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Background/Objectives: Computer-assisted mandibular reconstruction requires sophisticated technical expertise alongside surgical knowledge. This study aims to establish and validate an efficient collaborative protocol between oral and maxillofacial surgeons and bioengineers for virtual surgical planning in mandibular reconstruction. Methods: We developed a structured protocol with four sequential phases: (1) generation of 3D models from CT data, (2) virtual resection planning, (3) reconstruction design, and (4) surgical guide fabrication. Protocol efficiency was assessed through seven simulation trials measuring planning duration and required revisions. Clinical validation was performed in four mandibular reconstruction cases. Accuracy was evaluated by comparing virtual surgical plans to postoperative outcomes using 3-matic 13.0 software analysis. Results: Protocol implementation showed consistent efficiency across simulations with a mean planning duration of 2.86 working days (SD = 1.35). Only two of seven simulations required design revisions. Clinical application in four cases (three ameloblastomas, one odontogenic myxoma) demonstrated high precision with a mean virtual-to-actual discrepancy of 0.90 mm (SD = 0.34). Successful reconstructions were achieved across varying defect spans (29–53 mm) using both bicortical deep circumflex iliac artery (DCIA) flaps and monocortical iliac block bone grafts. The collaborative workflow resulted in optimized surgical guide design, reduced planning iterations, and improved surgical precision. Conclusions: The established surgeon–bioengineer collaborative protocol enhances the efficiency and accuracy of computer-assisted mandibular reconstruction while making advanced surgical planning techniques more accessible. While initial results are promising, future studies with larger patient cohorts and extended follow-up periods are needed to fully validate the protocol's long-term benefits and broader applicability. [ABSTRACT FROM AUTHOR]

Aim: The physiological effects and cellular mechanism of 25‐hydroxycholesterol (25‐HC), which is an oxysterol synthesized from cholesterol by cholesterol‐25‐hydroxylase (CH25H) expressed under inflammatory conditions, are still largely unknown during odontoclastogenesis. This study aimed to evaluate 25‐HC‐induced odontoclastogenesis and its cellular mechanisms in odontoblast‐like MDPC‐23 cells. Methodology: To investigate 25‐HC‐induced odontoclastogenesis of MDPC‐23 cells and its cellular mechanism, haemotoxylin and eosin staining, tartrate‐resistant acid phosphatase (TRAP) staining, dentine resorption assay, zymography, reactive oxygen species (ROS) detection, immunocytochemistry, and nuclear translocation were performed. The experimental values are presented as mean ± standard deviation and were compared using analysis of variance, followed by post hoc multiple comparisons (Tukey's test) using SPSS software version 22 (IBM Corp.). A p‐value <.05 was considered statistically significant. Results: Lipopolysaccharide or receptor activator of nuclear factor‐κB ligand (RANKL) induced the synthesis of 25‐HC via the expression of CH25H in MDPC‐23 cells (p <.01). Multinucleated giant cells with morphological characteristics and TRAP activity of the odontoclast were increased by 25‐HC in MDPC‐23 cells (p <.01). Moreover, 25‐HC increased dentine resorption through the expression and activity of matrix metalloproteinases in MDPC‐23 cells. It not only increased the expression of odontoclastogenic biomarkers but also translocated cytosolic nuclear factor‐κB (NF‐κB) to the nucleus in MDPC‐23 cells. Additionally, 25‐HC not only increased the production of ROS (p <.01), expression of inflammatory mediators (p <.01), pro‐inflammatory cytokines, receptor activator of NF‐κB (RANK), and RANKL but also suppressed the expression of osteoprotegerin (OPG) in MDPC‐23 cells. In contrast, CDDO‐Me, a chemical NF‐κB inhibitor, decreased TRAP activity (p <.01) and downregulated the expression of the odontoclastogenic biomarkers, including RANK and RANKL, in MDPC‐23 cells. Conclusion: 25‐HC induced odontoclastogenesis by modulating the RANK–RANKL–OPG axis via NF‐κB activation in MDPC‐23 cells. Therefore, these findings provide that 25‐HC derived from cholesterol metabolism may be involved in the pathophysiological etiological factors of internal tooth resorption. [ABSTRACT FROM AUTHOR]