical characteristics are not established; Drummond 2021 finds only the size > 1 cm as a reliable predictor of failure.⁷ Second, the heterogeneity of ESWT protocols (energy, number of shocks, frequency) makes comparisons difficult and prevents the establishment of a "gold standard" protocol.³ Finally, the strong tendency towards spontaneous resolution is a confounding factor in any evaluation of efficacy: trials must be interpreted in the light of the natural history.⁸

Management of RCCT does not end with resolution of the initial pain or fragmentation of the deposit. A long-term strategy is essential to guarantee lasting functional recovery and minimise the risk of recurrence, estimated at between 6% and 20% depending on the series, over follow-ups of several years.¹ Success rests on the transition from a passive approach towards active participation and empowerment of the patient. 🎓

How do you make the patient an active participant in their own recovery through self-management?

Self-management is the cornerstone of recurrence prevention. It aims to turn the patient into an expert in their own condition, able to recognise early warning signs and adapt their activities accordingly. Therapeutic patient education (TPE) significantly improves understanding, adherence and the sense of self-efficacy.² The integration of a personalised home exercise programme is documented as effective in the literature on subacromial pain.² The goals are:

• Cuff strengthening : infraspinatus and subscapularis for optimal humeral centring.²
• Strengthening of the scapular stabilisers : lower trapezius, serratus anterior, rhomboids.
• Maintaining a full pain-free range of motion.
• Learning progressive load management : modulating the volume, intensity and frequency of activities to avoid overloading the tendon, while applying enough stress to it for its adaptation.²,³

The recognition of overload symptoms (dull pain after exertion, prolonged morning stiffness, discomfort on elevation above 90°) is a key indicator for adjusting the programme and taking relative rest. The principle applied in tendon rehabilitation is that tolerable pain during and after exertion, which does not worsen within 24 h, remains compatible with continuing the activity ; beyond that, relative rest and a reduction in load are needed. ⚠️ Key point: even ESWT and UGN, which aim to fragment the deposit and make it resorb, do not correct the underlying biomechanical factors (subscapularis deficit, scapular dyskinesis, unfavourable postural pattern) that have contributed to the condition. That is why active engagement in post-intervention rehabilitation is non-negotiable to prevent recurrences.¹,²

When and how should you plan a safe return to sport and activities?

🎯 Return to sport (RTS) or to demanding occupational activities must be a process that is progressive and based on objective criteria, and not on mere elapsed time. A premature return is a major risk factor for recurrence. There is no specific international consensus on RTS after RCCT (as opposed to instability or cuff tears), but the general principles for cuff disorders apply. The decision-making process must be shared between the patient, the physiotherapist and the doctor, and rely on several criteria being met:

1. No pain : neither at rest, nor during ADLs, nor on palpation of the tendon.
2. Recovery of range of motion : active and passive, symmetrical with the contralateral side, without pain at end range.
3. Recovery of muscle strength : abductors, external and internal rotators reaching at least 90% of the unaffected side, measured objectively (handheld dynamometer).
4. Functional tests passed without pain or apprehension: sport-specific tests (simulated throw for overhead athletes, push-up for weight-bearing sports, etc.).
5. PROMs scores close to normal : SPADI, ASES, Constant or DASH depending on the tool used.

Once these criteria are met, the return takes place gradually: modified training → full training → competition. This "rehabilitation continuum" approach minimises the risk of relapse.

Criticism and controversy

Despite a growing consensus on the importance of active rehabilitation, clinical practice faces two challenges. First, the frequent discordance between imaging and symptoms : a patient can become completely asymptomatic while the calcification is still visible (Cho 2010), and vice versa. The fundamental question is therefore: is the therapeutic goal eradication of the calcification (radiological goal) or restoration of painless function (clinical goal)? Excessive focus on the image sometimes leads to needlessly aggressive treatments. Second, the "passive treatment bias" : procedures such as ESWT or UGN may be perceived as a "miracle solution", reducing the motivation to engage in active rehabilitation. Failure to prevent recurrences is then often not due to the ineffectiveness of the initial treatment but to the absence of correction of biomechanical deficits.¹,⁴

The diversity of clinical presentations of RCCT is immense, from the asymptomatic, incidentally discovered deposit to the resorptive hyperalgesic crisis with pseudo-fever and a massive biological inflammatory syndrome. Analysis of clinical cases published in the literature offers a concrete overview of this spectrum and illustrates classic diagnostic pitfalls.

