Calcium Hydroxyapatite Crystal Deposition Research Articles

Imaging of calcific tendinopathy: natural history, migration patterns, pitfalls, and management: a review.

Calcific tendinopathy is characterized by the deposition of calcium hydroxyapatite crystals in various tendons of the body. Terms like calcium tendinitis, tendinosis, and tendinopathy are used interchangeably. Calcific tendinopathy is a common and well-documented ailment in the literature. Although common, the natural history, aetiology, and progression of calcific tendinitis are poorly understood. The treatment options include conservative and interventional measures. However, these measures cannot be applied as a blanket and are often tailored depending on the stage/phase of the disease. Out of the recognized stages of the disease, the resorptive stage causes the utmost symptoms when the calcium is rather soft and unstable. During this stage, the calcium may migrate beyond expected resorption and get deposited in the adjacent tissues contiguous with the calcium focus. The common destinations include bursal migration, intraosseous migration, muscular migration, and other less common migration sites. Such atypical presentations can lead to dilemmas in the diagnosis, prolongation of the diagnostic pathway, unwarranted apprehension, and treatment delay. Radiologists' role in this situation is to correctly recognize the imaging findings of atypical presentations of calcific tendinopathy and prevent unnecessary diagnostic and interventional studies. In this review article, we describe the pathogenic pathway and natural history of calcific tendinopathy from a radiologist's perspective and discuss different migratory patterns of calcium in calcific tendinopathy not only around the shoulder but also in other areas of the body on different imaging modalities. We also show a few examples of mimics and pitfalls on imaging. Finally, we discuss the appropriate management option of this condition.

An Unusual Cause of Fever, Neck Pain, and Neck Stiffness: Acute Calcific Tendinitis of the Longus Colli Muscle

BackgroundAcute calcific tendinitis (ACT) of the longus colli muscle (LCM) is an inflammatory response due to deposition of calcium hydroxyapatite crystals. It is typically correlated with whiplash and overuse injuries. A common presentation of this inflammatory response is acute but progressive neck pain. It is a rare but important cause of neck pain that should be considered on a differential diagnosis when distinguishing between life-threatening conditions and non–life-threatening causes of neck pain. Case ReportA 51-year-old woman presented to the emergency department (ED) reporting a mild sore throat that progressed to acute neck pain and stiffness. She also reported fatigue, fever, myalgias, and nausea. In the ED, the patient was tachycardic, hypertensive, and mildly febrile with normal oxygen saturation. Examination revealed meningismus and was negative for lymphadenopathy, oropharyngeal findings, and neurologic deficits. Laboratory studies were significant for leukocytosis. Computed tomography (CT) neck was obtained and was notable for calcification of the superior left longus colli muscle with prevertebral and retropharyngeal space edema along the muscle body. Why Should an Emergency Physician Be Aware of This?ACT of the LCM is a benign, self-limited condition that can present with features overlapping emergent causes of acute neck pain. Correct diagnosis relies on characteristic radiographic findings on CT. Fortunately, patients may be discharged home with a short course of anti-inflammatories and corticosteroids with near-complete resolution of symptoms. Emergency physicians, therefore, can rule out life-threatening causes of neck pain, while also making a definitive diagnosis and initiating effective management for this pathology.

All that illuminates on radionuclide imaging is not a metastatic lesion: Role of complementary imaging

Radionuclide imaging is a non-invasive modality based on tracer physiology widely utilized in the diagnosis, staging, therapeutic evaluation, and monitoring of metastatic disease in a spectrum of malignancies. Calcific tendinopathy is a well-recognized disorder related to the deposition of calcium hydroxyapatite crystals within tendons. We describe a patient with urothelial carcinoma of the bladder revealing increased uptake at the left hip on 99mTc labeled methylene diphosphonate scintigraphy suggesting a metastatic lesion. Cross-sectional imaging with magnetic resonance imaging confirmed the accurate diagnosis of calcific tendinopathy of gluteus maximus insertion. This case report highlights the importance of a thorough clinical evaluation and complementary imaging in assessing benign pathologies which may mimic metastatic bone lesions.

Dördüncü ve Beşinci Parmak Metakarpofalangeal Eklemde Kalsiyum Depolanması

Acute calcium deposition disease is characterized by calcium hydroxyapatite crystal deposition within tendons and surrounding tissue of joints. It can manifest acute or chronic. It’s most common symptom is pain in affected area. Two patients applied to our outpatient clinic with complaints of hand pain. Calcific masses were detected by radiological imaging. After radiological imaging and laboratory examinations the patients diagnosed acute calcium deposition disease. One of the patients had ongoing symptoms for 2 years, the other one had ongoing symptoms for 3 years. Both of the patients had tried conservative treatment multiple times. These patients were treated surgically because of long-standing symptoms. Although acute calcium deposition disease usually resolves spontaneously with conservative treatment, patients with recurrent or persistent lesions can be treated surgically.

