Romosozumab Enhances Implant Stability in Glucocorticoid-Induced Osteoporotic Bone: A Rabbit Model Study

Implant fixation in osteoporotic bone presents substantial challenges due to reduced bone mass and compromised microarchitecture. This study investigated whether romosozumab, a sclerostin inhibitor, improves osseointegration and mechanical stability of cancellous bone screws in glucocorticoid-induced osteoporosis.

Fifty-five New Zealand white rabbits were enrolled. Osteoporosis was induced via either bilateral ovariectomy or weekly intramuscular glucocorticoid injections (4-8 mg/kg). Based on bone mineral density results, glucocorticoid injection was selected for experimental induction. Rabbits were divided into 5 groups: control, untreated osteoporosis, parathyroid hormone (PTH), PTH combined with denosumab, and romosozumab. Cancellous bone screws (4.0-mm diameter, titanium alloy) were bilaterally inserted into the iliac bones. Antiosteoporosis treatments were administered for 3-week postimplantation. Histomorphometric evaluation of bone-to-implant contact (BIC) and bone area fraction occupancy (BAFO) was performed using nondecalcified sectioning and Goldner trichrome staining. Biomechanical pull-out testing measured resistance at 1-mm displacement using a standardized setup on the MTS system.

The romosozumab-treated group exhibited superior outcomes. BIC reached 21.2%±18.1%, and BAFO was 56.9%±9.9%. Pull-out strength significantly increased to 275±55 N in the romosozumab group, outperforming PTH (184±61 N), PTH+denosumab (202±23 N), and untreated osteoporosis (120±33 N). Enhanced collagen structure and neobone formation were observed histologically around implants.

Romosozumab significantly enhances cancellous bone screw fixation strength and osseointegration in glucocorticoid-induced osteoporotic bone. These findings suggest its clinical potential as an adjuvant therapy in improving spinal implant outcomes in osteoporotic patients.