Maintenance of periodontal health or transition to a periodontal lesion reflects the continuous and ongoing battle between the vast microbial ecology in the oral cavity and the array of resident and emigrating inflammatory/immune cells in the periodontium. This war clearly signifies many 'battlefronts' representing the interface of the mucosal-surface cells with the dynamic biofilms composed of commensal and potential pathogenic species, as well as more recent knowledge demonstrating active invasion of cells and tissues of the periodontium leading to skirmishes in connective tissue, the locality of bone and even in the local vasculature. Research in the discipline has uncovered a concerted effort of the microbiome, using an array of survival strategies, to interact with other bacteria and host cells. These strategies aid in colonization by 'ambushing, infiltrating and outflanking' host cells and molecules, responding to local environmental changes (including booby traps for host biomolecules), communicating within and between genera and species that provide MASINT (Measurement and Signature Intelligence) to enhance sustained survival, sabotage the host inflammatory and immune responses and by potentially adopting a 'Fabian strategy' with a war of attrition and resulting disease manifestations. Additionally, much has been learned regarding the ever-increasing complexity of the host-response armamentarium at both cellular and molecular levels that is addressed in this review. Knowledge regarding how these systems fully interact requires both new laboratory and clinical tools, as well as sophisticated modeling of the networks that help maintain homeostasis and are dysregulated in disease. Finally, the triggers resulting in a 'coup de main' by the microbiome (exacerbation of disease) and the characteristics of susceptible hosts that can result in 'pyrrhic victories' with collateral damage to host tissues, the hallmark of periodontitis, remains unclear. While much has been learned, substantial gaps in our understanding of the 'parameters of this war' remain elusive toward fulfilling the Sun Tzu adage: 'If you know the enemy and know yourself, you need not fear the result of a hundred battles.'

Aim Peri-implant gingival healing following one-stage implant placement was investigated and compared to periodontal healing. Methods Healing at surgical sites (implant (I) and adjacent teeth (T+)) was compared to non-operated tooth (T-) in non-smokers receiving one-stage implant. Periodontal Indices (PI, GI) were recorded at surgery and up to 12 weeks postoperatively. Peri-implant (PICF) and gingival crevicular (GCF) fluids were analyzed for cytokines, collagenases and inhibitors. Data was analyzed by linear mixed model regression analysis and repeated measures ANOVA. Results 40 patients (22 female; 21-74 yrs old) completed the study. Surgical site GI, increased at week 1, decreased significantly during early healing (weeks 1-3; p=0.0003) and continually decreased during late healing (weeks 6-12) for I (p<0.01). PICF volume decreased 3-fold by week 12 (p=0.0003). IL-6, IL-8, MIP-1β, and TIMP-1 levels significantly increased at surgical sites at week one, significantly decreasing thereafter (P<0.016). Week one IL-6, IL-8 and MIP-1β levels were ~3-fold higher, and TIMP-1 levels 63% higher, at I compared to T+ (p=0.001). Conclusion Peri-implant gingival healing, as determined by crevicular fluid molecular composition, differs from periodontal healing. The observed differences suggest that peri-implant tissues, compared to periodontal tissues, represent a higher pro-inflammatory state.

Periodontitis is a chronic inflammation that destroys periodontal tissues caused by the accumulation of bacterial biofilms that can be affected by environmental factors. This report describes an association study to evaluate the relationship of environmental factors to the expression of periodontitis using the National Health and Nutrition Examination Study (NHANES) from 1999–2004. A wide range of environmental variables (156) were assessed in patients categorized for periodontitis (n = 8884). Multiple statistical approaches were used to explore this dataset and identify environmental variable patterns that enhanced or lowered the prevalence of periodontitis. Our findings indicate an array of environmental variables were different in periodontitis in smokers, former smokers, or non-smokers, with a subset of specific environmental variables identified in each population subset. Discriminating environmental factors included blood levels of lead, phthalates, selected nutrients, and PCBs. Importantly, these factors were found to be coupled with more classical risk factors (i.e. age, gender, race/ethnicity) to create a model that indicated an increased disease prevalence of 2–4 fold across the sample population. Targeted environmental factors are statistically associated with the prevalence of periodontitis. Existing evidence suggests that these may contribute to altered gene expression and biologic processes that enhance inflammatory tissue destruction.

Aim To investigate the role of Epstein–Barr virus (EBV), cytomegalovirus (CMV), and anaerobic bacteria in the progression of periodontitis. Methods Eighty‐one adults with generalized moderate to severe periodontitis were randomly assigned to: oral hygiene or scaling and root planning ± placebo or polyunsaturated fatty acids fish oil. Subgingival plaque samples collected from three healthy and three disease sites at weeks 0, 16, and 28 and from sites demonstrating disease progression were analysed for EBV, CMV, P. gingivalis (Pg), T. forsythia (Tf), and T. denticola (Td) DNA using quantitative polymerase chain reaction. Results Cytomegalovirus was detected in 0.3% (4/1454) sites. EBV was present in 12.2% of healthy sites (89/728) and 27.6% disease sites (201/726; p < .0001), but was in low copy number. Disease progression occurred in 28.4% of participants (23/81) and developed predominantly at sites identified as diseased (75/78; 96.2%). CMV and EBV were not associated with disease progression (p = .13) regardless of treatment. In contrast, disease sites were associated with higher levels of Pg, Td, Tf, and total bacteria, and sites that exhibited disease progression were associated with an abundance of Td and Tf (p < .04). Conclusion Disease progression was associated with Gram‐negative anaerobic bacteria; not EBV or CMV.

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