Sacroiliac joint (SIJ) anatomical variants are common on MRI and may complicate interpretation by mimicking inflammatory sacroiliitis; however, their relationship with inflammatory back pain (IBP)-like symptom patterns is not well defined in patients without axial spondyloarthritis (axSpA). To characterize inflammatory back pain (IBP)-like symptom patterns and accompanying MRI findings that may mimic sacroiliitis in patients with chronic low back pain (CLBP) and sacroiliac joint (SIJ) anatomical variants who did not fulfill classification criteria for axial spondyloarthritis (axSpA). In this cross-sectional study, consecutive patients younger than 45 years at the time of SIJ MRI/clinical evaluation, with chronic low back pain lasting at least 3 months, who underwent SIJ MRI between September 2023 and September 2025 were retrospectively screened for predefined SIJ anatomical variants and lumbosacral transitional anomalies. Patients with lumbosacral transitional anomalies were excluded at the screening stage. Those with at least one SIJ anatomical variant were invited for a standardized clinical assessment in which IBP features were captured using a single questionnaire covering the Calin, Rudwaleit (Berlin), and ASAS IBP criteria. All participants were systematically assessed against the ASAS classification criteria for axial spondyloarthritis (axSpA), and those who fulfilled these criteria were excluded from the final analysis. SIJ MRIs were read independently by two radiologists blinded to clinical data; agreement for variant detection was almost perfect (κ = 0.90). Bone marrow edema (BME) was evaluated according to the ASAS/OMERACT definition of MRI findings highly suggestive of active sacroiliitis, and structural changes were also recorded. Of 260 screened patients with CLBP, SIJ anatomical variants were identified in 108/260 (41.5%). After exclusions (n = 20), 88 patients were included in the final analysis; 75/88 (85.2%) were female, with a median age of 36 years (Q1-Q3: 28-39) and a median symptom duration of 3.0 years (Q1-Q3: 1.6-9.8). IBP positivity varied by criteria set: 51.1% (Calin), 34.1% (Berlin), and 27.3% (ASAS). Variants were predominantly bilateral (76/88, 86.4%). Among 98 recorded variant findings, accessory joint (n = 27) and iliosacral complex (n = 25) were the most frequent. ASAS/OMERACT-positive BME was present in 10/88 patients (11.4%); structural lesions included sclerosis in 22/88 (25.0%), erosions in 7/88 (8.0%), and fat metaplasia in 5/88 (5.7%). HLA-B27 positivity was observed in 4/69 tested patients (5.8%), and median CRP was 3.2 mg/L (Q1-Q3: 1.0-7.0). In a non-axSpA, variant-positive cohort, IBP-like symptom patterns were common, whereas ASAS/OMERACT-positive BME was infrequent. SIJ variants may therefore complicate clinical judgment because of symptom overlap in young patients within the typical age range for axSpA onset. Although infrequent, imaging features that mimic inflammatory disease highlight the need for careful clinical correlation to avoid misclassification as axSpA.

Rheumatoid arthritis (RA) is a chronic, inflammatory autoimmune disease characterized by progressive joint involvement. The disease is associated with reduced health-related quality of life, functional ability, work productivity, and daily activity, in addition to pain, fatigue, and inflammation-induced structural damage. RA emerges through a complex interplay of multiple factors, including the release of inflammatory cytokines. One such cytokine is tumor necrosis factor (TNF), which is inhibited by golimumab, an approved treatment for the disease. Golimumab is produced using a recombinant cell line that originated from genetically modified mice immunized with human TNF. This narrative review presents the efficacy and safety outcomes from the golimumab pivotal randomized controlled trials (RCTs) that evaluated the subcutaneous and intravenous formulations. Across the RCTs, treatment was associated with an American College of Rheumatology ≥ 20% improvement. A majority of participants reported at least one AE and the most frequent were upper respiratory infection, nasopharyngitis, and bronchitis. The review also presents data from post hoc analyses and real-world studies, which demonstrated benefits that included improvements in health-related quality of life and daily productivity, prolonged drug survival, and reduced fatigue, pain, disease activity, and structural damage. Lastly, data from meta-analyses, including RCTs and real-world studies, demonstrated that golimumab had an adverse event pattern similar to other TNF inhibitors. Collectively, these studies demonstrated that golimumab is an effective and safe treatment for RA when used according to the approved indication.

