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Periodontal diseases are associated with dysbiosis in the oral microbial communities. Managing oral biofilms is therefore key for preventing these diseases. Management protocols often include over‐the‐counter antimicrobial mouth rinses, which lack data on their effects on the oral microbiome's ecology, bacterial composition, metabolic activity, and dysbiosis resilience. This study examined the efficacy of antimicrobial mouth rinses to halt dysbiosis in in vitro oral biofilms under periodontitis‐simulating conditions. Multispecies oral biofilms were grown on hydroxyapatite discs (HADs) and rinsed daily with one of six mouth rinses. Positive and negative controls were included. After three rinses, biofilms were analyzed with viability quantitative polymerase chain reaction and visualized using scanning electron microscopy. Supernatants of rinsed biofilms were used for metabolic activity analysis. In addition, human oral keratinocytes were exposed to rinsed biofilms to assess their inflammatory response. All outputs were analyzed for correlation using Spearman coefficient. Product‐related changes were observed in the rinsed biofilms. Three of the six tested mouth rinses could significantly prevent dysbiosis with ≥30% reduction in pathobiont abundance relative to the control. These biofilms had lower metabolic activity, and the exposed human oral keratinocyte produced less interleukin‐8. Interleukin‐8 production correlated to both pathobiont quantity and the metabolic activity of the biofilms. Some mouth rinses could support biofilm resilience and stop dysbiosis evolution in the biofilm model, with a clear product‐related effect. Such mouth rinses can be considered for patients under maintenance/supportive periodontal therapy to prevent/delay disease recurrence. Others are more useful for different periodontal therapy stages.

The main aim of this study was to perform an integrative review on the enhanced bone healing by combining a flowable (injectable) platelet-rich fibrin (PRF) and bone graft porous materials. A bibliographical search was carried out on several databases (PubMed, Embase, Cochrane, Scopus, and Web of Science) for relevant studies on the combined effect of platelet-rich fibrin and bone substitutes for bone healing. The chemical, biologic, and physical properties of flowable PRF combined with bone graft biomaterials were discussed in this review. The repair of different bone defects was reported such as alveolar cleft reconstruction, sinus floor elevation, socket preservation, jaw defects, and impacted teeth. Regarding studies evaluating alveolar cleft defects, results showed potential benefits of PRF to enhance bone formation when mixed with autogenous bone graft. Two studies on socket preservation found enhanced bone growth when combining PRF to bone substitutes, although one study found similar results with or without bone substitutes. Also, the addition of PRF to demineralized bovine bone mineral improved the bone healing in the repair of jaw defects. No synergistic effect was reported in bone formation when PRF was associated to particulate bone graft in sinus floor elevation. The combination of PRF and bone graft materials revealed significant outcomes when compared to solely use of bone graft materials in alveolar cleft and jaw defects. In socket preservation, bone healing was improved when PRF and bone graft materials were applied in comparison to the solely use of PRF. On the reconstruction of larger bone defects, PRF can be mixed with a low resorption rate graft material to maintain biological and mechanical stability into the bone defect. In fact, PRF and particulate graft materials appear to exhibit a synergistic effect during bone tissue healing.

Periodontitis is a chronic inflammatory disease characterized by Gram‐negative bacteria responsible for the degradation of tissues surrounding tooth. Moreover, periopathogens can invade the bloodstream, disseminate and promote cardiovascular disease, such as the link between Porphyromonas gingivalisand atherosclerosis. The aim of this study was to explore the relationship between the severity of periodontitis and of abdominal aortic aneurysm (AAA). This cross‐sectional study compared patients with stable AAA (n = 30) and patients with unstable AAA (n = 31) based on aortic diameter, growth rate, and eligibility for surgical intervention. Periodontal clinical parameters were recorded as well as the Periodontal Inflamed Surface Area and the Periodontal Index for Risk of Infectiousness (PIRI). Microbiological analyses were performed on saliva and supragingival and subgingival plaque. Quantification of Tannerella forsythia (Tf), Porphyromonas gingivalis (Pg), Aggregatibacter actinomycetemcomitans (Aa), Fusobacterium nucleatum (Fn), and Prevotella intermedia (Pi)was done by quantitative polymerase chain reaction. The two AAA groups were homogeneous for age, sex, and most risk factors except hypertension and chronic obstructive pulmonary disease. Periodontal parameters were comparable but the proportion of patients with high PIRI scores was greater in those with unstable AAA (51.6% versus 23.3%). The probing depth (PD) and the proportion of PD >6 mm were positively correlated with AAA size and thrombus volume. Several associations were found between periopathogens such as Pgand AAA diameters and volumes, but no difference could be evidenced between stable and unstable AAA groups. Periodontitis was highly prevalent in both stable and unstable AAA patients. Severe and progressive periodontitis (stage IV and grade C) tended to be more frequent in the group of patients with unstable AAA. Moreover, Pgwas observed in all the samples (saliva, supragingival, and subgingival plaque) and was correlated with AAA diameters and volumes. The study evidenced potential relationships between periodontitis severity and size of AAA.

