Cementum is a calcified, avascular connective tissue that laminates the root of a tooth and plays a pivotal role in the development, homeostasis, and regeneration of a periodontal tissue. As a potential treatment for periodontal tissue defects in the patient with chronic periodontitis, much attention has been paid to tissue engineering combined with mesenchymal stem cells for regenerating periodontal tissues including cementum. However, limited information is available for the molecular factors that have impacts on the differentiation of mesenchymal stem cells into cementoblasts. Here, we focus on the effect of Wnt3a as a potential inducer and tested the effect of this protein in vitro using human bone marrow-derived mesenchymal stem cells. It was found that, when cells were cultured in an osteogenic medium containing Wnt3a, cementoblast-specific genes, such as cementum protein 1 and cementum attachment protein, as well as bone-related genes were significantly upregulated. These results suggest that Wnt3a promotes differentiation of the cells into cementoblast-like cells. Further experiments were carried out using inhibitors to gain deeper insights into molecular mechanisms underlying the observed differentiation. As a result, we conclude that Wnt3a-triggered differentiation into cementoblast-like cells is the consequence of the activation of the canonical Wnt signaling pathway with possible involvement of the non-canonical pathway.

Marine-derived tocopherol (MDT), which is typically found in marine organisms that inhabit cold water, is a monounsaturated tocol having vitamin E (VE) activity. To evaluate the functionality of this minor VE homolog, we have studied the influence of MDT on adipocyte differentiation and the production of inflammatory factors in mouse cell line 3T3-L1 adipocytes and mouse monocyte/macrophage cell line RAW264.7 cells. Treatment of 3T3-L1 adipocytes with 10 and 20 μM MDT during differentiation enhanced lipid accumulation and concurrently upregulated peroxisome proliferator activated receptor gamma and CCAAT/enhancer-binding protein expression. Compared to the control adipocytes, MDT treatment also increased the secretion and gene expression of adiponectin, while it decreased the secretion and gene expression of interleukin 6 (IL-6) and monocyte chemoattractant protein-1. Treatment with MDT resulted in higher adipogenesis activity and higher regulation of inflammatory factors than did treatment with α-and γ-tocopherol, the predominant homologous series of VE. MDT-treated RAW264.7 cells showed significantly decreased lipopolysaccharide-induced IL-6 and tumor necrosis factor alpha secretion compared to the control RAW264.7 cells. These results suggest that MDT could have a potential role for preventing obesityrelated inflammation progressing to metabolic disorders.

The aim of this study was to examine the anti-inflammatory effect of brain-derived neurotrophic factor (BDNF) on human dental pulp cells (HDPCs) and identify the intracellular signaling pathway involved. We investigated the effect of BDNF (50 ng/ml) on interleukin (IL)-6 and IL-8 expression in peptidoglycan (PGN)-treated HDPCs. An inhibition assay was performed with MAPK or NF-κB inhibitors to determine the possible signaling pathway. IL-6 and IL-8 mRNA, IL-6 and IL-8 protein, and phosphorylated p38 kinase activity were determined using real-time PCR, ELISA, and Western blot analysis, respectively. BDNF significantly attenuated PGN-induced IL-6 and IL-8 mRNA and protein levels in HDPCs. A p38 inhibitor also inhibited IL-6 and IL-8 mRNA transcription. PGN stimulated phosphorylated p38 kinase activity in HDPCs, which was inhibited by BDNF. Suppression of phosphorylated p38 kinase activity by BDNF in HDPCs inhibited increased IL-6 and IL-8 expression induced by PGN. Our findings suggest that BDNF regulates intracellular signaling molecule activities to exert its anti-inflammatory effect.

Key Clinical MessageDental radiography and cone‐beam computed tomography revealed the left mandibular first molar in a 68‐year‐old female patient with Heithersay Class 3 invasive cervical resorption (ICR). The inhibition of ICR progression and environmental improvement in and around the affected tooth through combined endodontic and periodontal treatments led to a favorable clinical outcome.