Biolife - Scientific Publisher

Biolife - Scientific Publisher

Journal of Orthopedics 2022; 14(2):July-December -/-


REVISITING THE STATE-OF-THE-ART KNOWLEDGE OF SHOULDER CALCIFIC TENDINITIS PATHOGENESIS, DIAGNOSIS, AND TREATMENT: AN EVIDENCE-BASED REVIEW

F. Pegreffi1, G. Merolla2, P. Paladini3, C. Barbato4, R.G. Bellomo5, N. Veronese6 and R. Saggini7

 

1Department for Life Quality Studies, Alma Mater Studiorum, University of Bologna, Bologna, Italy;
2Shoulder and Elbow Unit, Cervesi Hospital, Cattolica – AUSL Romagna, Cattolica, Italy;
3Shoulder and Elbow Unit, Cervesi Hospital, Cattolica – AUSL Romagna, Cattolica, Italy;
4Department of Biomolecular Science, Physical Medicine and Rehabilitation, Carlo Bo University Study of Urbino, Urbino, Italy;
5Department of Biomolecular Science, Physical Medicine and Rehabilitation, Carlo Bo University Study of Urbino, Urbino, Italy;
6Department of Internal Medicine, Geriatrics Section, University of Palermo, Palermo, Italy;
7Department of Theoretical and Applied Sciences, University E-Campus Novedrate, Italy

 

*Correspondence to:
Francesco Pegreffi, MD
Department for Life Quality Studies,
Alma Mater Studiorum,
University of Bologna,
Bologna, Italy
e-mail: f.pegreffi@gmail.com

 

Received: 21 September 2022
Accepted: 06 November 2022
 		 ISSN: 1973-6401
Copyright © by BIOLIFE (2022)
This publication and/or article is for individual use only and may not be further reproduced without written permission from the copyright holder. Unauthorized reproduction may result in financial and other penalties. Disclosure: All authors report no conflicts of interest relevant to this article.

 

ABSTRACT

 

Shoulder calcific tendinitis is a common debilitating disorder characterised by the presence of either single or multiple calcium deposits in the rotator cuff tendons or the subacromial-subdeltoid bursa. Although this disease tends to subside spontaneously, a large percentage of patients still report shoulder pain and dysfunction, even after therapy. Several treatment options are available for shoulder calcific tendinitis, but clear therapeutic guidelines are still lacking and clinical outcomes are often controversial, likely due to lack of understanding of its pathophysiology. This evidence-based narrative review aims to revisit the base of the pathogenesis, diagnosis, and treatment of calcific tendinitis affecting the shoulder rotator cuff, specifically focusing on the most recent scientific findings.

 

KEYWORDS: calcific tendinitis, shoulder, rotator cuff, diagnosis, therapeutic strategies

 

INTRODUCTION

 

Calcific tendinitis is a painful, self-limiting disorder most commonly observed in the shoulder girdle, and characterised by either single or multiple calcium deposits in the rotator cuff tendons or in the subacromial bursa (1).

Over the years, different terminology has been used to describe this disease. At first, the deposits in the subacromial bursa were described as the main radiological feature. Later, Codman (2) and Plenk (3) respectively identified the deposits inside the rotator cuff tendon and coined the term “calcifying tendinitis”.

 

Epidemiology

Shoulder calcific tendinitis occurs in 2.7% to 42% of the population worldwide (1, 4-7).  Deposits are bilateral in 10-20% of cases (1, 5, 8). Women are affected 60% more than men and it occurs more frequently in sedentary workers (9, 10). Calcific Tendinitis is typically seen in younger patients aged between 30-50 years (11), but it can rarely occur in the elderly as well (7, 12, 13). It is associated with metabolic disorders such as insulin-dependent diabetes (14), hyperlipidaemia, hypothyroidism, and disorders of estrogen metabolism (15). Biochemical features that play a role in the formation of calcium deposits include extracellular tendon matrix glycosylation observed in diabetic patients and genetic predisposition (14).

Among shoulder rotator cuff tendons, the supraspinatus is the most frequently affected (80% of the cases) (1, 3, 4, 16), while the infraspinatus and subscapularis are affected in 15% and 5% of the cases respectively, and the teres minor is only rarely affected (1, 4, 16). The right shoulder is the most commonly affected (16).

Although calcific tendinitis subsides spontaneously, in most cases, physical therapy and pain management, extracorporeal shock wave therapy, ultrasound-guided percutaneous lavage, orthobiologic therapy, and surgical debridement were demonstrated to relieve pain and restore shoulder function. Conservative treatment can accelerate recovery and healing; however, shoulder calcific tendinitis can be a recurring condition, which is a major clinical concern. In addition, despite treatment, pain and upper-arm disability are still a concern in many patients, reducing their quality of life.

This evidence-based narrative review aims to revisit the basis of the pathogenesis, diagnosis and treatment of calcific tendinitis affecting the shoulder rotator cuff, based on the most recent scientific literature. This will provide an update on the understanding of the pathogenesis of calcific tendinitis and the available therapeutic strategies.

 

Pathogenesis and natural history

Various authors have tried to explain the pathogenesis of calcium deposits; however, controversy still exists. Possible causes include degeneration due to overuse2, local tendon seat ischaemia (17), tenocytes necrosis due to apoptosis (18), and degenerative processes that involve necrotic changes in the tendon fibres that can progress into dystrophic calcification (19).

Analysing the anatomical and pathophysiological features of calcific tendinitis, literature reports the calcification within a viable and well vascularised rotator cuff tendon. It occurs within the structure of the rotator cuff, 1 to 2 cm proximal to its insertion.