Oral biofilms form on all hard and soft surfaces of the oral cavity. When the microbial balance in this biofilm is disturbed, pathogens can take the overhand, and this can lead to periodontitis (i.e. a chronic and inflammatory disease of the gum and tooth supporting tissues). In this work, a dual species community model containing one commensal bacterium and the most common periopathogen, is presented. The commensal bacterium is Streptococcus gordonii, the periopathogen is Porphyromonas gingivalis. Existing Genome-Scale Metabolic Models (GSMNs) are curated and transformed into planktonic Dynamic Flux Balance Analysis (dFBA) models in DFBAlab (Gomez et al., 2014). In the planktonic model for S. gordonii, split ratio’s are used to ensure correct flux distributions between the glycolysis and the pentose phosphate pathway and around the pyruvate node. The split ratios are required to simulate the suboptimal growth behaviour of this bacterium. Simulation results for the planktonic S. gordonii model are compared to experiments for pure cultures. The planktonic P. gingivalis model gives feasible results for biomass growth and nutrient uptake. Finally, both planktonic models are transformed into a biofilm model in DFBAlab by introduction of nutrient gradients over the depth of the biofilm. This first oral biofilm model predicted the partitioning of both bacteria in the biofilm, similar to what has been described in literature.

Periodontal health is defined by absence of clinically detectable inflammation. There is a biological level of immune surveillance that is consistent with clinical gingival health and homeostasis. Clinical gingival health may be found in a periodontium that is intact, i.e. without clinical attachment loss or bone loss, and on a reduced periodontium in either a non‐periodontitis patient (e.g. in patients with some form of gingival recession or following crown lengthening surgery) or in a patient with a history of periodontitis who is currently periodontally stable. Clinical gingival health can be restored following treatment of gingivitis and periodontitis. However, the treated and stable periodontitis patient with current gingival health remains at increased risk of recurrent periodontitis, and accordingly, must be closely monitored. Two broad categories of gingival diseases include non‐dental plaque biofilm–induced gingival diseases and dental plaque‐induced gingivitis. Non‐dental plaque biofilm‐induced gingival diseases include a variety of conditions that are not caused by plaque and usually do not resolve following plaque removal. Such lesions may be manifestations of a systemic condition or may be localized to the oral cavity. Dental plaque‐induced gingivitis has a variety of clinical signs and symptoms, and both local predisposing factors and systemic modifying factors can affect its extent, severity, and progression. Dental plaque‐induced gingivitis may arise on an intact periodontium or on a reduced periodontium in either a non‐periodontitis patient or in a currently stable “periodontitis patient” i.e. successfully treated, in whom clinical inflammation has been eliminated (or substantially reduced). A periodontitis patient with gingival inflammation remains a periodontitis patient (Figure 1), and comprehensive risk assessment and management are imperative to ensure early prevention and/or treatment of recurrent/progressive periodontitis. Precision dental medicine defines a patient‐centered approach to care, and therefore, creates differences in the way in which a “case” of gingival health or gingivitis is defined for clinical practice as opposed to epidemiologically in population prevalence surveys. Thus, case definitions of gingival health and gingivitis are presented for both purposes. While gingival health and gingivitis have many clinical features, case definitions are primarily predicated on presence or absence of bleeding on probing. Here we classify gingival health and gingival diseases/conditions, along with a summary table of diagnostic features for defining health and gingivitis in various clinical situations.

