Evaluation of the role of mitofusin-1 and mitofusin-2 in periodontal disease.

Background: Mitochondria and endoplasmic reticulum are key cellular organelles and create contact sites (mitochondria-endoplasmic reticulum contact [MERC]), which plays a major role in calcium metabolism, apoptotic processes, and inflammation. Previously, proteins that have been associated with these MERC contact sites mitofusin-1 (MFN1) and mitofusin-2 (MFN2) have been found to be downregulated in periodontal disease in vitro. Therefore, the aim of the current study was to evaluate MFN1 and MFN2 in gingival crevicular fluid (GCF) of patients with periodontal disease compared with healthy controls clinically.

Gene expression profiles of mitochondria-endoplasmic reticulum tethering in human gingival fibroblasts in response to periodontal pathogens.

Objective: The current study aimed to elucidate the potential involvement of mitochondria-endoplasmic reticulum contact genes in the pathogenesis of periodontal disease by monitoring levels of contact associated genes including Mitofusion 1 (MFN1) and MFN2, inositol 1,4,5-trisphosphate receptor (IP3R), chaperone glucose-regulated protein 75 (GRP75), sigma non-opioid intracellular receptor 1 (SIGMAR1) and phosphate and tensin homolog induced putative kinase 1 (PINK1) in human gingival fibroblasts in response to periodontal pathogens Fusobacterium nucleatum (F. nucleatum) and Porphyromonas gingivalis (P. gingivalis) in vitro.

Inflammasome dysregulation in human gingival fibroblasts in response to periodontal pathogens.

Objective: Uncontrolled production of Interleukin-1β (IL-1β), a major proinflammatory cytokine, is associated with tissue destruction in periodontal disease. IL-1β production is controlled by inflammasomes which are multiprotein regulatory complexes. The current study aimed to elucidate potential regulatory pathways by monitoring the effects of periodontal pathogens Fusobacterium nucleatum (Fn) and Porphyromonas gingivalis (Pg) on inflammasomes and their regulators in human gingival fibroblasts (HGFs) in vitro.

Dysregulation of Inflammasomes in Human Dental Pulp Cells Exposed to Porphyromonas gingivalis and Fusobacterium nucleatum.

Introduction: Interleukin-1β (IL-1β) is a major proinflammatory cytokine that plays a significant role in pulpal inflammation. The regulation of IL-1β as well as different cytokines and chemokines is controlled by multiprotein complexes named inflammasomes, which are known to be involved in pulpal inflammation. The goal of this study was to evaluate the effects of well-established endodontic bacteria and periodontal pathogens Fusobacterium nucleatum and Porphyromonas gingivalis on NLRP3 and AIM2 inflammasomes; the inflammasome regulatory proteins POP1, CARD16, and TRIM16; inflammasome components ASC and caspase-1; and IL-1β levels in human dental pulp cells (HDPCs) in vitro.

Effects of Porphyromonas gingivalis and Fusobacterium nucleatum on inflammasomes and their regulators in H400 cells.

Introduction: Inflammasomes are multiprotein complexes that regulate immune processes in response to infections and tissue damage. They modulate Interleukin-1beta (IL-1β) expression, a major proinflammatory cytokine. The inflammasome/IL-1β pathway is involved in head and neck squamous cell carcinoma (HNSCC) progression and the periodontal pathogens Fusobacterium nucleatum (Fn) and Porphyromonas gingivalis (Pg) have been reported to cause chronic inflammation in HNSCC.