Background: Adult patients with a thin buccal cortical plate and fragile periodontal phenotype are at high risk of dehiscence, fenestration and recession during transverse orthodontic expansion. Conventional mechanics often create a cervical compression-dominant environment that exceeds the adaptive capacity of the periodontal ligament (PDL)–bone complex. Objectives: This study proposes an integrative mechanobiological model in which a skeletal-anchorage-assisted loading protocol (Bone Protection System, BPS) transforms expansion into a tension-dominant regime that favours buccal phenotype preservation. Methods: Patient-specific finite element models were used to compare conventional expansion with a BPS-modified force system. Regional PDL stress patterns and crown/apex displacement vectors were analysed to distinguish tipping-dominant from translation-dominated mechanics. A pilot CBCT proof-of-concept (n = 1 thin-phenotype adult) with voxel-based registration quantified changes in maxillary and mandibular alveolar ridge width and buccal cortical plate thickness before and after BPS-assisted expansion. The mechanical findings were integrated with current evidence on compression- versus tension-driven inflammatory and osteogenic pathways in the PDL and cortical bone. Results: FEM demonstrated that conventional expansion concentrates high cervical compressive stress along the buccal PDL and cortical surface, accompanied by bending-like crown–root divergence. In contrast, the BPS protocol redirected forces to create a buccal tensile-favourable region and a more parallel crown–apex displacement pattern, indicative of translation-dominated movement. In the proof-of-concept (n = 1) CBCT case, BPS-assisted expansion was associated with preservation or increase of buccal ridge dimensions without radiographic signs of cortical breakdown. Conclusions: A tension-dominant orthodontic loading environment generated by a skeletal-anchorage-assisted force system may support buccal cortical preservation and vestibular phenotype reinforcement in thin-phenotype patients. The proposed mechanobiological model links these imaging and FEM findings to known molecular pathways of inflammation, angiogenesis and osteogenesis. It suggests a functional biomaterial-based strategy for widening the biological envelope of safe tooth movement.
Kuc et al. (Fri,) studied this question.