Conclusion
S. aureus bacteremia triggers local bone loss in murine arthritis, depending on both age and TLR2 expression.
Methods
We analyzed distal femoral BMD in young and old TLR2 knock-out and wild-type mice following intravenous S. aureus infection. BMD was measured in both total and trabecular bone in old and young mice to determine age and TLR2-dependent responses to infection.
Results
In non-infected mice, BMD in both total and trabecular bone was mainly age-related and TLR2-independent. Following S. aureus bacteremia, young wild-type mice with TLR2 expression showed decreased combined cortical and trabecular BMD. This effect was absent in aged mice or TLR2 deficient mice. Focal septic arthritis, induced by S. aureus bacteremia, emerged as the primary cause to bone loss in the femur metaphysis. TLR2 appears to play a crucial role in focal septic arthritis-induced bone loss, as evidenced by in vitro findings demonstrating that staphylococcal LPPs, known TLR2 agonists, increase the Tnfsf11/Tnfrsf11b ratio in mouse pariosteal osteoblasts.