Progranulin (PGRN) Facilitates Anti-Inflammation and Pulpitis Repair In Vivo and In Vitro Through TNFR2/14-3-3ε Signalling Complex.

Aim: To investigate the role and mechanism of progranulin (PGRN) in reparative dentinogenesis and inflammation control for rat pulpitis and inflammatory human dental pulp stem cells (hDPSCs).

Methodology: Eight-week-old male Wistar rats with irreversible pulpitis were treated with pulpotomy and divided into five groups: No treatment; Control; iRoot BP plus (BP); GelMA and recombinant human PGRN (rhPGRN) + GelMA (rhPGRN). Micro-computed tomography (Micro-CT) scans and histological and immunohistochemical staining were conducted to evaluate rhPGRN' anti-inflammation and pro-healing properties.

The pro-cancer and immunosuppressive activity of macrophage-transformed cancer-associated fibroblasts in oral squamous cell carcinoma.

Introduction: Cancer-associated fibroblasts (CAFs), as a crucial component of the tumor microenvironment (TME), exhibit heterogeneity, and macrophage-myofibroblast transition (MMT) has been demonstrated to be one of the origins of CAFs. However, the existence and functional features of MMT cells (MMTs) relative to general CAFs in tumors, especially in oral squamous cell carcinoma (OSCC), have not been fully revealed.

Objectives: This study is intended to understand the origin and functional features of MMT and the underlying mechanisms of its formation and functionality.

Porphyromonas gingivalis-Lipopolysaccharide Induced Gingival Fibroblasts Trained Immunity Sustains Inflammation in Periodontitis.

Aim: To investigate whether trained immunity occurs in gingival fibroblasts (GFs) and its relationship to the persistence of inflammation in periodontitis.

Methods: Periodontally healthy and inflammatory gingival fibroblasts (HGFs and IGFs) were cultured through continuous adherence subculture of tissue blocks. Trained immunity in HGFs was evaluated via a classic in vitro model, with relevant markers assessed via enzyme-linked immunosorbent assay, lactate content assay, glycolytic rate assay, and chromatin immunoprecipitation.

Periodontitis promotes tumor growth and immune evasion via PD-1/PD-L1.

Background: Our study investigated the role of experimental periodontitis on tumor growth, local and systemic immunosuppressive status, and programmed death receptor 1 (PD-1) / programmed death ligand 1 (PD-L1) expression in oral squamous cell carcinoma (OSCC) and prostate cancer.

Methods: Mouse oral or prostate cancer xenograft models were divided into control, periodontitis and periodontitis + anti-PD-1 groups. Tumor volume and weight were recorded and the levels of relevant immune-suppressive cells and T cells were detected by flow cytometry or immunofluorescence.