Mechanical loading modulates parathyroid hormone-promoted healing of mandibular condylar fractures: a mechanistic review
10.12016/j.issn.2096-1456.202660184
- Author:
CHEN Lingfeng
1
;
WANG Dongxiang
1
Author Information
1. Department of Oral and Maxillofacial Surgery, Guizhou Medical University Affiliated Stomatological Hospital
- Publication Type:Review
- Keywords:
mechanical loading;
mandibular condylar fractures;
parathyroid hormone;
osteoclast;
bone re⁃modeling;
PI3K/Akt/GSK3β/NFATc1 signal pathway;
mechanical dependence;
masticatory stress
- From:
Journal of Prevention and Treatment for Stomatological Diseases
2026;34(9):906-916
- CountryChina
- Language:Chinese
-
Abstract:
Mandibular condylar fractures are common injuries in oral and maxillofacial surgery. The unique anatomical structure and mechanical environment of the condyle render its fracture healing process distinct from that of long bones. Parathyroid hormone (PTH) and its active fragment PTH(1-34) (such as the drug teriparatide) are among the few clinically available agents with bone-anabolic properties, and have shown promise in fracture repair. However, the anatomical and mechanical discrepancies between the condyle and long bones raise doubts as to whether the efficacy of PTH observed in long bones can be directly extrapolated to condylar fractures. Elucidating how mechanical loading modulates the bone remodeling effects of PTH within the specific mechanical environment of the mandibular condyle thus constitutes a critical entry point for addressing this question. This review summarizes recent advances regarding how mechanical loading influences PTH-promoted healing of mandibular condylar fractures from three perspectives: the mechanical sensitivity of condylar fracture healing, the molecular mechanisms by which PTH regulates bone remodeling, and the synergy between mechanical and pharmacological interventions, with the aim of clarifying the existing molecular evidence for mechanical-PTH synergy derived from long-bone and in vitro models, and critically evaluating the feasibility and limitations of extrapolating these findings to condylar fractures. Evidence from long-bone fracture models and in vitro mechanical loading systems indicates that mechanical loading modulates the direction of PTH-mediated bone remodeling through the receptor activator of the nuclear factor-κB ligand (RANKL)/osteoprotegerin (OPG) axis and the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/glycogen synthase kinase-3β (GSK3β)/nuclear factor of the activated T-cells c1 (NFATc1) pathway, an effect that exhibits marked intensity- and time-dependent characteristics. Nevertheless, critical challenges remain in this field, including the standardization of quantitative mechanical loading parameters, the accumulation of direct evidence from condyle-specific fracture models, and the in-depth elucidation of the regulatory mechanisms governing mechanical-drug synergy. Future research should integrate finite element analysis, standardized mechanical loading techniques, and single-cell omics to establish a quantitative relationship between mechanical parameters, cellular responses, and PTH effects, thereby providing a theoretical basis for optimizing postoperative masticatory load management and PTH administration strategies in condylar fractures.
- Full text:2026091115315580736力学负荷调控甲状旁腺激素促进下颌骨髁突骨折愈合的机制综述.pdf