Acute calcific tendinitis of the FCR tendon in a 24-year-old male: A case report

Acute calcific tendinitis is an acute or chronic condition that typically affects the shoulder joint in patients 40 and older. Specifically caused by the deposition of calcium hydroxyapatite crystals in or around the tendon sheath, the cause is typically unknown but seems to be unrelated to underlying metabolic disturbances and pathologies. In this work, the case of left wrist pain in a 24-year-old male that was initially misdiagnosed but later identified as acute calcific tendinitis is highlighted.

Imaging of calcific tendinopathy in atypical sites by ultrasound and conventional radiography: A pictorial essay.

Calcific tendinopathy (CT) is a very common condition caused by the deposition of calcium hydroxyapatite crystals in tendons and it can be an incidental finding or associated with severe pain. CT can be easily detected by first level exams such as traditional radiography and ultrasound (US), which provide information on the site, extent and composition of the calcific formation. Classically, the most affected site is represented by the rotator cuff tendons, in particular the supraspinatus tendon. In this pictorial essay we illustrate various unusual localizations of CT detected by US and plain radiography, in order to provide an overview with the aim of preventing diagnostic delays and consequently CT complications.

Abstract 291: Phosphodiesterase 10A Regulates Medial Artery Calcification

Vascular calcification results from deposition of calcium hydroxyapatite crystals in the vessel wall. It is highly prevalent in patients with chronic kidney disease (CKD), diabetes, and peripheral artery disease (PAD). In lower extremity arteries, elevated calcification levels are associated with an increased risk of ischemic events including amputation. The cyclic nucleotides cAMP and cGMP, controlled by distinct cyclic nucleotide phosphodiesterase (PDE) isozymes, play important regulatory roles in a variety of human diseases. Using a qPCR PDE array, we found that PDE10A was the most highly induced isoform in a rodent model of arterial calcification. PDE10A was also markedly increased in calcifying vascular smooth muscle cells (VSMCs) in vitro , calcified arteries from rodents with CKD, and calcified human tibial arteries. Knockdown or inhibition of PDE10A markedly attenuated high phosphate-induced VSMC osteogenic transformation and calcification in both rat and human VSMCs. Importantly, deficiency of PDE10A significantly decreased arterial calcification in both ex vivo aortic ring and in vivo vitamin D 3 medial calcification models. Several labs including our own have previously demonstrated that matrix metallopeptidases (MMPs) are involved in vascular calcification. Using a loss-of-function strategy and bioinformatics analysis, we found that MMP-3 expression was regulated by PDE10A in calcifying VSMCs. Our further mechanistic studies showed that PDE10A could regulate vascular calcification by controlling p38 MAPK signaling and MMP-3 activity through cGMP/PKG signaling. These findings suggest that PDE10A plays a critical role in the development of medial artery calcification, and that targeting it may provide a novel therapeutic strategy to reduce medial calcification in patients with PAD and CKD with the ultimate goal of preventing major limb amputation.

Clinical evaluation and management of calcific tendinopathy: an evidence-based review

Calcific tendinopathy (CT) is an important musculoskeletal condition most commonly seen in the shoulder girdle, accounting for 10-42% of all shoulder pain. Despite the high prevalence within the shoulder region, CT has been demonstrated in many tendons throughout the axial and appendicular skeleton. Unlike degenerative tendinopathies, CT appears to be a self-limiting condition that affects otherwise-healthy tendon with deposition of calcium hydroxyapatite crystals between healthy tenocytes. In patients with functionally limiting symptoms or pain, the clinical course may be accelerated through a multitude of treatments including physical therapy and pain management, extracorporeal shock wave therapy, ultrasound-guided percutaneous lavage (UGPL), and operative debridement. Currently, the most efficacious and frequently utilized treatment for shoulder CT is UGPL due to its ability to effectively reduce calcium burden and pain while limiting soft-tissue damage. However, more evidence regarding the treatment and course of CT is needed before determining the most appropriate treatment at all potential sites of CT.

Recovery of limb perfusion and function after hindlimb ischemia is impaired by arterial calcification.

