Exosomes from Adipose-Derived Stem Cells Can Prevent Medication-Related Osteonecrosis of the Jaw.

The treatment measures of medication-related osteonecrosis of the jaw (MRONJ) is a worldwide challenge in oral and maxillofacial surgery because of its unclear pathogenesis. Previous studies suggested that mesenchymal stem cells played important roles in promoting MRONJ lesion healing, but the detailed mechanisms were unknown. Increasing numbers of studies have demonstrated that exosomes derived from mesenchymal stem cells, especially adipose-derived stem cells, have key roles in stem cell-based therapies by accelerating bone remodeling, facilitating angiogenesis, and promoting wound healing. We hypothesized that exosomes derived from adipose-derived stem cells can prevent MRONJ by accelerating gingival healing and enhancing bone remodeling processes. Our results may provide a promising therapeutic option for MRONJ clinical therapy.

Effects of carbodiimide dentin surface treatment on resin-dentin bonding.

PURPOSE: To assess the effects of ethanol-based 1-ethyl-3-(3-dimethyl-aminopropyl) carbodiimide (EDC) dentin surface treatment on resin-dentin bonding and dentin collagen fibril biodegradation. METHODS: Acid-etched dentin surfaces were pretreated with different concentrations of ethanol-based EDC solutions (0.01-2M) for 60 seconds, followed by two-step etch-and-rinse dentin adhesive application and resin composite bonding. Dentin surfaces pretreated with either ethanol alone or no pretreatment were used as controls. The specimens were subjected to microtensile bond strength testing after storage in 0.9% NaCl solution at 37°C for either 24 hours or 90 days. Furthermore, demineralized dentin slabs with and without ethanol-based EDC pretreatment were exposed to a collagenase solution for 24 hours, and subsequent hydroxyproline release was measured using ELISA. Data were analyzed with ANOVA and multiple comparison tests at α= 0.05. RESULTS: The bond strength values were significantly lower for dentin surfaces pretreated with 1 and 2 M ethanol-based EDC than for the control surfaces (P< 0.05). The 0.01, 0.1, and 0.3 M ethanol-based EDC pretreated groups obtained significantly higher bond strength values at 90 days compared to controls. Hydroxyproline release measurements revealed that there were significantly lower levels released in the 0.3 and 1 M ethanol-based EDC pretreated specimens than for controls (P< 0.05). CLINICAL SIGNIFICANCE: Pretreatment of dentin surfaces with ethanol-based EDC solution ≤ 0.3M before resin composite bonding can improve the stability of the resin-dentin bond and prevent dentin collagen fibril biodegradation.

[K (lysine) acetyltransferase 2A affects the osteogenic differentiation of periodontal ligament stem cells through the canonical Wnt pathway].

OBJECTIVE: This study aims to investigate the mechanism of K (lysine) acetyltransferase 2A (KAT2A) regulation and control on the osteogenic differentiation of periodontal ligament stem cells (PDLSCs). METHODS: The expression levels of KAT2A in PDLSCs were compared from each generation of the normal (H-PDLSCs) and periodontitis tissues (P-PDLSCs). The influences of KAT2A gene interference on the osteogenic differentiation of PDLSCs were also detected. In addition, the influences of the KAT2A gene interference to the canonical Wnt pathway and ligands were detected. The upstream and down-stream relationships between KAT2A and canonical Wnt pathway were also determined. RESULTS: The decreased expression of KAT2A in PDLSCs from the inflammatory tissue in each generation was compared with that in PDLSCs from the healthy tissue, and the difference was statistically significant (P<0.05). When the KAT2A gene was disrupted, the osteogenesis ability of PDLSC was declined, and the difference was statistically significant (P<0.05). The canonical Wnt pathway was activated, and the antagonist Dickkopf-1 (DKK-1) was reduced. After the DKK-1 addition, the osteogenic differentiation of the disturbed PDLSCs was recovered, and KAT2A was unaffected. CONCLUSIONS: The KAT2A expression in PDLSCs was decreased because of perio-dontitis. The classical Wnt pathway was activated to inhibit the osteogenic differentiation of the cells.

[Three-dimensional morphological analysis of corticotomy-assisted intrusion of premolars in Beagle dogs].

OBJECTIVE: This study aims to identify the effects of corticotomy-assisted orthodontic premolar intrusion andevaluate the changes of root resorption and the alveolar bone. METHODS: Both sides of the mandible of eight male Beagle dogswere randomly assigned into experimental and control groups. The third (P3) and fourth (P4) premolars were intruded withboth mini-screw implant anchorage (MIA) and corticotomy on the experimental side. By contrast, P3 and P4 were intrudedwith MIA alone on the control side. During pre-operation and after 2, 4, 8, and 12 weeks of orthodontic force applications,cone beam computed tomography was performed on every dog. The distance of tooth intrusion and root resorption of furcation, as well as the apex and height changes of the alveolar bone were measured and analyzed. RESULTS: The intrusion distanceof premolars on the experimental side was greater than that on the control side (P < 0.05). The root of furcation and apex onboth sides occurred in root resorption, and the root resorption of the apex on the experimental side was lighter than that onthe control side after 12 weeks of force application (P < 0.05). The alveolar bone height decreased, and the height reductiondistance on the experimental side was greater than that on the control side after 8 and 12 weeks of force application (P < 0.05). CONCLUSION: Corticotomy accelerates orthodontic molarintrusion and reduces root resorption.

Inhibition of the EGFR with nanoparticles encapsulating antisense oligonucleotides of the EGFR enhances radiosensitivity in SCCVII cells.

The aim of this study is to evaluate the effects of antisense epidermal growth factor receptor (EGFR) nanoparticles on cell survival and radiosensitivity in the head and neck squamous cell carcinoma cell line SCCVII. Experiments were performed using the murine head-and-neck tumor cell line, SCCVII. Nanoparticle encapsulated antisense EGFR oligonucleotides were combined with radiotherapy and the relative radiosensitivity of the cells was assessed in vitro by MTT and standard colony formation. The proportion of apoptotic cells and cell cycle stages were analyzed by flow cytometry. C3H/He mice with SCCVII tumor heterografts were treated with antisense-EGFR-nanoparticles or RT alone, or with combinations of concomitant and sequential therapy. The relative radiosensitivity of the tumors was assessed in vivo by growth delay assays. The SCCVII cells were resistant to anti-EGFR nanoparticles or radiation therapy alone, but a synergic inhibition effect was observed when the therapies were combined. When the SCCVII cells were pre-treated with 2 mug of antisense-EGFR nanoparticles for 24 h and X-irradiated (4 Gy), flow cytometry analysis revealed cell cycle arrest in G(1) phase and an increased proportion of apoptotic cells. Our results show that antisense EGFR nanoparticles enhance radiosensitivity by inhibition of EGFR-mediated mechanisms of radioresistance. Collectively, these findings may have therapeutic implications because EGFR inhibition may improve the therapeutic efficacy of radiation even in the tumor cells that are resistant to anti-EGFR therapy.