Background/Objectives: Patients with acute anterior uveitis (AAU) have a high prevalence of occult spondyloarthropathy (SpA). Only one previous study investigated ultrasonographic (US) changes at peripheral entheses and joints in patients with acute anterior uveitis (AAU) and no study has used these data in recognizing unknown SpA as defined by ASAS criteria. No previous study compared non-granulomatous (NGAU) with granulomatous uveitis (GAU) for these US features. The objective of this study was to investigate the prevalence of US enthesis and joint abnormalities in a consecutive series of GAU and NGAU patients and to use these data in recognizing unknown SpA as defined by ASAS criteria. Methods: A total of 152 consecutive patients diagnosed with AAU [103 NGAU (42 B27-, 61 B27+) and 49 GAU] from the Immunology Eye Unit (AUSL-IRCCS Reggio Emilia, Italy) were enrolled in this study. Six peripheral entheses as well as knee and ankle joints were bilaterally evaluated by US according to standard methods. The presence of any elementary lesion, structural damage and active enthesitis, according to OMERACT definitions, was recorded. ASAS classification criteria of SpA were integrated with the US data of active enthesitis and joint synovitis in defining the presence of enthesitis and arthritis. Results: NGAU patients had a higher prevalence of entheseal erosions (11.9% vs. 9%, P0 0.009), of enthesis exhibiting a PD signal (29.7% vs. 12.2%, p = 0.025) and of active enthesitis (23% vs. 8.2%, p = 0.026) compared with GAU group. Unknown SpA as defined by ASAS criteria was recognized in 29 patients by clinical and MR/Rx examination of sacroiliac joints and in 13 additional patients with the use of US data. Conclusions: Acute entheseal lesions and erosions are associated with NGAU, without apparent influence of HLA-B27 positivity. US examination helps to recognize previously unknown SpA and to define the disease phenotype of patients, moving toward more personalized treatment.

When assessing hip pain in athletes, it is important to focus on the extra-articular soft tissues that may clinically mimic joint pathology. One such extra-articular structure is the synovial bursa. Bursitis can clinically be misdiagnosed as joint-, tendon- or muscle-related pain. These pathological processes are a result of inflammation that is often secondary to acute trauma, overuse injuries, arthritis, or infection. Traumatic and overuse hip bursitis occur frequently in amateur and professional athletes and clinical presentation is often nonspecific. After clinical assessment, imaging plays an important role in diagnosis and in work-up of these lesions. Ultrasonography (US) is being increasingly used in the assessment of the hip because of the wide availability of US machines, the lower cost, and the unique real-time imaging capability which allows both static and dynamic evaluation as well as guidance of interventional procedures such as fluid aspiration and steroid injection. In order to obtain a correct diagnosis, an efficient US examination requires a thorough understanding of hip anatomy. In this setting, a structured approach based on identification of important US landmarks and compartmentalization of hip anatomy can significantly simplify the task. Sports physicians must be aware about the diagnostic and therapeutic possibilities offered by US in order to expedite rapid referral to a musculoskeletal specialist who can perform a point-of-care US examination of the hip by using a structured diagnostic approach. The purpose of this narrative review is to illustrate both the normal and pathological features of anterior and lateral hip compartments bursae using schematic diagrams and corresponding US images. We will concentrate on sport-related bursitis, of which we will discuss the etiology, clinic and principles of care management. Our aim is to promote the acquisition of these concepts in sports medicine in order to improve patient outcomes.

The primary objective of the minimally invasive Cotton osteotomy is to correct sagittal malalignment of the medial column by targeted plantarflexion, thereby restoring alignment and contributing to the reconstruction of complex pes planovalgus deformities within a joint-preserving surgical approach.

Most high-tech drugs and tissue engineering products based on human chondrocytes currently available on the market are aimed at restoring traumatic damage to cartilage tissue. However, in the presence of inflammation, their regenerative potential is significantly reduced, which limits their use in patients with osteoarthritis-one of the most common degenerative and inflammatory joint pathologies. The central element of the pathogenesis of osteoarthritis is inflammation-not classical acute inflammation, but rather chronic low-grade inflammation, primarily mediated by mechanisms of the innate immune response. Therefore, a key challenge is to enhance the anti-inflammatory effectiveness of cell-based drugs to broaden their indications to include degenerative diseases such as osteoarthritis and arthrosis. In recent years, cell-based drugs using stem cells, including mesenchymal stem cells (MSCs), hematopoietic stem cells (HSCs), and stromal vascular fraction (SVF) cells, have been actively studied. Despite their confirmed safety in inflammatory processes, meta-analyses of clinical trials show limited effectiveness in improving symptoms and MRI data in the treatment of osteoarthritis. A promising direction appears to be the development of combined cell-based drugs that combine MSCs with M2-polarized macrophages; however, data on their clinical effectiveness are still insufficient. This review explores key cellular effectors of inflammation and its molecular mechanisms, potential strategies for creating tissue engineering products that possess not only regenerative but also pronounced anti-inflammatory effects. The development of such products will expand their application in the treatment of inflammatory-degenerative joint diseases.

