Calcific Tendonitis: Symptoms, Types, Causes and Treatment

Calcific tendonitis is a common yet often misunderstood condition that can trigger acute or chronic pain and disrupt daily life. While most frequently associated with the shoulder—specifically the rotator cuff—it can affect many tendons throughout the body. This comprehensive guide explores the symptoms, types, causes, and modern treatment options for calcific tendonitis, drawing on current scientific evidence and advances in clinical practice.

Symptoms of Calcific Tendonitis

The first sign of calcific tendonitis is often pain, but the clinical picture is more complex. Understanding these symptoms can help patients and clinicians recognize the condition early and manage it effectively.

Symptom	Description	Frequency/Severity	Source(s)
Pain	Acute or chronic, often severe; may be sudden or develop gradually	Most common, can be disabling	1,3,7,8,15
Tenderness	Localized at tendon site	Common, especially when pressure is applied	1,7,10
Restricted Movement	Stiffness, limited range of motion	Variable, worse with severe pain	7,9,10,15
Swelling	Localized edema at affected site	Occasional, especially in acute phase	3,7,10
Asymptomatic	No symptoms, incidental finding	Up to 50% of cases	1,5,8

Table 1: Key Symptoms

Understanding the Symptoms

Calcific tendonitis often presents with a spectrum of symptoms that can range from completely silent to intensely painful.

Pain: The Hallmark Feature

• Acute Pain: Many patients report sudden, severe pain—often at night or after minor trauma. This is especially true during the resorptive phase, when inflammation peaks (3,7,15).
• Chronic Pain: Some experience a dull, persistent ache that gradually worsens, especially with movement or use of the affected tendon (8,10).

Other Symptoms

• Tenderness and Swelling: The area over the affected tendon may be tender to touch. Swelling or visible edema may develop, particularly during acute inflammatory flares (7,10).
• Limited Range of Motion: Pain and swelling can restrict movement. This is common in the shoulder, where patients may struggle to lift their arm or reach overhead (7,9,15).
• Asymptomatic Cases: Remarkably, up to half of those with calcific deposits experience no symptoms. These deposits are often discovered incidentally during imaging for unrelated issues (1,5,8).

Symptom Fluctuations

Symptoms may ebb and flow, with periods of relative quiet interrupted by sudden, intense exacerbations. This reflects the condition’s natural cycles of deposit formation and resorption (7,9,15). In rare cases, such as retropharyngeal calcific tendonitis, symptoms can mimic more serious illnesses, highlighting the need for accurate diagnosis (4).

Types of Calcific Tendonitis

Calcific tendonitis is not a uniform disease. It varies by location, underlying cause, and stage of progression. Understanding these types helps guide diagnosis and treatment.

Type	Location/Description	Distinguishing Feature	Source(s)
Rotator Cuff	Shoulder (supraspinatus, infraspinatus, etc.)	Most common site, often severe	1,7,8,9,15,16
Gluteal	Hip (gluteus medius/minimus)	Rare, may cause lateral hip pain	14
Retropharyngeal	Neck (longus colli muscle)	Mimics abscess, neck pain/swallowing issues	4
Tibialis Posterior	Foot (navicular tendon)	Extremely rare, foot pain	11
Idiopathic (Type I)	No identifiable cause	Most cases	6
Secondary (Type II)	Associated with endocrine/metabolic disorders	Younger onset, more severe course	6

Table 2: Main Types

A Closer Look at the Types

By Anatomic Location

• Shoulder/Rotator Cuff: The rotator cuff is by far the most frequent site, particularly the supraspinatus tendon. The condition is a leading cause of shoulder pain in adults, especially women in their 40s to 60s (7,8,9,15,16).
• Hip: The gluteus medius and minimus tendons can also develop calcific deposits, although this is far less common. When it does occur, it typically causes persistent lateral hip pain (14).
• Neck (Retropharyngeal): Calcific tendonitis of the longus colli muscle presents as acute neck pain, often with difficulty swallowing, and can be mistaken for infection (4).
• Foot: Rarely, tendons in the foot, like the tibialis posterior, are affected. Such cases may be overlooked due to their rarity (11).

By Etiology

• Idiopathic (Type I): Most cases have no clear cause and are considered idiopathic. These tend to follow a typical clinical course and often resolve on their own (6).
• Secondary (Type II): Some cases are linked to endocrine disorders—especially thyroid or estrogen metabolism problems. These tend to occur at a younger age, last longer, and are more likely to require surgery (6).

By Disease Phase and Morphology

• Formative, Resting, and Resorptive Phases: The disease progresses through a formative (deposit-building), resting (stable), and resorptive (breakdown/removal) phase. The most severe symptoms typically occur during the resorptive phase, marked by inflammation and pain (2,7,9).
• Morphological Types: Deposits can have various shapes—arc, fragmented, nodular, or cystic—each correlating with pain levels and disease stage (2).

Causes of Calcific Tendonitis

Why do some people develop calcific tendonitis while others do not? The answer involves interplay between cellular changes, mechanical stress, and sometimes, systemic conditions.

