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

ABSTRACT

Introduction: 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.

KEYWORDS:

• Gingivitis
• inflammation
• periodontal diseases
• periodontitis
• Porphyromonas gingivalis
• sTREM-1
• TREM-1
• TREM-2

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties.

Additional information

Funding

The research work of DK Agrawal is supported by research grants R01 HL112597, R01 HL116042, and R01 HL120659 from the National Institutes of Health, USA. The content of this review article is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health.