Abstract
Purpose: Over 100 single nucleotide variants (SNVs) contributing to osteoarthritis (OA) disease risk have now been reported. Risk-conferring variants typically operate by altering expression of a target gene and epigenetic mechanisms within chondrocytes can mediate this regulation. DNA methylation (DNAm) at CpG dinucleotides (CpGs) can correlate with SNV genotype, creating methylation quantitative trait loci (mQTLs). Previously, we have reported mQTLs associated with OA genetic risk loci in aged articular cartilage.
Published Version
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