Osteoarthritis (OA) is an age-related cartilage degenerative disease, and chondrocyte senescence has been extensively studied in recent years. Increased numbers of senescent chondrocytes are found in OA cartilage. Selective clearance of senescent chondrocytes in a post-traumatic osteoarthritis (PTOA) mouse model ameliorated OA development, while intraarticular injection of senescent cells induced mouse OA. However, the means and extent to which senescence affects OA remain unclear. Here, we review the latent mechanism of senescence in OA and propose potential therapeutic methods to target OA-related senescence, with an emphasis on immunotherapies. Natural killer (NK) cells participate in the elimination of senescent cells in multiple organs. A relatively comprehensive discussion is presented in that section. Risk factors for OA are ageing, obesity, metabolic disorders and mechanical overload. Determining the relationship between known risk factors and senescence will help elucidate OA pathogenesis and identify optimal treatments.

Osteoarthritis (OA) is a prevalent degenerative disease in elderly people that is characterized by cartilage loss and abrasion, leading to joint pain and dysfunction. The aetiology of OA is complicated and includes abnormal mechanical stress, a mild inflammatory environment, chondrocyte senescence and apoptosis, and changes in chondrocyte metabolism. Ferroptosis is a regulated cell death modality characterized by the excessive accumulation of lipid peroxidation and mitochondrial dysfunction. The role of ferroptosis in OA pathogenesis has aroused researchers’ attention in the past two years, and there is mounting evidence indicating that ferroptosis is destructive. However, the impact of ferroptosis on OA and how the regulators of ferroptosis affect OA development are unclear. Here, we reviewed the current understanding of ferroptosis in OA pathogenesis and summarized several drugs and compounds targeting ferroptosis in OA treatment. The accumulation of intracellular iron, the trigger of Fenton reaction, the excessive production of ROS, the peroxidation of PUFA-PLs, and mitochondrial and membrane damage are involved in chondrocyte ferroptosis. System X_c⁻ and GPX4 are the most important regulators that control ferroptosis. Several compounds, such as DFO and Fer-1, have been proven effective in preventing ferroptosis and slowing OA progression on animal models. Collectively, targeting ferroptosis shows great potential in treating OA.

With the increasing prevalence of obesity, there is growing awareness of the impact of overweight and obesity on total hip arthroplasty (THA). Research exploring the accuracy of acetabular component orientation in THA between robotic-assisted and manual techniques across different BMI categories is insufficient. This prospective study evaluated 221 patients who underwent THA with a Robotic Interactive Orthopaedic Arm system and 252 patients who underwent manual THA between March 2022 and January 2024. The patients were divided into four groups according to their BMI. We analysed whether there were differences in the accuracy of acetabular component positioning between robotic-assisted THA and manual THA across different BMI categories. In the overweight group, robotic-assisted THA achieved a significantly higher rate of abductions within the target range (73/6) than manual THA (62/28) (p = 0.000). Both abductions and anteversions within the target range were also significantly more frequent in the robotic-assisted THA group (69/10) than in the manual THA group (56/34) (p = 0.000). Among the obese patients, robotic-assisted THA showed a perfect record for anteversions within the target range (29/0), markedly outperforming manual THA (39/6) (p = 0.040). In the overweight (24 kg/m² ≤ BMI < 28 kg/m²) and obese (BMI ≥ 28 kg/m²) groups, robotic-assisted THA demonstrates significantly greater accuracy in acetabular component positioning compared to manual THA. This indicates that robotic-assisted technology may provide a more precise positioning of the acetabular component in overweight and obese patients.

Osteoarthritis (OA) is a common disease characterized by severe chronic joint pain, that imposes a large burden on elderly people. OA is a highly heterogeneous disease, and multiple etiologies contribute to its progression. Sirtuins (SIRTs) are Class III histone deacetylases (HDACs) that regulate a comprehensive range of biological processes such as gene expression, cell differentiation, and organism development, and lifespan. Over the past three decades, increasing evidence has revealed that SIRTs are not only important energy sensors but also protectors against metabolic stresses and aging, and an increasing number of studies have focused on the functions of SIRTs in OA pathogenesis. In this review, we illustrate the biological functions of SIRTs in OA pathogenesis from the perspectives of energy metabolism, inflammation, autophagy and cellular senescence. Moreover, we offer insights into the role played by SIRTs in regulating circadian rhythm, which has recently been recognized to be crucial in OA development. Here, we provide the current understanding of SIRTs in OA to guide a new direction for OA treatment exploration.