Dysregulation of myddosome complex genes its related to alendronate treatment failure in osteoporosis postmenopausal patients.

Some patients with osteoporosis (OP) do not respond to treatment with bisphosphonates; pathways that stimulate osteoclatogenesis may be involved in this failure, such as the myddosome pathway. A total of 40 OP patients and 20 controls were included in the group study. Patients treated with sodium alendronate (SA) for two years were classified according to bone mineral density (BMD) variations of the lumbar spine, femoral neck, and total hip, measured by the method of dual-energy x-ray absorptiometry (DXA) as responsive patients (OP-R) (n = 20) and non-responders (OP-NR) (n = 20), to evaluate the impact of the myddosome pathway gene expression profile in postmenopausal women with OP. The gene expressions were measured through real-time relative quantitative PCR with Taqman® probes; relative quantification was normalized to GAPDH and RPLP0 reference genes. Non-responders showed increased expression levels of MYD88 and IRAK3 compared to responders Fold change (FC) = 2.86±1.54, p=0.0002 e FC= 3.62±0.46, p<0.0001 respectively. Our results demonstrate the influence of the myddosome on OP maintenance and response to sodium alendronate (SA) treatment, highlighting the importance of this pathway as a potential target for new therapeutic approaches in postmenopausal OP.