Tendon Calcification Research Articles

Predictive Neuromarker Patterns for Calcification Metaplasia in Early Tendon Healing.

Unsuccessful tendon healing leads to fibrosis and occasionally calcification. In these metaplastic drifts, the mouse AT preclinical injury model represents a robust experimental setting for studying tendon calcifications. Previously, calcium deposits were found in about 30% of tendons after 28 days post-injury. Although a neuromediated healing process has previously been documented, the expression patterns of NF200, NGF, NPY, GAL, and CGRP in mouse AT and their roles in metaplastic calcific repair remain to be explored. This study included a spatiotemporal analysis of these neuromarkers during the inflammatory phase (7 days p.i.) and the proliferative/early-remodelling phase (28 days p.i.). While the inflammatory phase is characterised by NF200 and CGRP upregulation, in the 28 days p.i., the non-calcified tendons (n = 16/24) showed overall NGF, NPY, GAL, and CGRP upregulation (compared to 7 days post-injury) and a return of NF200 expression to values similar to pre-injury. Presenting a different picture, in calcified tendons (n = 8), NF200 persisted at high levels, while NGF and NPY significantly increased, resulting in a higher NPY/CGRP ratio. Therefore, high levels of NF200 and imbalance between vasoconstrictive (NPY) and vasodilatory (CGRP) neuromarkers may be indicative of calcification. Tendon cells contributed to the synthesis of neuromarkers, suggesting that their neuro-autocrine/paracrine role is exerted by coordinating growth factors, cytokines, and neuropeptides. These findings offer insights into the neurobiological mechanisms of early tendon healing and identify new neuromarker profiles predictive of tendon healing outcomes.

Alkaptonuria: From Molecular Insights to a Dedicated Digital Platform.

Alkaptonuria (AKU) is a genetic disorder that affects connective tissues of several body compartments causing cartilage degeneration, tendon calcification, heart problems, and an invalidating, early-onset form of osteoarthritis. The molecular mechanisms underlying AKU involve homogentisic acid (HGA) accumulation in cells and tissues. HGA is highly reactive, able to modify several macromolecules, and activates different pathways, mostly involved in the onset and propagation of oxidative stress and inflammation, with consequences spreading from the microscopic to the macroscopic level leading to irreversible damage. Gaining a deeper understanding of AKU molecular mechanisms may provide novel possible therapeutical approaches to counteract disease progression. In this review, we first describe inflammation and oxidative stress in AKU and discuss similarities with other more common disorders. Then, we focus on HGA reactivity and AKU molecular mechanisms. We finally describe a multi-purpose digital platform, named ApreciseKUre, created to facilitate data collection, integration, and analysis of AKU-related data.

Animal models of tendon calcification: Past, present, and future.

Tendon calcification is a common clinical condition that frequently occurs as a complication after tendon injury and surgery, or as an expression of fibrodysplasia ossificans progressiva. This condition can be referred to by various names in clinical practice and literature, including tendon ossification, tendon mineralization, heterotopic ossification, and calcific tendonitis. The exact pathogenesis of tendon calcification remains uncertain, but current mainstream research suggests that calcification is mostly cell mediated. To further elucidate the pathogenesis of tendon calcification and to better simulate the overall process, selecting appropriate experimental animal models is important. Numerous animal models have been utilized in various clinical studies, each with its own set of advantages and limitations. In this review, we have discussed the advancements made in research on animal models of tendon calcification, with a focus on the selection of experimental animals, the sites of injury in these models, and the methods employed for modeling.

Exploring the Link Between Autophagy-Lysosomal Dysfunction and Early Heterotopic Ossification in Tendons.

