Taken alongside data showing that TLR2- and TLR9-deficient osteoclast precursors undergo osteoclastogenesis upon intracellular infection with S. aureus, these data suggest that TLR2- and TLR9-independent pathways have the potential to modulate osteoclastogenesis during osteomyelitis. This evidence concerns the gene TLR9 and osteomyelitis.