Acute gouty arthritis (AGA) is a common inflammatory joint disease characterized by pain resulting from the deposition of monosodium urate (MSU) crystals into joints and surrounding tissues. RGFP966, a selective inhibitor of histone deacetylases 3 (HDAC3), can down-regulate the AIM2 inflammasomes. This study aimed to explore the mechanism of action of RGFP966 in MSU-induced AGA. MSU-induced AGA rats were treated with RGFP966 or colchicine, and physiological and pathological indicators were determined. The rat joint synovial tissues and kidneys pathological damage was observed by hematoxylin and eosin staining. Enzyme-linked immunosorbent assay (ELISA), Western blot, JC-1 staining, mitochondrial membrane potential (MMP) measurement, ATP assay, and immunofluorescence were applied to evaluate the effects of RGFP966 on the AIM2 inflammasomes and mitophagy. In MSU-induced AGA rats, RGFP966 significantly improved the gait score, the swelling degree and synovitis score. In addition, RGFP966 repressed the increased serum levels of IL-1β, IL-18, IL-6 and TNF-α, and reduced the protein levels of AIM2, Pro-caspase-1, Cleaved-caspase-1, ASC, Pro-IL-1β, and Cleaved-IL-1β in MSU-induced AGA rats. Furthermore, RGFP966 decreased the level of reactive oxygen species (ROS), increased the level of ATP and MMP, and promoted the levels of Pink1, Parkin and LC3-II. Collectively, RGFP966 significantly alleviated AGA, and the underlying mechanism is related to promote mitophagy by inhibiting the activation of the AIM2 inflammasomes.

This study aimed to develop a brucine (Bru) hydrogel-forming microneedle (Bru-HFM) delivery system that could achieve long-term, programmed drug release, through adjusting degree of cross-linking in polyvinyl alcohol (PVA)/carbomer 934P (CP) hydrogel. A one-way orthogonal experiment and a Franz diffusion cell were employed to optimize the preparation process. The resulting Bru-HFM exhibited favorable appearance, mechanical strength, and swelling properties. The drug release performance of the different drug-carrying sites of HFMs was compared. The results illustrated that in vivo drug release rate over 144 h was significantly higher in the needle body-carrying group (95.32%) than in the whole-microneedle (51.85%) and back-lining groups (57.39%). The amount of residue in the back-lining group was obvious, in line with expectations. The burst release rate of 78.81% could meet the high-dose demand during the acute phase of inflammation, whereas continuous release through the cross-linking network over 48-144 h achieved a total release rate of 95.32%. This covered the maintenance phase of chronic inflammation treatment, and the microneedles remained structurally intact at the end of drug release, permitting their detachable. The general pharmacodynamic evaluation results demonstrated that the pathological state of the ankle joints of rats with collagen-induced arthritis was significantly improved in the needle body-carrying group, which also exhibited significantly reduced serum levels of IL-6, IL-17, and TNF-α (all P < 0.05), indicating a significant therapeutic effect on rheumatoid arthritis. This study provides a new strategy and theoretical basis for designing HFMs for programmed drug release and inflammatory disease treatment.

The use of composite disease activity scores enables a pragmatic approach to the measurement of the level of disease activity in children with juvenile idiopathic arthritis (JIA). These tools are constructed through the combination of individual measures and provide a quantification of the absolute level of disease activity in one summary number on a continuous scale. The first composite score for JIA, named Juvenile Arthritis Disease Activity Score (JADAS), was published in 2009. It includes the following four variables: physician global assessment, parent/patient global assessment, active joints count, and an acute phase reactant. Its score is calculated as the arithmetic sum of the scores of its four items. Additional versions of the JADAS, which lack the acute phase reactant (clinical JADAS, cJADAS) or are specific to systemic JIA (systemic JADAS, sJADAS), were developed over the years. An important progress in the field has been represented by the definition of the cutoff values in the JADAS that distinguish the states of inactive disease or minimal, moderate, and high disease activity in JIA. These cutoffs may serve as therapeutic targets in the treat-to-target strategy. Recently, a JADAS version entirely composed of parent/patient-reported outcome measures has been developed and validated. This tool is well suited to implement remote patient monitoring, a form of telemedicine that may help to optimize disease control and reduce the pressure on healthcare systems. This review is aimed to describe the different versions of the JADAS and the main aspects of their developmental process.

