Rheumatoid arthritis (RA) is an autoimmune disease that involves T and B cells and their reciprocal immune interactions with proinflammatory cytokines. T cells, an essential part of the immune system, play an important role in RA. T helper 1 (Th1) cells induce interferon-γ (IFN-γ), tumour necrosis factor-α (TNF-α), and interleukin (IL)-2, which are proinflammatory cytokines, leading to cartilage destruction and bone erosion. Th2 cells primarily secrete IL-4, IL-5, and IL-13, which exert anti-inflammatory and anti-osteoclastogenic effects in inflammatory arthritis models. IL-22 secreted by Th17 cells promotes the proliferation of synovial fibroblasts through induction of the chemokine C-C chemokine ligand 2 (CCL2). T follicular helper (Tfh) cells produce IL-21, which is key for B cell stimulation by the C-X-C chemokine receptor 5 (CXCR5) and coexpression with programmed cell death-1 (PD-1) and/or inducible T cell costimulator (ICOS). PD-1 inhibits T cell proliferation and cytokine production. In addition, there are many immunomodulatory agents that promote or inhibit the immunomodulatory role of T helper cells in RA to alleviate disease progression. These findings help to elucidate the aetiology and treatment of RA and point us toward the next steps.Cite this article: Bone Joint Res 2022;11(7):426–438.

Chondrocytes are the sole cellular constituents of normal cartilage. The degeneration and apoptosis of these cells are considered the main cause of osteoarthritis (OA). Previous studies have suggested that the enhancement of autophagy in chondrocytes can delay the progression of osteoarthritis by affecting intracellular metabolic activity, i.e., by regulating the metabolism of nutrients, which can delay cell aging and death. In this review, we explored the relationship between autophagy and chondrocyte metabolism and provided new ideas for the prevention and treatment of OA.

The pathological manifestations of osteoarthritis (OA) involve the destruction of articular cartilage, synovial sac thickening, subchondral osteosclerosis and osteophyte formation. The types of cells involved in OA include chondrocytes, osteoblasts, osteoclasts, synovial fibroblasts, T cells, macrophages, and mesenchymal stem cells (MSCs). There are many effects of immune cells in OA, and innate immune cells such as dendritic cells and macrophages have significant roles in the pathogenesis of OA. On the other hand, the role of adaptive immune cells such as T-cell subsets, B-cell subsets, and NK cells is important in OA pathogenesis. MSCs not only play a key role in the dynamic balance and repair of OA tissue but also inhibit the immune system. Therefore, MSCs are a new potential therapeutic agent for OA. This review mainly summarizes the effects of various immune cells and cytokines on different cells in OA to find new effective therapeutic targets for OA therapy based on the immune system and cytokine activity sites to prevent the development of OA.

Osteoarthritis (OA) is mainly caused by ageing, strain, trauma, and congenital joint abnormalities, resulting in articular cartilage degeneration. During the pathogenesis of OA, the changes in subchondral bone (SB) are not only secondary manifestations of OA, but also an active part of the disease, and are closely associated with the severity of OA. In different stages of OA, there were microstructural changes in SB. Osteocytes, osteoblasts, and osteoclasts in SB are important in the pathogenesis of OA. The signal transduction mechanism in SB is necessary to maintain the balance of a stable phenotype, extracellular matrix (ECM) synthesis, and bone remodelling between articular cartilage and SB. An imbalance in signal transduction can lead to reduced cartilage quality and SB thickening, which leads to the progression of OA. By understanding changes in SB in OA, researchers are exploring drugs that can regulate these changes, which will help to provide new ideas for the treatment of OA.Cite this article: Bone Joint Res 2023;12(9):536–545.

Objective: Although previous studies have shown that gut microbiota may be involved in the occurrence of deep venous thrombosis (DVT), the specific link between the two remains unclear. The present study aimed to explore this question from a genetic perspective.Materials and methods: Genome-wide association study (GWAS) summary data of DVT were obtained from the UK Biobank (N = 9,059). GWAS summary data of the gut microbiota were obtained from the Flemish Gut Flora Project (N = 2,223) and two German cohorts (FoCus, N = 950; PopGen, N = 717). All the participants were of European ancestry. Linkage disequilibrium score (LDSC) regression has great potential for analyzing the heritability of disease or character traits. LDSC regression was used to analyze the genetic correlation between DVT and the gut microbiota based on the GWAS summary data obtained from previous studies. Mendelian randomization (MR) was used to analyze the genetic causal relationship between DVT and the gut microbiota. We used the random effects inverse variance weighted, MR Egger, weighted median, simple mode, and weighted mode to perform MR analysis. We performed a sensitivity analysis of the MR analysis results by examining heterogeneity and horizontal pleiotropy.Results: Linkage disequilibrium score analysis showed that Streptococcaceae (correlation coefficient = −0.542, SE = 0.237, P = 0.022), Dialister (correlation coefficient = −0.623, SE = 0.316, P = 0.049), Streptococcus (correlation coefficient = −0.576, SE = 0.264, P = 0.029), and Lactobacillales (correlation coefficient = −0.484, SE = 0.237, P = 0.042) had suggestive genetic correlation with DVT. In addition, the MR analysis showed that Streptococcaceae had a positive genetic causal relationship with DVT (P = 0.027, OR = 1.005). There was no heterogeneity or horizontal pleiotropy in the MR analysis (P > 0.05).Conclusion: In this study, four gut microbes (Streptococcaceae, Dialister Streptococcus, Lactobacillales) had suggestive genetic correlations with DVT, and Streptococcaceae had a positive causal relationship with DVT. Our findings provide a new research direction for the further study of and prevention of DVT.