AI Article Synopsis

  • Periodontal disease is a bacterial infection linked to inflammation that can contribute to various systemic health issues, making the development of new preventive measures crucial for the elderly in aging societies.
  • Research highlights the importance of the gingival epithelium as a barrier against bacteria and suggests that controlling cell interactions and inflammation may help prevent periodontal disease.
  • Several agents, including irsogladine maleate, azithromycin, amphotericin B, and a traditional Japanese herb (dokudami), have shown potential in enhancing the epithelial barrier and reducing neutrophil accumulation in the gums, indicating their possible use in preventing periodontal inflammation.

Article Abstract

Periodontal disease is a bacterial biofilm-associated inflammatory disease that has been implicated in many systemic diseases. A new preventive method for periodontal disease needs to be developed in order to promote the health of the elderly in a super-aged society. The gingival epithelium plays an important role as a mechanical barrier against bacterial invasion and a part of the innate immune response to infectious inflammation in periodontal tissue. The disorganization of cell-cell interactions and subsequent inflammation contribute to the initiation of periodontal disease. These make us consider that regulation of host defensive functions, epithelial barrier and neutrophil activity, may become novel preventive methods for periodontal inflammation. Based on this concept, we have found that several agents regulate the barrier function of gingival epithelial cells and suppress the accumulation of neutrophils in the gingival epithelium. We herein introduce the actions of irsogladine maleate, azithromycin, amphotericin B, and (dokudami in Japanese), which is commonly used in traditional medicine, on the epithelial barrier and neutrophil migration in gingival epithelial cells and , in order to provide support for the clinical application of these agents to the prevention of periodontal inflammation.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5944110PMC
http://dx.doi.org/10.1016/j.jdsr.2017.11.003DOI Listing

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