To investigate the effects of ficin on biofilm formation of conditionally cariogenic Streptococcus mutans (S. mutans). Biomass and metabolic activity of biofilm were assessed using crystal violet assay, colony‐forming unit (CFU) counting, and MTT assay. Extracellular polysaccharide (EPS) synthesis was displayed by SEM imaging, bacteria/EPS staining, and anthrone method while acid production was revealed by lactic acid assay. Growth curve and live/dead bacterial staining were conducted to monitor bacterial growth state in both planktonic and biofilm form. Total protein and extracellular proteins of S. mutans biofilm were analyzed by protein/bacterial staining and sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS‐PAGE), severally. qRT‐PCR was conducted to detect acid production, acid tolerance, and biofilm formation associated genes. Crystal violet assay, CFU counting, and MTT assay showed that the suppression effect of ficin on S. mutans biofilm formation was concentration dependent. 4 mg/mL ficin had significant inhibitory effect on S. mutans biofilm formation including biomass, metabolic activity, EPS synthesis, and lactic acid production (p < 0.05). The growth curves from 0 mg/mL to 4 mg/mL ficin were aligned with each other. There was no significant difference among different ficin groups in terms of live/dead bacterial staining result (p > 0.05). Protein/bacterial staining outcome indicated that ficin inhibit both total protein and biofilm formation during the biofilm development. There were more relatively small molecular weight protein bands in extracellular proteins of 4 mg/mL ficin group when compared with the control. Generally, ficin could inhibit biofilm formation and reduce cariogenic virulence of S. mutans effectively in vitro; thus, it could be a potential anticaries agent.

Dental pulp and periapical diseases make patients suffer from acute pain and economic loss. Although root canal therapies, as demonstrated through evidence-based medicine, can relieve symptoms and are commonly employed by dentists, it is still difficult to fully restore a dental pulp’s nutrition, sensory, and immune-regulation functions. In recent years, researchers have made significant progress in tissue engineering to regenerate dental pulp in a desired microenvironment. With breakthroughs in regenerative medicine and material science, bioactive scaffolds play a pivotal role in creating a suitable microenvironment for cell survival, proliferation, and differentiation, following dental restoration and regeneration. This article focuses on current challenges and novel perspectives about bioactive scaffolds in creating a microenvironment to promote dental pulp regeneration. We hope our readers will gain a deeper understanding and new inspiration of dental pulp regeneration through our summary.

Functional maturation of post‐extraction blood clots is the biological cornerstone for alveolar socket preservation, where fibrin‐mediated osteogenic cell recruitment and matrix mineralization dictate long‐term bone regeneration outcomes. To safeguard this critical process, we engineer an octopus‐inspired tissue‐adhesive nanofiber membrane (ANF) that actively stabilizes clots without occlusive disruption. Its bilayer architecture combines an outer hydrophobic nanofibrous layer that suppresses bacterial infiltration by 93.09 ± 0.55% and an inner charge‐heterogeneous Polyethyleneimine (PEI)/Polyacrylic acid (PAA) nanofiber network. Upon application, this system creates an adaptive tissue adhesive strength of 5.87 ± 0.57 kPa through biomimetic suction, which reaches 17.37 ± 3.26 kPa with hydrogen bonding on palatal tissues. At the same time, opposite‐charged interfaces of PEI/PAA nanofiber electrostatically enrich fibrinogen and coagulation factors. The blood clotting index was decreased to 1.43 ± 0.09%. Crucially, this non‐occlusive strategy avoids filler‐induced mechanical interference with natural clot retraction, while establishing a protective microenvironment for the re‐epithelialization of the gingiva. Rat anterior tooth extraction model confirms synergistic biological advantages: wound contraction is enhanced on days 7 and 14, respectively. ANF significantly improved alveolar ridge height reservation by 69.69 ± 2.53%, with a new bone area of 89.83 ± 2.06%. By accelerating hemostasis with unperturbed biological remodeling, this membrane transforms clot maturation into functional bone regeneration.

Periodontitis (PD) and type 2 diabetes mellitus (DM) are bidirectionally associated through shared chronic inflammatory mechanisms. Although monocytes serve as central immune mediators in both pathologies, their functional heterogeneity and dynamic alterations in diabetic periodontitis (PDDM) remain poorly characterized. Utilizing single-cell RNA sequencing (scRNA-seq) of peripheral blood mononuclear cells (PBMCs) from healthy controls, PD patients, and PDDM subjects, we systematically investigated the immunopathological crosstalk between these comorbidities. Our analysis revealed a significant shift in monocyte subpopulations, with PDDM patients exhibiting increased classical monocytes (CD14++CD16−) and decreased nonclassical monocytes (CD14 + CD16++) compared to PD counterparts. Functional profiling demonstrated PDDM-enriched classical monocytes upregulated oxygen transport pathways while suppressing chemotaxis and cytokine responses, whereas nonclassical monocytes showed impaired oxidative phosphorylation and nucleotide biosynthesis. Cell communication analysis identified reduced activity of TGF-β signaling and enhanced CCL pathway activation, collectively promoting chronic inflammation and tissue destruction. Regulatory network reconstruction revealed transcription factors (PBX1, TAL1, IRF9) governing monocyte differentiation defects and hyperinflammatory phenotypes. These results suggest mechanistic links how diabetic conditions exacerbate periodontal inflammation through monocyte reprogramming and signaling pathway dysregulation, providing a cellular roadmap for developing targeted immunotherapies in PDDM management.