Sclerostin antibody promotes alveolar bone regeneration after tooth extraction

Sclerostin is a key inhibitor of the Wnt signaling pathway, functioning by binding to the LRP5/6 receptor. This interaction inhibits beta-catenin expression, resulting in the downregulation of osteogenic markers, which contributes to the promotion of osteoporosis and an increase in osteoclast numbers. The primary objective of this research was to investigate the effects of sclerostin antibody (Scl-ab) on bone formation utilizing graft materials in tooth sockets, and to analyze the regulatory interaction between sclerostin and bone tissue through targeted sclerostin inhibition and stimulation of bone formation in tooth extraction sockets following local, single-dose administration. In this study, New Zealand male rabbits (3 months old, weighing 2.5-3 kg) were fully randomized to minimize bias. The experiments were conducted across five groups: a control group, a graft group, and three experimental groups receiving 100%, 75%, and 50% doses of Scl-ab. Calculated doses of Scl-ab were administered alongside the graft material in the extraction sockets, with results assessed at 2 and 4-week intervals. Cone-beam computed tomography indicated that the tooth extraction sockets treated with varying ratios of Scl-ab with graft material exhibited a statistically significant increase in the mean mandibular BV/TV ratio compared to the control and graft groups, with variations based on time and dosage. While bone volume improved over time, the most significant enhancement was observed in the 100% Scl-ab group. Additionally, the administration of different doses of Scl-ab significantly increased trabecular thickness of the alveolar bone compared to both the control (p < 0.001) and graft (p < 0.001) groups, with histological analysis corroborating these findings. The therapeutic application of Scl-ab facilitates early bone formation, and the localized inhibition of sclerostin secreted within the bone microenvironment targets potential bone regeneration.