Focal Septic Arthritis Elicits Age and TLR2-Dependent Periarticular Bone Loss.

INTRODUCTION

Septic arthritis, primarily caused by (), is a severe joint infection that leads to joint and bone damage. lipoproteins (LPPs) bind to Toll-like Receptor 2 (TLR2), inducing arthritis and localized bone loss. Aging affects TLR2 immune response to pathogens. While intra-articular injections of LPPs induces local bone resorption in mice, the influence of aging and TLR2 expression on bone mineral density (BMD) after bacteremia remains unclear.

METHODS

We analyzed distal femoral BMD in young and old TLR2 knock-out and wild-type mice following intravenous 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 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 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 ratio in mouse pariosteal osteoblasts.

CONCLUSION

bacteremia triggers local bone loss in murine arthritis, depending on both age and TLR2 expression.