Aims: To investigate the clinical performance of regenerative periodontal surgery in the treatment of furcation defects versus open flap debridement (OFD) and to compare different regenerative modalities.Material and Methods: A systematic search was conducted to identify RCTs evaluating regenerative surgical treatment of furcations with a minimum of 12‐month follow‐up. Three authors independently reviewed, selected and extracted data from the search conducted and assessed risk of bias. Primary outcomes were tooth loss, furcation improvement (closure/conversion) (FImp), gain of horizontal bone level (HBL) and attachment level (HCAL). Secondary outcomes were gain in vertical attachment level (VCAL), probing pocket depth (PPD) reduction, PROMs and adverse events. Data were summarized into Bayesian standard and network meta‐analysis in order to estimate direct and indirect treatment effects and to establish a ranking of treatments.Results: The search identified 19 articles, reporting on 20 RCTs (19 on class II, 1 on class III furcations) with a total of 575 patients/787 defects. Tooth loss was not reported. Furcation closure ranged between 0% and 60% (10 trials), and class I conversion from 29% to 100% (six trials). Regenerative techniques were superior to OFD for FImp (OR = 20.9; 90% CrI = 5.81, 69.41), HCAL gain (1.6 mm), VCAL gain (1.3 mm) and PPD reduction (1.3 mm). Bone replacement grafts (BRG) resulted in the highest probability (Pr = 61%) of being the best treatment for HBL gain. Non‐resorbable membranes + BRG ranked as the best treatment for VCAL gain (Pr = 75%) and PPD reduction (Pr = 56%).Conclusions: Regenerative surgery of class II furcations is superior to OFD. FImp (furcation closure or class I conversion) can be expected for the majority of defects. Treatment modalities involving BRG are associated with higher performance.

Oral bacteria are the main trigger for the development of periodontitis, and some species are known to modulate neutrophil function. This study aimed to explore the release of neutrophil extracellular traps (NETs), associated antimicrobial proteins, and reactive oxygen species (ROS) in response to periodontal bacteria, as well as the underlying pathways. Isolated peripheral blood neutrophils were stimulated with 19 periodontal bacteria. NET and ROS release, as well as the expression of NET-bound antimicrobial proteins, elastase, myeloperoxidase, and cathepsin G, in response to these species was measured using fluorescence-based assays. NET and ROS release was monitored after the addition of NADP (NADPH) oxidase pathway modulators and inhibitors of Toll-like receptors (TLRs). Moreover, bacterial entrapment by NETs was visualized microscopically, and bacterial killing was assessed by bacterial culture. Certain microorganisms, e.g., Veillonella parvula and Streptococcus gordonii , stimulated higher levels of ROS and NET release than others. NETs were found to entrap, but not kill, all periodontal bacteria tested. NADPH oxidase pathway modulators decreased ROS production but not NET production in response to the bacteria. Interestingly, TLR inhibitors did not impact ROS and NET release. These data suggest that the variability in the neutrophil response toward different bacteria may contribute to the pathogenesis of periodontal diseases by mechanisms such as bacterial avoidance of host responses and activation of neutrophils. Moreover, our results indicate that bacterium-stimulated NET release may arise in part via NADPH oxidase-independent mechanisms. The role of TLR signaling in bacterium-induced ROS and NET release needs to be further elucidated.

Neutrophils are amongst the most abundant immune cells within the periodontal tissues and oral cavity. As innate immune cells, they are first line defenders at the tooth-mucosa interface, and can perform an array of different functions. With regard to these, it has been observed over many years that neutrophils are highly heterogeneous in their behavior. Therefore, it has been speculated that neutrophils, similarly to other leukocytes, exist in distinct subsets. Several studies have investigated different markers of neutrophils in oral health and disease in recent years in order to define potential cell subsets and their specific tasks. This research was inspired by recent advancements in other fields of medicine in this field. The aim of this review is to give an overview of the current evidence regarding the existence and presence of neutrophil subsets and their possible functions, specifically in the context of periodontitis, gingivitis, and periodontal health.

Development of dysbiosis in complex multispecies bacterial biofilms forming on teeth, known as dental plaque, is one of the factors causing periodontitis. Fusobacterium nucleatum (F. nucleatum) is recognised as a key microorganism in subgingival dental plaque, and is linked to periodontitis as well as colorectal cancer and systemic diseases. Five subspecies of F. nucleatum have been identified: animalis, fusiforme, nucleatum, polymorphum, and vincentii. Differential integration of subspecies into multispecies biofilm models has been reported, however, biofilm forming ability of individual F. nucleatum subspecies is largely unknown. The aim of this study was to determine the single-subspecies biofilm forming abilities of F. nucleatum ATCC type strains. Static single subspecies F. nucleatum biofilms were grown anaerobically for 3 days on untreated or surface-modified (sandblasting, artificial saliva, fibronectin, gelatin, or poly-L-lysine coating) plastic and glass coverslips. Biofilm mass was quantified using crystal violet (CV) staining. Biofilm architecture and thickness were analysed by scanning electron microscopy and confocal laser scanning microscopy. Bioinformatic analysis was performed to identify orthologues of known adhesion proteins in F. nucleatum subspecies. Surface type and treatment significantly influenced single-subspecies biofilm formation. Biofilm formation was overall highest on poly-L-lysine coated surfaces and sandblasted glass surfaces. Biofilm thickness and stability, as well as architecture, varied amongst the subspecies. Interestingly, F. nucleatum ssp. polymorphum did not form a detectable, continuous layer of biofilm on any of the tested substrates. Consistent with limited biofilm forming ability in vitro, F. nucleatum ssp. polymorphum showed the least conservation of the adhesion proteins CmpA and Fap2 in silico. Here, we show that biofilm formation by F. nucleatum in vitro is subspecies- and substrate-specific. Additionally, F. nucleatum ssp. polymorphum does not appear to form stable single-subspecies continuous layers of biofilm in vitro. Understanding the differences in F. nucleatum single-subspecies biofilm formation may shed light on multi-species biofilm formation mechanisms and may reveal new virulence factors as novel therapeutic targets for prevention and treatment of F. nucleatum-mediated infections and diseases.