Calcific tendinitis of the shoulder: causes, symptoms, diagnosis and treatment

In clinical practice, the term "calcific tendinitis" almost always refers to calcific tendinopathy of the rotator cuff. Modern reviews emphasize that this is the pathological deposition of calcium hydroxyapatite crystals in the rotator cuff tendons, most commonly in the supraspinatus tendon. This makes this condition one of the most common causes of non-traumatic shoulder pain in adults. [1]

Today, this process is viewed not as a simple "salt deposit," but as a distinct form of tendinopathy with its own biology, stages, and often spontaneous progression. This is important for the patient, because severe pain does not always indicate a tendon rupture or the need for urgent surgery. For the physician, something else is important: the calcification can persist asymptomatically for a long time, then abruptly transition to a phase of severe inflammatory pain. [2]

Another fundamental point is that the term "tendinitis" is increasingly giving way to "tendinopathy" in international literature. This is because the disease involves not only inflammation but also tendon tissue remodeling, fibrocartilaginous changes, and the formation and resorption phases of calcium deposits. Nevertheless, the term "calcifying tendinitis" remains commonly used in coding systems and clinical language. [3]

Table 1. Key facts about the disease

Parameter	Brief description
What's happening	Calcium hydroxyapatite crystals are deposited in the tendon
Where is it most often found?	In the rotator cuff of the shoulder
The most common localization	Supraspinatus tendon
Typical age	From 30 to 60 years old
A typical clinic	Shoulder pain, night pain, limited motion
Important feature	Calcifications may be asymptomatic
Basic principle of treatment	First, conservative tactics, then minimally invasive methods, surgery only in resistant cases

The data for the table are based on current reviews and clinical guidelines. [4]

Code according to ICD 10 and ICD 11

In the International Classification of Diseases, 10th revision, the code M75.3 Calcific tendinitis of the shoulder is used for the shoulder variant. This is the most straightforward and commonly used code when referring specifically to the calcific process in the tendons of the shoulder region. [5]

The International Classification of Diseases, 11th revision, uses the code FB40.3 for calcific tendinitis as a tendon disorder. The code description states that this condition is characterized by the deposition of hydroxyapatite in any tendon of the body, leading to pain and inflammation, and anatomical detail can be added post-coordination. This means that for the shoulder, the International Classification of Diseases, 11th revision code defines the nosology, and the location is further specified if necessary. [6]

Table 2. Disease coding

Classification	Code	Meaning
International Classification of Diseases, 10th revision	M75.3	Calcific tendinitis of the shoulder
International Classification of Diseases, 11th revision	FB40.3	Calcific tendinitis
International Classification of Diseases, 11th revision	Post coordination	Further clarification of anatomical localization

Source for the table. [7]

Epidemiology

According to modern reviews and recent publications, the prevalence of calcific tendinopathy of the shoulder in the general population ranges from approximately 2.7% to 22%. This wide range is due to differences between studies, differences in imaging methods, and the fact that some people have calcifications without any complaints. [8]

Among asymptomatic adults, rotator cuff calcifications are found in approximately 7.8% of people, while among patients with chronic shoulder pain, such findings occur in 10% to 42% of cases. This is a very important epidemiological fact: a calcification on an X-ray can be either an incidental finding or a real source of pain, and these two situations should not be confused. [9]

The disease is more common in women, especially before menopause, and the typical age of onset is between 30 and 60 years. Furthermore, the process can be bilateral in approximately 10% of patients. The supraspinatus tendon is most commonly affected, although calcifications are also possible in other tendons of the rotator cuff or even in the subacromial-subdeltoid bursa. [10]

Table 3. Epidemiological landmarks

Indicator	Meaning
Prevalence in the general population	from 2.7% to 22%
Asymptomatic calcifications in adults	about 7.8%
Prevalence among patients with chronic shoulder pain	from 10% to 42%
Typical age	from 30 to 60 years old
Floor	More common in women
A two-way process	about 10%

Source for the table. [11]