Classically, the condition will end by spontaneous resolution, and it is uncommon to see other signs of degenerative changes (20). Discriminating between dystrophic calcification (calcification within a non-viable and poorly vascularized rotator cuff) and calcific tendinitis deposit (the deposition of calcium hydroxyapatite crystals within a pathologically healthy tendon (21) is of paramount importance. Unlike the calcification seen in degenerative tendinopathy, which is composed of a heterogenous mixture of calcium salts diffusely scattered throughout the tendon in areas of collagen degeneration or tear [add: 1a],  CT calcification (hydroxyapatite crystals) presents as a focal deposit in the ‘critical zone’ (1-2 cm from the insertion of a tendon) (22), “where there is thought to be high shear and stress forces that initiate the development of a focal calcific deposit between healthy collagen fibers” (21). CT typically involves the formation of a single foci of calcium hydroxyapatite crystals embedded between grossly healthy fibrils of collagen. On the other hand, degenerative tendinopathy results in the breakdown of type I collagen and subsequent diffuse intratendinous calcification (23).

In light of the aforementioned consideration, the prevalent theory for the development of CT is that of ‘failed cell-mediated healing’10, whereby repetitive microtrauma and excessive loading conditions trigger a non-physiological healing response and induce focal calcification formation. Previous authors described the progression of shoulder calcific tendinitis to follow distinct pathological stages correlated with disease presentation along with clinical features (22, 24). At first, the pre-calcific stage is characterised by the fibrocartilaginous metaplasia of tenocytes into chondrocytes inside the tendon, predisposition to an evolving situation. This stage is generally asymptomatic, and the patient does not realise that calcification may develop. The following calcific stage is subdivided into three phases: formative, resting, and reabsorption.

In the formative phase, a chronic process resulting from transient hypoxia that is commonly associated with repeated microtrauma responsible for inducing metaplasia into chondrocytes, the deposits develop into bone foci that later coalesce, typically with a chalk-like appearance (22, 24).

Incorrect differentiation of stem cells (TDSCs: tendon-derived stem cells), into osteoblasts or chondrocytes, could be the basis of calcification and the fibrocartilaginous transformation of tendon tissue (25). Once the calcification has formed, the patient enters into the painless resting phase that may last for a varied length of time before the resorption process starts.

During the resorptive phase, the acute inflammatory reaction to the calcific deposits is mediated through macrophages and multinucleated giant cells migration in the tendon, which infiltrate and phagocytose the calcific deposits, and vascularised tissue develops at the calcification periphery (26). This results in rising intratendinous pressure, consequent mechanical secondary impingement due to tendon size increase, and the onset of symptomatology.

The calcification at this phase resembles the consistency of toothpaste and can leak into nearby bursae, bone, or muscle, causing severe pain. Patients complain of symptoms progressing from diffuse pain to focal impingement, and finally, severe localized pain prior to resolution.

The last post-calcific/reparative/healing phase consists of reabsorption of the deposit and remodelling of the previously occupied space. Thus, calcium is substituted by type-II collagen and subsequently replaced within 12 to 16 months by Type I collagen, resulting in tendon restoration of both normal collagen pattern and architecture, and leading to complete rotator cuff tendon healing (27, 28).

 

Clinical presentation and natural history

The clinical manifestation of CT is highly variable. It can be asymptomatic, discovered serendipitously by X-rays, or progress from diffuse pain to focal impingement and finally severe localised, acute, disabling pain, prior to resolution. Furthermore, a clinical picture involving concomitant stiffness giving rise to a frozen shoulder can also be seen. The unpredictable clinical presentation was demonstrated to depend on both disease stage (at any stage patients may not display any symptoms), as well as the anatomic location in the shoulder (6, 7).

For this reason, clinical correlation with radiographic imaging findings is critical to ensure an accurate diagnosis by discriminating between the symptoms arising from severe acute inflammatory response and mechanical long-lasting impingement due to large calcific deposits, responsible for associated loss of shoulder range of motion.

Given that, the natural history of the disease can be divided in the three distinct clinical stages of acute, subacute, and chronic, despite the fact that symptomatology may vary significantly from patients who are completely asymptomatic to those presenting with acute, debilitating pain, which may or may not be associated with acute or gradual restriction of movements (29).

Clinical presentation, characterising the formative stage, consists of subacute, low-grade, general pain that may be more pronounced or noticeable at night or, with increased pressure in the area, provoked by shoulder movements, without localizable or specific findings (30).

Most patients progress into the resting stage after 3-6 months. However, remarkably, and inexplicably, the chronic formative phase may persist for months to years unless treated in about 10% of the patients (9, 15).

Symptoms become more mechanical in the resting phase, as stabilization of CT develops into a single calcified mass, causing secondary shoulder impingement and altering the intrinsic tendon’s elasticity. Consequently, patients may complain of snapping, clicking, or catching sensations, with localized pain in the joint (24, 31).

Although the deposits could be asymptomatic in about 20% of cases without symptoms at previous stages, classically, the resorptive stage is the most painful (11, 30, 32).

The pain may present acutely, accompanied by severe muscle spasms. Inflammation in nearby structures (subacromial bursa and long head of the biceps) is triggered by the extrusion of calcium and perpetrated by increased vascular flow, thus causing complications such as adhesive capsulitis, rotator cuff tear, long-head biceps pathology, and osteolysis of the greater tuberosity (33).

Even when a resorptive stage arises due to flare-ups of chronic tendinopathy, patients tend to complain of localized pain, swelling, and erythema,  associated with limited range of motion in their joints (33, 34).

During the transition from the resorptive to the last reparative stage, patients will experience diminishing signs and symptoms until normal tendon structure and joint mechanics are restored (27).

 

Conventional radiography

Conventional radiography, with standard joint-specific views,  is  the primary imaging modality used to visualize and localize calcific deposits, as well as characterize the phase of the disease.

Radiographs, “plain X-rays” in antero-posterior, outlet, and axillary view are reported to be viable to diagnose and follow-up CT, accessing the texture and morphology of deposits, identifying stages, and ruling out concomitant associated osseous abnormalities (29, 32).

Radiographic aspects of CT were the first used for classification by many authors for evaluating the deposits in terms of size and morphology, and for demonstrating that inter-observer variability is significantly high (35, 36-39).

