■牙周炎是由宿主对牙齿周围细菌沉积物的免疫反应引发的牙齿支撑结构的炎症状态。众所周知,促炎性白介素(IL)-6,IL-8,MCP-1以及含NOD样受体家族pyrin结构域3(NLRP3)炎性体,是激活这种反应的关键调节剂。掺铒钇铝石榴石(Er:YAG)激光器,固态晶体激光已普遍用于治疗牙周病。然而,人们对Er:YAG激光器的分子机制知之甚少,特别是针对牙周病原体引起的宿主免疫反应。因此,目前的研究主要集中于Er:YAG激光对牙周炎的保护作用,趋化因子和NLRP3炎性体表达。
■首先用来自牙龈卟啉单胞菌(Pg-LPS)的脂多糖(LPS)刺激人牙周膜成纤维细胞(PDLFs)以模拟牙周炎。然后用能量密度(3.6-6.3J/cm2)的Er:YAG激光照射细胞,然后进行细胞增殖和伤口愈合试验。接下来,研究了Er:YAG激光对IL-6,IL-8,MCP-1,NLRP3和裂解的GSDMD表达的影响。
■发现Pg-LPS可降低PDLF中细胞的增殖率和伤口愈合能力,并通过Er:YAG激光照射挽救。此外,LPS刺激导致IL-6,IL-8和MCP-1的分泌以及NLRP3和裂解的GSDMD蛋白的mRNA和蛋白质表达显着上调,而Er:YAG激光抑制了引起的现象。
■据我们所知,这是首次研究激光对牙周炎模型中NLRP3炎性体的影响。我们的研究揭示了Er:YAG激光通过调节IL-6,IL-8,MCP-1和NLRP3炎性体在改善牙周炎中的关键作用,并强调NLRP3炎性体的控制可能成为牙周炎的潜在方法。
UNASSIGNED: Periodontitis is an inflammatory condition of the tooth-supporting structures triggered by the host\'s immune response towards the bacterial deposits around the teeth. It is well acknowledged that pro-inflammatory interleukin (IL)-6, IL-8, MCP-1 as well as the NOD-like receptor family pyrin domain containing 3 (NLRP3) inflammasome, are the key modulators in the activation of this response. Erbium-doped yttrium-aluminium-garnet (Er:YAG) laser, a solid-state crystal laser have been commonly used in the treatment of periodontal diseases. However, little is understood about the molecular mechanism of the Er:YAG laser, especially in targeting the host immune response brought on by periodontal pathogens. Hence, the current study focused on the protective effects of Er:YAG laser on periodontitis in-vitro in terms of pro-inflammatory cytokines, chemokines and NLRP3 inflammasome expressions.
UNASSIGNED: Human periodontal ligament fibroblast (PDLFs) were first stimulated with lipopolysaccharides (LPS) from P. gingivalis (Pg-LPS) to simulate periodontitis. Cells were then irradiated with Er:YAG laser of ascending energy densities (3.6-6.3 J/cm2), followed by cell proliferation and wound healing assay. Next, the effects of Er:YAG laser on the expressions of IL-6, IL-8, MCP-1, NLRP3, and cleaved GSDMD were examined.
UNASSIGNED: Pg-LPS was found to reduce cell\'s proliferation rate and wound healing ability in PDLFs and these were rescued by Er:YAG laser irradiation. In addition, LPS stimuli resulted in a marked upregulation in the secretion of IL-6, IL-8 and MCP-1 as well as the mRNA and protein expression of NLRP3 and cleaved-GSDMD protein whereas Er:YAG laser suppressed the elicited phenomena.
UNASSIGNED: To our knowledge, this is the first study to look into the laser\'s implication on the NLRP3 inflammasome in periodontitis models. Our study reveals a crucial role of Er:YAG laser in ameliorating periodontitis in-vitro through the modulation of IL-6, IL-8, MCP-1 and the NLRP3 inflammasome and highlights that the control of the NLRP3 inflammasome may become a potential approach for periodontitis.