Table 2.
Sources | Characteristic | Diagnosis value | Relationship with OA | Ref. | |
---|---|---|---|---|---|
Blood | Plasma | Lower expression of miR-193b | Early diagnosis; | miR-193b is negatively correlated with inflammation | [44] |
Reflect the phenotypes | |||||
Serum | Higher expression of cathepsin F and lower lg α2 chain C | Early diagnosis | Cathepsin F may involve in the pathogenesis of OA | [122] | |
Plasma | Ratios of neutrophil-EVs to lymphocyte-EVs were positively correlated between plasma and SF | Early diagnosis; | Reflect OA joint inflammation and disease severity | [124] | |
Reflect the severity of OA | |||||
synovial fluid | Synovial fluid | Higher expression of HLA-DR,-DP, and -DQ | Reflect the severity of OA | Mainly originated from the immune cell infiltration in the OA joint | [124] |
Synovial fluid | Higher expression of PCGEM1 in late OA than in early OA | Reflect the stages of OA | PCGEM1 inhibited apoptosis, induced autophagy, and stimulated proliferation | [123,125] | |
Synovial fluid | Differential expression of miRNA between men and women | Reflect the subtype of OA | female specific miRNAs are estrogen responsive and target TLR signaling pathways. | [120] | |
Synovial fluid | Differential expression of miRNA before and after treatment | Evaluate the effect of treatment | Correlated with cartilage production (in young mice) and immune (in aged mice) | [48] | |
Tissue biopsies | Synovial fibroblasts | Differential expression of fifty miRNAs | Reflect the susceptibility of OA | miRNA expression patterns in exosomes are altered and miRNAs are selectively released; | [37] |
Chondrocytes | Nine proteins only present in OA-ACVs | Reflect the presence of stromal changes and predict OA | Differences in ECM proteins in OA and normal ACVs largely reflect known changes in OA ECM and increased catabolism | [126] |
*ACV: articular cartilage vesicles.