Scholarlink

<p>Periodontitis is characterized by the activity of neutrophil elastase, a host defense factor that leads to the destruction of the epithelial barrier and bacterial invasion of the periodontal tissue. Secretory leukocyte protease inhibitors (SLPI), predominantly secreted by epithelial cells, diffuse into the mucosal surface and inhibit excessive tissue loss caused by elastase during inflammation. The SLPI level is high in healthy gingiva and low in severe periodontitis. In this study, we hypothesized that intragingival administration of SLPI inhibits periodontal tissue destruction caused by periodontitis. Administration of SLPI significantly reduced neutrophil elastase activity in periodontal tissue and alleviated alveolar bone loss in mice. Real-time PCR analysis revealed that SLPI administration downregulated the transcription of pro-inflammatory cytokines and osteoclast-related factors in the gingival tissue. Furthermore, in vitro treatment of bone marrow macrophages with SLPI resulted in the downregulation of osteoclast differentiation. SLPI treatment of MC3T3-E1 cells promoted osteoblast differentiation and bone formation. These findings suggest that SLPI protects against periodontal tissue damage by suppressing inflammation and bone resorption and promoting bone regeneration.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Secretory leucocyte protease inhibitor regulates bone metabolism and inflammation in experimental mouse periodontitis

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年5月16日

查看全文
  • Karin Sasagawa,
  • Hisanori Domon,
  • Satoru Hirayama,
  • Tomoki Maekawa,
  • Toshihito Isono,
  • Koichi Tabeta,
  • Yutaka Terao

摘要

Periodontitis is characterized by the activity of neutrophil elastase, a host defense factor that leads to the destruction of the epithelial barrier and bacterial invasion of the periodontal tissue. Secretory leukocyte protease inhibitors (SLPI), predominantly secreted by epithelial cells, diffuse into the mucosal surface and inhibit excessive tissue loss caused by elastase during inflammation. The SLPI level is high in healthy gingiva and low in severe periodontitis. In this study, we hypothesized that intragingival administration of SLPI inhibits periodontal tissue destruction caused by periodontitis. Administration of SLPI significantly reduced neutrophil elastase activity in periodontal tissue and alleviated alveolar bone loss in mice. Real-time PCR analysis revealed that SLPI administration downregulated the transcription of pro-inflammatory cytokines and osteoclast-related factors in the gingival tissue. Furthermore, in vitro treatment of bone marrow macrophages with SLPI resulted in the downregulation of osteoclast differentiation. SLPI treatment of MC3T3-E1 cells promoted osteoblast differentiation and bone formation. These findings suggest that SLPI protects against periodontal tissue damage by suppressing inflammation and bone resorption and promoting bone regeneration.