Only recently the concept of prebiotics has been introduced in oral health. Few potential oral prebiotics have already been identified in dual species competition assays, showing a stimulatory effect on beneficial bacteria and by this suppressing the outgrowth of pathogenic species. This study aimed to validate the effect of previously identified potential prebiotic substrates on multispecies cultures by shifting the biofilm composition towards a more beneficial species dominated microbiota. A chemostat culture containing 14 model oral bacterial species was used to grow biofilms for 24 hours which subsequently were treated with prebiotic solutions three times a day for 3 consecutive days. Further the influence of environmental factors such as pH, nutrient availability, oxygen concentration and prebiotic dose on the efficacy of the prebiotic substances was investigated. Three potential prebiotic substrates N‐acetyl‐D‐mannosamine, succinic acid and Met‐Pro were able to bring the beneficial proportion to > 95%. While the pH of the prebiotic solution did not have an influence on the prebiotic effect, the interplay of nutrient availability, oxygen concentration and prebiotic treatment resulted in significant changes of the microbial composition identifying N‐acetyl‐D‐mannosamine as the most promising oral prebiotic substrate. Showing a clear dose dependent effect, concentrations of N‐acetyl‐D‐mannosamine of 1.0 and 1.5 M resulted in a biofilm composition of 97% beneficial species. Introducing the prebiotic concept in oral health might reveal a valid approach for treatment and prevention of oral diseases and promote oral health.

Background:There is growing interest in the use of probiotics in periodontal therapy; however, until now, most research has focused on lactobacilli probiotics. The aim of this study is to evaluate the effect of 4‐week use of yogurt supplemented with Bifidobacterium animalissubsp. lactisDN‐173010 versus a placebo yogurt, followed by a 5‐day non‐brushing period. Methods:Individuals were included in this single‐mask, randomized, controlled study if probing depth (PD) was ≤3 mm and attachment loss was ≤2 mm. After professional prophylaxis, they were randomized into two groups receiving yogurt containing either placebo or B. animalisfor 28 days, followed by a 5‐day non‐brushing period. Outcome measures were plaque index (PI), gingival index (GI), bleeding on probing (BOP), PD, gingival crevicular fluid (GCF) volume, and total amount and concentration of interleukin (IL)‐1β in GCF. These were measured at baseline, after 28 days of study product use, and subsequently after 5 days of plaque accumulation. Results:Fifty‐one patients were analyzed. No intergroup differences could be detected before and after intake of study products. However, after plaque accumulation, significantly better results for all parameters were seen in the probiotic group compared with the control group (P<0.001): lower PI and GI, less BOP, less increase in GCF volume, and lower IL‐1β total amount/concentration. Conclusion:The use of a probiotic yogurt supplemented with B. animaliscan have a positive effect on plaque accumulation and gingival inflammatory parameters after refraining from oral hygiene practices.

Dental implant failures occur mainly due to biofilm infections and mastication micro-movements or load stresses that may induce wear degradation. Dental implants’ microgaps are highly susceptible areas for biofilm formation and fluoride retention. Although fluoride is an antimicrobial agent widely used in caries prevention, its influence on biofilms under sliding wear remains unknown. The main aim of this work was to assess the effect of mixed biofilms and fluoride on the tribocorrosion behavior of titanium. Streptococcus mutansand Candida albicansmixed biofilms were cultured for 8 days on ground and polished commercially pure titanium. Biofilms’ formation was influenced by topography: higher roughness surfaces presented higher levels of biomass. Reciprocating sliding tests were performed on both surfaces, with and without biofilms, immersed in artificial saliva in the absence or presence of fluoride (30 and 227 ppm F−). The low friction coefficient registered indicated the lubricating effect of biofilms on titanium surfaces. Fluoride was also found to have lubricating properties on titanium during sliding, probably due to the precipitation of calcium fluoride (or like) salts. The presence of fluoride influenced the biotribological behavior of titanium surfaces covered with biofilms, facilitating their structural disruption and detachment. Nevertheless, open circuit potential tests reduced the corrosion of titanium in the presence of fluoride (227 ppm F−) and biofilms. In conclusion, it is highlighted that fluoride interaction with biofilms can significantly influence the tribological properties of commercially pure titanium in the oral cavity.

