Osteoblastogenesis and adipogenesis are higher in osteoarthritic than in osteoporotic bone tissue

New data show that increased adipogenesis in bone marrow may decrease osteoblastogenesis, resulting in osteoporosis (OP). Runt-related transcription factor 2 (RUNX2) and peroxisome proliferator-activated receptor γ (PPARγ) are two main transcriptional regulators controlling osteoblastogenesis and adipogenesis from the same precursor cell in bone-the mesenchymal stem cell. Because osteoarthritis (OA) and OP present the opposing bone phenotype, our aim was to determine whether the expression of selected adipogenic genes is lower in OA compared to OP bone tissue.

Bone samples were obtained from gender-matched OP (n = 54) and OA (n = 49) patients undergoing hip arthroplasty. Osteoblastogenesis and adipogenesis were estimated by gene expression analysis of RUNX2, PPARγ2 and their downstream genes.

In OA bone, significantly higher expression of PPARγ2 and adiponectin as well as RUNX2, osterix and osteocalcin were obtained, suggesting higher adipogenesis and osteoblastogenesis in OA than in OP. There were no differences in RUNX2/PPARγ2 and osteocalcin/adiponectin ratios between groups, suggesting similar balance of both processes. Higher perilipin 2, angiopoietin-like 4 and fatty-acid binding protein 4 mRNA levels in OP suggest activation of other transcription factors or hypoxic conditions in OP bone.

Regulation of bone formation by RUNX2 and PPARγ2 is modified in OA compared to OP, resulting in higher osteoblastogenesis and adipogenesis in OA. Both processes are similarly balanced in OP and OA but less active in OP.