The Affiliated Hospital of Qingdao University

Periodontitis drives alveolar bone loss, tooth mobility, and even tooth loss. Although orthodontic treatment can reposition compromised teeth and extend their functional lifespan, orthodontic tooth movement in patients with periodontitis occurs within a mechanoinflammatory microenvironment, where mechanical forces and persistent inflammation synergistically disrupt alveolar bone homeostasis and compromise stem-cell-mediated repair, culminating in bone loss. Breaking this vicious cycle demands a therapy that can simultaneously buffer physical stress and neutralize biochemical insults. Here we report injectable, stress-relaxing, and ROS-scavenging hydrogel microspheres that function as a protective microniche for dental follicle stem cells (DFSCs). Constructed from dopamine-modified hyaluronic acid and phenylboronic acid-modified gelatin, these viscoelastic microspheres rapidly dissipate mechanical stress while their catechol moieties mitigate oxidative damage. Under a combined mechanoinflammatory challenge, the microspheres preserved DFSC viability, stemness, osteogenic potential, and immunomodulatory function. Transcriptomic analysis revealed that the microspheres rescued the expression of the DNA repair enzyme OGG1, thereby preventing oxidative DNA damage and suppressing the downstream NF-κB inflammatory cascade. In a murine model of periodontitis-associated orthodontic tooth movement, DFSCs-loaded microspheres not only prevented bone loss but also restored a pro-regenerative osteoimmune homeostasis. Together, this study presents a viscoelastic and redox-active biomaterial-based strategy to safeguard stem cell function and restore osteoimmune balance in mechanically and immunologically challenged tissues.

Cardiac troponin I (cTnI) represents a highly specific biomarker for the detection of myocardial infarction. To meet the demand for accurate detection of cTnI, a ratiometric electrochemical biosensor based on graphene oxide-2-aminoanthraquinone (GO-AQ) and iron-based metal-organic frameworks‑gold nanoparticles (FeMOFs-Au NPs) was developed. GO possesses a large specific surface area and favorable biocompatibility, serving as an ideal carrier for subsequent antibody immobilization. Diazotized AQ was anchored onto the surface of GO via covalent bonds to generate stable electrochemical redox signals. Owing to their stable framework structure, FeMOFs can produce inherent and stable electrochemical redox peaks. The in-situ growth of Au NPs greatly enhances the conductivity of MOFs and accelerates interfacial electron transfer. With the self-calibration mechanism, the developed sensor could detect cTnI concentrations ranging from 0.001 to 100 ng mL^-1, and limit of detection was determined to be 0.36 pg mL^-1. Benefiting from superior signal stability, the sensor exhibited excellent intra-batch and inter-batch reproducibility. For practical samples, the sensor showed good recovery rates (99.92%-107.8%) and could distinguish patients from healthy individuals. The detection performance of the ratiometric sensor is significantly superior to that of single-signal modes, and the obtained results are highly consistent with those measured by commercial method.

Intervertebral disc degeneration (IDD) remains a major cause of chronic low back pain, yet effective disease-modifying therapies are lacking. Current advanced interventions, including cell-based therapies and matrix supplementation, often disrupt disc structural integrity and fail to achieve sustained regeneration. Here, we rationally designed and synthesized a series of arginine-based poly(ester amide)s (Arg-PEAs) as endplate-penetrating biomaterials for non-direct disc therapy. Unlike conventional intradiscal injection, Arg-PEAs were administered into the adjacent vertebral bodies, enabling trans-endplate delivery into the nucleus pulposus (NP). Among them, the lead polymer 8A6S demonstrated excellent biocompatibility and efficient accumulation within the NP, as confirmed by ex vivo and in vivo imaging. Mechanistically, 8A6S suppressed IL-17 signaling by attenuating TRAF6-mediated NF-κB activation, thereby reducing inflammatory catabolism (MMP13, ADAMTS5) and restoring anabolic extracellular matrix markers (ACAN, COL2A1, SOX9). This re-establishment of matrix homeostasis promoted NP regeneration in both rat and caprine models of IDD. Collectively, this study establishes Arg-PEAs as a new class of bioactive polymers capable of trans-endplate delivery and inflammation-modulating regeneration, providing a minimally invasive and structurally preserving strategy for IDD treatment.