BACKGROUND: Bearing dislocation is a unique complication of mobile-bearing unicompartmental knee arthroplasty (UKA), with diverse underlying mechanisms. This article reports a rare mechanism of bearing dislocation following mobile-bearing UKA, which was probably associated with the new-onset rheumatoid arthritis (RA) leading to anterior cruciate ligament (ACL) insufficiency—aiming to highlight this uncommon etiology and its implications for clinical practice. CASE PRESENTATION: A 53-year-old woman presented with acute right knee pain and restricted mobility one day prior to admission, who was treated by mobile-bearing UKA for anteromedial osteoarthritis two years ago. Radiographs revealed bearing dislocation in this patient. Laboratory evaluation revealed elevated inflammatory markers (CRP 71.59 mg/L, ESR 74 mm/h) and positive RA serology(anti-CCP 39.09 U/mL, RF 32.4 IU/mL). Periprosthetic joint infection was rigorously excluded through multiple methods. The patient responded well to short-term corticosteroids and underwent one-stage revision total knee arthroplasty. Intraoperatively, extensive chronic synovitis, bearing dislocation, and severe ACL erosion/laxity due to synovial proliferation were observed. Histopathology confirmed synovial hyperplasia with dense lymphoplasmacytic infiltration and lymphoid follicle formation. Following standardized anti-rheumatic therapy, the patient regained satisfactory knee function with normalized inflammatory markers at 12-month follow-up. CONCLUSION: This case highlights that in patients who was present with delayed pain and elevated inflammatory markers after UKA. Inflammatory joint diseases such as RA should be included in the differential diagnosis alongside infection. Appropriate serological screening and multidisciplinary collaboration with rheumatology are essential for optimal management. As a single case report, these findings are hypothesis-generating and warrant confirmation in larger studies.

OBJECTIVES: Osteoarthritis (OA) is the most prevalent joint disorder, whereas post-traumatic osteoarthritis (PTOA) denotes a form of arthritis that arises secondary to acute joint injury. METHODS: This was a combined bioinformatics and experimental validation study. We first analyzed single-cell RNA sequencing data (GSE200843) from murine knee joints following anterior cruciate ligament rupture to map granulocyte subpopulations. High-dimensional weighted gene co-expression network analysis (hdWGCNA) was used to identify PTOA-associated gene modules. Three machine learning algorithms (LASSO, SVM-RFE, and Random Forest) were applied to screen hub genes, followed by validation in external datasets (GSE26475, GSE112641) and by qRT-PCR in a mouse model (n = 6 per group). RESULTS: We identified five distinct granulocyte subpopulations, one of which (OA granulocytes) was significantly expanded in PTOA tissues. Through intersection of hdWGCNA-derived module genes and differentially expressed genes, combined with machine learning, Tgfbi and Mpp7 were identified as hub genes. These biomarkers could be developed into diagnostic assays for patients at risk of PTOA following acute joint injury. qRT-PCR confirmed that Tgfbi was significantly upregulated (p = 0.0014) and Mpp7 downregulated (p < 0.0002) in synovial tissues of the PTOA mouse model compared to controls. Immune infiltration analysis revealed significant correlations of these hub genes with naive B cells and M1 macrophages. CONCLUSIONS: This study identifies Tgfbi and Mpp7 as potential diagnostic biomarkers for PTOA. The findings suggest that assessing the expression of these genes may aid in early diagnosis and risk stratification, potentially enabling timely therapeutic intervention before irreversible joint damage occurs. These biomarkers could be developed into diagnostic assays for patients at risk of PTOA following acute joint injury.

Gout is among the most prevalent etiologies of chronic inflammatory arthritis in the United States, which is characterized by monosodium urate (MSU) monohydrate crystals deposition in the tissues.[1][2] Gout was first recognized even before the common era. Hence it is arguably the most understood and manageable disease among all rheumatic diseases.[3][4] 

The post-Covid-19 syndrome, also referred to as "Long Covid", can present with arthritic symptoms. A cross-sectional, prospective study was done on post Covid-19 patients at a tertiary centre in Telangana. This study included a total of 139 RT-PCR-confirmed Covid-19 patients, who were diagnosed with arthritis in the time interval between 1 to 6 months post Covid recovery. Demographic data, clinical data, blood investigations, inflammatory markers and imaging investigations were recorded. Majority of the patients (65.5%; n=91) were women and the mean age of the participants was 50.8 years. 77.0% (n=107) had arthralgia, 44.6% (n=62) had joint swelling, 25.2% (n=35) had myalgia and 5.8% (n=8) had fatigue. The most common joint affected was the knee (92.0%; n=128), followed by wrist (10.25%; n=4) and ankle (n=1). Abnormal Hb levels (43.9%; n=61), RBC counts (9.4%; n=13), WBC counts (13.7%; n=19) and ESR (26.6%; n=37), D-dimer (50.4%; n=70), LDH levels (49.6%; n=69), uric acid (36.0%; n=50), ferritin (35.5%; n=49) and rheumatoid factor (10.8%; n=15), were recorded in participants. Joint arthritic changes on radiographs and ultrasoundwere recorded in 77.0% had 95.7% of the participants respectively. Covid arthritis is one of the common features of Long Covid patients. Many patients suffer from joint aches and swelling which cause sufficient impairment causing majority of the individuals.