Osteoarthritis is the most common rheumatic disease, its incidence increases with age (Heideri, 2011). The economic cost of OA treatment is high (Zhang et al., 2016). It is characterized by articular cartilage loss, synovitis and bone resorption leading to functional failure (Ba?kan, et al., 2018) . Aberrant epigenetic changes regulate the pathogenesis of osteoarthritis and control molecular mediators of it (Hammaker and Firestein, 2017). Also, the epigenetic changes are linked to inflammation of the cartilage because inflammatory mediators affect the function of the enzymes involved in DNA methylation (Shen et al., 2017).
The current study showed a significant increase of the 5-mC level, a marker of global methylation in the blood of OA patients in comparison with the control group. This indicated that the OA pathogenesis is characterized by hypermethylation. To our knowledge, this might be the first study investigated the 5-mC concentration in the blood of OA patients. The results of the previous studies are inconsistent about the methylation status in OA. Epigenetic analysis of genes related to OA indicated that some genes may affected by hypermethylation as collagen gene(COL9A1) (Imagawa et al.,2014) while the expression of other genes is silenced by hypomethylation MMP genes (Roach et al.,2005). Alvarez?Garcia et al. (2016) identified increased methylation in OA cartilage than normal cartilage. as Bailey et al. (2013) reported that altered promoter DNA methylation levels of multiple genes in the peripheral blood mononuclear cells in patients with knee OA.
Our results are against some studies that assessed 5-mC level in cartilage and synovial fluid of OA joints. However, a non-significant change in general methylation levels in osteoarthritic chondrocytes was reported by Sesselmann et al. (2009). Results of other studies about the level of 5-mC in cartilage chondrocytes of OA detected unchanged level in comparison to non OA chondrocyte (Taylor et al., 2014). Also, the methylation of 31 genes related to bone and cartilage metabolism was measured in chondrocytes of knee OA in rats and significant decreases of methylation levels of C/ebp?-2, Cdk2, Bak1, and Fas genes which participate in the pathogenesis of Knee OA were found (Wang et al., 2017).
The findings of our study showed that the 5-mC level was not associated with clinical parameters of OA and not correlated with the KL grade of radiological severity or with a Lequensce index of clinical severity. This is not consistent with Rivas and Jeffries (2017) that showed that the methylation profile of blood with rapid progressive OA was found to correlated with radiographic cartilage loss.
In addition to the main pathology of the articular cartilage, remodeling of the bone is occurred in OA. This pathology involves subchondral bone as well as bone distal to the affected joint (Hopwood et al.,2009). The subchondral bone changes are strongly related to the severity of OA (Muratovic et al., 2018).
Our research indicated that the 5-mC concentration association with bone erosion not reached the statistical significance level (P=0.052), but was not associated with osteoporosis. Zhang et al. (2016) examined the genome-wide DNA methylation profiles of subchondral bone at the early, intermediate and late stages of OA using Human Methylation 450 BeadChip and reported that the DNA methylation changes occurred earlier in subchondral bone and different methylation patterns detected at the late stage of OA. DNA methylation was suggested to be associated with postmenopausal osteoporosis (Reppe et al., 2015).
The present study showed that the BMP-2 serum level was higher in knee OA patients when compared to control group (P


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