Aims. Developmental dysplasia of the hip (DDH) is a complex musculoskeletal disease that occurs mostly in children. This study aimed to investigate the molecular changes in the hip joint capsule of patients with DDH. Methods. High-throughput sequencing was used to identify genes that were differentially expressed in hip joint capsules between healthy controls and DDH patients. Biological assays including cell cycle, viability, apoptosis, immunofluorescence, reverse transcription polymerase chain reaction (RT-PCR), and western blotting were performed to determine the roles of the differentially expressed genes in DDH pathology. Results. More than 1,000 genes were differentially expressed in hip joint capsules between healthy controls and DDH. Both gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses revealed that extracellular matrix (ECM) modifications, muscle system processes, and cell proliferation were markedly influenced by the differentially expressed genes. Expression of Collagen Type I Alpha 1 Chain (COL1A1), COL3A1, matrix metalloproteinase-1 (MMP1), MMP3, MMP9, and MMP13 was downregulated in DDH, with the loss of collagen fibres in the joint capsule. Expression of transforming growth factor beta 1 (TGF-β1) was downregulated, while that of TGF-β2, Mothers against decapentaplegic homolog 3 (SMAD3), and WNT11 were upregulated in DDH, and alpha smooth muscle actin (αSMA), a key myofibroblast marker, showed marginal increase. In vitro studies showed that fibroblast proliferation was suppressed in DDH, which was associated with cell cycle arrest in G0/G1 and G2/M phases. Cell cycle regulators including Cyclin B1 (CCNB1), Cyclin E2 (CCNE2), Cyclin A2 (CCNA2), Cyclin-dependent kinase 1 (CDK1), E2F1, cell division cycle 6 (CDC6), and CDC7 were downregulated in DDH. Conclusion. DDH is associated with the loss of collagen fibres and fibroblasts, which may cause loose joint capsule formation. However, the degree of differentiation of fibroblasts to myofibroblasts needs further study. Cite this article: Bone Joint Res 2021;10(9):558–570

Wear induces osteolysis leading to periprosthetic bone loss and TJA loosening. Inflammatory immune cells can form an aggressive interface membrane activating osteoclasts. The current study shows the effect of metal particles and ions triggering cellular responses. Blood samples from primary and revision TJA were analysed for systemic inflammation. PBMCs were cultured on different implant materials. Cellular response was monitored by qRT-PCR. Furthermore, cells were exposed to increasing concentrations of metal particles (10-7 and 10–8 particles/ml) and CoCl2 (50 µM and 100 µM). Cellular response was measured using WST-1 reduction, MitoSox-fluorescence and TUNEL-staining. Cobalt ion influx into osteoblasts was measured using FURA2-staining, cellular effects for HIF-1alpha and qRT-PCR. No inflammatory parameters were detected in patients' blood from primary and revision TJA. Short inflammatory reaction of their PBMCs was observed in in vitro culture on ceramic implants, whereas there was no such reaction to other tested implant martials. In MM6 and Jurkat cells only metal ions induced oxidative stress but did not significantly reduce cell viability. An increase in HIF1-alpha was observed in tissue containing large amounts of metal wear in comparison to plastic wear containing tissues and OA synovial tissue without wear particles. Cobalt ions were stored by osteoblasts via a calcium channel inducing hypoxia. This effect could be blocked using a TRPM blocking agent. Ceramic induces a short inflammatory response that may induce periprosthetic inflammation. Ionic Cobalt induces oxidative stress and hypoxia. Ionic metal exerts a more intense reaction on cells than particles

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Interleukin (IL)-1β is one of the major pathogenic regulators during the pathological development of intervertebral disc degeneration (IDD). However, effective treatment options for IDD are limited. Suramin is used to treat African sleeping sickness. This study aimed to investigate the pharmacological effects of suramin on mitigating IDD and to characterize the underlying mechanism.

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This study aimed to determine if macrophages can attach and directly affect the oxide layers of 316L stainless steel, titanium alloy (Ti6Al4V), and cobalt-chromium-molybdenum alloy (CoCrMo) by releasing components of these alloys.

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Current treatments of prosthetic joint infection (PJI) are minimally effective against Staphylococcus aureus biofilm. A murine PJI model of debridement, antibiotics, and implant retention (DAIR) was used to test the hypothesis that PlySs2, a bacteriophage-derived lysin, can target S. aureus biofilm and address the unique challenges presented in this periprosthetic environment.