Medial artery calcification results from deposition of calcium hydroxyapatite crystals on elastin layers, and osteogenic changes in vascular smooth muscle cells. It is highly prevalent in patients with chronic kidney disease, diabetes, and peripheral artery disease (PAD), and when identified in lower extremity vessels, it is associated with increased amputation rates. This study aims to evaluate the effects of medial calcification on perfusion and functional recovery after hindlimb ischemia in rats. Medial artery calcification and acute limb ischemia were induced by vitamin D3 (VitD3) injection and femoral artery ligation in rats. VitD3 injection robustly induced calcification in the medial layer of femoral arteries in vivo. Laser Doppler perfusion imaging revealed that perfusion decreased and then partially recovered after hindlimb ischemia in vehicle‐injected rats. In contrast, VitD3‐injected rats showed markedly impaired recovery of perfusion following limb ischemia. Accordingly, rats with medial calcification showed worse ischemia scores and delayed functional recovery compared with controls. Immunohistochemical and histological staining did not show differences in capillary density or muscle morphology between VitD3‐ and vehicle‐injected rats at 28 days after femoral artery ligation. The evaluation of cardiac and hemodynamic parameters showed that arterial stiffness was increased while cardiac function was preserved in VitD3‐injected rats. These findings suggest that medial calcification may contribute to impaired perfusion in PAD by altering vascular compliance, however, the specific mechanisms remain poorly understood. Reducing or slowing the progression of arterial calcification in patients with PAD may improve clinical outcomes.

Therapeutics Development for Pseudoxanthoma Elasticum and Related Ectopic Mineralization Disorders: Update 2020.

Pseudoxanthoma elasticum (PXE), the prototype of heritable ectopic mineralization disorders, manifests with deposition of calcium hydroxyapatite crystals in the skin, eyes and arterial blood vessels. This autosomal recessive disorder, due to mutations in ABCC6, is usually diagnosed around the second decade of life. In the spectrum of heritable ectopic mineralization disorders are also generalized arterial calcification of infancy (GACI), with extremely severe arterial calcification diagnosed by prenatal ultrasound or perinatally, and arterial calcification due to CD73 deficiency (ACDC) manifesting with arterial and juxta-articular mineralization in the elderly; the latter disorders are caused by mutations in ENPP1 and NT5E, respectively. The unifying pathomechanistic feature in these three conditions is reduced plasma levels of inorganic pyrophosphate (PPi), a powerful endogenous inhibitor of ectopic mineralization. Several on-going attempts to develop treatments for these conditions, either with the goal to normalize PPi plasma levels or by means of preventing calcium hydroxyapatite deposition independent of PPi, are in advanced preclinical levels or in early clinical trials. This overview summarizes the prospects of treatment development for ectopic mineralization disorders, with PXE, GACI and ACDC as the target diseases, from the 2020 vantage point.

Síndrome de la apófisis odontoides coronada, una manifestación inusual de dolor cervical. Presentación de un caso

The calcium pyrophosphate dehydrate (CPPD) or hydroxyapatite (HA) crystal deposition disease can appear in any joint and the accumulation fo crystals in the cervical spine may be painful. Crowned dens syndrome is a rare clinical condition that involves crown-like calcification of the ligaments around the odontoid process. A 70-year-old man presented cervical pain, fever and a headache for over a week, therefore, a neurological condition was suspected. A CT scan revealed lentiform calcifications of the transverse ligament of the atlas. Steroid treatment and a non-steroidal anti-inflammatory diminished the symptoms. A proper clinical history and imaging studies avoid unnecessary procedures and makes it possible to include this entity as a differential diagnosis in acute cervical pain. Key words: Crystal deposition disease; acute cervical pain; crowned dens syndrome; Odontoid process

Acute calcific retropharyngeal tendinitis

A 44-year-old man with a 3-day history of limited range of motion of the bilateral shoulders, neck pain, dysphagia and mild fever presented to our emergency department. He had no...

Ultrasound Appearance of the Migration of Tendon Calcifications.

Calcific tendinopathy (CTe) is a frequent disorder related to the deposition of calcium hydroxyapatite crystals within tendons. Ultrasound has been shown to be an excellent imaging modality for the evaluation of CTe. During the resorptive phase of CTe, calcium deposits may migrate inside the tendons or in neighboring tissues and lead to local inflammation and severe pain. In this pictorial essay, we describe the ultrasound appearance of a spectrum of CTe migrations. Knowledge of the different migration patterns can help sonologists in their detection and in establishing the correct diagnosis.

