Periodontal disease (PD) is a chronic inflammation of the tooth supporting soft tissue and alveolar bone due to infection by a select group of gram negative microbes, and leads to tooth loss if untreated. Since mice deficient in CD4+ cells are resistant to infection-induced alveolar bone loss, Th cells have been implicated in bone destructive processes during PD. However, the extent to which different Th-cell subtypes play roles in pathogenesis or host protection remains to be defined, and is likely to vary depending on the dominant microorganism involved. By far the best studied periodontal microbe in PD is Porphyromonas gingivalis. Even though the gram negative anaerobe Tannerella forsythia is also a vital contributor to periodontal bone loss, almost nothing is known about immune responses to this organism. Previous studies from our laboratory have revealed that T. forsythia induces periodontal bone loss in mice, and that this bone loss depends on the bacterially-expressed BspA protein. In this study, we show that T. forsythia activates murine APCs primarily through TLR2-dependent signaling via BspA. Furthermore, T. forsythia infection causes a pronounced Th2 bias, evidenced by T cell expression of IL-5 but not IFN-γ or IL-17 in draining LN. Consistently, deficiencies in TLR2 or STAT6 result in resistance to T. forsythia-induced alveolar bone loss. Thus, TLR2 signaling and Th2 cells play pathogenic roles in T. forsythia-induced alveolar bone destruction.

Background Peri‐implantitis is a challenging condition to manage and is frequently treated using non‐surgical debridement. The local delivery of antimicrobial agents has demonstrated benefit in mild to moderate cases of peri‐implantitis. This study compared the safety and efficacy of chlorhexidine gluconate 2.5 mg chip (CHX chips) as an adjunctive treatment to subgingival debridement in patients afflicted with peri‐implantitis. Methods A multicenter, randomized, single‐blind, two‐arm, parallel Phase‐3 study was conducted. Peri‐implantitis patients with implant pocket depths (IPD) of 5‐8 mm underwent subgingival implant surface debridement followed by repeated bi‐weekly supragingival plaque removal and chlorhexidine chips application (ChxC group) for 12 weeks, or similar therapy but without application of ChxC (control group). All patients were followed for 24 weeks. Plaque and gingival indices were measured at every visit whereas IPD, recession, and bleeding on probing were assessed at 8, 12, 16, 24 week. Results A total of 290 patients were included: 146 in the ChxC group and 144 in the control. At 24 weeks, a significant reduction in IPD (P = 0.01) was measured in the ChxC group (1.76 ± 1.13 mm) compared with the control group (1.54 ± 1.13 mm). IPD reduction of ≥2 mm was found in 59% and 47.2% of the implants in the ChxC and control groups, respectively (P = 0.03). Changes in gingival recession (0.29 ± 0.68 mm versus 0.15 ± 0.55 mm, P = 0.015) and relative attachment gain (1.47 ± 1.32 mm and 1.39 ± 1.27 mm, P = 0.0017) were significantly larger in the ChxC group. Patients in the ChxC group that were < 65 years exhibited significantly better responses (P < 0.02); likewise, non‐smokers had similarly better response (P < 0.02). Both protocols were well tolerated, and no severe treatment‐related adverse events were recorded throughout the study. Conclusions Patients with peri‐implantitis that were treated with an intensive treatment protocol of bi‐weekly supragingival plaque removal and local application of chlorhexidine chips had greater mean IPD reduction and greater percentile of sites with IPD reduction of ≥2 mm as compared with bi‐weekly supra‐gingival plaque removal.

Baking soda and fluoride dentifrices, therefore, may perhaps be considered as a criterion standard for patients with routine oral hygiene needs.

Probiotics have been considered as an adjunct to prevent and treat a variety of diseases. The ease of administration of probiotics and the fact that no adverse outcomes have been reported in the literature has promoted increasing interest from the research community for this preventive approach in a number of diseases, including periodontal diseases. Several preliminary human clinical trials have been conducted and have yielded promising results. Vaccination is another biological strategy considered for use in the prevention of periodontal diseases. To date, no vaccine trials have been conducted in humans to determine if this strategy would prevent alveolar bone loss or bacterial colonization by target pathogens. Although the available research appears promising, the current body of evidence is incomplete for both strategies. This review attempts to summarize the present status of these 2 biological strategies for the prevention of periodontal diseases.

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