Reasons

The exact cause of calcific tendinitis remains unclear. Orthopedic and radiological reviews continue to describe the disease as multifactorial, rather than the result of a single mechanical overload. This is important because many patients develop the disease without any obvious injury or direct connection to heavy physical work. [12]

The modern concept attributes a key role to the local metaplasia of tenocytes into fibrocartilaginous tissue, followed by the deposition of hydroxyapatite crystals. In other words, at a certain stage, the tendon is restructured in such a way that calcium deposition becomes possible. This model better explains the phasic nature of the disease than the older concept of simple "salt deposition." [13]

Some publications link the disease to local hypoxia, microtrauma, and vascular and cellular disorders, but no single theory yet explains all cases. Therefore, the most accurate formulation remains the following: calcific tendinitis is a multifactorial tendon disease with an incompletely understood etiology. [14]

Risk factors

The most consistent associations relate to gender and age. Calcific tendinitis is more common in women, especially those between the ages of 30 and 60. This pattern is repeated in educational materials from the American Academy of Orthopaedic Surgeons, in 2025 reviews, and in recent disease reports. [15]

Additionally, data have accumulated on the association with metabolic factors. In a large population-based study, diabetes increased the risk of developing calcific tendinopathy of the shoulder by approximately 27% over an 8-year follow-up period. This does not mean that every patient with diabetes will necessarily develop calcifications, but it emphasizes the importance of metabolic background. [16]

However, the connection with physical activity itself turned out to be less straightforward than previously thought. Modern reviews note that the disease does not demonstrate the same obvious dependence on occupational stress as classic overuse tendinopathy. In other words, excessive activity may exacerbate symptoms, but it does not appear to be a universal explanation for the formation of calcifications. [17]

Table 4. Main risk factors and associations

Factor	What is known
Age	Most often from 30 to 60 years old
Floor	More common in women
Diabetes	The risk is approximately 27% higher in long-term follow-up
Metabolic background	Considered as a significant contributing factor
Mechanical load	May increase symptoms, but does not explain all cases.
Bilateral predisposition	Possible in approximately 10% of patients

Source for the table. [18]

Pathogenesis

The classical pathogenesis scheme includes precalcifying, calcifying, and postcalcifying stages. The calcifying stage, in turn, is divided into the formation phase, the quiescent phase, and the resorption phase. This staging is supported by modern reviews, radiological studies from 2025, and clinical guidelines. [19]

In the precalcification phase, tendon tissue undergoes fibrocartilaginous remodeling. During the formation phase, calcium material accumulates within this tissue. This can then be followed by a relatively quiet, resting phase, when calcification is already present, but there may be no pronounced symptoms at all. This partially explains the high proportion of asymptomatic findings on ultrasound and radiography. [20]

The most painful phase is the resorptive phase. During this period, the deposit becomes more friable, its contours often become unclear, and clinically, sharp pain, nocturnal pain, and sometimes an almost pseudo-paralytic picture appear, when the patient is unable to move the arm due to the intensity of symptoms. A modern study from 2025 using magnetic resonance imaging showed that it is precisely in the resorptive phase that deposits most often have an irregular shape, unclear edges, and a heterogeneous structure. [21]

This is followed by the post-calcification stage, when the tendon tissue is rebuilt and can partially or completely recover. Therefore, the disease is considered potentially self-limiting, although the rate of such natural resolution is highly variable. In some patients, the process subsides on its own, while in others it drags on for months and requires active intervention. [22]

Table 5. Process stages

Stage	What's happening	A typical clinic
Precalcifying	Fibrocartilaginous remodeling of tenocytes	Often asymptomatic
Calcification, formation phase	Formation of dense calcification	Often moderate or no pain
Calcifying, resting phase	The calcification is stable	An asymptomatic period is possible
Calcification, resorption phase	The calcification is loosened and resorbed	The most severe pain, night pain, limitation of movement
Postcalcifying	Tendon remodeling	Gradual reduction of symptoms

Source for the table. [23]

Symptoms

The most typical symptom is pain in the anterolateral shoulder, which worsens with arm elevation, abduction, overhead work, and lying on the affected side. The American Academy of Orthopaedic Surgeons also recommends pain in the front or side of the shoulder, severe stiffness, and decreased range of motion. [24]