A Rare Cause of Dysphagia to Consider: Calcific Tendinitis of the Longus Colli Muscle

Calcific tendinitis of the longus colli muscle is an acute inflammatory condition caused by the deposition of calcium hydroxyapatite crystals in the muscle's superior insertion point. It is a rare condition with a reported incidence of 1.31 per 100,000 person-years that most commonly presents during the third through sixth decades of life. Symptoms consist of acute neck pain characterized as stiffness with associated odynophagia; the condition is less frequently associated with dysphagia. A mild leukocytosis is typically present, which should prompt investigation to rule out other infectious etiologies first. Characteristic radiographic findings include calcifications in the superior fibers of the longus colli muscle tendons at the level of C1 or C2. This self-limiting condition usually resolves spontaneously with nonsteroidal anti-inflammatory agents. A 44-year old female patient with a medical history of gastroesophageal reflux disease, gastric ulcers, gastritis, gastric polyps, Schatzki ring, hiatal hernia, and benign thyroid nodules presented to the hospital with the complaint of progressive dysphagia to solid foods. This dysphagia developed after an isolated incident of food aspiration four weeks prior to her presentation. Three weeks after this event, she experienced persistent odynophagia with associated left-sided occipital headaches and neck pain radiating to the left ear and mastoid process. Physical examination was remarkable for decreased range of motion with neck flexion and extension, bilateral neck soft tissue tenderness to palpation, and thyromegaly. Laboratory data revealed a hemoglobin of 11.5, hematocrit of 34.8, and WBC of 11.88. An upper gastrointestinal series with barium swallow confirmed the presence of the patient's known Schatzki ring and hiatal hernia. A CT scan, MRI, and MRA of the brain was negative for acute abnormalities, however the CT scan of her neck was positive for calcified longus colli tendons just below the anterior ring of the C1 vertebrae. After an infectious etiology was ruled out, she underwent a trial of oral corticosteroids and NSAIDs that quickly improved her dysphagia and odynophagia. Though exceedingly rare, calcific tendinitis of the longus colli muscle must be considered in a differential diagnosis once the more common etiologies of acute dysphagia and odynophagia have been ruled out or do not correlate with the clinical presentation and/or patient's history. Since this patient's symptoms were progressive, persistent, and associated with a decreased range of motion in her neck along with soft tissue tenderness to palpation, her symptoms were not solely due to the presence of a Schatzki ring. These symptoms did indeed support the final diagnosis of calcific tendinitis of the longus colli muscle.

Intraosseous migration of tendinous calcifications: cortical erosions, subcortical migration and extensive intramedullary diffusion, a SIMS series.

Calcium hydroxyapatite crystal deposition is a common disorder, which sometimes causes acute pain as calcifications dissolve and migrate into adjacent soft tissue. Intraosseous calcium penetration has also been described. We illustrate the appearance of these lesions using a series of 35 cases compiled by members of the French Society of Musculoskeletal Imaging (Société d'Imagerie Musculo-Squelettique, SIMS). The first group in our series (7 cases) involved calcification-related cortical erosions of the humeral and femoral diaphyses, in particular at the pectoralis major and gluteus maximus insertions. A second group (28 cases) involved the presence of calcium material in subcortical areas. The most common site was the greater tubercle of the humerus, accompanying a calcifying tendinopathy of the supraspinatus. In addition, an extensive intramedullary diffusion of calcium deposits was observed in four of these cases, associated with cortical erosion in one case and subcortical lesions in three cases. Cortical erosions and intraosseous migration of calcifications associated with calcific tendinitis may be confused with neoplasm or infection. It is important to recognize atypical presentations of hydroxyapatite deposition to avoid unnecessary investigation or surgery.

Intra-osseous calcifying tendinitis of the infraspinatus tendon with erosion into the greater tuberosity

Calcific tendinitis is a condition characterised by the abnormal deposition of calcium hydroxyapatite crystals within the tendons of the rotator cuff. The characteristic appearance is that of acute or chronic shoulder pain combined with radiographic evidence of calcifications within the rotator cuff tendons. It is a specific disease entity which needs to be differentiated from other causes of rotator cuff calcium deposition. We present a case of calcific tendinitis with secondary erosion at the humeral insertion of the infraspinatus tendon. Conventional radiography proved unsuccessful in the initial diagnosis of the condition. Advanced modalities including both computed tomography (CT) and magnetic resonance imaging (MRI) proved to be both diagnostic and pivotal in the further management of the patient.

