The resource utilization of keratin waste has garnered significant attention, yet the processing of yak hair keratin in underdeveloped regions such as Tibet and Qinghai in China remains challenging. This study addresses these concerns by carbonizing yak hair keratin waste using a steam flash explosion (SFE) technique for 150 s, which is followed by activation with KOH at various ratios and subsequent to produce activated carbon (AC) samples. The AC was then combined with sodium alginate (Alg) at different ratios, pH and applied voltage to yield AC−Alg gel microbeads using an electrospinning method. The characterization of the AC and AC–Alg gel microbeads was conducted using SEM, BET, TG, and FT-IR analysis. In adsorption studies, AC−Alg_0.5U gel microbeads prepared with optimized conditions (pH 7, 11 kV, 19 G needle) were used to remove dyes (methylene blue (MB) and methyl orange (MO)) and antibiotic minocycline hydrochloride (MH). Various parameters such as temperature, pH, and adsorbent dose were optimized to obtain the maximum adsorption performance under model concentrations. The experimental results showed that the AC−Alg_0.5U gel microbeads can effectively adsorb MB and MO with adsorption capacities of 1038.9 mg/g and 206.2 mg/g, respectively. Moreover, the microbeads had the best adsorption performance for MH (1694.2 mg/g), with the kinetics most accurately represented by the pseudo-second-order kinetic model (R² = 0.999), and the isotherm followed the Langmuir model (R² = 0.984). The microbeads maintained a high adsorption capacity of 75% after six cycles. The composite gel microbeads not only utilize yak hair keratin waste but also will be used as durable and favorable adsorbents for the removal of pollutants.

Metabolic dysfunction-associated steatotic liver disease (MASLD) affects over 30% of adults globally, yet no pharmacotherapies are approved for its early stages. Emerging evidence from preclinical models and limited observational studies suggests that periodontitis may represent a biologically plausible, modifiable risk factor for MASLD through proposed direct oral--hepatic pathways; however, causal relationships remain to be established, and these pathways are currently insufficiently validated in humans. This narrative review synthesizes evidence ranging predominantly from in vitro and animal studies to limited human observational and interventional data consistent with three proposed mechanistic pathways by which periodontal pathogens and their derivatives may potentially contribute to MASLD pathogenesis: (i) disruption of hepatocyte lipid homeostasis through TLR4-mediated inflammatory signaling, (ii) amplification of hepatic inflammation via activation of Kupffer cells and liver sinusoidal endothelial cells, and (iii) promotion of fibrogenesis through hepatic stellate cell activation. We emphasize that these pathways remain largely hypothetical, derived principally from preclinical models, and await robust validation in human populations. Preclinical studies further suggest that reactive oxygen species (ROS) and associated inflammasome signaling—particularly NLRP3 pathway activation—may function as interconnected integrative nodes linking these processes, although the relative contribution of NLRP3-mediated mechanisms within this proposed framework remains to be systematically defined. Clinical evidence is currently limited to a single small prospective interventional study (n = 40) reporting that periodontal treatment may improve hepatic steatosis and inflammatory markers in patients with comorbid periodontitis and MASLD; these preliminary findings should be regarded as hypothesis-generating rather than confirmatory, and require independent replication in larger, adequately powered randomized controlled trials before any definitive clinical conclusions can be drawn. We critically appraise the current evidence base, highlighting the predominance of monomicrobial Porphyromonas gingivalis models, the lack of standardized methodologies, and the absence of human interventional studies capable of distinguishing direct from gut-mediated pathways. We explicitly note that the proposed oral-hepatic mechanisms are predominantly supported by preclinical data and remain insufficiently validated in humans, and we propose a standardized framework to advance causal inference and clinical translation.

