Oral pathogen aggravates atherosclerosis by inducing smooth muscle cell apoptosis and repressing macrophage efferocytosis.

Periodontitis imparting the increased risk of atherosclerotic cardiovascular diseases is partially due to the immune subversion of the oral pathogen, particularly the Porphyromonas gingivalis (P. gingivalis), by inducing apoptosis. However, it remains obscure whether accumulated apoptotic cells in P.

Association of the Inferior Alveolar Nerve Position and Nerve Injury: A Systematic Review and Meta-Analysis.

Background: We aimed to compare the relationship between the buccal and lingual positions of the inferior alveolar nerve canal (IAC) relative to the lower third molar (LM3) and the rate of the inferior alveolar nerve (IAN) injury.

Methods: A systematic search was performed in the following databases: PubMed, Cochrane Central Register of Controlled Trials (CENTRAL), Web of Science, and Journals@Ovid. No language or publication status restrictions were set.

Differential expression profiles and function prediction of tRNA-derived fragments in fibrous dysplasia.

Objective: Fibrous dysplasia (FD) is a bone disease featuring that normal bone matrix is replaced by fibrous tissue and immature bone tissue. Transfer RNA-derived RNA fragments (tRFs) and tRNA halves (tiRNAs) are types of small non-coding RNA that produced by specific shearing of mature tRNA. Here, we conducted a comparative analysis of the expression of tRFs/tiRNAs in BMSCs and FD BMSCs.

LncRNA NEAT1 controls the lineage fates of BMSCs during skeletal aging by impairing mitochondrial function and pluripotency maintenance.

Aged bone marrow mesenchymal stem cells (BMSCs) exhibit aberrant self-renewal and lineage specification, which contribute to imbalanced bone-fat and progressive bone loss. In addition to known master regulators of lineage commitment, it is crucial to identify pivotal switches governing the specific differentiation fate of aged BMSCs. Here, we profiled differences in epigenetic regulation between adipogenesis and osteogenesis and identified super-enhancer associated lncRNA nuclear-enriched abundant transcript 1 (NEAT1) as a key bone-fat switch in aged BMSCs.

A CREB1-miR-181a-5p loop regulates the pathophysiologic features of bone marrow stromal cells in fibrous dysplasia of bone.

Background: Fibrous dysplasia (FD) is a bone marrow stromal cell (BMSC) disease caused by activating mutations of guanine nucleotide-binding protein alpha-stimulating activity polypeptide (GNAS) and is characterized by increased proliferative activity and disrupted osteogenesis of BMSCs. However, the molecular mechanisms regulating the pathophysiologic features of BMSCs in FD remain unknown. This study aimed to identify and verify the roles of the CREB1-miR-181a-5p regulatory loop in FD pathophysiology.

Effects of oligopeptide simulating DMP-1/mineral trioxide aggregate/agarose hydrogel biomimetic mineralisation model for the treatment of dentine hypersensitivity.

Dentine hypersensitivity (DH) occurs when dentine is exposed to stimuli from the oral environment due to a lack of enamel or cementum. The use of biomimetic mineralisation in occluding exposed dentinal tubules and regenerating enamel-like tissues on dentine surfaces is preferred for a long-lasting treatment. In this study, we established a biomimetic mineralisation model composed of oligopeptide stimulating dentine matrix protein 1 (DMP-1), mineral trioxide aggregate (MTA) and an agarose hydrogel biomimetic mineralisation model (AHBMM); the proposed model is thus referred to as DMP-1@MTA@AHBMM.