Regulation of RIP1-Mediated necroptosis via necrostatin-1 in periodontitis.

Objective: To explore the mechanism of receptor-interacting protein 1 (RIP1)-mediated necroptosis during periodontitis progression.

Background: RIP3 and mixed lineage kinase domain-like protein (MLKL) have been detected to be upregulated in periodontitis models. Because RIP1 is involved in necroptosis, it might also play a role in the progression of periodontitis.

Inhibition of Rgs10 aggravates periodontitis with collagen-induced arthritis via the nuclear factor-κB pathway.

Objective: To explore the role of the Rgs10-associated nuclear factor (NF)-κB signalling pathway in periodontitis with rheumatoid arthritis.

Methods: Porphyromonas gingivalis and collagen were locally applied to mice to establish in vivo periodontitis and rheumatoid arthritis models, respectively. Both agents were administered together to establish the comorbid group.

Inhibition of regulator of G protein signaling 10, aggravates rheumatoid arthritis progression by promoting NF-κB signaling pathway.

Rheumatoid arthritis (RA) is the most common inflammatory arthropathy, with evidence pointing to an immune-mediated etiology that propagates chronic inflammation. Although targeted immune therapeutics and aggressive treatment strategies have substantially improved, a complete understanding of the associated pathological mechanisms of the disease remains elusive. This study aimed at investigating whether regulator of G protein signaling 10 (RGS10) could affect rheumatoid arthritis (RA) pathology by regulating the immune response.

Inhibition of yes-associated protein dephosphorylation prevents aggravated periodontitis with occlusal trauma.

Background: Occlusal trauma can aggravate periodontitis, but the mechanism remains unclear. Yes-associated protein (YAP), a mechanical stressor protein, may play an important role in this process.

Methods: Western blot and quantitative real-time polymerase chain reaction (qRT-PCR) were applied to detect the expression of YAP and inflammatory factors in patients with periodontitis accompanied with or without occlusal trauma.

Inhibition of Cathepsin K Alleviates Autophagy-Related Inflammation in Periodontitis-Aggravating Arthritis.

Rheumatoid arthritis (RA) and periodontitis share many epidemiological and pathological features, with emerging studies reporting a relationship between the two diseases. Recently, RA and periodontitis have been associated with autophagy. In the present study, we investigated the effects of cathepsin K (CtsK) inhibition on RA with periodontitis in a mouse model and its immunological function affecting autophagy.

Inhibition of Ctsk modulates periodontitis with arthritis via downregulation of TLR9 and autophagy.

Objectives: The mechanisms underlying the effects of Toll-like receptor 9 (TLR9) and autophagy on rheumatoid arthritis (RA)-aggravated periodontitis are unclear. We aimed to explore a novel target, cathepsin K (Ctsk)-mediated TLR9-related autophagy, during the progress of periodontitis with RA.

Materials And Methods: DBA/J1 mouse model of periodontitis with RA was created by local colonization of Porphyromonas gingivalis (Pg) and injection of collagen.