Time-course Investigation of Bone and Disc Degeneration in a Rat Model of Pyogenic Spondylodiscitis

化脓性脊柱炎大鼠模型中骨骼和椎间盘退变的时间进程研究

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Abstract

BACKGROUND/AIM: Pyogenic spondylodiscitis causes rapid endplate destruction followed by bone remodeling; however, the time-course of bone loss and recovery remains incompletely defined. This study aimed to characterize longitudinal changes in vertebral bone and intervertebral disc pathology in a rat tail pyogenic spondylodiscitis model. MATERIALS AND METHODS: Male Sprague-Dawley rats (n=16) were allocated to 2-, 4-, or 6-week observation groups. Staphylococcus aureus ATCC 29213 (10(7) CFU/ml, 100 μl) was injected into the C6/7 disc space (Discitis segment), and phosphate-buffered saline (100 μl) was injected into C9/10 as an internal Control segment. Micro-computed tomography was performed at baseline and at sacrifice to quantify the bone destruction rate, disc height ratio, cancellous Hounsfield units (HU), and trabecular microarchitecture (bone volume fraction, trabecular thickness, trabecular number, and trabecular separation). Histology (TRAP and osteocalcin staining) and bone histomorphometry [osteoclast surface per bone surface (Oc.S/BS), osteoclast number per bone surface (Oc.N/BS), and osteoblast surface per bone surface (Ob.S/BS)] were evaluated. RESULTS: The bone destruction rate was significantly higher in the Discitis segment than in the Control segment at all time points, indicating persistent endplate damage. The disc height ratio decreased at 2 weeks but did not differ from controls at 4-6 weeks. Cancellous HU and trabecular parameters showed a biphasic pattern: decreased bone mass at 2 weeks, followed by recovery/reconstruction at 4-6 weeks. Histomorphometry demonstrated increased osteoclast activity (Oc.S/BS, Oc.N/BS) and osteoblast surface (Ob.S/BS) in the acute phase, with osteoclast indices decreasing over time, whereas osteoblast surface remained relatively elevated. CONCLUSION: This model demonstrated a biphasic bone metabolic response characterized by increased osteoclast-mediated bone resorption followed by bone formation and trabecular remodeling. Moreover, this model may serve as an experimental platform to investigate the optimal timing and strategies of therapeutic interventions.

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