Host modulation: controlling the inflammation to control the infection

Abstract

Historically, periodontal disease (gingivitis and periodontitis) has been recognized as being primarily of bacterial origin. However, recent evidence indicates that while bacteria are necessary for disease development they are not sufficient for the clinical manifestation of the many and varied forms of periodontal disease. It is becoming increasingly apparent that it is the host inflammatory response to the subgingival bacteria that is responsible for the tissue damage and, most likely, progression of the disease. We explore the concept that it is the subgingival microenvironment modified by the inflammatory response that leads to a change from a commensal to pathogenic microbiota. In this review, we examine the evidence for the emerging paradigm supporting the central role of inflammation rather than specific microbiota in the pathogenesis of periodontitis, and that by controlling the inflammation, it is possible to control the infection. As an extension of this, we propose a working model for the ongoing monitoring of periodontal patients using the medical model of 'treat to target'.

Real-time PCR quantification of 9 periodontal pathogens in saliva samples from periodontally healthy Korean young adults

“…In addition to a microbial shift favoring pathogenic species, a suitable environment and ‘susceptible’ host are essential for periodontitis to manifest clinically [1]. Periodontitis is no longer regarded as an infectious disease caused by bacteria.…”

“…Periodontal disease occurs because of interactions between host inflammatory and immune systems and bacterial complexes [12]. These bacterial complexes are also found in periodontally healthy individuals, and disease occurs when the balance between host defense and bacterial complexes is disrupted [3].…”

Biological response to peri‐implantitis treatment

“…Recent studies involving the pathogenesis of peri‐implant diseases have investigated putative oral biomarkers, similar to those detected with periodontitis that could aid in the diagnostic process . In as much as PIP involves a robust host response to a substantial oral bacterial burden, with an imbalance between pro‐ and anti‐inflammatory responses and tissue destruction of the periodontium (soft and hard tissue damage), analysis of cytokine levels representing these responses in peri‐implant crevicular fluid (PICF) could assist in identifying early biological responses that might presage disease. Biomarkers linked to PIP include an array of pro‐inflammatory cytokines (tumor necrosis factor‐α, interferon‐γ, interleukin (IL)‐1β, IL‐6, anti‐inflammatory cytokines (IL‐4 and IL‐10), chemokines (IL‐8, monocyte chemoattractant protein (MCP)‐1 and macrophage inflammatory protein (MIP‐1α), and tissue destructive enzymes (matrix metalloproteinases (MMP‐8) .…”

IL‐22–expressing CD4+AhR+ T lymphocytes are associated with RANKL‐mediated alveolar bone resorption during experimental periodontitis

“…Periodontitis is a chronic inflammatory disease in which the disruption of the balance between the host's immune response and the subgingival bacterial biofilm plays a pivotal role in the onset and progression of the disease . Periodontitis results from polymicrobial synergy and dysbiosis; however, periodontal tissue breakdown is mainly determined by the host's immune response, where the T‐lymphocyte subpopulations play a central role in the alveolar bone resorption that leads to tooth loss .…”