摘要
Introduction Rheumatoid arthritis(RA)is a chronic autoimmune disease that results in a series of inflammatory reactions in the joints,marked by pathologies such as articular bone destruction and erosive synovial inflammatory cartilage[1].The bone destruction in RA arises from an imbalance between bone resorption by osteoclasts and bone formation by osteoblasts[2].The pathogenesis of RA remains unknown,and studies have indicated its close relationship with genetics,the environment,immune response,and other factors.Potential genes linked to RA susceptibility include major histocompatibility complex genes,like the single nucleotide polymorphism rs9277535 in the HLA-DP subunit HLA-DPB1,which is strongly associated with RA susceptibility in the Western Chinese population[3].Furthermore,studies have also identified a correlation between major genes encoding the inflammatory CASPs(CASP1,CASP4,and CASP5)and RA[4].Environmental factors,including smoking,diet,obesity,and infections,have the ability to trigger RA in susceptible individuals[5,6].Regarding the immune response,both immune dysregulation and overactivity can result in an inflammatory response,leading to excessive proliferation of synovial tissue,imbalanced distribution of osteoblasts and osteoclasts,and an irregular proportion of immune cells,culminating in the disease.
