Exploring the role of gut microbiota in the pathogenesis of Kashin-Beck Disease: A Focus on selenium deficiency and T-2 toxin exposure

Abstract

Kashin-Beck disease (KBD) is a chronic degenerative osteochondral condition endemic to certain regions, with its etiology and pathogenesis yet to be fully understood. Research indicates that low selenium levels and exposure to T-2 toxin are recognized environmental risk factors associated with KBD. The gut microbiota, a complex assemblage of microorganisms residing in the human gastrointestinal tract, engages in intricate interactions with its metabolites and the host organism, which can have either beneficial or harmful impacts on host health. These interactions may contribute to or influence the development and progression of various diseases. Clinical investigations into osteoarthritis (OA) have demonstrated alterations in the gut microbiota of patients, which are closely associated with the onset of OA. Notably, KBD exhibits clinical and pathological similarities to OA. In light of the relationship between gut microbiota and bone-related diseases, we propose the hypothesis that selenium deficiency and T-2 toxin exposure induce dysbiosis of the gut microbiota, thereby contributing to the pathogenesis of KBD. We hypothesize that the gut microbiota and its metabolites may play a role in the injury or necrosis of chondrocytes induced by inflammatory responses, as well as in the degradation of the chondrocyte extracellular matrix (ECM), via the “cartilage-gut-microbiome” axis. This interaction could result in pathological changes in chondrocytes. Understanding this mechanism may offer novel insights for the treatment and management of KBD.