Background and Objective It has been reported that long non‐coding RNAs (lncRNAs), such as metastasis‐associated lung adenocarcinoma transcript 1 (MALAT1), act as key regulators of the development of inflammatory diseases. However, it is unclear whether MALAT1 regulates the function of human gingival fibroblasts (HGFs) in periodontitis. This study is to explore the role of MALAT1 on inflammatory cytokine production of HGFs. Material and Methods Primary HGFs were harvested from human gingiva. MALAT1 was detected in inflammatory and healthy gingival tissues via quantitative real‐time PCR (qRT‐PCR). Bioinformatics analysis, dual‐luciferase reporter assay, and RNA‐binding protein immunoprecipitation (RIP) were used to detect the relationship among MALAT1, toll‐like receptor 4 (TLR4), and microRNA (miR) ‐20a. After transfection LPS‐treated HGFs with MALAT1 siRNA (si‐MALAT1), miR‐20a mimic or overexpression MALAT1 plasmid (sno‐MALAT1), the levels of MALAT1, miR‐20a, TLR4, IL‐6 and IL‐8 were analyzed by qRT‐PCR, enzyme‐linked immunosorbent assay, or western blot assay. Results MALAT1 up‐regulated in inflammatory gingival tissues of chronic periodontitis. MiR‐20a was bound with MALAT1 and TLR4 3′‐UTR in RNA‐protein complex with Ago2, respectively. Moreover, MALAT1, TLR4, IL‐6, and IL‐8 increased while miR‐20a decreased after 1 μg/mL Porphyromonas gingivalis lipopolysaccharide (LPS) or Escherichia coli LPS stimulation. MiR‐20a inhibited the expression of proinflammatory cytokines via binding to TLR4 3′‐UTR. In addition, MALAT1 increased TLR4 level and the secretion of inflammatory cytokines. Conclusion MALAT1 enhances inflammatory cytokine production through sponging miR‐20a and releasing TLR4, indicating a regulatory role of MALAT1 in periodontal inflammation.

Objective: This study aimed to fabricate hyaluronic acid (HA)/parecoxib-loaded PLGA microspheres for the treatment of temporomandibular disorders (TMD) and investigate the in vitro and in vivo effect of the microsphere system so as to solve the issues of poor drug delivery and short duration on drug concentration in conventional TMD therapy. Method: The microspheres were prepared by the double emulsion (w/o/w) method. Various formulations were compared in terms of particle size, drug loading rate and encapsulation rate. Scanning electron microscopy (SEM), differential Scanning Calorimetry (DSC) and FT-IR spectroscopy were performed to evaluate physicochemical properties. The drug release be-havior of microspheres and toxicity assay on synovial cells were investigated. The in vitro anti-inflammatory effect on in-flammatory markers such as IL-1β, TNF-α and COX-2 was assessed by real-time PCR. Then the in vivo therapeutic effect of microspheres was investigated using mechanically-induced rat synovitis model. Protein levels of inflammatory cytokines (IL-1β, TNF-α and COX-2) from TMJ periarticular tissues were quantified by enzyme-linked immunosorbent assay (ELISA). Results: The results showed that microspheres were morphological regular, smooth and non-cohesive. The average particle size of the microspheres was (25.32±1.01) μm. The drug loading rate of parecoxib was 17.12%-20.95 % with encapsulation efficiency reaching 51.9%-54.7%. In vitro drug release tests showed a successful sustained release over 28 days with a burst of 19.98% of the total drug substance. Treatment with HA/parecoxib-loaded PLGA microspheres declined the mRNA ex-pression of IL-1β, TNF-α and COX-2 induced by LPS in articular synovial cells. Moreover, in vivo results demonstrated that the intra-articular microspheres significantlyreduced protein levels of inflammatory cytokines (IL-1β, TNF-α and COX-2) for more than two weeks and stopped the mechanically-induced synovitis in its tracks in rat models. Conclusion: The study presented new and potential insights into treatments of TMD using PLGA microspheres loaded with HA and parecoxib as a successful drug delivery system.

Background Serum amyloid A (SAA) has been identified to trigger inflammation response, and play a crucial role in chronic inflammatory diseases. However, the regulatory mechanism of SAA still remains unclear during the development of periodontitis Methods SAA mRNA and protein expression were detected in healthy and inflammatory gingival tissues using real‐time polymerase chain reaction (PCR) and immunohistochemistry. Human recombinant SAA (Apo‐SAA), Pam3CSK4 (a Toll‐like receptor (TLR) 2 ligand), siRNA‐SAA, or TLR2 neutralizing antibody was applied to treat human gingival fibroblasts, respectively, or combined. SAA, TLRs, and inflammatory cytokines interleukin (IL)‐6 and IL‐8 were analyzed by real‐time PCR, western blotting, or enzyme‐linked immunosorbent assay. Results SAA expression increased in human inflammatory gingival tissues from patients with periodontitis (P <0.05). Apo‐SAA could increase not only the mRNA expression of TLR2 (P <0.05), but also IL‐6 and IL‐8 mRNA and protein levels (P <0.05) which was suppressed by TLR2 antibody in human gingival fibroblasts. Pam3CSK4 increased SAA, IL‐6, and IL‐8 levels (P <0.05). However, the expression of SAA, IL‐6, and IL‐8 decreased after transfection of siRNA‐SAA (P <0.05). Conclusion SAA not only increases in inflammatory gingiva, but also triggers inflammatory cytokine secretion via interacting with TLR2 pathway in human gingival fibroblasts, which indicates that SAA is involved in periodontal inflammation.

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