Selenium, Selenoprotein P, and Gut Dysbiosis are Associated with Cartilage Damage in Osteoarthritis Patients.

The objective of the present study was to evaluate markers of selenium (Se) metabolism and taxonomic characteristics of gut microbiota, as well as their relationship to markers of inflammation and cartilage damage in patients with osteoarthritis (OA). The study enrolled 50 healthy controls, 45 patients with knee OA (kOA), and 41 patients with knee and one-sided hip OA (khOA). Serum selenoprotein P (SELENOP), cartilage oligomeric matrix protein (COMP), lipopolysaccharide (LPS), C-reactive protein (CRP), as well as C3 and C5a complement components were assessed. Serum, hair, and urinary Se levels were evaluated using inductively coupled plasma-mass spectrometry (ICP-MS). Fecal microbiota taxonomy was evaluated by high-throughput sequencing. Patients with kOA and especially khOA were characterized by higher COMP and CRP levels. LPS concentration also tended to be higher in khOA patients. The lowest serum Se and SELENOP levels were observed in khOA patients. The richness of Bacteroidota phylum, classes Bacteroidia and Negativicutes was increased, whereas the abundance of Coriobacteriia was lower in OA patients compared to controls. The relative abundance of families Actinomycetaceae, Anaerovoracaceae, Clostridiaceae, Eggerthellaceae, Lactobacillaceae, Peptostreptococcaceae, Streptococcaceae, and unclassified_Clostridia UCG-014 was reduced in OA patients, while Oscillospiraceae and Prevotellaceae were enriched. Significant group differences were also observed in the richness of certain bacterial genera. Multiple linear regression analysis revealed inverse association between SELENOP and LPS concentrations, while COMP concentration was associated with C5a and SELENOP levels in a positive and negative manner, respectively. Certain bacterial taxa were also considered significant predictors of SELENOP and COMP levels. Therefore, these novel data establish that gut dysbiosis is associated with both cartilage damage and altered Se metabolism in OA.