The oral cavity is a complex environment where corrosive substances from dietary, human saliva, and oral biofilms may accumulate in retentive areas of dental implant systems and prostheses promoting corrosion at their surfaces. Additionally, during mastication, micromovements may occur between prosthetic joints causing a relative motion between contacting surfaces, leading to wear. Both processes (wear and corrosion) result in a bio-tribocorrosion system once that occurs in contact with biological tissues and fluids. This review paper is focused on the aspects related to the corrosion and wear behavior of titanium-based structures in the oral environment. Furthermore, the clinical relevance of the oral environment is focused on the harmful effect that acidic substances and biofilms, formed in human saliva, may have on titanium surfaces. In fact, a progressive degradation of titanium by wear and corrosion (tribocorrosion) mechanisms can take place affecting the performance of titanium-based implant and prostheses. Also, the formation of wear debris and metallic ions due to the tribocorrosion phenomena can become toxic for human tissues. This review gathers knowledge from areas like materials sciences, microbiology, and dentistry contributing to a better understanding of bio-tribocorrosion processes in the oral environment.

ABSTRACTThe outgrowth of Porphyromonas gingivaliswithin the inflammatory subgingival plaque is associated with periodontitis characterized by periodontal tissue destruction, loss of alveolar bone, periodontal pocket formation, and eventually, tooth loss. Potential virulence factors of P. gingivalisare peptidylarginine deiminase (PPAD), an enzyme modifying free or peptide-bound arginine to citrulline, and the bacterial proteases referred to as gingipains (Rgp and Kgp). Chemokines attract leukocytes during inflammation. However, posttranslational modification (PTM) of chemokines by proteases or human peptidylarginine deiminases may alter their biological activities. Since chemokine processing may be important in microbial defense mechanisms, we investigated whether PTM of chemokines by P. gingivalisenzymes occurs. Upon incubation of interleukin-8 (IL-8; CXCL8) with PPAD, only minor enzymatic citrullination was detected. In contrast, Rgp rapidly cleaved CXCL8 in vitro. Subsequently, different P. gingivalisstrains were incubated with the chemokine CXCL8 or CXCL10 and their PTMs were investigated. No significant CXCL8 citrullination was detected for the tested strains. Interestingly, although considerable differences in the efficiency of CXCL8 degradation were observed with full cultures of various strains, similar rates of chemokine proteolysis were exerted by cell-free culture supernatants. Sequencing of CXCL8 incubated with supernatant or bacteria showed that CXCL8 is processed into its more potent forms consisting of amino acids 6 to 77 and amino acids 9 to 77 (the 6-77 and 9-77 forms, respectively). In contrast, CXCL10 was entirely and rapidly degraded by P. gingivalis, with no transient chemokine forms being observed. In conclusion, this study demonstrates PTM of CXCL8 and CXCL10 by gingipains of P. gingivalisand that strain differences may particularly affect the activity of these bacterial membrane-associated proteases.

Background:The aim of the current study is to compare the prevalence of commensal bacteria, with beneficial properties, for healthy and diseased individuals and additionally to examine the inhibitory effect of some commercial dietary probiotics on periodontopathogens, comparing this inhibitory effect to that of orally derived beneficial bacteria. Methods:Subgingival plaque samples from 35 patients (healthy and periodontitis patients) were analyzed. Growth inhibition of the periodontal pathogens Porphyromonas gingivalis, Prevotella intermedia, Fusobacterium nucleatum, and Aggregatibacter actinomycetemcomitanswas examined using the agar overlay technique and agar well diffusion method. The quantification of the inhibitory effect was checked with the agar well diffusion method. Results:Using the agar overlay technique, the prevalence of strains antagonistic toward P. gingivalis, A. actinomycetemcomitans,and F. nucleatumwas found to be higher in healthy individuals than in individuals with periodontitis, but this could not be validated by the agar well diffusion assay. Compared with the antagonistic activity of the isolated strains, the probiotic strains overall showed a stronger inhibition of the periodontal pathogens. Conclusion:It was shown that some oral bacteria can cause antagonism toward periodontopathogens, and these observations underline the therapeutic potential of applications that stimulate oral health by the application of beneficial effector strains.

