Adolescent idiopathic scoliosis (AIS), defined by an age at presentation of 11 to 18 years, has a prevalence of 0.47% and accounts for approximately 90% of all cases of idiopathic scoliosis. Despite decades of research, the exact aetiology of AIS remains unknown. It is becoming evident that it is the result of a complex interplay of genetic, internal, and environmental factors. It has been hypothesized that genetic variants act as the initial trigger that allow epigenetic factors to propagate AIS, which could also explain the wide phenotypic variation in the presentation of the disorder. A better understanding of the underlying aetiological mechanisms could help to establish the diagnosis earlier and allow a more accurate prediction of deformity progression. This, in turn, would prompt imaging and therapeutic intervention at the appropriate time, thereby achieving the best clinical outcome for this group of patients.

Cite this article: Bone Joint J 2022;104-B(8):915–921.

Aims

To evaluate inducing osteoarthritis (OA) by surgical destabilization of the medial meniscus (DMM) in mice with and without a stereomicroscope.

Both osteochondritis dissecans and coxa plana are diseases with identical pathological changes, namely avascular necrosis. Although the etiology is not known in either case, it seems likely that when the etiological factors are fully determined they will prove to be applicable to either condition. The relative importance of each etiological factor in the multiple pathogenesis of these two conditions is almost certainly different in each disease process, and probably in each individual case. Present day concepts suggest that there is an underlying constitutional disturbance, which is associated with other factors (of which trauma is almost universally accepted as being one; perhaps the only one), to predispose the individual to these conditions. It is hoped that further studies along these lines will not only help to provide a better understanding of the two conditions mentioned above, but will also be of value in the appreciation of the pathogenesis and etiology of a large number of disturbances including such varied conditions as dysplasia epiphysialis multiplex congenita, cretinoid dysgenesis of the capital femoral epiphysis, adolescent coxa vara, transient synovitis of the hip, and the recently discussed (Merle d'Aubigné 1964) idiopathic avascular necrosis of the femoral head in adults. That there is an etiological relationship between osteochondritis dissecans and coxa plana seems clear, but much more work is required before we will have at hand the patho-physiological evidence that will permit an accurate correlation of these two conditions

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We aimed to develop a gene signature that predicts the occurrence of postmenopausal osteoporosis (PMOP) by studying its genetic mechanism.

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Post-traumatic osteoarthritis (PTOA) is a subset of osteoarthritis (OA). The gut microbiome is shown to be involved in OA. However, the effect of exercise on gut microbiome in PTOA remains elusive.

Adamantinoma is a rare tumour of long bones that occurs most commonly in the tibia. Its pathogenesis is unknown. It is locally aggressive and recurrences are common after resection. Metastases have been reported in 10% to 20% of cases, most commonly in the lungs and rarely in the lymph nodes. We report a patient who developed a skeletal metastasis four years after resection of the primary tumour. There was no evidence of recurrence at the primary site or of secondary deposits in the lungs

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The aim of this study was to compare outcomes of guided growth and varus osteotomy in treating Kalamchi type II avascular necrosis (AVN) after open reduction and Pemberton acetabuloplasty for developmental dysplasia of the hip (DDH).

Perthes’ disease is an osteonecrosis of the juvenile hip, the aetiology of which is unknown. A number of comorbid associations have been suggested that may offer insights into aetiology, yet the strength and validity of these are unclear. This study explored such associations through a case control study using the United Kingdom General Practice Research database. Associations investigated were those previously suggested within the literature. A total of 619 cases of Perthes’ disease were included, as were 2544 controls. The risk of Perthes’ disease was significantly increased with the presence of congenital anomalies of the genitourinary and inguinal region, such as hypospadias (odds ratio (OR) 4.04 (95% confidence interval (CI) 1.41 to 11.58)), undescended testis (OR 1.83 (95% CI 1.12 to 3.00)) and inguinal herniae (OR 1.79 (95% CI 1.02 to 3.16)). Attention deficit hyperactivity disorder was not associated with Perthes’ disease (OR 1.01 (95% CI 0.48 to 2.12)), although a generalised behavioural disorder was (OR 1.55 (95% CI 1.10 to 2.17)). Asthma significantly increased the risk of Perthes’ disease (OR 1.44 (95% CI 1.17 to 1.76)), which remained after adjusting for oral/parenteral steroid use. Perthes’ disease has a significant association with congenital genitourinary and inguinal anomalies, suggesting that intra-uterine factors may be critical to causation. Other comorbid associations may offer insight to support or refute theories of pathogenesis

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Alcoholism is a well-known detrimental factor in fracture healing. However, the underlying mechanism of alcohol-inhibited fracture healing remains poorly understood.

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In the repair of condylar cartilage injury, synovium-derived mesenchymal stem cells (SMSCs) migrate to an injured site and differentiate into cartilage. This study aimed to confirm that histone deacetylase (HDAC) inhibitors, which alleviate arthritis, can improve chondrogenesis inhibited by IL-1β, and to explore its mechanism.