Heterotopic ossification (HO), the pathological formation of bone within soft tissues such as tendon and muscle, is a notable complication resulting from severe injury. While soft tissue injury is necessary for HO development, the specific molecular pathology responsible for trauma-induced HO remains a mystery. The previous study detected abnormal autophagy function in the early stages of tendon HO. Nevertheless, it remains to be determined whether autophagy governs the process of HO generation. Here, trauma-induced tendon HO model is used to investigate the relationship between autophagy and tendon calcification. In the early stages of tenotomy, it is observed that autophagic flux is significantly impaired and that blocking autophagic flux promoted the development of more rampant calcification. Moreover, Gt(ROSA)26sor transgenic mouse model experiments disclosed lysosomal acid dysfunction as chief reason behind impaired autophagic flux. Stimulating V-ATPase activity reinstated both lysosomal acid functioning and autophagic flux, thereby reversing tendon HO. This present study demonstrates that autophagy-lysosomal dysfunction triggers HO in the stages of tendon injury, with potential therapeutic targeting implications for HO.

Exploring shoulder joint pain: a comparative analysis of dynamic ultrasonography and magnetic resonance imaging

BACKGROUND: To evaluate shoulder joint pain, the study concentrated on evaluating the diagnostic accuracy of ultrasonography and magnetic resonance imaging. AIM: By comparing the results from both modalities within the same patient group, the study aimed to identify potential challenges in image interpretation, underscoring the limitations of ultrasonography and magnetic resonance imaging. MATERIALS AND METHODS: Patients with shoulder joint pain were included through purposive sampling. These patients underwent ultrasonography and magnetic resonance imaging, and the results were correlated. Various shoulder pathologies, including tendon tears, bursitis, degenerative changes, calcifications, and impingement, were analyzed. RESULTS: The study comprised 35 patients who underwent ultrasonography and magnetic resonance imaging detecting pathologies such as subscapularis and supraspinatus tendon injuries, partial and full-thickness tears, peribicipital tendon fluid, subcoracoid and subacromial-subdeltoid bursitis, acromioclavicular joint degeneration, tendon calcification, and impingement. Comparative analysis showed varying sensitivities, specificities, positive predictive values, negative predictive values, and accuracy for different pathologies. CONCLUSION: Compared with ultrasonography, magnetic resonance imaging demonstrated greater sensitivity and specificity in identifying conditions causing shoulder pain. Ultrasonography’s affordability, real-time capabilities, and ability to compare results with the unaffected side make it a useful first diagnostic step for shoulder pain. Ultrasonography, although a quick and cost-effective initial diagnostic tool, has limitations, including operator dependence and lower sensitivity in certain conditions. In contrast, magnetic resonance imaging is employed as a confirming measure or in instances where diagnosis is challenging. The study emphasized the complementary roles of ultrasonography and magnetic resonance imaging in the diagnosis of shoulder joint pain, with magnetic resonance imaging as the more accurate and complete imaging modality.

Clinical and ultrasonographic evaluation of uninjured dominant shoulder in amateur rugby players vs a control group: a pilot study

BackgroundRugby is a sport involving a great number of shoulder collisions. Traumatic stress of the shoulder can weaken the static stabilizers and promote major injuries as dislocation or full-thickness tears of the rotator cuff. The goal of this study is to evaluate the clinical and ultrasonographic dominant shoulder factures in a group of amateur rugby players, with no history of shoulder injuries, and to compare them with those of a control group.Methods52 male subjects join in the study: 26 amateur rugby players and 26 subjects, which did not practice rugby or competitive sport. Clinical history was obtained from all subjects, followed by dominant shoulder physical and ultrasonographic exams.ResultsRugby players showed a higher prevalence of positive clinical test, suggesting subacromial impingement than control group (p = 0.01).Among rugby group, five players (19,2%) showed positive test for radiculopathy (p = 0,02), and ten players (73,1%) reported shoulder pain needing pain-reliever drugs at list one time in the last six months (p = 0.001). In rugby group, ultrasound exams showed 23,1% degenerative changes and 30,8% tendon calcifications in supraspinatus tendons (p < 0.05).ConclusionsUninjured dominant shoulder of rugby players shows higher prevalence of clinical and ultrasound changes compare to control. Some rugby players without history of cervical symptoms show positive clinical test of cervical radiculopathy. Clinical and ultrasonographic monitoring of the shoulder can play a role in prevention and knowledge of silent shoulder damage in these athletes.