Although there is no classification that perfectly matches the radiographic findings and clinical presentation, the morphological characteristics of the deposits correlated with the histologic stage could be described as follows: the resting phase is recognizable when observing well-circumscribed and dense deposits, while the formative phase is circumscribed with an inhomogeneous structure or poorly circumscribed with a homogeneous structure, and the resorptive phase is defined when calcium appears poorly circumscribed and is radiographically translucent (36).

 

Ultrasound

Ultrasound (US), also called sonography or diagnostic sonography, is a complementary diagnostic imaging modality of choice for CT that is extremely useful in the diagnosis and treatment of calcific tendinitis (36, 40). In fact, the use of high-resolution US has demonstrated superior ability to visualize CT at all stages and to guide therapeutic interventions (41).

Over the years, the role of US has turned from purely diagnostic to concretely operative, making sonography a therapeutic tool of paramount importance for carrying out percutaneous procedures (bursal lavage and tendon needling).

Ultrasonography is considered safe but highly operator-dependent, and in the hands of a skilful operator it can be used to easily identify the deposits’ location, size and texture, and detect associated lesions. Furthermore, US is extremely useful not only for identifying the calcification, but also for  staging the deposits, by means of correlation shadow cones, with the pathological state (42, 43). To go into further detail: CT sonographic features are characterized by hyperechoic focus within the fibular pattern of the healthy tendon, with posterior acoustic shadowing.

In the resting phase, the deposits appear hyperechoic and arc shaped, whereas in the resolving phase, they appear non arc shaped (fragmented/punctate, cystic, nodular). These appearances can also be correlated to the symptomatic and asymptomatic phases of the disease44. Some authors divided the deposits into three types: hyperechoic focus with a well-defined shadow, hyperechoic focus with a faint shadow, and hyperechoic focus with no shadow (36). Doppler examination during the reabsorption phase shows increased vascularity around the deposits due to phagocyte activity around the deposits (45).

Ultrasonographic findings associated with symptomatic CT include fragmentation, power Doppler signal, and distention or extrusion of calcium into surrounding bursal structures (36, 42). In addition, although ultrasound is most commonly utilized for CT surrounding the shoulder and distal extremities due to the superficial locations, it may still be diagnostic for deeper structures. Newer scanning techniques, including compound scanning technology and elastography, hold promise for the evaluation of CT but need more investigation before routine use (46).

 

Magnetic Resonance Imaging

Magnetic Resonance Imaging (MRI) is a useful, but not essential, imaging tool for two reasons: first, because it does not give any additional information in most of the cases (47, 48), and second, because it is difficult to visualize calcium deposit with standard MRI due to the similar signal hypointensity of calcifications compared to normal tendon, thus leading to false-negatives and missed deposits or false-positives of normal hypointense, healthy tendons (48, 49). Nevertheless, MRI is useful to rule out other local joint and soft tissue pathology that may cause similar symptoms including tendon tears, osteoarthritis, and chondral or labral injury.

Areas of increased signal intensity can be found around the deposits in T2 images, signifying oedema around the deposits in the resorptive phase. This area of increased signal intensity can be misinterpreted as a RC lesion (49, 50). The accuracy of MRI in identifying calcific deposits is around 95%, but it is more useful in cases of chronic CT which could be associated with RC tears (Fig. 2), adhesive capsulitis, and osteolysis of the great tuberosity (33, 51).

Nevertheless, clinical correlation with imaging findings is critical to ensure an accurate diagnosis, especially when the CT is associated with other conditions, like shoulder stiffness, occurring in an acute stage of the disease that should be differentiated from both primary adhesive capsulitis and secondary stiffness following RC tears. Additionally, MRI has a high specificity for tendon and ligament tears as well as cartilaginous injuries that are important to identify and may be amenable to surgical repair or addressed intraoperatively. In chronic forms associated with TO, imaging assessment can allow for the differentiation from those occurring in association with dystrophic calcification and in tumours (52).

The employment of specialty sequences, including susceptibility weighted imaging, has allowed for the improved diagnostic ability of MR in comparison with conventional radiography, respectively 98% (sensitivity ) and of 96% (specificity), for the identification of calcifications when compared with radiography, thus leading to better diagnostic performance than standard shoulder MRI protocols (53).                                           

 

Conservative treatment

Considering the natural course of the calcific tendinitis, conservative therapy focused on symptomatic relief and shoulder functional improvement is the first line option of a stepwise algorithm including anti-inflammatory medications (NSAIDs administration), physical therapy, activity modification, UGN (Ultrasound Guided Needling), and ESWT (Extra Corporeal Shock Wave Therapy) (54).

Although literature reports little evidence regarding the individual efficacy of any particular treatment, treatment can be modulated to include the following, depending upon the presence of specific negative prognostic factors in the early phase of the disease associated with high prevalence of  “failure of nonoperative therapy” (persistence of symptomatic CT of the shoulder after a minimum of 6 months of treatment):  bilateral calcific deposit, location close to the acromion, medial (subacromial) extension and large size of the calcific deposit (54).

Usually, the acute phase requires oral NSAIDs that are commonly prescribed due to their ability to provide pain relief through analgesia and a reduction in inflammation (55). Given no direct comparison studies, even topical NSAIDs, which have been demonstrated to result in lower systemic complications, are recommended. Appropriate physiotherapy can be utilized as a co-intervention to reduce pain and avoid shoulder stiffness, thus limiting NSAIDs administration and consequently reducing long-term gastrointestinal, renal, and cardiovascular side effects (55).

Physiotherapy, as reported, could be beneficial to preserve articular and tendon mobility, prevent gleno-humeral stiffness, and optimize joint mechanics, thereby decreasing dynamic tendon impingement (56, 57). Range-of-motion exercises and periscapular and rotator cuff strengthening performed in combination may restore the biomechanics of any tendon affected by CT, but there is currently not sufficient evidence to guide rehabilitation protocols (56, 58, 59).

