This paper provides a review of the years of experience of hip sonography since the first ultrasound (US) course in Italy in 1987. Clinical and US findings were correlated in 1,000 newborns examined consecutively in a study in 1991. Developmental dysplasia of the hip (DDH) was present even in the absence of clinical signs, including the Ortolani sign. The percentage of US diagnosis of DDH in newborns was 2.8%, while instability according to the Ortolani test was present in 0.75%. After recommendations from the American Academy of Pediatrics against universal US screening, early diagnosis decreased from 74.4% in the period 1992–2002 (43,418 hips examined) to 52.7% in 2013–2014 (5,598 hips examined). In order to answer the question of whether early treatment of DDH has better outcomes, the acetabulum maturation was studied in 93 type III hips. The statistical analysis showed a strong dependency (P < 0.001) between the alpha-angle gain and the age at which treatment was started. The first 2 weeks of life is the optimum time for early diagnosis and treatment; after 6 weeks of life, treatment is less effective and the results are less predictable. Furthermore, the role of the labrum and its morphological changes was analyzed in 86 unstable dysplastic hips (13 type D, 49 type III and 24 type IV) in patients with an average age of 53 days (range 1–134 days) at DDH diagnosis and the beginning of treatment. The labrum was never inverted and underwent a statistically significant increase in echogenicity and dimensions with a frequency of 97% and 96% respectively, suggesting the labrum’s stabilizing role. Abnormal findings such as in achondroplasia, cleidocranial dysplasia, other rare osteochondrodysplasias and in coxa vara are underlined. Uncommon findings such as incomplete acetabular bony rim and eccentric position of the femoral head nucleus are also described.

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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.

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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.

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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.

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Rheumatoid arthritis (RA) is an inflammatory arthritis that affects synovial joints, and it is not surprising that the temporomandibular joint (TMJ), a synovial joint, is also affected. However, TMJ is rarely the first affected joint in the course of RA. Often, RA patients come to the physician with more focus on complaints in other peripheral joints. Therefore, asking TMJ complaints and symptoms, and TMJ examination in RA patients is often neglected by doctors too, because they focus more on other joints. This neglect may cause serious damage to the joints and cause disability. Examination of TMJs, which is a crucial component of vital activities such as nutrition and speech, should be added to the routine. Also, further studies may be focused on adding TMJ assessment to disease activity scales and health assessment questionnaires.

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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.

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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.

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Gout is the most common inflammatory arthritis and a global health problem. In addition to joint involvement, urate crystals induce chronic inflammation, leading to increased cardiovascular risk in gout. Thus, cardiovascular disease is the leading cause of death in gout and numerous studies have revealed an increase in cardiovascular-related mortality in these patients. However, despite the efficacy of urate-lowering therapies, such as allopurinol and febuxostat, suboptimal management of gout and poor adherence continue to make it difficult to achieve better outcomes. Treat-to-target strategy may help change this, as in other diseases such as rheumatoid arthritis. Nevertheless, even with a well-defined clinical target (absence of flares and tophi disappearance), the numerical target [serum uric acid (SUA) < 5 mg/dL or < 6 mg/dL] still varies depending on current guidelines and consensus documents. Recently, several trials [Long-Term Cardiovascular Safety of Febuxostat Compared with Allopurinol in Patients with Gout (FAST), REasons for Geographic And Racial Differences in Stroke (REGARDS)] have shown better cardiovascular outcomes in those patients who achieve SUA levels < 5 mg/dL. Likewise, some observational studies, mostly based on imaging tests such as ultrasound and dual-energy computed tomography, have found better results in the magnitude and speed of reduction of urate joint deposition when SUA < 5 mg/dL is achieved. Based on an analysis of the available evidence, SUA < 5 mg/dL is postulated as a more ambitious target within the treat-to-target approach for the management of gout to achieve better joint and cardiovascular outcomes in patients with cardiovascular risk or severe disease.

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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.

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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.

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