Calcific tendinitis is particularly characterized by nocturnal pain, sometimes very intense. Recent reviews emphasize that during the resorptive phase, the pain can be so severe that the patient is almost unable to use the arm and perceives the condition as an acute traumatic injury, although no injury has occurred. [25]

In some patients, symptoms are chronic and nagging, while in others, they begin acutely or subacutely. A 2025 clinical summary of the signs of calcific tendinopathy emphasizes that nocturnal pain, acute or subacute onset, and decreased active and passive range of motion, especially during resorption, are typical. [26]

If reactive subacromial-subdeltoid bursitis is present, the pain becomes even more diffuse and is triggered by almost any shoulder movement. Sometimes, it is the bursal reaction that explains why the symptoms seem more severe than would be expected based on the size of the calcification. [27]

Table 6. The most typical symptoms

Symptom	How typical is it?
Pain in the anterolateral shoulder	Very characteristic
Night pain	Very characteristic, especially in the resorptive phase
Increased pain when raising the arm	Often
Stiffness and limited movement	Often
Pseudoparalytic picture due to pain	Possible in severe acute phase
Reactive bursitis	Possible and increases symptoms

Source for the table. [28]

Classification, forms and stages

From a practical standpoint, calcific tendinitis is conveniently divided into asymptomatic and symptomatic. This simple distinction has significant clinical significance, as not every calcification requires treatment. If a calcification is discovered incidentally and does not cause pain, active intervention may not be necessary at all. [29]

The second important classification is related to the stages of the process: the pre-calcifying stage, the calcifying stage with its formation, rest, and resorption phases, and then the post-calcifying stage. It is this phased nature of the disease that best explains why one patient can live for a long time with a dense deposit with virtually no symptoms, while another suddenly experiences severe, acute pain. [30]

From a radiological perspective, calcifications are also described by size, density, clarity of contours, and location. Research from 2025 emphasizes that radiography and ultrasound are used not only to confirm the diagnosis but also to assess the morphology of the deposit, which helps to predict the phase of the process. [31]

Table 7. Practical classification

Principle	Options
By symptoms	Asymptomatic, symptomatic
By biological stage	Precalcifying, calcifying, postcalcifying
By the calcification stage	Formation, rest, resorption
By visualization	Dense and clear deposit, loose and fuzzy deposit, migration to the bursa

Source for the table. [32]

Complications and consequences

In most cases, the condition does not destroy the joint or lead to catastrophic consequences, but it can significantly impair quality of life. Nighttime pain, the inability to raise the arm, limitations in work and sports, sleep disturbances, and constant pain with normal everyday movements make calcific tendinitis one of the most uncomfortable forms of non-traumatic shoulder pain. [33]

Potential complications include reactive subacromial-subdeltoid bursitis, extratendinous migration of calcium material, and long-term chronic shoulder dysfunction. Furthermore, long-term observations indicate that calcific tendinitis may be associated with rotator cuff tears and late development of shoulder osteoarthritis, although the causal relationship is not always straightforward.[34]

Another consequence is overtreatment. Due to severe pain, patients sometimes quickly switch from one minimally invasive method to another, although the disease is often self-limiting. Modern randomized and review studies are important precisely because they encourage caution in the use of procedures whose effectiveness has long been considered almost self-evident. [35]

When to see a doctor

It's advisable to consult a doctor if shoulder pain persists for more than a few weeks, interferes with sleep, limits arm movement, or returns after brief periods of improvement. It's especially important not to delay if the pain is so severe that it's difficult to move the arm even slightly, or if the person has already begun to avoid movement due to fear of pain. [36]

A more urgent evaluation is necessary after an injury, with significant deformity, noticeable weakness, fever, redness, general malaise, or persistent swelling. These signs are less consistent with typical calcific tendinitis and require the exclusion of tendon rupture, infection, fracture, or other shoulder pathology. [37]