Overall, many adjunctive conservative modalities been evaluated for the treatment of CT, such as osteopathic manipulative therapy and/or friction massage , therapeutic ultrasound, transcutaneous electrical nerve stimulation (TENS), and acetic acid iontophoresis (60-62). Although in most cases, conservative treatment is enough for resolution of symptoms, there is limited evidence to recommend one specific treatment over another (46, 63).

 

Minimally invasive treatment

Minimally invasive procedures include isolated bursal or peritendinous injections and ultrasound (US)-guided procedures (injections and barbotage or needling and lavage). US is currently accepted as guidance when performing shoulder musculoskeletal procedures (64).

As previously mentioned, calcium deposition may be extruded from the tendons cranially towards the sub-bursal space and subacromial bursa. Intrabursal penetration, causing acute microcrystalline bursitis during active resorption of calcification, does not allow the patient to perform therapeutic exercises due to excessive pain. In this sense, the use of steroid injections, despite being a debatable topic, have demonstrated to be effective in relieving pain due to subacromial impingement and bursitis, but not in stopping deposit reabsorption (65, 66).

For this reason, US-guided percutaneous aspiration of calcific tendinopathy (US-PICT) is superior to subacromial bursa injections in this setting, and when associated with US-guided barbotage (needling and lavage) of the calcific deposition, the two are the main therapeutic options in this phase (67).

In addition, a two-step procedure involving US-guided lavage of the intratendinous calcific deposit (first step to reduce intra-tendinous pressure and promote/accelerate the clearance of hydroxyapatite crystals from the rotator cuff tendons) followed by a corticosteroid injection of the subacromial bursa (second step to reduce the risk of post-procedural bursitis) would be considered the best approach for this phase of calcific tendinopathy (64).

Needling procedure effectiveness was first demonstrated using fluoroscopy (68)  and in association with lavage and needling, nowadays a common intervention in clinical practice, while performed under local anaesthesia and without requiring hospitalisation (69). This procedure is more useful in treating fluid calcifications characterising the acute phase, as showed in published a study of 121 patients with a 2-year follow-up that reported satisfactory results after 3 months (70).

A recent systematic review on UGN in CT concluded that due to the low quality of evidence, the efficacy of UGN could not be firmly established and additional randomized trials are required (71).

 

Extra corporeal shock wave therapy

ESWT is an option for the management of CT that has been used for medical treatment since the 90s, although the exact underlying mechanism of the therapeutic effect is still debated.

Regarding the direct mechanical effect, ESWT induces calcium deposit fragmentation due to the increasing pressure inside the deposit itself, while regarding its molecular effect, it seems to be related to the phagocytosis of calcium deposits induced by a neo-vascularization inflammatory response and leukocyte chemotaxis (72).  This method is based on the application of repetitive pulses over the affected shoulder, which ca be low-energy (below0.08 mJ/mm2), medium-energy (0.08-0.28 mJ/mm2) and high-energy shock waves (0.28-0.60 mJ/mm2 (73).

The shock waves can be generated through electrohydraulic, electromagnetic, or piezoelectric mechanisms and are applied tailoring the dose on the patient. It was seen that between one single dose of 0.3 mJ/mm2 and two doses of 0.2 mJ/mm2, the former dose was more effective (74), and a 0.20 mJ/mm2 dosage was found to be more effective than 0.10mJ/mm2 (75). Furthermore, literature reported a study in that was in favour of high dose therapy, though the follow-up was of only 3 months, and they did not find any significant differences in the size of deposits on X-rays (76). In a RCT where the control group was given sham treatment, the results were better in the ESWT group. The researchers also suggested other forms of treatment to patients who did not respond to ESWT after 6 months (72). Krasny et al. (59) compared ESWT alone and ESWT combined with UGN, and found that the combined treatment was more effective in relieving symptoms and that less patients in the combined treatment group required surgery (77). Daecke et al. (78), published a long-term follow-up in patients managed with ESWT which showed that 20% of overall patients required surgery and 70% of patients were treated successfully and no long-term complications were seen. Lee et al. (61) did a systematic review to find out midterm effectiveness of ESWT but due to the variability of treatment and reliability of the available studies, they were not able to conclude a particular dosage of treatment. Kim et al. (63) did a comparative study between UGN and ESWT and found better radiological and clinical outcomes in the UGN group, although both the groups showed improvement from the initial findings. As reported by literature, association with needling procedure could lead to better clinical results compared with ESWT alone (79).

 

Surgical approach

Arthroscopy is regarded as the last remaining modality in chronic cases in which conservative or less invasive approaches have failed. Once calcium deposits are arthroscopically identified by observing the “calcific bulging sign” within tendon structure, calcium removal is carried on. Literature describes different techniques regarding the type of tendon incision and the instrumentation used to remove the calcium deposit (29).

Open surgery should be considered a further option, given the fact that arthroscopic removal of deposits has been shown to give similar results as open surgery with less morbidity of the deltoid. However, surgery requires hospitalization, general anaesthesia or sedation, and quite a long rehabilitation period after treatment (80).

Some concerns arise about calcification size, as correlated deposits larger than 1 cm measured by X-ray were less susceptible to treatment with PT, corticosteroid injection, and ultrasound-guided aspiration, and were 2.8 times more likely to require surgical intervention.

One of the great advantages of surgery is that, while removing the calcification, the surgeon may also perform other procedures, such as subacromial decompression and thorough cleaning of the joint. In addition, many debatable issues regarding surgical technique are discussed: repairing versus leaving the defect created, complete versus incomplete removal of the deposits, removal of deposits versus acromioplasty only.

Ark et al. (81), published a report of 23 patients in which they suggested that complete removal of the deposits is not essential, and they did not attempt to repair the defects created following the removal of deposits. Other researchers suggested a similar approach. Jerosch et al. concluded in their study that repair is not required following removal of deposits, but they insisted on complete removal of the deposits (82-84).

