What this is
Qi, Wang, Xie, Ma, Li, Tang, Sun, and Chang, a group at the Hospital of Stomatology of Jilin University in Changchun, have published a broad review of orofacial mechanobiology in the International Journal of Oral Science (volume 18, article 58, published 27 August 2026). It is a framework review, not a new experiment: the authors organize the field into three levels, tissue responses to mechanical load, the molecular networks that transduce it, and therapies designed around mechanical cues, and they apply the scheme to oral mucosa, the dentin-pulp complex, periodontal ligament, alveolar bone, and the temporomandibular joint. This piece reads only the dentin-pulp complex sections, because that is the tracked route (/programs/pulp-dentin-repair/).
The physics the pulp lives with
The review pulls together measured numbers that rarely travel outside specialist papers. Intrapulpal pressure in healthy pulp sits near 25 mmHg and can rise toward 40 mmHg under inflammatory conditions (the review cites the Van Hassel physiology summary, Journal of Endodontics 2021, DOI 10.1016/j.joen.2021.03.001). Substrate stiffness changes cell fate: on a 2 kPa substrate, DPSCs kept pluripotency markers NANOG and OCT4 higher and senesced more slowly than on 50 kPa (Ghaffari and Shrestha, Journal of Endodontics 2025, DOI 10.1016/j.joen.2025.01.004). The response is dose-shaped, not linear: tensile strain from 0 to 15 percent raised odontogenic marker expression up to a peak at 12 percent and then suppressed it (Lee et al., Life Sciences 2010, DOI 10.1016/j.lfs.2009.11.013), and compressive stress between 17 and 22 kPa first enhanced and then nearly abolished dentin-formation markers (Miyashita et al., Journal of Tissue Engineering and Regenerative Medicine 2017, DOI 10.1002/term.1928). The review also notes that aging softens pulp, and reads that as one explanation for why DPSCs from older donors regenerate less.
How pulp cells sense force
The molecular core will not surprise anyone who follows pulp biology, but the review assembles it cleanly. Piezo1 channels sit on odontoblasts and DPSCs; direct indentation, cyclic stretch, or shear opens them, calcium enters, and odontogenic differentiation accelerates, with a Piezo1-inhibitor experiment showing the channel is also needed for calcium signals to pass between neighboring odontoblasts (Sun et al., Journal of Endodontics 2022, DOI 10.1016/j.joen.2022.02.005; Matsunaga et al., Frontiers in Physiology 2021, DOI 10.3389/fphys.2021.704518). Low-intensity pulsed ultrasound works through TRPV1 and TRPM7 (Zuo et al., Ultrasound in Medicine and Biology 2018, DOI 10.1016/j.ultrasmedbio.2017.09.006). A 45 Hz vibration arresting hDPSCs in G0/G1 and driving differentiation through BMP2-p-ERK-RUNX2 is in the stack (Lee et al., International Journal of Molecular Sciences 2021, DOI 10.3390/ijms221810167). The most speculative layer is a proposed mechano-metabolic-epigenetic axis: micropatterned culture with 1:2 and 1:4 aspect ratios reshapes nuclei, leaves persistent histone marks in passaged cells, and improves nerve regeneration in rats, which the authors frame as pulp cells holding a mechanical memory (Li et al., Advanced Functional Materials 2023, DOI 10.1002/adfm.202302829).
Where it touches the repair route
The translational sections are the reason this belongs on the record. A 3D double-network hydrogel matching native pulp stiffness outperformed 2D culture on matrix production, collagen deposition, and vascularization through TGF-beta1/Smad3 (Han et al., ACS Applied Materials and Interfaces 2023, DOI 10.1021/acsami.2c20848). A “young-mechanical niche” hydrogel with higher stiffness and viscoelasticity pushed hDPSC proliferation and odontogenic differentiation through YAP/TEAD1/CTGF/Cyr61 (Zhang et al., Chemical Engineering Journal 2024, DOI 10.1016/j.cej.2024.157483). Most concretely, a hyaluronic-acid-modified mineralized collagen scaffold with modulus and hardness close to natural dentin regenerated dentin in a beagle dog model (Jin et al., Chemical Engineering Journal 2023, DOI 10.1016/j.cej.2023.141800). The angiogenesis evidence is genuinely split: shear stress steers SHED toward endothelial differentiation via VEGF-DLL4/Notch-EphrinB2 (Wang et al., International Journal of Molecular Medicine 2018, DOI 10.3892/ijmm.2018.3761), yet flow-exposed hDPSCs in a pericyte-like state formed fewer tubes and downregulated VEGF, ANGPT1, and eNOS (Bertani et al., Stem Cell Research and Therapy 2023, DOI 10.1186/s13287-023-03254-2). The review says both, and the honest read is that no one yet knows which regime a regenerating pulp needs.
What it does not show
This is a conceptual framework built from other groups’ experiments, most of them in vitro, with the dog dentin study the only in vivo result cited in the dentin-pulp sections. The three-level scheme is the authors’ organizing proposal, not a validated model, and the smart self-adaptive biomaterials it ends on are aspirations. One citation deserves a flag: the claim that mechanical stimulation shifts DPSC metabolism toward glycolysis, with lactate suppressing HDAC1/2 and raising H3K27ac, is referenced to a cancer-metabolism paper on histone lactylation (Zhang et al., Clinical and Translational Medicine 2024, DOI 10.1002/ctm2.1614), not to a pulp study. Read that mechano-metabolic-epigenetic axis as a hypothesis the field has not yet tested in pulp cells.
Where we differ from the coverage
We found no press or popular coverage of this review to differ from. The review’s own closing framing, which points toward intelligent mechanoresponsive materials and oral interventions for systemic disease, outruns a literature whose strongest in vivo entry is one dog study; the defensible content is the compiled physics and the named scaffold experiments.
Provenance: grounded in the full open-access text of Qi et al. (2026), International Journal of Oral Science 18:58, read in full via Europe PMC (PMC13522602); underlying studies cited above checked against their own records by DOI. Method and sourcing standard at /method/.