In order for chairside diagnostic testing to make an impact on dental therapy, practitioners require a better understanding of genetic mutations contributing to the pathophysiology of periodontal disease. Commensal and pathogenic bacterial colonization in oral cavity tissues produces a cascade of proinflammatory signaling pathways ultimately detrimental to host tissues. Resolving inflammation is a multifactorial process involving the downregulation of proinflammatory cytokines while allowing commensal bacterial levels to return to normal. Because of the complicated nature of commensal bacteria and oral health homeostasis, the emphasis of dental therapy should place renewed focus on limiting destructive inflammation rather than solely eliminating bacteria. Salivary diagnostics are an easy, non‐invasive way to assess inflammatory markers. Inflammatory cytokine levels can help determine the subclinical health of a patient, showing the transition from health to gingivitis, or periodontitis, prior to clinical presentation. Single nucleotide polymorphism mutations can aid in determining increased risk of developing periodontitis. Taken together, and alongside regular clinical evaluations, chairside diagnostics help individualize treatment plans to slow, or halt, the progression of disease—before tissue destruction can take place. While more studies are needed analyzing specific mutations across periodontal categories, chairside diagnostics present an exciting adjunct to improve patient care.

Introduction: Sepsis is a disease process characterized by an extreme inflammatory response followed by a period of severe immunosuppression. In recent years, there has been improved survival in the initialimmune response during systemic inflammatory response syndrome, and compensatory anti-inflammatory response, yet is mostly unchanged with 18–30% mortality during the laterstage of sepsis despite numerous Phase 3 clinical trials. Areas covered: This review article presents a critical evaluation of the most promising newer studies aimed at improving the immunosuppressive stage of sepsis. Administration of DHEA/AED/AET show promise in improving survival. Blockade of signaling pathways for PD-1/PD-L1/CTLA-4, and partial blockade of TREM-1 signaling, and modification to sTREM-1 and the JAK/STAT pathway are promising methods of restoring host immune response and improving survival. While there has been significant progress, currently no findings have been translated into effective clinical interventions. Expert Commentary: Clinical success by immunomodulation with individual immune mediator is encouraging and should progress to evaluating combined methods of immunoregulation. Since most of the animal studies do not reproduce human sepsis, development of better animal models and moving toward human studies for intervention will lead to the most beneficial findings in translational science.

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.