Posterior fixation without debridement for pyogenic spondylodiscitis can promote infection control: initial evaluation of a pyogenic spondylodiscitis posterior fixation rat model

Abstract Purpose Pyogenic spondylodiscitis is a significant health concern, particularly in older individuals. Minimally invasive surgical techniques, such as posterior fixation, are promising for infection control; however, their mechanisms remain unclear. This study aimed to clarify how posterior fixation promotes infection control in an animal model. Methods Thirty female Wistar rats were used to create a pyogenic spondylodiscitis model by injecting methicillin-sensitive Staphylococcus aureus into the intervertebral space between the 6th and 7th coccygeal vertebrae. Three days post-injection, rats were divided into fixation and control groups. The fixation group underwent posterior fixation with an external fixator, whereas the control group underwent screw insertion alone. Bone destruction was assessed via microcomputed tomography on postoperative days (POD) 7, 14, and 21. Immunohistochemistry for cathepsin K and receptor activator of nuclear factor-kappa B ligand (RANKL) was performed on POD 7 samples to assess osteoclast activity. Results The fixation group showed less bone destruction than the control group at POD 14 (35% vs. 56%, p = 0.0007) and POD 21 (30% vs. 52%, p < 0.0001). The cathepsin K-positive area was significantly reduced in the fixation group ( p = 0.027). RANKL expression was localized within the intervertebral disc in the fixation group, whereas RANKL was strongly expressed on the bone surface adjacent to the disc in control. The RANKL-positive area was also reduced in the fixation group ( p = 0.041). Conclusions Our combined model of pyogenic spondylodiscitis and posterior fixation supports the theory that posterior fixation stability suppresses RANKL and osteoclast expression, promoting infection control.