Limb salvage using free tissue transfer in patients with rare autoinflammatory syndromes is poorly described, and the safety of microvascular reconstruction in this population remains uncertain. Hereditary pyogenic arthritis, pyoderma gangrenosum, and acne (PAPA) syndrome is characterized by dysregulated inflammation, pathergy, and impaired wound healing, raising concern for flap compromise and postoperative complications. We report a rare case of lower extremity free tissue transfer in a patient with PAPA syndrome. A 66-year-old woman with rheumatoid arthritis and PAPA syndrome presented with rapid wound breakdown, violaceous ulceration, exposed hardware, and periprosthetic joint infection following left total knee arthroplasty (TKA). Examination revealed an approximately 9 × 7 cm anterior knee defect with subtotal patellar tendon necrosis. After multidisciplinary optimization, she underwent single-stage irrigation and debridement, hardware removal, revision TKA with patellar tendon reconstruction using gracilis autograft, and immediate coverage with a 22 × 14 cm free latissimus dorsi (LD) muscle flap. The flap was anastomosed end-to-side to the anterior tibial artery with venous outflow via the venae comitantes and loosely inset to preserve future surgical access. The donor site was closed primarily. A 21 × 13 cm staged split-thickness skin graft was performed 1 week later, with adjunctive postoperative hyperbaric oxygen therapy (HBOT). Initial healing was uncomplicated, with complete graft take and donor-site healing. Four months postoperatively, the patient developed chronic sinus tracts and recurrent periprosthetic infection requiring flap re-elevation, debridement, and hardware exchange; the flap pedicle was preserved, and coverage maintained. At one-year follow-up, all wounds had healed; flap coverage was durable with acceptable cosmesis, and the patient was ambulatory for short distances without assistance. She was last seen infection-free and full-weightbearing 4 months later. This case demonstrates that microvascular limb salvage is feasible in PAPA syndrome when guided by multidisciplinary planning and strategic flap design.

Background/Objectives: Osteoarthritis is a chronic joint disorder involving the progressive breakdown of articular cartilage, which leads to joint pain and impaired mobility. The present study investigated the effects of curcuminoids phospholipid (CP) on osteoarthritis progression, assessed its cartilage-protective effects, and elucidated the underlying mechanisms. Methods: Male Sprague-Dawley rats were randomly allocated to six experimental groups. One group received an intra-articular saline injection as the normal control (NC), while the remaining five groups were injected with monosodium iodoacetate (MIA) and consisted of an MIA control group (MC), a positive control group treated with celecoxib (PC, 3 mg/kg), and three groups treated with CP (31.25, 62.5, or 125 mg/kg). Results: Compared with the MC group, CP administration significantly improved pain-related behavior, as assessed by weight-bearing measurements. Micro-computed tomography and histological analyses demonstrated that CP administration mitigated subchondral bone erosion and preserved cartilage integrity. Additionally, the CP treatment significantly reduced markers associated with cartilage degradation, including matrix metalloproteinases and cartilage oligomeric matrix proteins; downregulated the expression of matrix-degrading enzymes; and restored aggrecan expression. Serum levels of inflammatory mediators, including nitric oxide; prostaglandin E2; C-reactive protein; and pro-inflammatory cytokines, including interleukin (IL)-6, tumor necrosis factor (TNF)-α, and IL-1β, were reduced following CP administration. Furthermore, CP decreased the activation of nuclear factor kappa B (NF-κB) signaling. Conclusions: These findings suggest that CP may be a promising functional agent for osteoarthritis, demonstrating beneficial effects on pain-related outcomes and cartilage integrity, potentially mediated by its anti-inflammatory activity.

