Calcific Tendinopathy: A Brief Overview

Calcific tendinopathy (CT) of the shoulder is a common but often under-recognised condition that can cause significant discomfort and disability. In this blog post, we’ll explore what it is, its underlying pathology, how it is diagnosed, and the latest management strategies

What Is Calcific Tendinopathy?

Calcific tendinopathy is characterised by the deposition of calcium hydroxyapatite crystals within a tendon, most frequently affecting the supraspinatus tendon in the rotator cuff. Studies suggest that calcific tendinopathy accounts for 10–42% of shoulder pain presentations and is typically seen in patients aged between 30 and 50 years, with a higher incidence in women. It is often associated with metabolic and endocrine disorders, such as diabetes and thyroid dysfunction, and usually presents without any history of trauma.

Epidemiology and Risk Factors

Calcific Tendinopathy is notably prevalent in the shoulder region, and while many patients experience spontaneous resolution, the acute phases can be debilitating. Risk factors include:

• Age and Gender: Most patients present in their 30s to 50s, with women more commonly affected.
• Metabolic Conditions: Endocrine disorders, particularly diabetes and thyroid issues, have been linked to an increased risk.
• Repetitive Stress: Chronic overuse and repetitive microtrauma can initiate an aberrant healing response that leads to calcium deposition.

Recent research has further investigated the role of systemic inflammation and metabolic dysregulation in Calcific Tendinopathy, suggesting that improved management of these underlying conditions may help mitigate the severity of symptoms.

Understanding the Pathophysiology

The development of Calcific Tendinopathy is generally explained through the stages described by Uhthoff, which include:

1. Precalcific Phase

This phase involves an abnormal healing response to repetitive microtrauma and overloading. The failed cell-mediated healing theory suggests that these factors initiate the formation of calcium deposits in an otherwise healthy tendon.

2. Calcific Phase

Divided into three sub-stages:

• Formative Phase: Calcium crystals begin to form and merge into larger deposits, often with a chalk-like appearance.
• Resting Phase: The calcifications become stable, encapsulated by a fibrocartilaginous “cap” that borders the deposit.
• Resorptive Phase: An intense inflammatory reaction occurs as the body attempts to break down the deposits. Vascular tissue forms around the calcification, which may leak into adjacent tissues and cause severe pain.

3. Post-Calcific Phase

In this reparative phase, fibroblasts gradually replace the calcium with Type III collagen, which is then remodeled into stronger Type I collagen. This process ultimately restores the tendon’s structure and function.

Recent studies have underscored the importance of inflammation in the resorptive phase and have investigated pharmacological interventions that target specific inflammatory pathways to reduce pain and accelerate healing.

Diagnostic Imaging

Ultrasound is the diagnostic imaging modality of choice for CT due to its ability to visualize calcifications at various stages and to guide therapeutic procedures. On ultrasound, Calcific Tendinopathy appears as a hyperechoic focus that disrupts the normal tendon architecture. Plain radiographs are also useful, though MRI/MRA may be less sensitive given the similar signal intensity of calcifications and normal tendon tissue.

Recent advancements in ultrasound technology and elastography have enhanced the sensitivity and specificity of Calcific Tendinopathy diagnosis, allowing for earlier and more accurate detection of the disease.

Clinical Assessment and Differential Diagnosis

Patients typically report:

• Acute, severe pain: Especially during the resorptive phase, often worse at night.
• Range of Motion Deficits: Both active and passive range of motion can be affected, particularly during abduction and forward flexion.
• Joint Sounds: Clicking or snapping sensations may occur during movement.

The clinical picture of Calcific Tendinopathy must be differentiated from other shoulder conditions such as:

• Adhesive Capsulitis: Unlike Calcific Tendinopathy, passive range of motion is limited in adhesive capsulitis.
• Long Head Biceps Tendinopathy: Often associated with normal radiographs.
• Degenerative Tendinopathy: Characterised by pain with resisted movements and passive stretching.
• Tendon Tear: Although acute pain can be similar, patients with Calcific Tendinopathy usually retain a full active range of motion, albeit painfully.
• Acute Synovitis/Septic Arthritis: These conditions typically present with systemic symptoms and abnormal laboratory results, unlike Calcific Tendinopathy

Management Strategies

Management of calcific tendinopathy is often multimodal, depending on the stage of the disease:

Conservative Management

• Physiotherapy and Rehabilitation: Focuses on restoring range of motion and strengthening the shoulder.
• Corticosteroid Injections: Particularly useful in the resorptive phase to alleviate pain.
• Suprascapular Nerve Block: Provides additional pain relief.

Interventional Treatments

• Barbotage Under Ultrasound Guidance: This procedure involves needling the deposit and aspirating the calcium to relieve pain.
• Shockwave Therapy: Although its availability is limited, research shows promising results in breaking up calcific deposits.

Surgical Interventions

For patients who do not respond to conservative measures, surgical options such as arthroscopic removal of calcific deposits, bursectomy, debridement, and subacromial decompression may be considered. In cases where a tendon tear is present due to Calcific Tendinopathy, repair may also be necessary.

Recent literature emphasizes that early intervention, particularly during the resorptive phase, may reduce the need for surgical intervention. Emerging research is also looking into regenerative therapies that could improve tendon healing and restore function more rapidly.

Emerging Research and Future Directions

Current research is exploring the molecular pathways involved in Calcific Tendinopathy, with studies focusing on:

• Inflammatory Mediators: Targeting cytokines and other inflammatory molecules may open up new pharmacological treatments.
• Biologic Agents: There is ongoing investigation into the use of biologics to modulate tendon healing and reduce calcific deposition.
• Advanced Imaging Techniques: New imaging modalities are being developed to better characterise the biochemical and structural properties of calcific deposits, potentially leading to more personalised treatment plans.

These advancements offer hope for more effective treatments and better outcomes for patients suffering from this painful condition.

Conclusion

Calcific tendinopathy of the shoulder is a multifaceted condition with distinct phases that impact both diagnosis and management. With a robust body of research supporting various treatment modalities—from conservative physiotherapy to innovative interventional techniques—the outlook for patients continues to improve. As our understanding of the underlying pathophysiology expands, future therapies may provide even more targeted and effective relief.

References

• Ricci, V., Mezian, K., Chang, K.-V. and Özçakar, L. (2022) 'Clinical/Sonographic Assessment and Management of Calcific Tendinopathy of the Shoulder: A Narrative Review', Diagnostics, 12, p. 3097.
• Guido, F., Venturin, D., De Santis, A., Giovannico, G. and Brindisino, F. (2024) 'Clinical features in rotator cuff calcific tendinopathy: A scoping review', Shoulder & Elbow, 0(0), pp. 1–9.
• McNally, E. (2005) Practical MSK ultrasound.
• Catapano, M., Robinson, D.M., Schowalter, S. and McInnis, K.C. (2022) 'Clinical evaluation and management of calcific tendinopathy: an evidence-based review', Journal of Osteopathic Medicine, 122(3), pp. 141–151.