Rapid wound healing of oral soft tissue may reduce the opportunity of infection and discomfort of patients. Previous studies have demonstrated that enhancement of angiogenesis is an effective way to accelerate wound repair. In this study, to enhance angiogenesis and healing of palatal wounds, dimethyloxalylglycine (DMOG) was applied to a rat palatal wound model. DMOG is known to inhibit oxygen-dependent degradation of hypoxia inducible factor-1 alpha (HIF-1α), which can lead to up-regulation of angiogenesis markers, favoring wound repair. We also evaluated the effects of DMOG on cell migration and HIF-1α expression of rat palatal (RP) cells. Furthermore, mRNA and protein expression of vascular endothelial growth factor (VEGF) were analyzed in DMOG-treated RP cells. Primary cultures of rat palatal (RP) cells were obtained from Sprague–Dawley (SD) rats. Effects of DMOG on cell viability and migration of RP cells were evaluated by using a formazan and culture insert, respectively. VEGF mRNA was observed by real-time PCR, and VEGF and HIF-1α proteins were detected by Western blotting. For the animal study, excisional wounds, 3 mm in diameter, were made at the central part of the palate of SD rats. DMOG with hyaluronic acid ointment was topically applied three times during 1 week, and then wound closures were quantitated photographically and histologically. DMOG was cytotoxic to RP cells at concentrations higher than 2 mM and did not affect cell migration at non-cytotoxic concentrations. mRNA and protein expression of VEGF were significantly stimulated by DMOG treatment. The protein level of HIF-1α was also stabilized in RP cells by DMOG. In the animal study, groups treated with 1 mg/ml DMOG showed an increase of rat palatal wound contractures. DMOG enhanced wound healing of rat palatal mucosa, which was likely due to the angiogenic effect of the agent.

Background: Dental resin monomers that are leached from the resin matrix due to incomplete polymerization can affect the viability and various functions of oral tissues and cells. In this study, the effects of triethylene glycol dimethacrylate (TEGDMA) and 2-hydroxyethyl methacrylate (HEMA) on odontogenic differentiation of human dental pulp cells (HDPCs) were examined. To mimic clinical situations, dental pulp cells were treated with resin monomers for 24 h prior to the analysis of alkaline phosphatase (ALP) activity and mRNA expression of genes related to pulp cell differentiation. To elucidate the underlying signaling pathways, regulation of mitogen-activated protein (MAP) kinases by resin monomers was also investigated. Results: The ALP activity of HDPCs was reduced by TEGDMA and HEMA at noncytotoxic concentrations. The mRNA expression of dentin sialophosphoprotein (DSPP), osteocalcin (OCN), and osteopontin (OPN) was also downregulated by resin monomers. However, DSPP expression was not affected by hydrogen peroxide (H ₂ O ₂ ). Among the MAP kinases examined, ERK activation (ERK phosphorylation) was not affected by either resin monomers or H ₂ O ₂ , whereas JNK was phosphorylated by TEGDMA and HEMA. Phospho-p38 was upregulated by HEMA, while TEGDMA and H ₂ O ₂ suppressed p38 phosphorylation. Conclusions: Exposure to TEGDMA and HEMA for a limited period suppresses differentiation of HDPCs via different signaling pathways.

Macrophage polarization has become increasingly important for the improvement of the biocompatibility of biomaterials. In this study, we coated Ti discs with phospholipids (phosphatidylserine/phosphatidylcholine [4:1 mole/mole]) by evaporating the solvent under vacuum, and observed the polarization of RAW 264.7 cells cultured on the discs. The coated discs were hydrated before cell culture was added. The shape of the hydrated phospholipids varied with the concentration of loaded phospholipids: a perforated layer (0.1 mM), tubules and spheres (1 mM), and spheres (10 mM). RAW 264.7 cells exhibited different morphologies, depending on the concentration of phospholipids. On the coated discs, the gene expression and protein release of TGF-β1, VEGF, Arg-1, and TNF-α were downregulated, especially with 10 mM phospholipids. The stimulation of mRNA expression and the protein release of those genes by IL-4 and LPS were also disturbed on the phospholipid-coated discs. In conclusion, the polarization of RAW 264.7 cells was prevented by hydrated phospholipids on Ti discs.

Ji-A Park, Deok-Young Park, Hyun-Jun Yoo, Byoung-Jin Lee, Sol Han, Hee-Chul Park, Bo-Hyoung Jin. J Korean Acad Oral Health 2023;47:140-50. https://doi.org/10.11149/jkaoh.2023.47.3.140

본 연구에서는 Mineral Trioxide Aggregate(MTA)의 생체적합성에 대한 dicalcium phosphate dihydrate (DCPD)의 영향을 평가하고자 하였다. MTA 경화 시 발생하는 pH 상승을 억제하고자 DCPD를 OrthoMTA에 첨가하여 세포독성과 피하염증반응의 변화를 관찰하였다. 인산완충생리식염수에 침지한 OrthoMTA와 DCPD-OrthoMTA의 pH를 측정한 결과, OrthoMTA와 DCPD-OrthoMTA는 측정 1일째에 각각 12.5와 12.0의 pH를 보였다. 마지막 측정시점인 19일에 OrthoMTA는 평균 11.6을 보인 반면, DCPD-OrthoMTA는 8.8을 나타내었다. NIH 3T3 섬유아세포에 대한 세포독성은 높은 농도의 용출액(50% 이상)에서 DCPD가 OrthoMTA의 세포독성을 억제하는 효과를 보였다(p 0.05). 마우스 피하이식 시험에서는 ProRoot MTA, OrthoMTA, DCPD-OrthoMTA 간의 염증반응의 차이는 발생하지 않았다. 따라서 DCPD의 MTA 세포독성을 낮추는 효과와 본 실험 조건에서의 피하염증발생에 대한 영향은 서로 유의한 상관관계를 보이지 않는 것으로 사료된다.