Analysis of a classic case: from assessment to resolution.

A typical case often involves a woman aged 40-60 presenting with shoulder pain of sudden onset, intense (VAS 8-10), sleep-disturbing, with no history of trauma. Clinical examination finds near-total functional loss, exquisite tenderness on palpation of the greater tuberosity, and all impingement tests (Neer, Hawkins) are positive but poorly discriminating.¹ Imaging settles it: the radiograph shows a dense opacity above the humeral head. Ultrasound characterises the deposit, often flocculent and fragmented, with peri-calcific hyperaemia on power Doppler, suggestive of the resorption phase.² In the face of such a crisis, several therapeutic options are available:

• Ultrasound-guided aspiration-lavage (UGN, Aina 2001, Radiology): Aina and colleagues described this minimally invasive technique in 30 consecutive shoulders (23 women / 7 men, mean age 47.4 years), with chronic pain averaging 43 months that was refractory to medical treatment. The method fragments and then aspirates the pasty ("toothpaste") deposit. Near-immediate reduction of pain and rapid functional recovery in the majority of patients.³
• Two-needle technique (Serafini 2009, Radiology): a technical refinement using two needles, with a non-randomised 10-year follow-up confirming long-term efficacy.⁴
• High-energy focused ESWT : non-invasive alternative, with efficacy supported by evidence of very low certainty, considered mainly for dense chronic deposits (Gartner Type I).⁵

The diagnostic challenge: when RCCT mimics an emergency.

🦠 The most dangerous diagnostic trap is that of pseudo-septic arthritis. The resorption phase can be accompanied by a systemic inflammatory reaction mimicking an infection. The case report by Aljumaan 2025 (published in Cureus) perfectly illustrates this trap:⁶

• Patient presenting to the emergency department with acute shoulder pain, redness, oedema, and fever.
• Blood tests: leucocytosis, raised CRP.
• Initial suspicion: septic arthritis (a surgical emergency).
• Empirical IV antibiotics started.
• MRI (or ultrasound depending on context) : calcific deposit in the supraspinatus + reactive bursitis, without infected effusion.
• Antibiotics stopped, diagnosis reattributed to a resorptive hyperalgesic crisis of RCCT.

This trap is not anecdotal: it is a reminder of the importance of systematic early imaging in the face of an acute hyperalgesic shoulder crisis, even in the presence of systemic inflammatory signs. The joint aspiration (if doubt persists) remains the reference examination to exclude infection.⁶

Study of a complex case: intra-osseous migration, giant forms, bilaterality.

RCCT can take atypical forms that are rare but clinically significant:

• Intra-osseous migration : a rare phenomenon in which calcific material migrates from the tendon into the underlying bone. Marinetti and colleagues (2018, Skeletal Radiology) described two cases with cortical erosion and intramedullary migration. The MRI presentation can be mistaken for a bone tumour (osteoblastoma, osteoid osteoma) or osteomyelitis. Knowing about this entity avoids unnecessary biopsies.⁷,⁸
• Bilateral forms : bilaterality, synchronous or asynchronous, suggests a systemic predisposition (metabolic, genetic). Its frequency remains poorly estimated.
• Giant calcifications (> 2-3 cm): pose particular challenges through their mechanical mass effect and the difficulty of treating them with simple ultrasound-guided lavage. A size > 1 cm is in itself a predictor of failure of conservative treatment (Drummond 2021, OR 2.86).⁹
• Non-rotator cuff RCCT : deposits in the pectoralis major, along the neck, along the epicondyle, rare entities that present with atypical pain (Aljumaan-related cases in the literature).

