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DOI 10.1080/1744666x.2017.1392855

Медицинская библиотека · Expert review of clinical immunology · 2017

Triggering receptor expressed on myeloid cells in the pathogenesis of periodontitis: potential novel treatment strategies.

Rudick Courtney P, Miyamoto Takanari, Lang Melissa S, Agrawal Devendra K

СтатьяОбзорПоддержка NIH: внешняя программаПеревод в очереди

Аннотация

Periodontal diseases are polymicrobial inflammatory disorders of the tissue, ligament, and bone structures supporting teeth. Periodontitis (inflammation with corresponding loss of attachment) affects 40-50% of adults. Recently, members of the Triggering Receptor on Myeloid Cell (TREM) family have been studied to determine their relationship to these diseases. Areas covered: TREM-1 is a receptor expressed on the surface of PMNs, monocytes, macrophages, dendritic cells, vascular smooth muscle cells, and keratinocytes upregulated in the presence of periodontal inflammation. TREM-1 expression can be upregulated by oral bacterium Porphyromonas gingivalis that can be abrogated by a sub-antimicrobial dose of doxycycline. When cleaved from the cell surface, a soluble form of TREM-1 (sTREM-1) can be used as a biomarker of inflammation and might also provide a link between oral and systemic inflammation. While less understood, TREM-2 has a role in osteoclastogenesis which could contribute to the alveolar bone destruction seen in more advanced periodontitis. Expert commentary: Additional studies to simulate biofilm microenvironment in TREM research are warranted. Longitudinal studies determining TREM-1, sTREM-1, and TREM-2 levels in tissues over time and progression of periodontal diseases would provide valuable information in the role of TREM receptors as indicators of or contributors to the disease process.

Для цитирования: Rudick Courtney P, Miyamoto Takanari, Lang Melissa S, Agrawal Devendra K. Triggering receptor expressed on myeloid cells in the pathogenesis of periodontitis: potential novel treatment strategies.. Expert review of clinical immunology. 2017. DOI: 10.1080/1744666x.2017.1392855.

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