Background:Microgravity is associated with an increase in peroxidative damage. The effect is more pronounced after long‐duration space flights and can even last for several weeks after landing. The objective of the study is to determine the influence of simulated microgravity on the periodontal status and salivary and serum oxidant/antioxidant status of the body in simulated microgravity (−6° head‐down‐tilt [HDT) bed rest). Methods:Twenty healthy male volunteers were studied before and after 60 days of simulated microgravity (−6° HDT bed rest). We measured salivary and serum oxidative markers, such as malondialdehyde (MDA), 8‐oxo‐7,8 dihydro‐2 deoxyguanosine (8‐OHdG), and vitamins C and E, and clinical periodontal parameters (probing depth [PD] and clinical attachment level [CAL]). Results:Serum and salivary vitamin C and E concentrations were significantly decreased, whereas MDA and 8‐OHdG levels were significantly increased after 60 days of simulated microgravity. Serum and salivary markers showed a strong and significant correlation. CAL and PD were higher but not statistically significant in simulated microgravity. Conclusions:This study suggests that oxidative stress in the microgravity environment was increased but did not significantly influence periodontal parameters after 2 months. Also, this study indicates the possibility that the findings may have a broader clinical relevance to patients on bed rest or who are physically inactive. Studies on larger patient samples and follow‐up for a longer time are required to verify the relationship between antioxidant status in the space microgravity condition and periodontal health.

Background:In the past few decades, more patients have been treated orthodontically, but no longitudinal study has compared orthodontic bands and brackets microbiologically and clinically. Methods:This longitudinal trial (split‐mouth design) included 24 patients. Microbiology (sub‐ and supragingival), probing depth (PD), bleeding on probing (BOP), and gingival crevicular fluid flow (GCF) were assessed at baseline (band placement) and at weeks 18 (bracket bonding) 20, 24, and 36. A statistical comparison was made over time and among the banded, bonded, and control sites. Results:The aerobe/anaerobe ratio of sub‐ and supragingival colony forming units decreased significantly (relatively more anaerobes) over the study period for the banded and bonded sites (P<0.001). This decrease was accompanied by significant elevations in PD, BOP, and GCF. These changes occurred faster after bonding compared to banding. No significant changes were observed 18 weeks after banding with the exception of increased PD (P<0.001). At week 36, all microbial and clinical variables at the bonded site had changed significantly in the negative direction (P<0.001) compared to week 18. The control sites did not show any significant changes over time, indicating that the effects were localized. Conclusions:The placement of fixed orthodontic appliances had a significant impact on microbial and clinical variables. The changes occurred faster at the bonded sites compared to the banded sites, probably because wire insertion caused difficulties in approximal cleaning. Over the long term, banding did not lead to more adverse microbial and periodontal effects than bonding.

Background:Since smoking is an established risk factor for the development of periodontitis, the present study investigated whether nicotine and cotinine can make epithelial cells more prone to colonization by periodontopathogens. Methods:Primary epithelial cell mono‐layers were inoculated with nicotine and cotinine prior to adhesion experiments with Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis. The number of bacteria associated with cells inoculated or not with nicotine or cotinine were assessed by an indirect culture viability assay. The same experimental set‐up was used for assessing HeLa cells exposed to cigarette smoke extract (CSE). Results:Primary epithelial cells inoculated with concentrations of nicotine and cotinine, found in smokers and non smokers, did not show significant differences (P>0.05) in colonization susceptibility to A. actinomycetemcomitans. When these concentrations were increased to 1 mg/ml, a significant (P<0.05) and species‐specific effect of the colonization susceptibility of epithelial cells was observed: It increased for A. actinomycetemcomitans, while it decreased for P. gingivalis. For both species the effects were more pronounced for nicotine, although this was not statistically significant. The change in colonization susceptibility did not result from alterations of the bacterial viability due to nicotine or cotinine. Treatment of HeLa cells with CSE also led to a species‐specific variation in colonization tendency; i.e., increased for A. actinomycetemcomitans(P<0.05), but not for P. gingivalis. Conclusions:The susceptibility of epithelial cells to become colonized by either A. actinomycetemcomitansor P. gingivaliscould be altered by nicotine, cotinine, or CSE in a time‐dependent, species‐specific manner. Whether these findings that support the hypothesis of an increased patient susceptibility for bacterial adhesion to epithelial cells in smokers are clinically relevant remains to be proven. J Periodontol 2005;76:1315‐1322.