Diagnostics

Diagnosis begins with a medical history and physical examination. The doctor clarifies the nature of the pain, its nocturnal component, whether it is acute or gradual in onset, the presence of injury, whether it is triggered by movement, and the degree of functional limitation. Clinical guidelines for rotator cuff pathology emphasize that, even at the initial stage, it is necessary to assess not only shoulder pain but also range of motion, strength, associated cervical symptoms, and the overall clinical picture. [38]

Radiography and ultrasound are considered the primary methods for confirming calcifications. Recent publications explicitly state that the diagnosis of calcific tendinopathy of the shoulder is usually based on these two methods. Ultrasound allows one to visualize the calcification, acoustic shadowing, signs of bursitis, and sometimes suggest the stage of the process, while conventional radiography clearly shows dense deposits in the typical area. [39]

For chronic shoulder pain, radiography remains the typical initial imaging modality. The American College of Radiology indicates that radiography is typically the first imaging test performed for chronic shoulder pain, and if radiographs are normal or equivocal and rotator cuff pathology is suspected, ultrasound or magnetic resonance imaging may be the next step. [40]

Conventional magnetic resonance imaging (MRI) is not considered the best initial method for detecting calcium. The American College of Radiology notes that hydroxyapatite may be poorly visualized on standard MRI due to low contrast between the calcium and the adjacent tendon. However, MRI is useful when evaluating a concomitant rotator cuff tear, significant bursitis, atypical location, or other alternative explanations for pain. [41]

An interesting new diagnostic approach involves zero-echo sequences. In a 2025 study by ZTE, magnetic resonance imaging was better than conventional sequences at detecting calcifications and better at distinguishing between the resorptive and formative phases. While this is not yet a widely used standard, it shows promise for more accurate phase assessment of the process. [42]

Laboratory tests are not usually the primary diagnostic tool. They are not used to confirm calcific tendinitis, but rather when an infection, systemic inflammatory disease, or other rare cause of pain is suspected. Typically, the diagnosis is made based on clinical findings and imaging, not blood tests. [43]

Table 8. Step-by-step diagnostics

Step	What are they doing?	Why is this necessary?
1	They collect anamnesis and evaluate night pain	A typical clinical pattern is identified
2	They examine the shoulder and measure the range of motion	Determine the severity of the restriction
3	They are performing an x-ray	Confirm the presence of dense calcification
4	They are doing an ultrasound examination	Specify the size, shape, phase, bursitis
5	If necessary, magnetic resonance imaging is prescribed.	They are looking for an accompanying rupture or atypical pathology
6	If the picture is atypical, laboratory tests are prescribed.	Infection and systemic inflammation are ruled out

Source for the table. [44]

Differential diagnosis

Calcific tendinitis must first be differentiated from simple rotator cuff tendinopathy without calcifications, subacromial-subdeltoid bursitis, partial tendon tears, adhesive capsulitis, and long head biceps brachii pathology. These conditions can cause very similar pain, especially if the physician relies solely on the patient's complaints rather than imaging. [45]

It is also important to remember that calcification may be an incidental finding. If the clinical picture is not consistent with typical calcific tendinitis, other sources of pain should be sought, including cervical radiculopathy, acromioclavicular pathology, shoulder instability, and inflammatory diseases. Particular caution should be exercised when interpreting images in older patients, who often have a mixed degenerative shoulder background. [46]

Treatment

Treatment begins with understanding the stage of the disease and the severity of symptoms. Since the disease is self-limiting in some patients, the initial approach is usually conservative. Modern reviews and guidelines emphasize that during painful episodes, the first step is usually rest from the provoking load, pain relief, nonsteroidal anti-inflammatory drugs, and supervised rehabilitation. [47]

Complete shoulder rest is not considered a good strategy today. It is more important to temporarily reduce abrupt and painful overhead movements, but maintain gentle activity to prevent further stiffness. The 2025 Rotator Cuff Clinical Guideline recommends an active rehabilitation program as the initial treatment for shoulder pain associated with the rotator cuff, including those with calcification. [48]