Cause	Mechanism/Role	Key Features	Source(s)
Cell-Mediated Process	Tendon cells transform, deposit apatite	Active, not passive process	9,10
Microtrauma	Repetitive minor injury	Triggers tendon healing response	7,9,10
Hypoxia	Decreased oxygen to tendon	Promotes cell changes	7,9
Inflammation	Immune response to deposits	Neovascularization and new nerves	3,5,9
Endocrine Disorders	Thyroid, estrogen imbalance	Higher risk, younger onset	6
Unknown/Idiopathic	No clear trigger	Most cases	6,8

Table 3: Main Causes

Unpacking the Causes

Cellular and Molecular Triggers

• Active Cellular Process: Calcific tendonitis is not just a matter of passive mineral buildup. Research shows tendon cells (tenocytes) can transform into chondrocyte-like cells, which actively deposit calcium apatite into the tendon matrix (9,10).
• Role of Matrix Vesicles and Proteins: Proteins such as osteopontin may regulate deposit formation. The composition of the deposits changes over time, reflecting different stages of disease (2,9).
• Phases of Calcification: The process involves:
  • Formative Phase: Cells lay down poorly crystalline calcium apatite.
  • Resting Phase: Deposits stabilize.
  • Resorptive Phase: The body mounts an inflammatory response, breaking down the deposit (2,7,9).

Mechanical and Environmental Factors

• Repetitive Microtrauma: Chronic overuse or repetitive minor injuries can disrupt tendon healing, leading to abnormal mineralization (7,9,10).
• Transient Hypoxia: Decreased oxygen supply during repetitive stress alters tendon cell behavior, promoting calcification (7,9).

Inflammation and Pain Generation

• Immune Response: As the body tries to resorb the deposit, an intense inflammatory response occurs. There is infiltration of macrophages, mast cells, and new blood vessels, along with nerve ingrowth, which directly correlates with pain severity (3,5,9).
• Inflammasome Activation: The breakdown of apatite crystals triggers the release of inflammatory mediators like IL-1β, amplifying pain and swelling (9).

Systemic/Secondary Causes

• Endocrine Disorders: Diseases affecting thyroid and estrogen metabolism increase risk, especially in younger women. These cases are more resistant to conservative treatment (6).
• Other Factors: While metabolic abnormalities of calcium and phosphorus are rarely implicated, there are many unanswered questions about what initiates and resolves the disease in different people (8,10).

Treatment of Calcific Tendonitis

Treatment depends on the severity, duration, and impact on daily life. Most cases resolve with conservative measures, but persistent or severe cases may need advanced interventions.

Treatment	Description/Indication	Effectiveness/Notes	Source(s)
Conservative	Rest, NSAIDs, physical therapy	First-line, often effective	7,8,15,16
Corticosteroid Injection	Reduces inflammation and pain	Good for acute flares	1,7,15,12
Ultrasound-Guided Needling (UGN)/Barbotage	Needle aspiration/fragmentation of deposits	Highly effective, especially combined with steroid injection	1,12,13
Extracorporeal Shock Wave Therapy (ESWT)	Non-invasive, breaks deposits	Effective, especially high-energy; best for chronic cases	12,13
Surgery (Arthroscopic removal)	For refractory cases only	Minimally invasive, complete removal not always necessary	7,14,15,16

Table 4: Treatment Options

Exploring Treatment in Depth

Conservative Approaches

• Rest and NSAIDs: Most patients start with rest, nonsteroidal anti-inflammatory drugs (NSAIDs), and sometimes ice or heat. This approach is often adequate, as many cases resolve spontaneously (7,8,15).
• Physical Therapy: Targeted exercises help maintain range of motion and strength, especially in the shoulder (15,16).

Minimally Invasive Interventions

• Corticosteroid Injections: Injecting steroids into the subacromial bursa or around the affected tendon can rapidly reduce pain and inflammation. Best results are seen in patients with clear signs of local inflammation or bursal widening (1,7,12).
• Ultrasound-Guided Needling (Barbotage/UGN): This technique uses ultrasound to guide a needle into the deposit, allowing aspiration or fragmentation. Combining this with a corticosteroid injection improves pain relief and accelerates deposit resolution (1,12,13).
• Extracorporeal Shock Wave Therapy (ESWT): High-energy sound waves are used to break up calcific deposits. Radial and focused ESWT are both effective, particularly in chronic cases. Combining ESWT with barbotage or steroid injection offers the best outcomes for pain and deposit clearance (12,13).

Surgical Options

• When Surgery Is Needed: Surgery is reserved for cases that fail to improve with conservative and minimally invasive measures. Arthroscopic removal is preferred, as it is minimally invasive and allows rapid recovery (7,14,15,16).
• Extent of Removal: Complete removal of the deposit is not always necessary; partial removal can suffice, as the body finishes resorbing the rest (7,15).

Special Considerations

• Chronic/Refractory Cases: Patients with underlying endocrine disorders may require more aggressive treatment and are more likely to need surgery (6).
• Other Sites: Rare locations (e.g., neck, foot, hip) may need tailored approaches, but the general principles remain the same—start conservatively, escalate as needed (4,11,14).

Conclusion

Calcific tendonitis is a multifaceted disorder that can cause significant pain and functional impairment, yet often resolves spontaneously. Recognition of its symptoms, understanding the different types and causes, and a stepwise approach to treatment can dramatically improve patient outcomes.

Key points:

• Symptoms range from silent deposits to acute, disabling pain, often with restricted movement and localized swelling.
• Types are defined by location (shoulder, hip, neck, foot), underlying cause (idiopathic vs. secondary), and disease phase (formative, resting, resorptive).
• Causes involve active cell-mediated processes, repetitive microtrauma, inflammation, and sometimes endocrine disorders.
• Treatment starts with conservative measures, progresses to corticosteroid injections, ultrasound-guided needling, or ESWT, and rarely requires surgery.

A patient-centered, evidence-based approach ensures that most individuals with calcific tendonitis can return to pain-free, active lives with minimal intervention.