On the contrary, Porcellini et al. recommended complete removal of deposits followed by repair of the defect in the tendon using simple side to side sutures or suture anchors, depending upon the size of the residual defect (85). They argued that repair gives similar results without the fear of propagation of the tear and also helps in early rehabilitation of patients. Tillander et al. (86) compared the outcome of acromioplasty in 50 patients, 25 of which had CT and another 25 which had other causes of impingement syndrome. They did not find any significant difference between the constant scores of both groups at 2 years and recommended that the deposits should be left alone. Most of the authors recommended informing patients about delayed recovery post-surgery and were of the opinion that surgical treatment should be reserved for patients not responding to conservative treatment for more than 6 months.

 

Complications in the treatment of calcific tendinitis of the shoulder

Various complications associated with calcific tendinitis were described as additional complications, such as secondary adhesive capsulitis and rotator cuff tears, both of which could occurring during the primary disease or post-surgical intervention, as well as ossifying tendinitis, which is an extremely rare condition following surgical removal of the calcium deposits87. Osteolysis of the greater tuberosity has been described as an occurrence along with calcific tendinitis of the rotator cuff (33, 88) (Fig. 3).

 

CONCLUSIONS

 

CT of the RC is a controversial pathology with several treatment modalities, depending on the stage of the disease. Although it reabsorbs spontaneously in the majority of the cases, a subset of patients displays persistent pain in their shoulder, requiring conservative or operative management. In addition, some complications such as TO, adhesive capsulitis, or ossifying tendinitis (very rare) may give rise to prolonged pain that is resistant to common conservative therapies. UGN is indicated in the acute phase, but good results have also been found in patients with chronic calcific deposits. ESWT can be used reasonably successfully in chronic calcific cases, even in combination with UGN. Surgical treatment should be considered when conservative measures have failed or in cases of US or MRI evidence of RC tears.

 

REFERENCES

 

