Jia Mengying, Lv Yaoguang, Xu Yingjie, Gong Zhongcheng
Oncology Department of Oral and Maxillofacial Surgery of The First Affiliated Hospital of Xinjiang Medical University, Urumqi, 830054, Xin Jiang Province, China.
The Stomatology College of Xinjiang Medical University, Urumqi, 830054, Xin Jiang Province, China.
BMC Musculoskelet Disord. 2021 Feb 26;22(1):229. doi: 10.1186/s12891-021-04092-0.
The nucleotide-binding oligomerization domain-like receptor pyrin domain containing 3 (NLRP3) inflammasome signaling pathway is a highlighted topic in the field of inflammation. However, there is little research on the relationship between the NLRP3 inflammasome pathway and temporomandibular joint osteoarthritis (TMJOA). The aim of this study was to examine the expression of inflammatory mediators related to the NLRP3 inflammasome in the synovial fluid of patients with condylar cartilage degeneration and verify the clinical effects of sodium hyaluronic acid (HA) treatment on TMJOA.
Patients diagnosed with temporomandibular joint internal derangement (TMJID) without condylar defects and TMJOA with condylar defects were divided into two groups. There were thirty patients in each group, and inflammatory mediators related to the NLRP3 inflammasome, including interleukin-1 beta (IL-1β), IL-18, NLRP3, and cysteinyl aspartate specific proteinase 1 (CASP1), in synovial fluid were measured by enzyme-linked immunosorbent assay (ELISA). Eighteen patients in the TMJOA group were retested after two HA treatments to evaluate the therapeutic effects of HA.
IL-1β, IL-18, NLRP3 and CASP1 were all positive in the two groups, and TMJOA patients with condylar defects had higher expression of these molecules than TMJID patients (P < 0.05). IL-1β, IL-18, and NLRP3 were decreased after two HA treatments (P<0.05), but there was no significant difference in CASP1 after two HA injections (P = 0.549).
The NLRP3 inflammasome signaling pathway may be involved in condylar degeneration. HA could reduce some inflammatory molecules to alleviate inflammation.
核苷酸结合寡聚化结构域样受体吡啉结构域含3（NLRP3）炎性小体信号通路是炎症领域的一个热点话题。然而，关于NLRP3炎性小体通路与颞下颌关节骨关节炎（TMJOA）之间的关系研究较少。本研究旨在检测髁突软骨退变患者滑液中与NLRP3炎性小体相关的炎症介质表达，并验证透明质酸钠（HA）治疗TMJOA的临床效果。
将诊断为无髁突缺损的颞下颌关节内紊乱（TMJID）和有髁突缺损的TMJOA患者分为两组。每组30例，采用酶联免疫吸附测定（ELISA）法检测滑液中与NLRP3炎性小体相关的炎症介质，包括白细胞介素-1β（IL-1β）、IL-18、NLRP3和半胱天冬酶-1（CASP1）。TMJOA组18例患者在接受两次HA治疗后再次检测，以评估HA的治疗效果。
两组患者IL-1β、IL-18、NLRP3和CASP1均呈阳性，有髁突缺损的TMJOA患者这些分子的表达高于TMJID患者（P<0.05）。两次HA治疗后IL-1β、IL-18和NLRP3降低（P<0.05），但两次HA注射后CASP1无显著差异（P = 0.549）。
NLRP3炎性小体信号通路可能参与髁突退变。HA可降低一些炎症分子以减轻炎症。
