Chemical Stability and Antimicrobial Activity of Plasma-Sprayed Cerium Oxide-Incorporated Calcium Silicate Coating in Dental Implants.

PURPOSE: The aim of this study is to investigate the biological activity and antibacterial property of cerium oxide-incorporated calcium silicate coatings (CeO2-CS) in dental implants. MATERIALS AND METHODS: In this study, MC3T3-E1 cells cultured on the plastic, Ti-6Al-4V, and the cerium oxide-incorporated calcium silicate coatings (CeO2-CS) coating served as the blank, control, and CeO2-CS groups, respectively. A cell counting kit-8 (CCK-8) and flow cytometry were used to evaluate the biocompatibility. The osteoblastic differentiation of the MC3T3-E1 cells was also analyzed by quantitative real-time polymerase chain reaction analysis. The CCK-8 and counts of colony-forming units (CFUs) were used to detect the antibacterial activity of the coating on Enterococcus faecalis. The study showed that the cerium oxide-incorporated calcium silicate coating (CeO2-CS) has better biocompatibility. Meanwhile, the ALP, OCN, and BSP mRNA expression levels in the CeO2-CS group were significantly upregulated (P < 0.05). The number of viable bacteria and the CFU results were significantly reduced in the CeO2-CS group (P < 0.05). CONCLUSION: The cerium oxide-incorporated calcium silicate coatings (CeO2-CS) may promote the osteoblastic differentiation of osteoblasts. Meanwhile, the cerium oxide-incorporated calcium silicate coating (CeO2-CS) showed strong antimicrobial activity on E. faecalis, with good biocompatibility.

From Bone Remodeling to Wound Healing: An miR-146a-5p-Loaded Nanocarrier Targets Endothelial Cells to Promote Angiogenesis.

Wound healing is a complex challenge that demands urgent attention in the clinical realm. Efficient angiogenesis is a pivotal factor in promoting wound healing. microRNA-146a (miR-146a) inhibitor has angiogenic potential in the periodontal ligament. However, free microRNAs (miRNAs) are poorly delivered into cells due to their limited tissue specificity and low intracellular delivery efficiency. To address this hurdle, we developed a nanocarrier for targeted delivery of the miR-146a inhibitor into endothelial cells. It is composed of a polyethylenimine (PEI)-modified mesoporous silica nanoparticle (MSN) core and a pentapeptide (YIGSR) layer that recognizes endothelial cells. In vitro, we defined that the miR-146a inhibitor and adiponectin (ADP) can modulate angiogenesis and the remodeling of periodontal tissues by activating the ERK and Akt signaling pathways. Then, we confirm the specificity of YIGSR to endothelial cells, and importantly, the nanocarrier effectively delivers the miR-146a inhibitor into endothelial cells, promoting angiogenesis. In a C57 mouse skin wound model, the miR-146a inhibitor is successfully delivered into endothelial cells at the wound site using the nanocarrier, resulting in the formation of new blood vessels with strong CD31 expression. Additionally, no significant differences are found in the expression levels of inflammatory markers interleukin-6 and tumor necrosis factor-α. This outcome not only brings new strategies for angiogenesis but also exhibits broader implications for bone remodeling and wound healing. The breakthrough holds significance for future research and clinical interventions.

C1 Silencing Attenuates Inflammation and Alveolar Bone Resorption in Endodontic Disease.

INTRODUCTION: Endodontic disease, 1 of the most prevalent chronic infectious diseases worldwide, occurs when the dental pulp becomes infected and inflamed, leading to bone destruction around the tooth root, severe pain, and tooth loss. Although many studies have tried to develop therapies to alleviate the bone erosion and inflammation associated with endodontic disease, there is an urgent need for an effective treatment. METHODS: In this study, we used a gene-based therapy approach by administering recombinant adeno-associated virus (AAV)-mediated Atp6v1c1 knockdown to target both periapical bone resorption and inflammation in the mouse model of endodontic disease. RESULTS: The results showed that Atp6v1c1 knockdown is simultaneously capable of reducing bone resorption by 70% through impaired osteoclast activation, inhibiting inflammation by decreasing T-cell infiltration in the periapical lesion by 75%, and protecting the periodontal ligament from destruction caused by inflammation. Notably, AAV-mediated gene therapy of Atp6v1c1 knockdown significantly reduced proinflammatory cytokine expression, including tumor necrosis factor α, interleukin 1α, interleukin 17, interleukin 12, and interleukin 6 levels in periapical tissues caused by bacterial infection. Quantitative real-time polymerase chain reaction revealed that Atp6v1c1 knockdown reduced osteoclast-specific functional genes (ie, Ctsk) in periapical tissues. CONCLUSIONS: Our results showed that AAV-mediated Atp6v1c1 knockdown in periapical tissues slowed endodontic disease progression, prevented bone erosion, and alleviated inflammation in the periapical tissues and periodontal ligament potentially through regulation of toll-like receptor signaling, indicating that targeting Atp6v1c1 may facilitate the design of novel therapeutic approaches to reduce inflammation and bone erosion in endodontic disease.

[Experimental study on constructing a tissue engineered epidermis for replacement of skin irritation in vitro].

OBJECTIVE: To investigate the method of constructing a tissue engineered epidermis with human epidermal cells and polycarbonate membrane, and to establish a tissue engineered epidermis with barrier function which is intended to be the replacing model in vitro of skin irritation test. METHODS: The tissue engineered epidermis was constructed by using polycarbonate membrane as scaffold and stratified differentiated epidermis derived from human keratinocytes. The tissue engineered epidermis was cultured on an inert polycarbonate filter at the air-liquid interface. After 13 days of culture, the composition and structure of tissue engineered epidermis were observed by HE staining, immunofluorescence staining of keratin 10 (K10) & K13, K14, laminin, involucrin, and filaggrin, and transmission electronic microscope. The half maximal inhibitory concentration of a substance (IC50) of SDS was determined in the penetration test of tissue engineered epidermis cultured in the absence (control group) or the presence (experimental group) of lipid supplement for 18 hours. RESULTS: The constructed epidermis was similar to normal epidermis, which was consisted of a proliferating basal layer, differentiated spinous layer, granular layer, and stratum corneum. The IC50 values of tissue engineered epidermis cultured in the control group and experimental group were 0.072% (2.36 mmol/L) and 0.183% (6.00 mmol/L), respectively. CONCLUSION: The tissue engineered epidermis constructed on polycarbonate membrane has normal composition and structure and barrier function corresponding to the normal epidermis.