We have carefully studied your recent publication entitled “Romosozumab Enhances Implant Stability in Glucocorticoid-Induced Osteoporotic Bone: A Rabbit Model Study.” [1] This study systematically evaluates the effects of romosozumab on peri-implant bone microarchitecture and mechanical stability under glucocorticoid-induced osteoporotic conditions. By integrating micro-computed tomography analysis, histological observation, and pull-out mechanical testing, the authors establish a coherent experimental framework that provides valuable preclinical insight into the potential application of osteoanabolic agents in implant-related settings.

While fully acknowledging the innovation and experimental rigor of this work, we would like to offer supplementary reflections from two perspectives: the temporal dimension and treatment sequence, and the definition of implant stability, with the aim of further refining the interpretation and translational relevance of the findings.

First, the skeletal effects of romosozumab are well recognized to be time-dependent and sequence-dependent. By inhibiting sclerostin and activating the Wnt/β-catenin signaling pathway, romosozumab induces a distinct early “anabolic window,” characterized by rapid increases in bone formation markers and bone mass. However, this anabolic predominance is transient, with bone formation rates gradually declining thereafter and bone resorption relatively increasing [2]. Accordingly, long-term improvements in bone structure and mechanical competence in clinical practice generally rely on subsequent consolidation with antiresorptive therapy. This concept is supported by randomized clinical evidence showing that, although romosozumab rapidly improves bone density and reduces fracture risk, maintenance of its benefits depends on appropriate treatment sequencing [3]. In the present rabbit model, romosozumab was applied as a single intervention with observations focused on an early time point, which is well suited for evaluating early implant fixation but suggests that the conclusions may be best framed within the context of early effects.

Second, implant stability itself represents a hierarchical and time-sensitive concept. The use of peri-implant bone volume/total volume, trabecular thickness, and increased pull-out force provides robust evidence for improved early mechanical stability. Nevertheless, long-term bone-implant integration depends not only on bone quantity but also on bone tissue maturity, mineralization quality, and sustained remodeling. Previous studies indicate that bone newly formed during early romosozumab treatment is predominantly woven and relatively less mineralized, requiring subsequent remodeling to achieve optimal material properties [1]. Thus, the enhanced pull-out strength observed here may primarily reflect improved early mechanical anchorage rather than complete long-term biological integration.

In summary, this study offers strong experimental evidence that romosozumab enhances early implant stability in glucocorticoid-induced osteoporotic bone. Further consideration of temporal dynamics, treatment sequence, and the hierarchical nature of implant stability may help to more precisely define its role in long-term clinical translation.

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