Aseptic loosening is a major cause of failure of total hip arthroplasty. The adverse tissue response to prosthetic wear particles, with activation of cytokine and prostanoid production, contributes to bone loss around the implants. We have investigated the possibility that inducible nitric oxide synthase (iNOS) and cyclo-oxygenase-2 (COX-2) are expressed in macrophages in the pseudomembrane at the bone-implant interface, thereby contributing to the periprosthetic bone resorption. We also assessed whether peroxynitrite, a nitric oxide (NO)-derived oxidant associated with cellular injury, is generated in the membrane. Enzymatic activity of iNOS was measured using the arginine-citrulline assay technique and prostaglandin E. 2. (PGE. 2. ), as an indicator of COX-2 activity, was measured using an enzyme immunoassay. Cellular immunoreactivity for iNOS, nitrotyrosine (a marker of peroxynitrite-induced cellular injury) and COX-2 was assessed by quantitative peroxidase immunocytochemistry while immunofluorescence methods were used for subsequent co-localisation studies with CD68. +. macrophages. The presence of calcium-independent iNOS activity and PGE. 2. production was confirmed in the homogenized interface membrane. Immunocytochemistry showed that periprosthetic CD68. +. wear-debris-laden macrophages were the most prominent cell type immunoreactive for iNOS, nitrotyrosine and COX-2. Other periprosthetic inflammatory and resident cell types were also found to immunolocalise nitrotyrosine thereby suggesting peroxynitrite-induced protein nitrosylation and cellular damage not only in NO-producing CD68. +. macrophages, but also in their neighbouring cells. These data indicate that both iNOS and COX-2 are expressed by CD68. +. macrophages in the interface membrane and peroxynitrite-induced cellular damage is evident in such tissue. If high-output NO and peroxynitrite generation were to cause macrophage cell death, this would result in the release of phagocytosed wear debris into the extracellular matrix. A detrimental cycle of events would then be established with further phagocytosis by newly-recruited inflammatory cells and subsequent NO, peroxynitrite and prostanoid synthesis. Since both NO and have been implicated in the induction and PGE. 2. maintenance of chronic inflammation with resulting loss of bone, and peroxynitrite in the pathogenesis of disease states, they may be central to the pathogenesis of aseptic loosening

This review of the literature presents the current understanding of Scheuermann’s kyphosis and investigates the controversies concerning conservative and surgical treatment. There is considerable debate regarding the pathogenesis, natural history and treatment of this condition. A benign prognosis with settling of symptoms and stabilisation of the deformity at skeletal maturity is expected in most patients. Observation and programmes of exercise are appropriate for mild, flexible, non-progressive deformities. Bracing is indicated for a moderate deformity which spans several levels and retains flexibility in motivated patients who have significant remaining spinal growth. The loss of some correction after the completion of bracing with recurrent anterior vertebral wedging has been reported in approximately one-third of patients. Surgical correction with instrumented spinal fusion is indicated for a severe kyphosis which carries a risk of progression beyond the end of growth causing cosmetic deformity, back pain and neurological complications. There is no consensus on the effectiveness of different techniques and types of instrumentation. Techniques include posterior-only and combined anteroposterior spinal fusion with or without posterior osteotomies across the apex of the deformity. Current instrumented techniques include hybrid and all-pedicle screw constructs

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To develop an early implant instability murine model and explore the use of intermittent parathyroid hormone (iPTH) treatment for initially unstable implants.

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To investigate whether idiopathic osteonecrosis of the femoral head (ONFH) is related to impaired osteoblast activities.

Rheumatoid arthritis (RA) is an autoimmune disease characterized by symmetrical and chronic polyarthritis. Fibroblast-like synoviocytes are mainly involved in joint inflammation and cartilage and bone destruction by inflammatory cytokines and matrix-degrading enzymes in RA. Approaches that induce various cellular growth alterations of synoviocytes are considered as potential strategies for treating RA. However, since synoviocytes play a critical role in RA, the mechanism and hyperplastic modulation of synoviocytes and their motility need to be addressed. In this review, we focus on the alteration of synoviocyte signalling and cell fate provided by signalling proteins, various antioxidant molecules, enzymes, compounds, clinical candidates, to understand the pathology of the synoviocytes, and finally to achieve developed therapeutic strategies of RA.

Cite this article: Bone Joint Res 2021;10(4):285–297.

Aims

Rheumatoid arthritis (RA), which mainly results from fibroblast-like synoviocyte (FLS) dysfunction, is related to oxidative stress. Advanced oxidation protein products (AOPPs), which are proinflammatory mediators and a novel biomarker of oxidative stress, have been observed to accumulate significantly in the serum of RA patients. Here, we present the first investigation of the effects of AOPPs on RA-FLSs and the signalling pathway involved in AOPP-induced inflammatory responses and invasive behaviour.

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Osteoarthritis (OA) is characterized by persistent destruction of articular cartilage. It has been found that microRNAs (miRNAs) are closely related to the occurrence and development of OA. The purpose of the present study was to investigate the mechanism of miR-486 in the development and progression of OA.

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This study aimed to evaluate sagittal spinopelvic alignment (SSPA) in the early stage of rapidly destructive coxopathy (RDC) compared with hip osteoarthritis (HOA), and to identify risk factors of SSPA for destruction of the femoral head within 12 months after the disease onset.

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The aim of this prospective study was to assess the long-term clinical, radiological, functional, and quality of life (QoL)-related outcome of patients treated with the synthetic Ligament Advanced Reinforcement System (LARS) device for anterior cruciate ligament (ACL) rupture.