Laboratory study reveals that respiratory shear forces promote soft-tissue integration of chest wall PEEK implants via cellular crosstalk, highlighting a mechanical driver of implant success.
Clinical studies have demonstrated that the infection rate at the incision site of polyetheretherketone (PEEK) implant in the craniomaxillofacial region is significantly higher than that in the chest wall. This difference is primarily attributable to the cyclic respiratory shear forces to which chest wall PEEK implants are subjected. However, the mechanisms by which cyclic respiratory shear force influences soft-tissue integration around the PEEK interface have rarely been reported. Herein, we constructed an in vitro dynamic culture system to simulate the respiration-induced shear force at the PEEK-soft tissue interface. Our results showed that moderate alternating shear force promoted fibroblast proliferation and M2 macrophage polarization. Co-culture experiments revealed that activated L929 fibroblasts induced M2 polarization of macrophages via paracrinally produced transforming growth factor beta 1 (TGF-β1). Inversely, macrophages facilitated L929 fibroblast adhesion and migration by secreting TGF-β1. Molecular tension probe measurements further demonstrated that integrin β1 (ITGB1) was activated at 12 pN. Animal experiments confirmed superior soft-tissue integration around chest wall PEEK implants compared with craniomaxillofacial implants. These findings elucidate the core molecular mechanisms by which dynamic shear force mediates soft tissue integration at the PEEK-tissue interface, thereby providing theoretical support for the clinical application of PEEK implants.
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Huang et al. (2026) studied this question.
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