Exercise remains a central part of treatment, although it does not directly "dissolve" calcium. Its purpose is to reduce pain, maintain mobility, restore rotator cuff strength and scapular mechanics, and facilitate a safer return to weight-bearing activity. A 2025 network meta-analysis found that comprehensive physical therapy was the leading method for improving function among non-surgical interventions. [49]

If pain is severe, oral painkillers and nonsteroidal anti-inflammatory drugs are temporarily used. Their role is symptomatic: to alleviate the condition in the acute or subacute phase and enable the patient to move and engage in rehabilitation. However, no modern source considers pills as a way to eliminate the deposit itself. [50]

Shockwave therapy remains one of the most widely discussed non-surgical treatments. A 2025 clinical guideline specifically states that it can be used to reduce pain and disability in calcific rotator cuff tendinopathy, and a separate review of the same guideline noted that high-energy shockwave therapy is superior to low-energy shockwave therapy in reducing pain and disability. [51]

However, shockwave therapy is not completely risk-free and does not guarantee success for everyone. A review of evidence from the UK's National Institute for Health and Care Excellence, updated in 2026, showed improved function and increased calcification resolution in a number of studies, but also recorded a higher rate of adverse events compared with placebo, primarily pain, redness, bruising, and temporary worsening of symptoms. Serious complications were rarely reported. [52]

Ultrasound-guided lavage or aeration has long been considered a near-standard minimally invasive option for refractory lesions. The 2025 Rotator Cavity Guidelines still allow it for refractory calcific tendinopathy after initial treatment and note that it may reduce pain and limitation more than corticosteroid injection or shockwave therapy alone in some studies. [53]

But the data on lavage are no longer as clear-cut as they once were. A randomized, double-blind, sham-controlled trial published in 2023 and available through The BMJ showed no benefit for either ultrasound-guided corticosteroid lavage or sham-assisted corticosteroid lavage compared to sham alone over 24 months. This suggests that the role of lavage today requires a more critical reassessment, especially when it is proposed as a nearly mandatory procedure. [54]

Corticosteroid injections can be used as a short-term way to reduce inflammation and pain, especially if there is concomitant bursitis. However, current evidence does not support the idea of endless repeat injections or consider them a permanent solution. Even in a 2023 sham-controlled study, the corticosteroid injection did not provide convincing long-term superiority over sham alone. [55]

Biologics and injectables, such as platelet-rich plasma or hyaluronic acid, have not yet become standard treatments specifically for calcific tendinitis. The 2025 rotator cuff guidelines allow them as options for certain forms of shoulder pain, but the evidence base remains mixed, and the benefits over exercise, placebo, or simpler approaches do not appear convincing enough to warrant routine recommendation for everyone. [56]

Surgery is reserved for persistent, truly resistant forms. Contemporary reviews emphasize that surgery is considered after months of unsuccessful conservative treatment and minimally invasive attempts, and the surgery itself is usually aimed at removing the calcification, sometimes with additional tendon repair. A 2024 systematic review and meta-analysis found that all surgical approaches generally significantly reduced pain and improved function, but no significant differences were found between calcification removal, removal with subacromial decompression, and removal with tendon repair. [57]

Table 9. Modern treatment tactics

Method	Modern assessment
Limiting the provocative load	The starting step
Exercise and rehabilitation	Base of conservative treatment
Nonsteroidal anti-inflammatory drugs	For short-term pain control
High-energy shock wave therapy	Acceptable and better than low-energy for calcifications
Laser therapy	It may be considered, but the evidence is not the strongest.
Therapeutic ultrasound	Not recommended for calcific tendinopathy
Ultrasound-guided lavage	Possible in refractory cases, but data are conflicting
Corticosteroid injection	Temporary relief, not a radical solution
Platelet-rich plasma	Not first line standard
Operation	For chronic resistant cases

Source for the table. [58]

Prevention

There is no specific prophylaxis that can reliably prevent the formation of calcifications. This is because the cause of the disease remains multifactorial and not fully understood. Therefore, prevention in the strict sense is limited. [59]

However, it is possible to reduce the likelihood of an asymptomatic or inactive process becoming painful. To do this, it is wise to avoid sudden increases in shoulder stress, promptly treat prolonged shoulder pain, maintain shoulder girdle mobility and strength, and pay attention to the management of metabolic diseases, especially diabetes. [60]