  1. Bosworth BM. Calcium deposits in the shoulder and subacromial bursitis: a survey of 12122 shoulders. JAMA. 1941;116. doi:10.1001/jama.1941.02820220019004
  2. Codman EA. The Shoulder. Thomas Todd; 1934.
  3. Plenk HP. Calcifying tendinitis of the shoulder. Radiology. 1952;59. doi:10.1148/59.3.384
  4. Bosworth BM. Examination of the shoulder for calcium deposits. Technique of fluoroscopy and spot film roentgenography. J Bone Jt Surg. 1941;23.
  5. Welfling J, Kahn MF, Desroy M, Paolaggi JB, de Sèze S. [Calcifications of the shoulder. II. The disease of multiple tendinous calcifications]. Rev Rhum Mal Osteoartic. 1965;32(6):325-334.
  6. Darrieutort-Laffite C, Blanchard F, Le Goff B. Calcific tendonitis of the rotator cuff: From formation to resorption. Joint Bone Spine. 2018;85(6):687-692. doi:10.1016/j.jbspin.2017.10.004
  7. Sansone V, Consonni O, Maiorano E, Meroni R, Goddi A. Calcific tendinopathy of the rotator cuff: the correlation between pain and imaging features in symptomatic and asymptomatic female shoulders. Skeletal Radiol. 2016;45(1):49-55. doi:10.1007/s00256-015-2240-3
  8. DePalma AF, Kruper JS. Long term study of shoulder joints afflicted and treated for calcific tendinitis. Clin Orthop. 1961;20.
  9. Louwerens JKG, Kuijer PPFM, Sierevelt IN, et al. The Impact of Minimally Invasive Treatment for Rotator Cuff Calcific Tendinitis on Self-Reported Work Ability and Sick Leave. Arthrosc Sports Med Rehabil. 2020;2(6):e821-e827. doi:10.1016/j.asmr.2020.07.021
  10. Oliva F, Barisani D, Grasso A, Maffulli N. Gene expression analysis in calcific tendinopathy of the rotator cuff. Eur Cell Mater. 2011;21.
  11. Depalma AF, Kruper JS. Long-term study of shoulder joints afflicted with and treated for calcific tendinitis. Clin Orthop. 1961;20:61-72.
  12. Lippmann RK. Observations concerning the calcific cuff deposit. Clin Orthop. 1961;20.
  13. McLaughlin HL. Lesions of the musculotendinous cuff of the shoulder: III. Observations on the pathology, course and treatment of calcific deposits. Ann Surg. 1946;124. doi:10.1097/00000658-194608000-00020
  14. Mavrikakis ME, Drimis S, Kontoyannis DA, Rasidakis A, Moulopoulou ES, Kontoyannis S. Calcific shoulder periarthritis (tendinitis) in adult onset diabetes mellitus: a controlled study. Ann Rheum Dis. 1989;48. doi:10.1136/ard.48.3.211
  15. Harvie P, Pollard TC, Carr AJ. Calcific tendinitis: natural history and association with endocrine disorders. J Shoulder Elbow Surg. 2007;16. doi:10.1016/j.jse.2006.06.007
  16. Depalma AF, Kruper JS. Long-term study of shoulder joints afflicted with and treated for calcific tendinitis. Clin Orthop. 1961;20:61-72.
  17. Sandstrom C. Peridentinis calcarea: common disease of middle life. Its diagnosis, pathology and treatment. Am J Roentgenol. 1938;40.
  18. Mohr W, Bilger S. Basic morphologic structures of calcified tendinopathy and their significance for pathogenesis. Z Rheumatol. 1990;49.
  19. Hedberg-Oldfors C, Meyer R, Nolte K, et al. Loss of supervillin causes myopathy with myofibrillar disorganization and autophagic vacuoles. Brain. 2020;143(8):2406-2420. doi:10.1093/brain/awaa206
  20. Uhthoff HK, Sarkar K. Calcifying tendinitis. Baillière’s Clinical Rheumatology. 1989;3(3):567-581. doi:10.1016/S0950-3579(89)80009-3
  21. Riley GP, Harrall RL, Constant CR, Cawston TE, Hazleman BL. Prevalence and possible pathological significance of calcium phosphate salt accumulation in tendon matrix degeneration. Annals of the Rheumatic Diseases. 1996;55(2):109-115. doi:10.1136/ard.55.2.109
  22. Uhthoff HK, Loehr JW. Calcific Tendinopathy of the Rotator Cuff: Pathogenesis, Diagnosis, and Management. JAAOS – Journal of the American Academy of Orthopaedic Surgeons. 1997;5(4):183.
  23. Zhang Y, Johnson K, Russell RG, et al. Association of sporadic chondrocalcinosis with a -4-basepair G-to-A transition in the 5′-untranslated region of ANKH that promotes enhanced expression of ANKH protein and excess generation of extracellular inorganic pyrophosphate. Arthritis Rheum. 2005;52. doi:10.1002/art.20978
  24. Gosens T, Hofstee DJ. Calcifying tendinitis of the shoulder: Advances in imaging and management. Curr Rheumatol Rep. 2009;11(2):129-134. doi:10.1007/s11926-009-0018-0
  25. Rui YF, Lui PP, Chan LS, Chan KM, Fu SC, Li G. Does erroneous differentiation of tendon-derived stem cells contribute to the pathogenesis of calcifying tendinopathy? Chin Med J (Engl). 2011;124.
  26. Merolla G, Bhat MG, Paladini P, Porcellini G. Complications of calcific tendinitis of the shoulder: a concise review. J Orthopaed Traumatol. 2015;16(3):175-183. doi:10.1007/s10195-015-0339-x
  27. Fouda MB, Thankam FG, Dilisio MF, Agrawal DK. Alterations in tendon microenvironment in response to mechanical load: potential molecular targets for treatment strategies. Am J Transl Res. 2017;9(10):4341-4360.
  28. Uhthoff H, Sarkar K, Maynard J. Calcifying tendinitis: a new concept of its pathogenesis. Clin Orthop Relat Res. 1976;118.
  29. McKendry RJ, Uhthoff HK, Sarkar K, Hyslop PS. Calcifying tendinitis of the shoulder: prognostic value of clinical, histologic, and radiologic features in 57 surgically treated cases. J Rheumatol. 1982;9.
  30. de Witte PB, van Adrichem RA, Selten JW, Nagels J, Reijnierse M, Nelissen RGHH. Radiological and clinical predictors of long-term outcome in rotator cuff calcific tendinitis. Eur Radiol. 2016;26(10):3401-3411. doi:10.1007/s00330-016-4224-7
  31. Mole´ D, Kempf JF, Gleyze P, Rio B, Bonnomet F, Walch G. Results of endoscopic treatment of non-broken tendinopathies of the rotator cuff. Calcifications of the rotator cuff [in French]. Rev Chir Orthop. 1993;79.
  32. Siegal DS, Wu JS, Newman JS, del Cura JL, Hochman MG. Calcific Tendinitis: A Pictorial Review. Can Assoc Radiol J. 2009;60(5):263-272. doi:10.1016/j.carj.2009.06.008
  33. Porcellini G, Paladini P, Campi F, Pegreffi F. Osteolytic lesion of greater tuberosity in calcific tendinitis of the shoulder. Journal of Shoulder and Elbow Surgery. 2009;18(2):210-215. doi:10.1016/j.jse.2008.09.016
