Downregulation of odontogenic ameloblast-associated protein in the progression of periodontal disease affects cell adhesion, proliferation, and migration.

OBJECTIVE: This work aimed to examine changes in odontogenic ameloblast-associated protein (ODAM) expression during the progression of periodontal disease and to investigate the effect of ODAM deficiency in vitro by RNA sequencing. DESIGN: Gingival tissue samples were collected from three groups, including healthy control, gingivitis and periodontitis patients, and ODAM expression was assessed by immunohistochemistry and quantitative reverse transcription PCR (qRT-PCR). Then, an Odam-knockdown cell line was established by lentiviral infection of small guide RNAs (sgRNAs) into an immortalized ameloblast-lineage cell line. RNA sequencing was carried out in Odam-knockdown and empty lentiviral vector-transfected cells. Differentially expressed genes were compared between these two cell groups to analyze functional enrichment, and a protein-protein interaction network was built. RESULTS: ODAM expression levels in gingival tissue samples were significantly lower in patients with periodontitis than in healthy controls as determined by immunohistochemistry and qRT-PCR. Transcriptomic analysis of Odam-knockdown cells identified 2801 differentially expressed genes, which were enriched in cell-substrate adhesion, proliferation, and migration pathways. The expression of a core of differentially expressed genes was confirmed by qRT-PCR in Odam-knockdown cells and by immunohistochemistry in clinical samples. Knocking down Odam significantly reduced cell adhesion but increased cell proliferation and migration capacity in vitro. CONCLUSIONS: ODAM is important in cell adhesion, proliferation, and migration, and its downregulation may contribute to periodontitis progression in humans.

Semaphorin 3A promotes the osteogenic differentiation of rat bone marrow-derived mesenchymal stem cells in inflammatory environments by suppressing the Wnt/ß-catenin signaling pathway.

After periodontal treatment, the local inflammatory environment surrounding periodontal tissues cannot be entirely eliminated. The means by which alveolar bone repair and regeneration are promoted in inflammatory environments have important clinical significance. As a powerful protein that promotes the differentiation of osteocytes, semaphorin 3A (Sema3A) shows potential for bone regeneration therapy. However, the effect of Sema3A on osteogenic differentiation in an inflammatory environment, as well as the underlying mechanism, have not yet been explored. We used lentivirus to transduce rat bone marrow-derived mesenchymal stem cells (rBMSCs) to stably overexpress Sema3A. Lipopolysaccharide from Escherichia coli (E. coli LPS) was used to stimulate rBMSCs to establish an inflammatory environment. ALP staining, Alizarin red staining, ALP activity tests, quantitative RT-PCR (qRT-PCR), and Western blotting were used to elucidate the effect of Sema3A on the osteogenesis of rBMSCs in inflammatory environments. XAV939 and LiCl were used to determine whether the Wnt/ß-catenin signaling pathway was involved in attenuating the inhibition of Sema3A-induced osteogenic differentiation by LPS. The qRT-PCR and Western blot results demonstrated that the lentiviral vector (LV-NC) and lentiviral-Sema3A (LV-Sema3A) were successfully transduced into rBMSCs. An inflammatory environment could be established by stimulating rBMSCs with 1 µg/ml E. coli LPS. After Sema3A overexpression, mineral deposition was exacerbated, and the BSP and Runx2 gene and protein expression levels were increased. Furthermore, E. coli LPS activated the Wnt/ß-catenin signaling pathway and decreased rBMSC osteogenesis, but these effects were attenuated by Sema3A. In conclusion, Sema3A could protect BMSCs from LPS-mediated inhibition of osteogenic differentiation in inflammatory environments by suppressing the Wnt/ß-catenin pathway.

Multiple idiopathic cervical root resorption involving all permanent teeth.

Multiple idiopathic external cervical root resorption is a rare condition with numerous predisposing factors that have not yet been clearly elucidated. In addition, its diagnosis and treatment pose challenges for clinicians, and thus, the extraction of the involved teeth is commonly performed. Here, we report a 29-year-old pregnant woman with no contributory medical or family/social history who experienced cervical root resorption that progressed aggressively and involved all permanent teeth. This case is unique owing to the involvement of all teeth. Reports of multiple idiopathic external cervical root resorption are rare in the literature, and the pathogenesis of the condition is poorly understood. This report aims to add an additional case to the existing literature, analyse the underlying mechanisms and provide clinicians with some guidance in diagnosing cervical root resorption.