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Xanthogranulomatous inflammation is a rare chronic inflammatory condition. It has been described in the long bones, and can affect various organs, including the salivary glands, gallbladder, kidneys, and gastrointestinal tract. The diagnosis is made throught histopathology which reveales foamy macrophages alongside polymorphonuclear leukocytes, plasma cells, and polyclonal lymphocytes arranged in a mosaic-like pattern. Here, we present the case of a 16-year-old boy in good general health who was referred by his orthodontist to the oral surgery department at Bretonneau Hospital for an asymptomatic multipartite image of the left mandibular angle that was discovered incidentally on a panoramic radiograph. The clinical examination was unremarkable. Cone beam computed tomography revealed a multipartite osteolytic lesion of the left mandibular angle, but this that was not specific enough for a diagnosis. Magnetic resonance imaging ruled out a vascular malformation. A biopsy revealed xanthogranulomatous osteomyelitis. In summary, this is the second case of xanthogranulomatous osteomyelitis localised to the mandible. This highlights a crucial point : radiological images of xanthogranulomatous osteomyelitis do not allow for a diagnosis; a biopsy is essential to rule out an aggressive or a malignant tumor.

Background Chronic recurrent multifocal osteomyelitis (CRMO) is a little known inflammatory bone disease occurring primarily in children and adolescents. Delays in referral and diagnosis may lead to prolonged courses of antibiotics with in-patient care, unnecessary radiation exposure from multiple plain radiographs or bone scans and repeated surgery including bone biopsies. Children (aged < 18 years) diagnosed with CRMO between January 2005 and December 2012, reviewed at Bristol Royal Hospital for Children were included and all available data collected. Information regarding CRMO was sent to all orthopaedic surgeons in the region in 2009. The aim of the study was to examine the features of the cohort, to examine the length of time to diagnosis and to explore the criteria used for diagnosis with and without biopsy. Findings Over an 8 year period, 41 patients were diagnosed with CRMO. Symptom onset occurred at a median of 9 years of age and time to diagnosis had a median of 15 months (range 0–92). Correlation coefficient analysis for time to diagnosis by year showed statistical significance with a decreasing trend. From the cohort data, diagnostic criteria were developed; applied retrospectively, 34 (83 %) children may have been diagnosed using the criteria, without a biopsy. Conclusions The data suggest that increasing knowledge of this condition may shorten time to diagnosis. Use of the Bristol diagnostic criteria by an experienced clinician may obviate the need for biopsy in some patients.

Chronic nonbacterial osteomyelitis (CNO) is a primary autoinflammatory bone disease that presents more frequently in children and is characterized by inflammatory bone lesions in the absence of an infectious etiology. There is little information of this disease in Latin America. The objective of the study was to evaluate demographic, clinical, laboratory, imaging, histopathology characteristics, and treatment responses of pediatric CNO patients. The clinical records of 19 patients with CNO diagnosed between 2007 and 2019 at three tertiary centers in Santiago, Chile were reviewed. The median age of onset was 10 years and 47% were female. Median delay in diagnosis was 12 months. All patients had a pattern of recurrent multifocal disease. 37% of patients had positive antinuclear antibodies and 16% HLA-B27 positivity. 21% of patients presented arthritis or other rheumatologic comorbidity, although no association with psoriasis, inflammatory bowel disease (IBD) or palmoplantar pustulosis (PPP) was observed. Eighteen patients received treatment with nonsteroidal anti-inflammatory drugs with partial response. Twelve patients received methotrexate, and half of them received steroids at the same time reaching remission in 50%. Of the five patients who received bisphosphonates, 60% achieved remission. All four patients who received adalimumab had comorbid arthritis and 75% achieved remission. In a series of Chilean children with CNO, all patients presented with multifocal lesions. Comorbid autoimmune diseases including arthritis were frequent, but no association was observed with psoriasis, IBD, or PPP.