  34. Flemming DJ, Murphey MD, Shekitka KM, Temple HT, Jelinek JJ, Kransdorf MJ. Osseous Involvement in Calcific Tendinitis: A Retrospective Review of 50 Cases. American Journal of Roentgenology. 2003;181(4):965-972. doi:10.2214/ajr.181.4.1810965
  35. Uhthoff HK, Loehr JW. Calcific tendinopathy of the rotator cuff: pathogenesis, diagnosis, and management. J Am Acad Orthop Surg. 1997;5. doi:10.5435/00124635-199707000-00001
  36. Farin PU. Consistency of rotator-cuff calcifications. Observations on plain radiography, sonography, computed tomography, and at needle treatment. Invest Radiol. 1996;31. doi:10.1097/00004424-199605000-00010
  37. Gartner J, Simons B. Analysis of calcific deposits in calcifying tendinitis. Clin Orthop. 1990;254.
  38. Maier M, Schmidt-Ramsin J, Glaser C, Kunz A, Küchenhoff H, Tischer T. Intra- and interobserver reliability of classification scores in calcific tendinitis using plain radiographs and CT scans. Acta Orthop Belg. 2008;74.
  39. Gartner J, Heyer A. Calcific tendinitis of the shoulder. Orthopäde. 1995;24.
  40. Papatheodorou A, Ellinas P, Takis F, Tsanis A, Maris I, Batakis N. US of the shoulder: rotator cuff and non-rotator cuff disorders. Radiographics. 2006;26. doi:10.1148/rg.e23
  41. Erickson JL, Jagim AR. Ultrasonic tenotomy and debridement for calcific tendinopathy of the shoulder: a pilot case series. J Prim Care Community Health. 2020;11. https://doi.org/10.1177/2150132720964665New case series showing ultrasonic tenotomy and debridement may be effective for CT and needs further study.
  42. Chiou HJ, Chou YH, Wu JJ, Hsu CC, Huang DY, Chang CY. Evaluation of calcific tendonitis of the rotator cuff: role of color Doppler ultrasonography. J Ultrasound Med. 2002;21.
  43. Chianca V, Albano D, Messina C. Rotator cuff calcific tendinopathy: from diagnosis to treatment. Acta Biomed. 2018;89. doi:10.23750/abm.v89i1-S.7022
  44. Le Goff B, Berthelot JM, Guillot P, Glémarec J, Maugars Y. Assessment of calcific tendonitis of rotator cuff by ultrasonography: Comparison between symptomatic and asymptomatic shoulders. Joint Bone Spine. 2010;77(3):258-263. doi:10.1016/j.jbspin.2010.01.012
  45. Chiou HJ, Chou YH, Wu JJ, Hsu CC, Huang DY, Chang CY. Evaluation of calcific tendonitis of the rotator cuff: role of color Doppler ultrasonography. J Ultrasound Med. 2002;21.
  46. Chiou HJ, Chou YH, Wu JJ, et al. The role of high resolution ultrasonography in management of calcific tendonitis of the rotator cuff. Ultrasound Med Biol. 2001;27. doi:10.1016/S0301-5629(01)00353-2
  47. Loew M, Sabo D, Wehrle M, Mau H. Relationship between calcifying tendinitis and subacromial impingement: a prospective radiography and magnetic resonance imaging study. J Shoulder Elbow Surg. 1996;5. doi:10.1016/S1058-2746(96)80059-0
  48. Zubler C, Mengiardi B, Schmid MR, Hodler J, Jost B, Pfirrmann CWA. MR arthrography in calcific tendinitis of the shoulder: diagnostic performance and pitfalls. Eur Radiol. 2007;17(6):1603-1610. doi:10.1007/s00330-006-0428-6
  49. Bachmann GF, Melzer CH, Heinrics CM, Möhring B, Rominger MB. Diagnosis of rotator cuff lesions: comparison of US and MRI on 38 joint specimens. Eur Radiol. 1997;7. doi:10.1007/s003300050133
  50. Rutten MJ, Jager GJ, Blickman JG. From the RSNA refresher courses: US of the rotator cuff: pitfalls, limitations and artifacts. Radiographics. 2006;26. doi:10.1148/rg.262045719
  51. Maier M, Schmidt-Ramsin J, Glaser C, Kunz A, Küchenhoff H, Tischer T. Intra- and interobserver reliability of classification scores in calcific tendinitis using plain radiographs and CT scans. Acta Orthop Belg. 2008;74.
  52. Brown KE, Stickler L. Shoulder pain and dysfunction secondary to neural injury. Int J Sports Phys Ther. 2011;6(3):224-233.
  53. Bachmann GF, Melzer CH, Heinrics CM, Möhring B, Rominger MB. Diagnosis of rotator cuff lesions: comparison of US and MRI on 38 joint specimens. Eur Radiol. 1997;7. doi:10.1007/s003300050133
  54. Ogon P, Suedkamp NP, Jaeger M, Izadpanah K, Koestler W, Maier D. Prognostic factors in nonoperative therapy for chronic symptomatic calcific tendinitis of the shoulder. Arthritis Rheum. 2009;60. doi:10.1002/art.24845
  55. Zheng XQ, Li K, Wei YD, Tie HT, Yi XY, Huang W. Nonsteroidal Anti-Inflammatory Drugs Versus Corticosteroid for Treatment of Shoulder Pain: A Systematic Review and Meta-Analysis. Archives of Physical Medicine and Rehabilitation. 2014;95(10):1824-1831. doi:10.1016/j.apmr.2014.04.024
  56. Abdulla SY, Southerst D, Côté P, et al. Is exercise effective for the management of subacromial impingement syndrome and other soft tissue injuries of the shoulder? A systematic review by the Ontario Protocol for Traffic Injury Management (OPTIMa) Collaboration. Manual Therapy. 2015;20(5):646-656. doi:10.1016/j.math.2015.03.013
  57. Ahmed S, Khattab S, Haddad C, Babineau J, Furlan A, Kumbhare D. Effect of aerobic exercise in the treatment of myofascial pain: a systematic review. J Exerc Rehabil. 2018;14(6):902-910. doi:10.12965/jer.1836406.205
  58. Dilek B, Gulbahar S, Gundogdu M, et al. Efficacy of Proprioceptive Exercises in Patients with Subacromial Impingement Syndrome. American Journal of Physical Medicine & Rehabilitation. 2016;95(3):169-182. doi:https://doi.org/10.1097/phm.0000000000000327
  59. Calamita SAP, Biasotto-Gonzalez DA, De Melo NC, et al. Evaluation of the immediate effect of acupuncture on pain, cervical range of motion and electromyographic activity of the upper trapezius muscle in patients with nonspecific neck pain: study protocol for a randomized controlled trial. Trials. 2015;16:100. doi:10.1186/s13063-015-0623-3
  60. Pfefer MT, Cooper SR, Uhl NL. Chiropractic Management of Tendinopathy: A Literature Synthesis. Journal of Manipulative & Physiological Therapeutics. 2009;32(1):41-52. doi:10.1016/j.jmpt.2008.09.014
  61. Leduc BE, Caya J, Tremblay S, Bureau NJ, Dumont M. Treatment of calcifying tendinitis of the shoulder by acetic acid iontophoresis: a double-blind randomized controlled trial. Arch Phys Med Rehabil. 2003;84. doi:10.1016/S0003-9993(03)00284-3