Osteoarthritis (OA) is a chronic, progressive joint disease characterized by degenerative changes in articular cartilage, subchondral bone sclerosis, accompanied by synovitis and chondrocyte apoptosis. With the aging of society, it has become one of the major factors endangering the mobility of middle-aged and elderly people worldwide. The pathogenesis of OA remains unclear, and current treatments can only control symptoms without effectively repairing damaged cartilage. Ferroptosis, a novel form of programmed cell death proposed and confirmed in 2012, is characterized by iron-dependent accumulation of lipid peroxides, mitochondria-specific damage, and imbalance in antioxidant defense capacity. In recent years, it has been proven to be involved in regulating the process of cartilage degradation in OA. This review mainly focuses on the key biological processes of chondrocyte ferroptosis, elaborating on the interactions between iron homeostasis disorders, oxidative stress and inflammation, as well as the research progress on chondrocyte ferroptosis induced by dysregulation of important signaling pathways in the pathological environment of OA. In summary, it systematically analyzes the relationship between ferroptosis and other forms of programmed cell death, summarizes the research progress of OA therapeutic strategies targeting chondrocyte ferroptosis, and puts forward the existing contradictions and development trends in current research, aiming to provide new clues and directions for exploring the mechanism of OA occurrence and development and clinical personalized treatment.

Background and objective Reactive arthritis (ReA), formerly termed Reiter's syndrome, is an autoimmune inflammatory arthritis that develops in response to a gastrointestinal or genitourinary infection. Although nearly two-thirds of patients have a self-limited course, the remaining patients go on to develop chronic symptoms and complications. In the absence of a curative treatment, the treatment goal remains the alleviation of symptoms, for which diverse treatments have been used with variable responses. Apremilast, an oral phosphodiesterase 4 (PDE4) inhibitor typically used for psoriatic arthritis and plaque psoriasis, appears to be a promising therapeutic option for ReA. This study aimed to evaluate the efficacy and safety of oral apremilast as an adjuvant therapy in patients with treatment-refractory ReA. In this study, adjuvant therapy refers to the addition of apremilast to ongoing conventional treatment with the aim of improving disease control and facilitating the reduction or discontinuation of concomitant medications such as corticosteroids and non-steroidal anti-inflammatory drugs (NSAIDs). Material and methods This was a retrospective, observational pilot study conducted at a tertiary care center. Medical records of 12 adult patients with treatment-refractory ReA, defined according to the criteria of the Third International Workshop on Reactive Arthritis (1996), who received oral apremilast as adjuvant therapy for 40 weeks between June 2024 and May 2025, were reviewed. Apremilast was administered at a dose of 30 mg twice daily following one week of dose titration. Treatment efficacy was primarily assessed using the American College of Rheumatology 20% improvement criteria (ACR20) along with secondary outcomes including ACR50/70 responses, changes in swollen and tender joint counts, inflammatory markers, improvement in functional outcomes measured by the Health Assessment Questionnaire-Disability Index (HAQ-DI) status, and evaluation of the corticosteroid-sparing effect. Results The mean age of the patients at the time of diagnosis was 26.91 years (range 19-36 years). Of the patients receiving apremilast (n=12), 10 (83.33%) achieved an ACR20 response at week 40. Although observed in a smaller proportion of patients, the higher-efficacy outcome measures, such as ACR50 and ACR70 responses, were sustained over 40 weeks in eight (66.67%) and five (41.67%) patients with continued treatment. The mean swollen joint count (SJC) and tender joint count (TJC) improved by 79.3% and 68.8%, respectively, at week 40. Around two-thirds of the treated patients (n=8, 66.67%) achieved a HAQ-DI minimal clinically important difference of ≥0.35 at 40 weeks. No serious infections or any other severe adverse effects were recorded in any of the patients. Conclusions Apremilast appears to be an efficacious and safe novel therapeutic option for treatment-refractory ReA. In addition to providing direct and substantial improvements in joint-related symptoms and beneficial effects on extra-articular manifestations, its corticosteroid-sparing effect makes it a promising candidate as an adjuvant in the treatment of ReA. The results of this study warrant further validation in larger controlled trials.

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]