Introduction Chronic non-bacterial osteomyelitis (CNO) is an autoinflammatory bone-disease of unknown origin. The National Pediatric Rheumatologic Database (NPRD) collects long-term data of children and adolescents with rheumatic diseases including CNO. Objective To assess characteristics, courses, and outcomes of CNO with onset in childhood and adolescence and to identify outcome predictors. Methods From 2015 to 2021 patients with a confirmed diagnosis of CNO, who were registered in the NPRD during their first year of disease and at least one follow-up visit, were included in this analysis and observed for up to 4 years. Results Four hundred patients with recent diagnosis of CNO were enrolled in the NRPD during the study period. After 4 years, patient data documentation was sufficient to be analyzed in 81 patients. A significant decline of clinical and radiological lesions is reported: at inclusion in the registry, the mean number of clinical lesions was 2.0 and 3.0 MRI lesions per patient. A significant decrease of manifestations during 4 years of follow-up (mean clinical lesions 0.5, p  < 0.001; mean MRI lesions 0.9 ( p  < 0.001)) was documented. A significant improvement of physician global disease activity (PGDA), patient-reported overall well-being, and childhood health assessment questionnaire (C-HAQ) was documented. Therapeutically, an increase of disease-modifying anti-rheumatic drugs over the years can be stated, while bisphosphonates rather seem to be considered as a therapeutic DMARD option in the first years of disease. Only 5–7% of the patients had a severe disease course as defined by a PGDA >  = 4. Predictors associated with a severe disease course include the site of inflammation (pelvis, lower extremity, clavicle), increased erythrocyte sedimentation rate, and multifocal disease at first documentation. The previously published composite PedCNO disease activity score was analyzed revealing a PedCNO70 in 55% of the patients at 4YFU. Conclusion An improvement of physician global disease activity (PGDA), patient reported overall well-being and imaging-defined disease activity measures was documented, suggesting that inactivity of CNO disease can be reached. PedCNO score and especially PGDA, MRI-defined lesions and in a number of patients also the C-HAQ seem to be reliable parameters for describing disease activity. The identification of risk factors at the beginning of the disease might influence treatment decision in the future.

Unless acute osteomyelitis in children is diagnosed promptly and treated appropriately, it can be a devastating or even fatal disease. This review summarizes the current approach to the treatment of acute osteomyelitis in children. Bacteria may reach bone through direct inoculation from traumatic wounds, by spreading from adjacent tissue affected by cellulitis or septic arthritis, or through hematogenous seeding. In children, an acute bone infection is most often hematogenous in origin. 1 In high-income countries, acute osteomyelitis occurs in about 8 of 100,000 children per year, 2 but it is considerably more common in low-income countries. Boys are affected twice as often as girls. 2 , 3 Unless acute osteomyelitis is diagnosed promptly and treated appropriately, 4 it can be a devastating or even fatal disease with a high rate of sequelae, especially in resource-poor countries where patients present . . .

Mycoplasma phocimorsus is an identified zoonotic agent of musculoskeletal infections. Osteomyelitis developed in a patient after injury sustained while skinning a bear, and he experienced delayed diagnosis after ineffective treatments. Clinicians should use doxycycline or moxifloxacin therapy in treatment-refractory cases with exposure to seals, cats, or bears while awaiting molecular diagnostics results.

Staphylococcus aureus (S. aureus) has been identified as a hindrance to osteoblast differentiation, thereby contributing significantly to the development of osteomyelitis. Consequently, exploring pharmaceutical interventions targeting osteoblast differentiation mediated by S. aureus may present a novel approach for treating osteomyelitis. It has been reported that N6‐methyladenosine (m6A) methylation is highly associated with infection. Moreover, studies continue to validate that short‐chain fatty acids play an important role in transcriptional modification and have been considered as a potential treatment for S. aureus infection. Our research aimed to examine the impact and underlying mechanism of butyrate, a short‐chain fatty acid, in reducing the inhibitory influence exerted by S. aureus on osteoblast differentiation. The concentration of butyrate beneficial to MC3T3‐E1 cell viability was screened by Cell Counting Kit‐8 (CCK8) assay. Reverse transcription‐quantitative PCR (RT‐qPCR), Western blotting, and alkaline phosphatase (ALP)staining were used to verify the osteogenic indexes and the expression levels of m6A methylation‐related proteins in MC3T3‐E1 cells infected with S. aureus at different time points. Besides, the same methods were used to verify the effects of butyrate stimulation and METTL3 knockdown on the osteogenic ability of MC3T3‐E1 cells. H&E staining, Goldner staining, and immunohistochemical staining were used to verify the effect of butyrate on mice with endo‐plant associated S. aureus osteomyelitis. The potential mechanisms of METTL3 and autophagy in MC3T3‐E1 cells were studied by Western blotting. In vitro experiments, we found that butyrate significantly enhanced the expression of osteogenic‐related genes down‐regulated by infection in MC3T3‐E1 cells induced by S. aureus, including RUNX2, OCN, and ALP. In addition, METTL3, an important m6A methyltransferase, was significantly up‐regulated in S. aureus‐infected MC3T3‐E1 cells, but its expression could be down‐regulated by butyrate. Inhibiting the expression of METTL3 by siRNA could effectively rescue the osteogenic markers down‐regulated by S. aureus infection in MC3T3‐E1 cells, which was similar to the results of butyrate treatment. In vivo experiments had shown that butyrate could alleviate inflammation and osteogenic activity in implant‐associated osteomyelitis. The construction of bone marrow METTL3 low‐expression mice using siRNA also showed similar effects on osteogenic activity. Additionally, Western blotting confirmed that knocking down METTL3 rescued the autophagy imbalance caused by S. aureus infection in MC3T3‐E1 cells. In general, our research demonstrated that butyrate effectively alleviated the hindrance of osteoblast activity induced by S. aureus infection by suppressing the expression of METTL3, suggesting that butyrate may be a novel treatment for S. aureus osteomyelitis.