Aims

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).

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Biofilm-related infection is a major complication that occurs in orthopaedic surgery. Various treatments are available but efficacy to eradicate infections varies significantly. A systematic review was performed to evaluate therapeutic interventions combating biofilm-related infections on in vivo animal models.

MicroRNAs (miRNAs ) are small non-coding RNAs that regulate gene expression. We hypothesised that the functions of certain miRNAs and changes to their patterns of expression may be crucial in the pathogenesis of nonunion. Healing fractures and atrophic nonunions produced by periosteal cauterisation were created in the femora of 94 rats, with 1:1 group allocation. At post-fracture days three, seven, ten, 14, 21 and 28, miRNAs were extracted from the newly generated tissue at the fracture site. Microarray and real-time polymerase chain reaction (PCR) analyses of day 14 samples revealed that five miRNAs, miR-31a-3p, miR-31a-5p, miR-146a-5p, miR-146b-5p and miR-223-3p, were highly upregulated in nonunion. Real-time PCR analysis further revealed that, in nonunion, the expression levels of all five of these miRNAs peaked on day 14 and declined thereafter. . Our results suggest that miR-31a-3p, miR-31a-5p, miR-146a-5p, miR-146b-5p and miR-223-3p may play an important role in the development of nonunion. These findings add to the understanding of the molecular mechanism for nonunion formation and may lead to the development of novel therapeutic strategies for its treatment. Cite this article: Bone Joint J 2015; 97-B:1144–51

Aims

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

In this study of 41 patients, we used proteomic, Western blot and immunohistochemical analyses to show that several reactive oxygen species scavenging enzymes are expressed differentially in patients with primary osteoarthritis and those with non-loosening and aseptic loosening after total hip replacement (THR). The patients were grouped as A (n = 16, primary THR), B (n = 10, fixed THR but requiring revision for polyethylene wear) and C (n = 15, requiring revision due to aseptic loosening) to verify the involvement of the identified targets in aseptic loosening. When compared with Groups A and B, Group C patients exhibited significant up-regulation of transthyretin and superoxide dismutase 3, but down-regulation of glutathione peroxidase 2 in their hip synovial fluids. Also, higher levels of superoxide dismutase 2 and peroxiredoxin 2, but not superoxide dismutase 1, catalase and glutathione perioxidase 1, were consistently detected in the hip capsules of Group C patients. We propose that dysregulated reactive oxygen species-related enzymes may play an important role in the pathogenesis and progression of aseptic loosening after THR

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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.

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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.

Posterolateral rotatory instability is the most common type of symptomatic chronic instability of the elbow. In this condition the forearm complex rotates externally in relation to the humerus, causing posterior subluxation or dislocation of the radial head. The lateral ligament complex, radial head and coronoid process are important constraints to posterolateral rotatory instability, and their disruption is involved in the pathogenesis of this condition. The diagnosis relies on a high index of clinical suspicion, active and passive apprehension tests, and examination under anaesthesia. Surgical treatment has given consistently successful results. Open reconstruction of the lateral ligaments with a tendon graft has been the procedure of choice, with arthroscopic techniques emerging as a potential alternative

Previous perfusion studies of the rotator cuff have demonstrated an area of hypovascularity in the distal part of the supraspinatus tendon. This has been implicated in the pathogenesis of its rupture. We performed a quantitative histological analysis of the vascularity of the tendons of supraspinatus and infraspinatus. Vessel number, size and the percentage of the tendon occupied by vessels were measured at 5 mm intervals from the humeral insertions to the muscle bellies. Both tendons were hypovascular in their distal 15 mm. No significant difference was demonstrated between the vascularity of supraspinatus and infraspinatus. We conclude that factors other than vascularity are important in the pathogenesis of supraspinatus rupture

Our aim was to analyse the influence of the size, shape and number of particles on the pathogenesis of osteolysis. We obtained peri-implant tissues from 18 patients having revision surgery for aseptically loosened Freeman total knee replacements (10), Charnley total hip replacements (3) and Imperial College/London Hospital double-cup surface hip replacements (5). The size and shape of the polyethylene particles were characterised using SEM and their concentration was calculated. The results were analysed with reference to the presence of radiological osteolysis. The concentration of polyethylene particles in 6 areas with osteolysis was significantly higher than that in 12 areas without osteolysis. There were no significant differences between the size and shape of the particles in these two groups. We conclude that the most critical factor in the pathogenesis of osteolysis is the concentration of polyethylene particles accumulated in the tissue

Aims

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

Ischaemia resulting from increased joint pressure may play a role in the pathogenesis of necrosis of the femoral head epiphysis. We studied the effect of temporary vascular occlusion on this epiphysis in young rabbits. Occlusion for six hours resulted in necrosis of trabecular bone and of intertrabecular marrow and vascular tissue, later followed by revascularisation and repair, as has been demonstrated previously. In contrast, raised intra-articular pressure lasting for only two hours resulted in a more complex picture: trabecular osteocytes were dead, whereas the bone-forming marrow was shown by fluorochrome labelling to remain viable, and to form appositional repair bone throughout the epiphysis. We concluded that transient vascular occlusion may cause the death of trabeculae despite intact perfusion of the bone. This type of change may be important in the pathogenesis of Perthes' disease

1. The capsular changes in osteoarthritis of the hip and their pathogenesis are described, and it is concluded that symptoms are due mainly to this abnormality. 2. The clinical significance and pathogenesis of subchondral sclerosis, cysts, osteophytes, secondary subluxation and new bone formation on the lower border of the femoral neck are discussed. 3. These bony features which can be seen in the radiograph may, under certain circumstances, be correlated with the symptoms. 4. The influence of joint debris and capsular fibrosis upon the symptoms arising in other osteoarthritic joints is considered. 5. The mechanism by which osteoarthritis develops in hip joints with an anatomical abnormality is discussed in relation to the normal functional anatomy of the hip. 6. The evolution of osteoarthritis in dysplasia of the hip is considered with special reference to its diagnosis, prognosis and early treatment. 7. The supposition that osteoarthritis is commonly due to progressive ischaemia in the femoral head has been investigated and is rejected. 8. The cause of idiopathic osteoarthritis remains obscure but the evidence suggests that constitutional rather than local conditions in the joint account for many of these cases

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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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.

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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.

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