Introducing reversible covalent linkages, such as Schiff base bonds and disulfide bonds, into natural polymer networks like chitosan and hyaluronic acid has become an important research direction in the hydrogel field. This strategy seeks to reconcile the limited strength of physically crosslinked gels with the poor adaptability of permanently crosslinked gels. Although dynamic covalent networks, self-healing natural-polymer hydrogels, and injectable oral or periodontal materials have each been reviewed, these topics are often treated separately. The unresolved question addressed here is how to select dynamic bonds and regulate their exchange kinetics under the coupled constraints of the oral cavity, including salivary washout, masticatory friction, local pH/ROS/glucose fluctuations, required retention and degradation periods, and manufacturability. This review therefore focuses on dynamic covalent-crosslinked hydrogels built from natural polymer backbones and evaluates three mainstream bond types: Schiff base bonds, disulfide bonds, and boronic ester bonds. Following an oral-specific design framework of “pathological signals—bond response—property trade-offs—scenario fit—translation bottlenecks”, it examines local drug delivery and tissue-repair applications in periodontitis and oral ulcers and discusses dentin hypersensitivity and pulp protection only as potential extension directions. Diagnostic sensing, molecular imaging, and receptor-mediated targeting are outside the evidence base of this review and are not claimed as established applications. The review summarizes trade-off rules between mechanical performance and dynamic functions and identifies bottlenecks in multi-network regulation, sterilization, and clinical translation. Its added value lies in linking bond chemistry to oral-specific design constraints, rather than cataloguing hydrogel examples alone.

Established oral squamous cell carcinoma (OSCC) remains constrained by local recurrence, inadequate lesion exposure, systemic toxicity, and therapy resistance. This narrative review evaluates a proposed microneedle–small extracellular vesicle (sEV) system for localized adjunctive treatment in three preclinical contexts: postoperative residual-disease control, local immunomodulation/checkpoint combination, and chemoradiotherapy sensitization. Direct evidence for the combined microneedle–sEV system in OSCC is not yet available; the analysis therefore integrates OSCC-specific sEV mechanisms with oral-mucosal microneedle and cross-disease engineering studies. We focus on whether the proposed microneedle–sEV system can preserve sEV potency, achieve reproducible local delivery, and meet oncologic-safety, manufacturing, and repeated-dose oral-safety requirements. The review provides a preclinical decision framework and comparator-based development criteria rather than a claim of clinical readiness.

The functions of most proteins encoded by the African swine fever virus (ASFV) remain largely unknown, although several have been reported to possess immunomodulatory properties. Among these, we identified that the DP71L protein exerts an inhibitory effect on inflammatory bowel disease. To investigate its protective role in murine colitis, we constructed and expressed a recombinant DP71L protein. Colitis was induced in mice using DSS, and the effects of DP71L treatment were evaluated by assessing histopathological changes, inflammatory cytokine profiles, oxidative stress markers, colonic tissue pathology, and the expression of tight-junction proteins (claudin-1, occludin, and ZO-1). Our results showed that DP71L intervention significantly attenuated body weight loss and organ damage and ameliorated DSS-induced colonic histopathological injury. Moreover, DP71L treatment markedly increased superoxide dismutase (SOD) activity and reduced malondialdehyde (MDA) content in colonic tissues. Mechanistically, DP71L suppressed both DSS-induced NF-κB and JAK-STAT activation and concurrently inhibited DSS-induced epithelial cell apoptosis. These events likely underlie the observed reduction in pro-inflammatory cytokines (IL-1β, IL-6, IFN-γ, and TNF-α) and the restoration of tight-junction protein expression, as DP71L treatment effectively prevented DSS-induced downregulation of claudin-1, occludin, and ZO-1, while also promoting the anti-inflammatory cytokines IL-10 and TGF-β. Collectively, our findings demonstrate that DP71L effectively inhibits the progression of murine colitis through coordinated anti-inflammatory and anti-apoptotic mechanisms. This study suggests that DP71L may function as a potential immunosuppressant, opening new avenues for the application of viral proteins in the treatment of immune-related disorders.