Rectus Femoris Tendon Calcification: Arthroscopic Excision in 6 Top Amateur Athletes.

Background:Since it was developed, hip arthroscopy has become the favored treatment for femoroacetabular impingement. Due to recent considerable improvements, the indications for this technique have been widely extended. Injuries of the rectus femoris tendon origin, after an acute phase, could result in a chronic tendinopathy with calcium hydroxyapatite crystal deposition, leading to pain and loss of function. Traditionally, this condition is addressed by local injection of anesthetic and corticosteroids or, when conservative measures fail, by open excision of the calcific lesion by an anterior approach.Purpose:To assess whether arthroscopic excision of calcification of the proximal rectus is a safe and effective treatment.Study Design:Case series; Level of evidence, 4.Methods:Outcomes were studied from 6 top amateur athletes (age range, 30-43 years; mean, 32.6 years) affected by calcification of the proximal rectus who underwent arthroscopic excision of the calcification. Patients were preoperatively assessed radiographically, and diagnosis was confirmed by a 3-dimensional computed tomography scan. To evaluate the outcome, standardized hip rating scores were used pre- and postoperatively (at 6 and 12 months): the Hip disability and Osteoarthritis Outcome Score, Oxford Hip Score, and Modified Harris Hip Score. Moreover, visual analog scales (VAS) for pain, sport activity level (SAL), and activities of daily living (ADL) were also used.Results:One year after surgery, all patients reported satisfactory outcomes, with 3 of 6 rating their return-to-sport level as high as preinjury level, and the remaining 3 with a percentage higher than 80%. Five patients ranked their ability to carry on daily activities at 100%. Statistical analysis showed significant improvement of the Oxford Hip Score, the Modified Harris Hip Score, and all 3 VAS subscales (pain, SAL, and ADL) from pre- to latest postoperative assessment (P < .05).Conclusion:Arthroscopic excision of rectus femoris tendon calcification yields satisfying results with few risks to the patient as well as rapid recovery.Clinical Relevance:The recent improvements in hip arthroscopy give the opportunity to address an increasing number of hip conditions effectively and safely, with rapid recovery for the patient. Arthroscopic excision of rectus femoris tendon calcification can be considered a feasible option, with few risks to the patient, rapid recovery, and satisfying outcomes.

The Structural Consequences of Calcium Crystal Deposition

Calcium pyrophosphate dihydrate and basic calcium phosphate (BCP) crystals are the most common calcium-containing crystals associated with rheumatic disease. Clinical manifestations of calcium crystal deposition include acute or chronic inflammatory and degenerative arthritides and certain forms of periarthritis. The intra-articular presence of BCP crystals correlates with the degree of radiographic degeneration. Calcium crystal deposition contributes directly to joint degeneration. Vascular calcification is caused by the deposition of calcium hydroxyapatite crystals in the arterial intima. These deposits may contribute to local inflammation and promote further calcification, thus aggravating the atherosclerotic process. Calcium crystal deposition results in substantial structural consequence in humans.

A Simple Technique to Restore Needle Patency During Percutaneous Lavage and Aspiration of Calcific Rotator Cuff Tendinopathy

Calcific rotator cuff tendinopathy caused by symptomatic calcium hydroxyapatite crystal deposition is a well-established cause of shoulder pain. In refractory or acutely symptomatic cases, sonographically guided percutaneous lavage and aspiration can significantly reduce pain in approximately 60%-92% of cases. Although the complication rate of sonographically guided percutaneous lavage and aspiration is apparently low, needle clogging attributable to impacted calcific debris has been described by several authors and in our experience can occur in daily practice. Traditionally, an inability to relieve the obstruction via needle repositioning or increased syringe plunger pressure has required needle removal and replacement. In this article, we outline a simple technique that can be used to restore patency of the obstructed lavage needle without necessitating needle removal and replacement.

A Case of Retropharyngeal Calcific Tendinitis in a Patient with Ankylosing Spondylitis

Retropharyngeal calcific tendinitis, also known as calcific tendinitis of the longus colli muscle, was first described by Hartley in 1964. It is caused by deposition of calcium hydroxyapatite crystals in the longus colli muscles from C1 to C3. Retropharyngeal calcific tendinitis is diagnosed radiologically by the detection of amorphous calcification and pre-vertebral soft tissue swelling. Twelve cases of retropharnygeal calcific tendinitis have been reported in the Korean literature, but no cases with ankylosing spondylitis. In this case, we report an unusual case of retropharyngeal calcific tendinitis with ankylosing spondylitis.