Forecast

Overall, the prognosis for many patients is favorable, as calcific tendinitis is considered a potentially self-limiting disease. Modern radiological and review publications explicitly refer to it as a self-resolving disease, meaning a process that, in some cases, can result in the natural resorption of the deposit and tendon remodeling. [61]

But the prognosis isn't the same for everyone. For some patients, the pain resolves within months, for others it lingers, and still others require a step-by-step approach, progressing from conservative care to shockwave therapy, lavage, or surgery. This is why prognoses are now formulated cautiously: the disease is often benign, but its course can be very painful and unpredictable in duration. [62]

Long-term follow-up also shows that some patients develop rotator cuff tears and signs of shoulder osteoarthritis years later. This does not mean that every calcification necessarily leads to such consequences, but it emphasizes the need for careful monitoring in patients with a protracted or recurrent course. [63]

Table 10. What influences the prognosis

Factor	How does it affect
Self-limiting flow	Improves prognosis
Severe resorptive phase	It causes very strong, but not always long-lasting pain.
Reactive bursitis	May increase and prolong symptoms
Refractory to conservative therapy	Increases the likelihood of procedures or surgery
Associated rotator cuff tear	May worsen functional outcome

Source for the table. [64]

FAQ

Can calcific tendonitis go away on its own?

Yes. Modern reviews and radiological studies indicate that the disease often has a self-limiting course, especially after the resorptive phase. However, it is difficult to predict the time of natural resolution in a particular patient. [65]

Does a calcification on an X-ray always indicate the cause of pain?

No. In some adults, calcifications are discovered incidentally and cause no symptoms. Therefore, the diagnosis is made not based on a single radiograph, but rather on a combination of clinical and imaging findings. [66]

What is better for diagnosis: X-ray or ultrasound?

In practice, these methods complement each other. Radiography clearly shows dense calcification, while ultrasound is better at assessing its structure, stage, and reactive bursitis, and helps plan procedures. [67]

Does all patients need MRI?

No. Conventional magnetic resonance imaging is not the best initial test specifically for calcium. It is used primarily in complex clinical situations, where there is a suspicion of a concomitant tendon rupture or other shoulder pathology. [68]

Does shock wave therapy help?

Yes, it helps some patients, especially those with the calcific form. Current guidelines from 2025 allow its use, and the high-energy version appears more effective than the low-energy version, although tolerability and the risk of temporary pain increase should also be considered. [69]

Should everyone do lavage?

No. Earlier reviews suggested lavage for persistent cases, but a 2023 sham-controlled study did not confirm its superiority over the sham procedure. Therefore, it cannot be considered a universally required method. [70]

When is surgery considered?

Surgery is usually considered only after months of persistent pain and the failure of conservative and minimally invasive treatments. It is an option for truly resistant pain, not for the first episode of pain. [71]

Key points from experts

François Demeule, PhD, physiotherapist, professor at the School of Rehabilitation at the University of Montreal, and researcher in orthopedic and rehabilitation care, is important in that he views calcific tendinopathy not as an automatic indication for invasive treatment, but as part of a spectrum of shoulder pain, where active rehabilitation remains the mainstay of therapy. The practical implication: even in the presence of calcification, treatment should not automatically begin with a procedure. [72]

Sun Jin Shin, MD, PhD, professor in the Department of Orthopedic Surgery at Ewha Womans University, highlights one important point: the phase of calcific tendinitis matters because it is associated with treatment decisions and symptom severity. The practical implication is that similarly named "calcifications" can behave differently depending on whether they are in the formation or resorption phase. [73]

Jens Ivar Brox, MD, PhD, consultant and professor at II Oslo University Hospital. His group demonstrated in a 2023 sham-controlled study that ultrasound-guided corticosteroid lavage was no better than sham treatment over 24 months. The practical implication of this study is crucial: even a popular and technically attractive procedure should be validated with placebo controls, and treatment algorithms should be regularly reviewed. [74]