Surgical excision of P3 fragments in 86 declawed cats: case series (2013-2023).

This case series describes the clinical findings and surgical intervention of 86 declawed cats; 52 from a shelter or rescue and 34 owned cats. Historical reports from owners and shelter staff included house-soiling, biting behavior, repelling behavior, barbering, lameness, chronic digit infection and nail regrowth. All the cats had fragments of the third phalanx (P3) of varying sizes diagnosed on radiographs. Pathology visible on examination included digital subcutaneous swelling, ecchymosis, malaligned digital pads, ulcerations, exudate, tendon contracture, nail regrowth and callusing. Surgery was pursued in these cases to remove the P3 fragments, relieve tendon contracture and reposition the digital pads with an anchoring suture. Gross findings intraoperatively included fragmented growth of cornified and non-cornified nail tissue, osteophytes on the surface of the second phalanx, deep digital flexor tendon calcification, and both bacterial and sterile exudate. The most common complication 14 days postoperatively was mild (14%) to moderate (1%) lameness. All historical parameters recorded improved in both populations of cats (house-soiling, biting behavior, repelling behavior, barbering, lameness, tendon contracture and chronic digit infection). Postoperatively, 1/47 cats exhibited continued malalignment of two digital pads and there were no reports of long-term postoperative lameness. Two methods of declawing cats are detailed in the veterinary literature, including partial amputation of P3 and disarticulation of the entire P3 bone. The novel information in this report includes historical and clinical signs of declawed cats with P3 fragments, intraoperative gross pathology, surgical intervention and the postoperative follow-up results.

Calcified apoptotic vesicles from PROCR+ fibroblasts initiate heterotopic ossification.

Heterotopic ossification (HO) comprises the abnormal formation of ectopic bone in extraskeletal soft tissue. The factors that initiate HO remain elusive. Herein, we found that calcified apoptotic vesicles (apoVs) led to increased calcification and stiffness of tendon extracellular matrix (ECM), which initiated M2 macrophage polarization and HO progression. Specifically, single-cell transcriptome analyses of different stages of HO revealed that calcified apoVs were primarily secreted by a PROCR+ fibroblast population. In addition, calcified apoVs enriched calcium by annexin channels, absorbed to collagen I via electrostatic interaction, and aggregated to produce calcifying nodules in the ECM, leading to tendon calcification and stiffening. More importantly, apoV-releasing inhibition or macrophage deletion both successfully reversed HO development. Thus, we are the first to identify calcified apoVs from PROCR+ fibroblasts as the initiating factor of HO, and might serve as the therapeutic target for inhibiting pathological calcification.

An analysis of reported cases shoulder injury related to vaccine administration of after COVID-19 vaccination.

To prevent COVID-19, the COVID-19 vaccine has been widely administered worldwide, but various complications accompany this vaccine. The aim of this study was to investigate the demographic patterns, clinical features, diagnostic findings, and treatment outcomes associated with shoulder injury related to vaccine administration (SIRVA). This study examined 22 patients with SIRVA following COVID-19 vaccination from the Web of Science (WOS) and PubMed databases. The patients were categorized based on sex, age, type of COVID-19 vaccine received, dose administered, latency of symptom onset, and the presence of specific clinical manifestations. Patients, evenly distributed by sex (12 females, 10 males), and aged 21 to 84 years (mean age 46.6), were analyzed. SIRVA cases were reported across all age groups. The Pfizer - BioNTech COVID-19 vaccine had the highest incidence (n = 8), followed by the Oxford/AstraZeneca COVID-19 vaccine (n = 4). Symptoms, primarily shoulder pain (n = 22) and shoulder mobility disorders (n = 18), occurred within three days post-vaccination. Some patients also reported shoulder swelling (n = 5) and fever (n = 2). Imaging revealed nonspecific X-ray findings, supraspinatus tendon calcification (n = 2), and shoulder edema and inflammation on MRI (n = 12). This study provides insights into the clinical aspects of SIRVA related to COVID-19 vaccination. Recognition and appropriate management of these complications are crucial for optimal patient outcomes.

Pathological calcification in canine tendon-derived cells is modulated by extracellular ATP

Tendon calcification is a commonly associated with degenerative tendinopathy of the Achilles tendons in dogs. It is characterised by the formation of calcific deposits and is refractory to treatment, often re-forming after surgical removal. Little is known about its pathogenesis and therefore the aims of this study were to develop an in vitro model of canine tendon calcification and use this model to investigate mechanisms driving calcification. Cells from the canine Achilles tendon were cultured with different calcifying media to establish which conditions were best able to induce specific, cell-mediated calcification. Once optimum calcification conditions had been established, the effect of ATP treatment on calcification was assessed. Results revealed that 2 mM di-sodium phosphate combined with 2 mM calcium chloride provided the optimum calcifying conditions, increasing calcium deposition and expression of osteogenic-related genes similar to those observed in tendon calcification in vivo. ATP treatment inhibited calcification in a dose-dependent manner, reducing calcium deposition and increasing cell viability, while osteogenic-related genes were no longer upregulated. In conclusion, the in vitro model of canine tendon calcification developed in this study provides the ability to study mechanisms driving tendon calcification, demonstrating that ATP plays a role in modulating tendon calcification that should be explored further in future studies.

Minimally invasive surgeries for insertional Achilles tendinopathy: A commentary review.

Studies of minimally invasive surgery for insertional Achilles tendinopathy are limited. To establish this surgery, the following techniques must be minimally invasive: Exostosis resection at the Achilles tendon insertion, debridement of degenerated Achilles tendon, reattachment using anchors or augmentation using flexor hallucis longus (FHL) tendon transfer, and excision of the posterosuperior calcaneal prominence. Studies on these four perspectives were reviewed to establish minimally invasive surgery for insertional Achilles tendinopathy. Techniques for exostosis resection were demonstrated in one case study, where blunt dissection around the exostosis was performed, and the exostosis was resected using an abrasion burr under fluoroscopic guidance. Techniques for debridement of degenerated Achilles tendon were demonstrated in the same case study, where the space left after resection of the exostosis was used as an endoscopic working space, and the degenerated Achilles tendon and intra-tendinous calcification were debrided endoscopically. Achilles tendon reattachment techniques using suture anchors have been demonstrated in several studies. However, there are no studies on FHL tendon transfer techniques for Achilles tendon reattachment. In contrast, endoscopic posterosuperior calcaneal prominence resection is already established. Additionally, studies on ultrasound-guided surgeries and percutaneous dorsal wedge calcaneal osteotomy as minimally invasive surgery were reviewed.

Reinsertion of the Achilles Tendon with Bony Anchor in Insertional Achilles Tendinitis with Haglund’s Deformity

Haglund’s deformity is a common cause of hindfoot pain in adults and functional disability. Conservative treatment is effective often. Surgery is required only in intractable cases. Many surgical treatments in a Haglund deformity have been described. After resect and debridement, an anchor suture may use to reattach Achille’s tendon. This study aims to show the place of the suture anchor to improve the reinsertion of the Achilles tendon in an insertional Achilles tendinitis and Haglund’s deformity. We report a 54-year-old male complains of 2 years of chronic right heel pain while strength training. A focused exam of the left ankle showed a bump on the posterior heel with inflammation to the anterior and posterior Achilles tendon. A lateral X-ray and CT scan of the left ankle showed a bone spur and intratendinous calcification of the Achilles tendon with the Philip – Fowler angle at 87°. The Bohler’s ankle was at 27°. After the failure of at least 6 months of conservative treatment, surgical management was indicated. It has consisted of a midline incision. Bursectomy and, resection of the posterosuperior tuberosity of the calcaneus was performed. Then, debridement of necrotic tissue and calcifications in the tendon and any posterior osteophytes were carried out. The tendon had been reinserted at its central part with single-row anchor. The lower leg was immobilized in 20° plantar flexion, this was switched to a walking boot with adjustable plantar flexion. Partial support was allowed at the 6th postoperative week. Full rehabilitation was prescribed after the removal of the cast. At 2-year follow-up, the patient is very satisfied and had no pain when standing on the toes of the operated leg. Dorsiflexion was symmetric. The effective return to full-sport activities was at 6 months at the same level.

Association of Haglund Deformity Size and Insertional Achilles Tendinopathy.

We aimed to investigate the effect of Haglund deformity size on insertional Achilles tendinopathy (IAT) using a new measurement system and identify independent risk factors of IAT with Haglund deformity. We reviewed medical records of patients with IAT and age/sex-matched patients with diagnoses other than Achilles tendinopathy. Radiographs were reviewed to identify posterior heel spur, plantar heel spur, and intra-Achilles tendon calcification, and to measure Fowler-Philip angle, calcaneal pitch angle, and Haglund deformity angle and height. We introduced a new measurement system for Haglund deformity angle and height and evaluated its intraobserver and interobserver reliability. Multivariate logistic regression analysis was performed to identify independent risk factors of IAT with Haglund deformity. Fifty patients (55 feet) were enrolled in the study group, equaling the size of the age/sex-matched control group. The new Haglund deformity measurement system showed excellent intraobserver and interobserver reliability. No significant differences between the 2 groups were noted in Haglund deformity angle and height: 6.0 degrees in both groups, and 3.3 mm vs 3.2 mm in the study and control group, respectively. The study group had significantly higher calcaneal pitch angle, incidence of posterior heel spur, plantar heel spur, and intra-Achilles tendon calcification: 5.2 vs 23.1 degrees (P = .044), 81.8% vs 36.4% (P < .001), 76.4% vs 34.5% (P = .003), and 67.3% vs 5.5% (P < .001), respectively. Multivariate logistic regression analysis identified independent risk factors of IAT: posterior heel spur (OR = 3.650, 95% CI = 1.063, 12.532), intra-Achilles tendon calcification (OR = 55.671, 95% CI = 11.233, 275.905), and increased calcaneal pitch angle (OR = 6.317). Based on our results, the actual size of Haglund deformity as we have reliably measured was not associated with IAT, suggesting a routine Haglund deformity resection may be unnecessary in the surgical treatment of IAT. If patients with Haglund deformity have posterior heel spur, intra-Achilles tendon calcification, or increased calcaneal pitch angle, a higher chance of IAT can be predicted. Level III, retrospective cohort study.

Structural features of the Achilles tendon in men with dyslipidemia and atherosclerosis

Highlights. A large number of studies are devoted to changes in connective tissues in persons with familial hypercholesterolemia. Studies that are focused on these changes in patients with dyslipidemia without family history of dyslipidemia are few, and most of them are based on ultrasound methods. The data presented in the article make it possible to timely assess the presence of minor changes in the Achilles tendons and thereby obtain additional information about the mechanism of lipid deposition in various tissues.Aim. To determine structural features of the Achilles tendon in men with dyslipidemia and atherosclerosis.Methods. The study included 138 men aged 45–65 years with or without atherosclerosis of the common carotid artery or the abdominal aorta and their aortic branches verified by multislice computed tomography.Results. In individuals with atherosclerosis, the frequency of calcification of the Achilles tendon was 2.5 times higher than in individuals without atherosclerosis. In individuals with carotid artery atherosclerosis, the cross-sectional area of the Achilles tendon was 1.2 times larger than in individuals with abdominal aortic atherosclerosis. In individuals with carotid artery atherosclerosis, the density of the Achilles tendon was 1.1 times higher than in individuals with abdominal aortic atherosclerosis. In individuals with carotid artery atherosclerosis, the frequency of calcification of the Achilles tendon was 2.0 times higher than in individuals with abdominal aortic atherosclerosis. An increase in the cross-sectional area of the tendon and its density, regardless of other factors, including the localization of the atherosclerosis, is directly associated with the total blood cholesterol. The presence of lipid and calcium deposition in the tendons, regardless of other factors, is directly associated with the total blood cholesterol and some of its fractions. The presence of lipid deposition in the tendons is inversely associated with the level of level of phosphate in the blood. The thickening of the tendon and the increase in its density is directly associated with the age of men.Conclusion. The study results revealed that persons with dyslipidemia and atherosclerosis present with changes in the connective tissues – in the structure of tendons, regardless of family history.

ODP137 Achilles Tendon Size and Characteristics for Diagnosis of Familial Hypercholesterolemia Among Thai Patients

Abstract Background The presence of tendon xanthomas, defined as thickening or nodularities of tendons, is subjective and remains largely undetected in patients with familial hypercholesterolemia (FH) in clinical practice. This study aimed to determine Achilles tendon thickness cutoff values associated with the highest diagnostic accuracy for identifying FH among Thai patients. Methods 63 subjects with possible, probable or definite FH according to the Dutch Lipid Clinic Network criteria, 58 subjects with hypercholesterolemia not compatible with FH and 55 normolipidemia subjects were recruited. Achilles tendon thickness was measured on each side separately at the point of maximum thickness using Lange skinfold calipers, Slim Guide skinfold calipers, plain radiograph of lateral ankles and ultrasonography. Ultrasonographic characteristics of the tendons were also recorded. The diagnostic performance of the maximum Achilles tendon thickness (maximum value of either left or right Achilles tendon of each person) obtained by each method was determined by Receiver-Operating Characteristic curves and optimal cut-points determined by Youden's index. Spearman rank-order correlation coefficient assessed factors associated with Achilles tendon thickness. Results Of all subjects, the mean age was 47 (±13) years, and 45% were male. The study groups were comparable in baseline characteristics except for a higher LDL cholesterol burden, a longer duration of lipid lowering therapy and a higher percentage of subjects receiving high intensity statins and ezetimibe in the FH group. Both types of skinfold calipers demonstrated 61% accuracy for diagnosing FH. An anteroposterior (AP) diameter on plain radiographs ≥7.7 mm had an 80% accuracy with 75% sensitivity and 82% specificity, whereas ultrasonographic thickness ≥6.4 mm. showed a 76% accuracy with 46% sensitivity and 93% specificity. Tendon border irregularities, diffuse hypoechogenicity and calcification were reported in a higher percentage of patients with FH, compared with the other 2 groups. Factors showing a significant correlation with Achilles tendon thickness in the FH group were years since FH diagnosis, a higher Dutch Lipid Clinic Network score and a higher body mass index (BMI). In the overall cohort, factors showing a significant correlation were higher LDL cholesterol burden and higher BMI. Conclusion Achilles tendon thickness measured by calipers showed low accuracy for FH diagnosis. An AP diameter on plain radiographs demonstrated highest sensitivity, whereas ultrasonographic thickness and area of Achilles tendon showed high specificity. Tendon irregularities, diffuse hypoechogenicity and calcification might serve as supportive findings. Presentation: No date and time listed

Scavenging of reactive oxygen species can adjust the differentiation of tendon stem cells and progenitor cells and prevent ectopic calcification in tendinopathy

Tendinopathy is a common disorder that leads to pain and impaired quality of life. Recent studies revealed that osteogenic differentiation of tendon stem/progenitor cells (TSPCs) played an important role in the pathogenesis of tendon calcification and tendinopathy. In this study, we found that the growth hormone-releasing hormone agonist (GA) can prevent matrix degradation and osteogenic differentiation in TSPCs. As oxidative stress is a key factor in the osteogenic differentiation of TSPCs, we used bovine serum albumin/heparin nanoparticles (BHNPs), which have biocompatibility and drug loading capacity, to scavenge reactive oxygen species (ROS) and achieve sustained release of GA at the site of inflammation. The newly developed BHNPs@GA had a synergetic effect on reducing ROS production in TSPCs. In addition, BHNPs@GA effectively inhibited tendon calcification and promoted collagen formation in a rat model of tendinopathy. Focusing on the ROS underlying the differentiation and dedifferentiation of TSPCs, this work demonstrated that sustained release of GA targeting ROS and ectopic ossification is a practical therapeutic strategy for treating tendinopathy. Statement of SignificanceOsteogenic differentiation of tendon stem/progenitor cells (TSPCs) plays an important role in the pathogenesis of ectopic calcification in tendinopathy. In this study, we found that growth hormone-releasing hormone agonist (GA) can reduce reactive oxygen species (ROS) production and adjust TSPCs differentiation. Bovine serum albumin/heparin nanoparticles (BHNPs) were developed to encapsulate GA and achieve sustained release of GA at the site of inflammation. The developed compound, BHNPs@GA, with a synergistic effect of inhibiting ROS and thus, can effectively adjust TSPCs differentiation, inhibit tendon calcification, and promote collagen formation in tendinopathy. This study highlighted the role of ROS underlying the differentiation and dedifferentiation of TSPCs in tendinopathy, and findings may help to identify new therapeutic targets and develop novel strategy for treating tendinopathy.

Whose team do you ski for? The simultaneous presence of Klippel-Feil syndrome and diffuse idiopathic hyperostosis mimics clinical presentation of advanced ankylosing spondylitis.

Introduction: Klippel-Feil syndrome (KFS) is a congenital fusion of two or more cervical vertebrae. Diffuse idiopathic hyperostosis (DISH) is a disorder in which there is calcification of ligaments and tendons, primarily of the spinal column. The simultaneous occurrence of DISH and ankylosing spondylitis (AS) has seldom been described in the literature. Coexistence of KFS and DISH clinically resembling “skier’s posture” of the advanced AS, to the best of our knowledge has never been described before in literature. Case Report: 59-years old male was examined by rheumatologist due to inflammatory back pain and prolonged morning stiffness in spinal joints. He had “skier’s posture” which could be clinical sign of advanced axial disease in AS. Functional measurements had also spoken in favor of spondyloarthropathy. Spinal joints radiography described 2nd and 3rd cervical vertebral fusion along with prominent osteophytes and dorsal spine hyperostosis. Sacroiliac joints had no inflammatory or degenerative radiographic changes. Hip joints ultrasound excluded synovitis and effusion. Conclusion: Patient has two joint diseases, resulting in severe spinal degenerative changes, together resembling clinical presentation of advanced AS.

The Prevalence of Shoulder Disorders among Professional Bullfighters: A Cross-Sectional Ultrasonography Study.

We aimed to investigate clinical and ultrasound signs of shoulder overuse injuries in professional bullfighters; side-to-side differences (dominant vs. non-dominant); and to determine potential differences according to bullfighters’ categories. An observational cross-sectional study was conducted. Thirty professional and active bullfighters were assessed. A bilateral ultrasound assessment of the subacromial bursa, long biceps head tendon (LHBT), and rotator cuff was performed to determine the presence of bursitis, subluxation, partial or total tendon rupture, tenosynovitis, or calcification. Supraspinatus tendon thickness was measured. Finally, a battery of clinical orthopedic tests (Yergason, Jobe, infraspinatus, Gerber, and bursa tests) were also performed. Most identified ultrasound findings were located in the dominant side, being the presence of bursitis (n = 9; 30%), LHBT tenosynovitis (n = 8; 26.7%), and subscapularis tendon calcification (n = 5; 16.7%) the most prevalent. No side-to-side or between-categories differences were found for supraspinatus tendon thickness (all, p > 0.05). The most frequent positive signs were the infraspinatus test (40.0%), Gerber lift-off test (33.3%), and bursitis, Jobe, and Yergason tests (all, 26.7%). Ultrasound signs were commonly found at LHBT, subacromial bursa, and rotator cuff in professional bullfighters without difference between categories and sides. No side-to-side or between-categories differences were found. Positive clinical test signs suggestive of bursitis, LHBT, and rotator cuff tendinopathy were frequently observed.

Ultrasonographic assessment of entheseal sites of upper and lower extremities in hemodialysis patients using Madrid Sonography Enthesitis Index

BackgroundThere is no much information about the entheseal involvement among hemodialysis (HD) patients. The aim of this study was to assess the frequency and distribution of ultrasonographic (US) entheseal alterations in HD patients and to evaluate the association between US abnormalities and both clinical and laboratory data.MethodsThis study was conducted on 41 HD patients and 23 sex- and age- matched controls. All participants were evaluated clinically for any signs of enthesopathy. Six entheses sites were scanned bilaterally using grey scale (GS) and power Doppler (PD) US and were scored using Madrid Sonography Enthesitis Index (MASEI) scoring system.ResultsIn HD patients, at least one clinical sign suggestive of enthesopathy was found in 69 (14%) of 492 entheses. HD patients had statistically significant higher scores of structural tendon abnormalities (p < 0.001), enthesis thickening (p < 0.001), bone erosions (p < 0.001) and calcification (p = 0.037) than the healthy controls. Total MASEI score was higher in HD patients than healthy controls (median;18 vs 8, p < 0.001), also, MASEI-inflammatory (median;11 vs 3, p < 0.001) and damage scores (median;6 vs 0, p < 0.001). There was a statistically significant positive association between total MASEI score and both age (p = 0.032) and duration of HD (p = 0.037). Duration of HD was predictive for both MASEI-damage component (p = 0.004) and total MASEI score (p = 0.014).ConclusionThere is a high prevalence of subclinical enthesopathy in HD patients. The entheseal US alterations is much higher in HD patients than in healthy subjects. The duration of HD is the significant predictor of enthesopathy in HD patients.

Efficacy of Ultrasound-Guided Percutaneous Lavage and Biocompatible Electrical Neurostimulation, in Calcific Rotator Cuff Tendinopathy and Shoulder Pain, A Prospective Pilot Study.

Calcific tendinopathy of the shoulder (CTS) is the most common cause of shoulder pain. Conservative treatment is considered as the first therapeutic choice for CTS. The main objective of this study was to assess the effect of US-guided needling (UGN) compared to UGN plus Biocompatible Electrical Neurostimulation (BEN) in the treatment of the CTS. Pilot, prospective, non-interventional, monocentric, and observational study of patients treated for calcific rotator cuff tendinopathy and shoulder pain. Patients’ selection, enrollment and interventions were conducted at the Chiparo Physical Medicine and Rehabilitation outpatient facility. Forty adult patients (aged 40–60 years) with a diagnosis of CTS in the acute and colliquative phase were recruited and enrolled into the study. Participants were assessed for self-perceived pain through the Numerical Rating Scale (NRS), and for functional limitation through the Shoulder Pain and Disability Index score (SPADI) at baseline (T0), after 15 days (T1), and after 40 days (T2). As a possible confounding factor between the two treatments’ response, the dimension of the tendon calcification was also assessed by US-examination. Through the study, both groups improved their perceived functional performance of the arm (p-value < 0.001). AT T1, the SPADI score decreased by half in both groups, and the improvement remained stable at T2. A multiplicative effect (Time × Treatment) was demonstrated (p-value < 0.001). An improvement in the NRS score was measured at T1, and it remained stable at T2, a multiplicative effect was also reported (p-value < 0.001). The main results of this pilot study provide evidence that UGN plus BEN increases functional performance and reduces shoulder pain in individuals with CTS. Moreover, the tendon calcification dimension at the baseline and the percentage of drainage of the lesion were associated with a functional performance recovery and pain reduction detected after intervention.