5ɑ-Dihydrotestosterone Upregulates Interferon Signaling in Osteoclast Differentiation During Inflammatory State

In RA, the differentiation of osteoclast precursor cells (OCPs) into bone-resorbing osteoclasts is stimulated by the inflammatory environment, causing significant erosive disease. Notably, androgen, the dominant sex hormone in males, is protective against this inflammation-driven bone loss.

To investigate how androgen regulates osteoclastogenesis in an inflammatory state, bone marrow-derived cells were treated with or without androgen in a TNF-mediated osteoclast culture. 5ɑ-dihydrotestosterone (DHT)-treated and vehicle-treated cells were collected, analyzed, and compared with single-cell RNA-sequencing which determined differences in cell populations, gene expression, functional gene ontology, and differentiation.