  62. Perron M, Malouin F. Acetic acid lontophoresis and ultrasound for the treatment of calcifying tendinitis of the shoulder: A randomized control trial. Archives of Physical Medicine and Rehabilitation. 1997;78(4):379-384. doi:10.1016/S0003-9993(97)90229-X
  63. Lee KW, Kim WH. Effect of thoracic manipulation and deep craniocervical flexor training on pain, mobility, strength, and disability of the neck of patients with chronic nonspecific neck pain: a randomized clinical trial. J Phys Ther Sci. 2016;28(1):175-180. doi:10.1589/jpts.28.175
  64. Ricci V, Mezian K, Chang KV, Özçakar L. Clinical/Sonographic Assessment and Management of Calcific Tendinopathy of the Shoulder: A Narrative Review. Diagnostics (Basel). 2022;12(12):3097. doi:10.3390/diagnostics12123097
  65. Orlandi D, Mauri G, Lacelli F, Corazza A, Messina C, Silvestri E, et al. Rotator cuff calcific tendinopathy: randomized comparison of US-guided percutaneous treatments by using one or two needles. Radiology. 2017;285:518–27. https://doi.org/10.1148/radiol.2017162888Trial showing similar outcomes of one versus two-needle UGPL techniques with trend towards more subacromial bursitis in one-needle group.
  66. Darrieutort-Laffite C, Varin S, Coiffier G, et al. Are corticosteroid injections needed after needling and lavage of calcific tendinitis? Randomised, double-blind, non-inferiority trial. Ann Rheum Dis. 2019;78(6):837-843. doi:10.1136/annrheumdis-2018-214971
  67. Jo H, Kim G, Baek S. Calcific tendinopathy of the gluteus medius mimicking lumbar radicular pain successfully treated with barbotage: a case report. Ann Rehabil Med. 2016;40.
  68. Comfort TH, Arafiles R. Barbotage of the shoulder with image-intensified fluoroscopic control of needle placement for calcified tendinitis. Clin Orthop Relat Res. 1978;135.
  69. Castillo-González FD, Ramos-Álvarez JJ, Rodríguez-Fabián G, González-Pérez J, Calderón-Montero J. Treatment of the calcific tendinopathy of the rotator cuff by ultrasound-guided percutaneous needle lavage. Two years prospective study. Muscles Ligaments Tendons J. 2014;4.
  70. Moya D, Gómez D, Velóz Serrano D, Bernáldez Domínguez P, Dallo Lazzarini I, Gómez G. Treatment Protocol for Rotator Cuff Calcific Tendinitis Using a Single-Crystal Piezoelectric Focused Shock Wave Source. J Vis Exp. 2022;(190). doi:10.3791/64426
  71. Vignesh KN, McDowall A, Simunovic N, Bhandari M, Choudur HN. Efficacy of ultrasound-guided percutaneous needle treatment of calcific tendinitis. AJR Am J Roentgenol. 2015;204. doi:10.2214/AJR.13.11935
  72. Hsu CJ, Wang DY, Tseng KF, Fong YC, Hsu HC, Jim YF. Extracorporeal shock wave therapy for calcifying tendinitis of the shoulder. J Shoulder Elbow Surg Br. 2008;17. doi:10.1016/j.jse.2007.03.023
  73. Rompe JD, Kirkpatrick CJ, Kullmer K, Schwitalle M, Krischek O. Dose-related effects of shock waves on rabbit tendo Achillis: a sonographic and histological study. J Bone Jt Surg Br. 1998;80. doi:10.1302/0301-620X.80B3.8434
  74. Farr S, Sevelda F, Mader P, Graf A, Petje G, Sabeti-Aschraf M. Extracorporeal shockwave therapy in calcifying tendinitis of the shoulder. Knee Surg Sports Traumatol Arthrosc. 2011;19(12):2085-2089. doi:10.1007/s00167-011-1479-z
  75. Ioppolo F, Tattoli M, Di Sante L, et al. Extracorporeal Shock-Wave Therapy for Supraspinatus Calcifying Tendinitis: A Randomized Clinical Trial Comparing Two Different Energy Levels. Physical Therapy. 2012;92(11):1376-1385. doi:10.2522/ptj.20110252
  76. Saggini R, Di Stefano A, Saggini A, Bellomo RG. CLINICAL APPLICATION OF SHOCK WAVE THERAPY IN MUSCULOSKELETAL DISORDERS: PART I. J Biol Regul Homeost Agents. 2015;29(3):533-545.
  77. Krasny C, Enenkel M, Aigner N, Wlk M, Landsiedl F. Ultrasound-guided needling combined with shock-wave therapy for the treatment of calcifying tendonitis of the shoulder. J Bone Jt Surg Br. 2005;87. doi:10.1302/0301-620X.87B4.15769
  78. Daecke W, Kusnierczak D, Loew M. Long-term effects of extracorporeal shockwave therapy in chronic calcific tendinitis of the shoulder. J Shoulder Elbow Surg. 2002;11. doi:10.1067/mse.2002.126614
  79. Anwar N, Li S, Long L, et al. Combined effectiveness of extracorporeal radial shockwave therapy and ultrasound-guided trigger point injection of lidocaine in upper trapezius myofascial pain syndrome. Am J Transl Res. 2022;14(1):182-196.
  80. Rubenthaler F, Ludwig J, Wiese M, Wittenberg RH. Prospective randomized surgical treatments for calcifying tendinopathy. Clin Orthop Relat Res. 2003;410. doi:10.1097/01.blo.0000063786.32430.22
  81. Ark JW, Flock TJ, Flatow EL, Bigliani LU. Arthroscopic treatment of calcific tendinitis of the shoulder. Arthroscopy. 1992;8. doi:10.1016/0749-8063(92)90034-9
  82. Seil R, Litzenburger H, Kohn D, Rupp S. Arthroscopic treatment of chronically painful calcifying tendinitis of the supraspinatus tendon. Arthrosc – J Arthrosc Relat Surg. 2006;22. doi:10.1016/j.arthro.2006.01.012
  83. Balke M, Bielefeld R, Schmidt C, Dedy N, Liem D. Calcifying tendinitis of the shoulder: midterm results after arthroscopic treatment. Am J Sports Med. 2012;40. doi:10.1177/0363546511430202
  84. Jerosch J, Strauss JM, Schmiel S. Arthroscopic treatment of calcific tendinitis of the shoulder. J Shoulder Elbow Surg. 1998;7. doi:10.1016/S1058-2746(98)90180-X
  85. Porcellini G, Paladini P, Campi F, Paganelli M. Arthroscopic treatment of calcifying tendinitis of the shoulder: clinical and ultrasonographic follow-up findings at two to five years. J Shoulder Elbow Surg. 2004;13. doi:10.1016/j.jse. 2004.04.001
  86. Tillander BM, Norlin RO. Change of calcifications after arthroscopic subacromial decompression. J Shoulder Elbow Surg. 1998;7. doi:10.1016/S1058-2746(98)90047-7
  87. Merolla G, Bhat MG, Paladini P, Porcellini G. Complications of calcific tendinitis of the shoulder: a concise review. J Orthopaed Traumatol. 2015;16(3):175-183. doi:10.1007/s10195-015-0339-x
  88. Cocco G, Ricci V, Boccatonda A, Iannetti G, Schiavone C. Migration of calcium deposit over the biceps brachii muscle, a rare complication of calcific tendinopathy: ultrasound image and treatment. J Ultrasound. 2018;21. doi:10.1007/s40477-018-0336-z

 

Tags: