Gout often presents as acute arthritis but may also present with chronic joint inflammation. For the diagnosis of an acute gout attack with its typical symptoms, the differentiation towards a bacterial joint infection is critical and mandatory. The detection of intracellular uric acid crystals in the synovial fluid of affected joints is important for the initial diagnosis of gout. In the case of a chronic course with polyarticular joint involvement, the differentiation from other inflammatory rheumatic diseases such as rheumatoid arthritis (RA) can be challenging. The case presented here is of interest because the patient initially had characteristic clinical symptoms of tophaceous gout including a typical medical history—even though rheumatoid factor and anti-citrullinated protein antibodies (anti-CCP) were positive. The course of the disease and the critical evaluation of all findings also, and most interestingly, including histological results finally suggested a main diagnosis of RA.

Congenital fused/blocked vertebrae are an incidental finding in most cases. It remains asymptomatic unless there is a traumatic event or there is an increased biomechanical load which may be attributed to a task that is not typically performed by the individual. Symptomatic cases can present with several musculoskeletal symptoms including neck pain. Physiotherapy management strategies may help patients recover from the mechanical strains on the cervical neuromuscular structures. The present case is of a 21-year-old male engineering student who was referred for physiotherapy, he presented with complaints of neck pain (non-radiating in nature) for a week. The intensity of the pain had been intermittently increasing/decreasing for about a year and there were about 2–3 episodes in a month for approximately one year. He presented with an X-ray that showed C3–C4 cervical vertebrae synostosis (block vertebrae). The patient was managed using pain education and exercises along with ergonomic advice. Patient-reported pain decreased significantly from the initial visit and he was able to sit for a longer duration and had a considerable improvement in function.

Following anterior cruciate ligament (ACL) injury of the knee, the functional hop test (an averaging of 4 component hop tests including single-hop, triple-hop, cross-over-hop, and 6-meter-hop) is commonly used by sports medicine physicians, doctors of physical therapy, and athletic trainers in return-to-practice and return-to-play decision making. In this case report, the functional hop test was applied to a 31-year-old recreational basketball player status-post full-tear of the anterior talofibular ligament (ATFL) to examine the applicability of a standardized, efficient, and easy-to-administer functional test in making return-to-play decisions following an ankle injury. The functional hop test was administered 5 times across a treatment course of 11 physical therapy sessions emphasizing pain-free range of motion, baseline strength, weight-bearing loading, and sport-specific training. The functional hop test was found to be a helpful (albeit imperfect) tool for clinical decision-making following an ankle injury. Specifically, improvements in landing skill/confidence of single hop accounted for the greatest gains in total score in the early phase of rehabilitation, while momentum and plyometric skill/control of triple hop accounted for the greatest gains in total score in the later phase of rehabilitation. Modification of the functional hop test to include sub-component tests of strength, endurance, and/or lateral hops are discussed.

Hyperuricemia is known to be a necessary and causal condition for gout, but much more prevalent than gout. Medicine has standardized treatments for gout, but has no such determination for asymptomatic hyperuricemia. Nevertheless, people with hyperuricemia, gouty or not, too often continue to be at risk for shortened lifespans from life-threatening comorbidities, all of which are known to be consequences of obstructive sleep apnea (OSA), which is shown herein to cause most hyperuricemia. This review also presents the wide variety of OSA consequences, many of which are irreversible and life-threatening, as the rationale for treating all hyperuricemia (gouty and asymptomatic) by diagnostic testing and effective treatment for OSA as soon as hyperuricemia is detected. It advocates frequent ultrasonic screening for aggregated urate crystals. Multiple epidemiological studies have found OSA to be significantly more prevalent in those people with gout diagnosed with OSA than it is in those never diagnosed with it. A clinical study shows an even higher prevalence of OSA in people with gout. The pathophysiology of hypoxia from OSA explains how it would lead to both the overproduction and the underexcretion of uric acid, leading to hyperuricemia and the precipitation of monosodium urate crystals which cause a gout flare. Resolving OSA has been shown to prevent or even reverse life-threatening diseases that are recognized comorbidities of hyperuricemia and gout, and can prevent further gout flares. In order to extend the length and quality of life of people with gout or hyperuricemia, when either first manifests a patient sleep study is recommended, followed by effective OSA treatment as warranted.

Soft tissue sarcoma (STS) is a rare malignancy with a high incidence. Early diagnosis can reduce the rate of amputations and increase survival, however, this is typically delayed. The diagnosis and treatment of smaller lesions have a better prognosis; nonetheless, patients present to physicians when the soft tissue mass is large with obvious signs of red flags. In addition, the symptoms of this disease are highly non-specific and overlap greatly with benign conditions, resulting in a lack of clinical suspicion and low awareness among practitioners and the general public. Thusly, it is entitled as “the loneliest cancer”. This can make an accurate diagnosis difficult, with a great proportion of misdiagnoses leading subsequent inadvertent to incomplete STS excision, affecting the overall prognosis of the disease and devastating consequences in the disease process. A timely and precise diagnosis is essential because half of people with STS progress toward quietly aggressive illness. The purpose of this review is to raise awareness of STSs so that early recognition, accurate work-up, overview of conventional treatment plans, and appropriate referral to a tumor center can be achieved, avoiding whoop situations, and improving patient outcomes. In addition, insight into the advances in immunotherapy, nanotechnology, and artificial intelligence (AI) can lead to STS diagnosis and treatment prognosis.

Diffuse idiopathic skeletal hyperostosis (DISH) is a systemic condition characterized by the new bone formation and enthesopathies of the axial and peripheral skeleton. The diagnosis of DISH currently relies upon the end-stage radiographic criteria of Resnick and Niwayama, in which bridging osteophytes are present over at least four thoracic vertebras. The pathogenesis of DISH is not well understood, and it is currently considered a non-inflammatory condition with an underlying metabolic derangement. However, an inflammatory component was suggested due to the similarities between DISH and spondyloarthritis (SpA) in spinal and peripheral entheseal new bone formation. Magnetic resonance imaging (MRI) is the imaging modality of choice in the diagnostic work-up and follow-up of patients with SpA, as well as in understanding its pathogenesis. The aims of the current review were to evaluate the current and future role of MRI in imaging DISH.

It has been suggested that diffuse idiopathic skeletal hyperostosis (DISH), a skeletal disease characterized by the ligamentous ossification of the anterolateral spine, is a radiological entity with no clinical implications; however, many patients suffer from chronic back pain, decreased spinal mobility, and postural abnormalities. Additionally, the pathological new bone formation at the cervical and thoracic levels may mainly produce dysphagia and breathing disturbances. Over the last 20 years, a close association between DISH, obesity, diabetes mellitus (DM), and metabolic syndrome (MS) has emerged. However, a causal relationship has not yet been established. It has been suggested that the longer life expectancy and the growing incidence of MS in Western populations, associated with the tendency of DISH to manifest in later life, may increase the DISH prevalence rates in the following decades. Future investigations should focus on the early DISH phase to clarify pathogenetic mechanisms and identify targeted therapies.

Rheumatoid arthritis (RA) is a chronic immune-mediated inflammatory disease of unknown origin. Although it mainly affects joints, it can have extra-articular manifestations, with the lung being one of the most affected organs. The estimated incidence of diffuse interstitial lung disease (ILD) is 4 cases to 4.5 cases/1000 patient-years. The most common forms are usual interstitial pneumonia (UIP) and nonspecific interstitial pneumonia (NSIP; 44–46% and 33–44%, respectively), although there have been reports of cases involving all the histopathologic forms described for the disease. RA-ILD is associated with specific risk factors, such as male sex, older age, smoking, and positive rheumatoid factor (RF) and anti-citrullinated peptide antibody (ACPA) levels. The clinical course of ILD ranges from asymptomatic forms to rapidly progressive disease in a minority of cases. It has been estimated that the risk of death is up to 3-fold higher in patients with RA-ILD than in those without ILD, making RA-ILD the second most common cause of death after cardiovascular disease. Treatment of RA has improved considerably in recent years with the advent of biologics; however, the use of these agents has been restricted in patients with ILD owing to safety concerns. Many doubts continue to surround the treatment of patients with RA-ILD. Therefore, the objective of this review is to examine the current management of affected patients in terms of diagnosis, treatment, and follow-up.

Bone formation is a complex process that occurs throughout life, and is normally limited to the skeletal system. In bone formation, osteoprogenitor cells follow several developmental stages, including differentiation in osteoblasts, proliferation, matrix maturation, and mineralization. The mechanisms involved in the mineralization process of bone, such as in the new bone formation, are extremely complex and have been under intense investigation for many years. Bone formation follows two distinct processes, intramembranous and endochondral ossification; both are regulated by signaling pathways involving numerous genes. Disturbance of these signaling pathways may cause a large spectrum of skeletal diseases characterized by new bone formation and bone growth anomalies. This review will only focus on the key genetic pathways involved in heterotopic bone formation. Wingless/integrated (Wnt), hedgehog (HH), and transforming growth factor beta (TGFβ)/bone morphogenetic protein (BMP) signaling pathways are described and illustrated; their relation with new bone formation is demonstrated through their involvement in bone formation disorders.

Gout is common in people with chronic kidney disease and in general is sub-optimally managed. Lack of evidence due to the exclusion of people with chronic kidney disease from the majority of clinical trials, concerns about adverse effects and conflicting gout management guidelines all contribute to suboptimal management. Herein we review the evidence for the pharmacological treatment of gout, both flares and long-term urate-lowering, in people with concomitant chronic kidney disease.

Rheumatoid arthritis (RA) is the most common rheumatologic disease characterized by inflammation with a definite relationship with heart disease. Impaired immunity, chronic inflammation, genetic susceptibility, autonomic nervous system (ANS) dysfunction, altered metabolic profile have been blamed for ischemic and non-ischemic heart diseases in RA patients. Medications used in RA treatment can also modify the risk of heart diseases by different mechanisms. Understanding the pathogenesis is essential to prevent early cardiac dysfunction in RA patients. Fundamental cellular and molecular mechanisms of pathogenesis await further elucidation. Disease management is of great importance since the cardiovascular (CV) events are known to be reduced with low disease activity. Discovery of new mechanisms will pave the way for the development of novel treatment modalities. This review highlights the epidemiology, pathogenesis, risk factors, diagnosis and screening methods and management of CV comorbidities in RA patients. Besides impact of RA medications and exercise on CV risk are summarized.

Rheumatology, the medical specialty dealing with the diagnosis and treatment of rheumatic and musculoskeletal diseases (RMDs), is evolving with the emergence of digital health technologies, such as electronic health records (EHRs), virtual visits, mobile health (mHealth), wearable medical devices, social media, websites, digital therapeutics, artificial intelligence (AI) and machine learning. These technologies offer new opportunities to improve essential aspects of care, such as care access or disease management. They can significantly reduce the risk of errors and the workload of rheumatologists, while enhancing communication between physicians and patients, resulting in better quality of care. Moreover, digital health technologies can significantly improve research outcomes. However, digital health technologies in rheumatology also face specific barriers such as privacy, security concerns, incremental costs as well as limited digital health literacy and access. Therefore, further analysis, actions and strategies are needed to overcome these barriers. This article explores the impact of digital health technologies on rheumatology practice and highlights their contributions and challenges. By understanding the immense potential and overcoming the obstacles, the way for a future where digital health technologies are integrated into daily rheumatology care may be envisioned, in order to empower patients and healthcare providers.

Diffuse idiopathic skeletal hyperostosis (DISH) and axial spondyloarthritis (axSpA) are diseases with inflammatory involvement of the axial skeleton that can result in new bone formation that may lead to total ankylosis of the spine and functional impairment of different extent in individual patients. In these diseases, the new bone formation may lead to total ankylosis of the spine and impaired mobility with functional impairment. This review will highlight the similarities and differences of these two conditions. In axSpA, the genetic background with the association with human leukocyte antigen-B27 (HLA-B27) is known for 50 years, while in DISH, a genetic contribution is not yet proven. The phenotype of new bone formation and its anatomic features are different between these diseases. In axSpA symmetric, thin and marginal syndesmophytes representing an ossification of enthesitic inflammation at the area of the attachment of the annulus fibrosus that may extend to the adjacent deeper layers anterior longitudinal ligament and are typical, while in DISH the so-called “chunky bridging osteophytes” grow as an additional layer on the anterior longitudinal ligament. Besides distinct anamnestic and clinical features, magnetic resonance imaging is helpful differentiating the two diseases since inflammatory changes with the typical pattern of axSpA are reliably visualized. Similar in both diseases is the high prevalence of vertebral fractures, which are mainly caused by the local osteoporosis and decreased flexibility of the affected bones, and therefore may occur even after minor traumata. The presence of extraarticular manifestations like uveitis, inflammatory bowel disease or psoriasis are only linked to axSpA. In contrast, DISH is associated with obesity, diabetes mellitus, and other metabolic diseases. Although DISH and axSpA are distinct conditions, the cooccurrence of these two diseases exists in some patients. Various therapeutic options are becoming available for axSpA, but no therapy has been approved for DISH yet.

Upon self-reflection, some clinicians privately confess a lack of confidence in being able to safely perform trigger point dry needling (TrPDN) or trigger point injection (TrPI) on craniofacial muscles. Procedural performance anxiety seems to be more pronounced relative to those muscles that cannot be palpated and/or have an increased risk of iatrogenic injury to neurovascular structures. Participatory action ultrasound imaging (PAUI) can be a useful tool in enhancing clinician confidence. A clinician-subject with a left lateral pterygoid trigger point was dry-needled under ultrasound guidance by a clinician-needler with extensive training and experience relative to evaluation and treatment of patients with craniofacial pain. Prior to PAUI, both the clinician-needler and clinician-observer describe low-to-moderate anxiety in the performance of TrPDN of the lateral pterygoid, using a lateral-to-medial approach. By contrast, both the clinician-needler and clinician-observer expressed high anxiety, objectively confirmed by the state-trait anxiety inventory (STAI) form Y-1 (STAI Y-1), in the performance of a newly learned cephalo-caudal approach. Following an initial round of clinical training without PAUI, subjective anxiety remained high despite a lower theoretical risk to the maxillary artery using the cepalo-caudal approach. A second round of training was performed with the addition of PAUI; the clinician-needler was able to reach the target tissue within 2 min in each of 3 attempts. Upon visual inspection and interpretation of the images and cine, the clinician-needler and clinician-observer both expressed a “significant” decrease in self-reported anxiety in performing the cephalo-caudal approach, objectively verified by improvements in the STAI Y-1 score of both clinicians. This case report presents PAUI as a means for future research and clinician education regarding risk assessment of TrPDN or TrPI of muscles with risk of iatrogenic injury.

Psoriasis is a chronic immune-mediated disorder affecting about 2% of the population worldwide which is associated with significant morbidity. The disease usually presents as raised, well-demarcated erythematous plaques with adherent silvery scales. Psoriasis can appear at any age but it has two peaks occurring at 15–20 and 55–60 years of age. It affects males and females equally. Despite the multitude of investigations about psoriasis and even development of drugs with satisfactory results, its pathogenesis is not fully understood yet and its course is unpredictable. Various environmental triggers, e.g., obesity, stress and drugs may induce disease in genetically susceptible patients. Although psoriasis was considered primarily as a disease of the skin, more investigations have been revealed its systemic nature. Psoriatic arthritis (PsA) may complicate up to one-third of cases of psoriasis vulgaris (PV). Also, the association between psoriasis and a variety of other immune-mediated disorders such as inflammatory bowel disease (IBD) and celiac disease (CD) has been confirmed in various studies. Moreover, a growing body of evidences indicates that psoriasis shares some common histological and phenotypical properties with the spectrum of osteoimmunological diseases such as Paget’s disease of bone (PDB). Thus, exploring the common molecular and genetic mechanisms underlying psoriasis and related disorders is of paramount importance for better elucidating disease pathogenesis and designing more targeted treatments.

Calcium pyrophosphate deposition disease (CPPD) is a cause of inflammatory arthropathy that increases in prevalence with increasing age, presents in acute and chronic forms, and is characterized by the finding of positively birefringent crystals on polarized microscopy of synovial fluid. This review finds that although strides are being made in CPPD diagnosis and classification, CPPD remains a poorly understood, unrecognized, and debilitating disease. As a consequence, treatment options usually lack supportive evidence and there has been little progress in novel drug development for the condition. This article aims to discuss the updated evidence on treatment options for CPPD and identifies promising future areas for improvement.

Medical attention to uric acid (UA) has been increasing in recent years, mainly because this molecule has been shown to be associated with increased cardiovascular risk, both in the general population and in the hypertensive patients. A growing body of clinical and experimental data supports this view and prompts reconsideration of the role of UA in the development of atherosclerosis and the genesis of cardiovascular disease. It is known that this substance, in certain plasma concentrations, induces increased oxidative stress, a chronic inflammatory state, and a whole series of other modifications that are potentially deleterious at the cardiovascular level leading to hypertension, atherosclerosis, atrial fibrillation (AF), and other metabolic changes such as diabetes, metabolic syndrome, non-alcoholic fatty liver disease and kidney failure. Despite this epidemiologic and mechanistic evidence, the current guidelines from international cardiology scientific societies do not give precise indications in this regard, and some of them only suggest UA evaluation as part of an initial screening of the hypertensive patient. The purpose of this review is to briefly describe the main clinical and epidemiological evidence supporting the role of hyperuricemia as a possible emerging cardiovascular risk factor and to analyze the potential pathophysiological mechanisms through which elevated UA levels may exert a detrimental effect on the cardiovascular system.