Criticism and controversies

Analysis of clinical cases, although instructive, carries a major publication bias : spectacular cases (atypical presentations, therapeutic successes) are over-represented, whereas ordinary courses (quiet spontaneous resolution, treatment failure) are under-reported.¹⁰ It is important to keep in mind that classic RCCT is often unspectacular and progresses favourably within a few months under conservative treatment. Another controversy lies in the excessive focus on removal of the deposit (the "radiological symptom") rather than on the underlying tendon function. The modern approach integrates the focal intervention into a global rehabilitation pathway aimed at restoring the load capacity of the tendon.

Applying the evidence in clinical practice is the bridge between science and tangible improvement in patients' health. This transition is not limited to knowing the latest studies but requires concrete strategies for referral, objective measurement of progress and the removal of systemic and individual barriers.

When, and to which other healthcare professionals, should you refer?

🧭 The physiotherapist in a first-line role must be able to recognise situations that fall outside their scope. The detection of red flags is central. The review by Finucane 2020 (JOSPT 50(7):350-372) on musculoskeletal red flags provides a reference framework applicable to the shoulder.¹

The multidisciplinary collaboration is decisive for complex cases:

• Interventional radiologist or sports physician practising ultrasound for UGN/barbotage.
• Rheumatologist for the aetiological work-up in cases of bilaterality, metabolic syndrome, or suspected associated rheumatological disease.
• Endocrinologist in cases of poorly controlled diabetes or suspected thyroid dysfunction (RCCT risk factors).
• Clinical psychologist for patients with marked catastrophising or kinesiophobia.
• Orthopaedic surgeon (shoulder) as a last resort after failure of conservative and minimally invasive treatments.

The shared decision-making (Légaré 2018 Cochrane CD006732), presenting the options (ESWT vs UGN vs corticosteroids), discussing advantages and drawbacks, deciding together, significantly increases adherence to treatment and satisfaction.²

How do you measure outcomes and overcome barriers to implementation?

📈 The systematic use of PROMs questionnaires is a cornerstone of evidence-based practice. For RCCT, the validated tools include:

• SPADI (Shoulder Pain and Disability Index): 13 items (5 pain + 8 function), score 0-100, MCID ≈ 8-13 points. Excellent effort-to-information ratio.
• Constant-Murley score : mixed clinical + PROM score (15 pain + 20 ADLs + 40 range of motion + 25 strength = 100), a classic in orthopaedics.
• ASES (American Shoulder and Elbow Surgeons): 50% pain + 50% function, 0-100.
• QuickDASH : 11 items, quicker than the DASH (30 items), focused on the whole upper limb.

🚧 Implementation runs up against several barriers documented in the literature:

• Clinicians : lack of time, limited critical appraisal, beliefs that contradict the recommendations.
• Patients : unrealistic expectations ("operate to remove the calcification"), poor adherence, preference for passive treatment.
• System : reimbursement unfavourable to prolonged supervised exercise, a culture that favours the short technical procedure.

Effective strategies for knowledge translation are active and multifaceted: interactive training, mentoring, local clinical champions, integration of recommendations into patient records. Passive dissemination of guidelines has little impact.³

Criticism and controversy: the tension between standardisation and personalisation

🧠 Promoting evidence-based practice must be reconciled with the principle of person-centred care. Guidelines, by definition, are based on averages of populations studied in trials with strict inclusion/exclusion criteria; they do not always represent the complexity of the real patient.⁴ The controversy is not about rejecting the evidence but about properly integrating clinical reasoning + experience + patient preferences. Clinical expertise consists of navigating between the general recommendation and the individual reality, using the evidence as a compass rather than a GPS route. Sometimes the best evidence-based decision is to depart judiciously from a standard protocol to meet the specific needs of a patient.⁴,⁵