Periodontal disease is a microbially-mediated inflammatory disease of tooth-supporting tissues that leads to bone and tissue loss around teeth. Although bacterially-mediated mechanisms of alveolar bone destruction have been widely studied, the effects of a polymicrobial infection on the periodontal ligament and microbiome/virome have not been well explored. Therefore, the current investigation introduced a new mouse model of periodontal disease to examine the effects of a polymicrobial infection on periodontal ligament (PDL) properties, changes in bone loss, the host immune response, and the microbiome/virome using shotgun sequencing. Periodontal pathogens, namely Porphyromonas gingivalis, Treponema denticola, Tannerella forsythia, and Fusobacterium nucleatum were used as the polymicrobial oral inoculum in BALB/cByJ mice. The polymicrobial infection triggered significant alveolar bone loss, a heightened antibody response, an elevated cytokine immune response, a significant shift in viral diversity and virome composition, and a widening of the PDL space; the latter two findings have not been previously reported in periodontal disease models. Changes in the PDL space were present at sites far away from the site of insult, indicating that the polymicrobial radius of effect extends beyond the bone loss areas and site of initial infection and wider than previously appreciated. Associations were found between bone loss, specific viral and bacterial species, immune genes, and PDL space changes. These findings may have significant implications for the pathogenesis of periodontal disease and biomechanical properties of the periodontium. This new polymicrobial mouse model of periodontal disease in a common mouse strain is useful for evaluating the features of periodontal disease.

The effects of probiotic supplementation on systemic health and gastrointestinal diseases have been investigated in numerous studies. The aim of this review is to provide an overview of probiotics and their effects on periodontal health. Probiotics show beneficial effects as adjunctive therapeutics and as stand‐alone agents in the treatment and prevention of gingivitis as well as specific clinical parameters of periodontitis. This review focuses on the clinical and microbiological aspects of probiotics in the context of health, gingivitis, and periodontitis. In addition, a special focus on nisin‐producing probiotics and nisin itself showcase their significant potential for oral and systemic use.

Background: Oral dysbiosis is an imbalance in the oral microbiome and is associated with a variety of oral and systemic diseases, including periodontal disease, caries, and head and neck/oral cancer. Although antibiotics can be used to control this dysbiosis, they can lead to adverse side effects and superinfections. Thus, novel strategies have been proposed to address these shortcomings. One strategy is the use of probiotics as antimicrobial agents, since they are considered safe for humans and the environment. Specifically, the Grampositive Lactococcus lactis, a species present in the oral and gut microbiota, is able to produce nisin, which has been used worldwide for food preservation. Objective: The objective of this study was to test whether a nisin probiotic can promote a healthier oral microbiome in pathogen-spiked oral biofilms. Results: We found that L. lactis can prevent oral biofilm formation and disrupt 24-h and 48h pre-formed biofilms. Finally, we demonstrate that both treatments, a nisin-producing L. lactis probiotic and nisin can decrease the levels of pathogens in the biofilms and return the diversity levels back to control or 'healthy' levels. Conclusion: A nisin-producing probiotic, can be used to treat 'disease-altered' biofilms and promote healthier oral biofilms, which may be useful for improving patient oral health.

Recent studies revealed culturable periodontal keystone pathogens are associated with preterm low birth weight (PLBW). However, the oral microbiome is also comprised of hundreds of ‘culture-difficult’ or ‘not-yet-culturable’ bacterial species. To explore the potential role of unculturable and culturable periodontitis-related bacteria in preterm low birth weight (PLBW) delivery, we recruited 90 pregnant women in this prospective study. Periodontal parameters, including pocket probing depth, bleeding on probing, and clinical attachment level were recorded during the second trimester and following interviews on oral hygiene and lifestyle habits. Saliva and serum samples were also collected. After delivery, birth results were recorded. Real-time PCR analyses were performed to quantify the levels of periodontitis-related unculturable bacteria (Eubacterium saphenum, Fretibacterium sp. human oral taxon(HOT) 360, TM7 sp. HOT 356, and Rothia dentocariosa), and cultivable bacteria (Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, Fusobacterium nucleatum and Prevotella intermedia) in saliva samples. In addition, ELISA analyses were used to determine the IgG titres against periodontal pathogens in serum samples. Subjects were categorized into a Healthy group (H, n = 20) and periodontitis/gingivitis group (PG, n = 70) according to their periodontal status. The brushing duration was significantly lower in the PG group compared to the H group. Twenty-two of 90 subjects delivered PLBW infants. There was no significant difference in periodontal parameters and serum IgG levels for periodontal pathogens between PLBW and healthy delivery (HD) groups. However, ordinal logistic regression analysis revealed that a higher abundance of Treponema denticola, Prevotella intermedia, Fretibacterium sp. HOT360 and lower levels of Rothia dentocariosa were significantly associated with the presence of periodontal disease during pregnancy. Moreover, the amount of Eubacterium saphenum in saliva and serum IgG against Aggregatibacter actinomycetemcomitans were negatively correlated with PLBW. Taken together, unculturable periodontitis-associated bacteria may play an important role both in the presence of periodontal inflammation during pregnancy and subsequent PLBW.

No abstract

The bidirectional relationship between diabetes mellitus (DM) and periodontal disease has drawn great attention; however, the mechanisms underlying their association remain unclear. In this study, we aimed to develop a rhesus monkey model of diabetic periodontitis and explore the potential mechanisms by which DM affects the progression of periodontal disease. Three healthy rhesus monkeys were selected as the control group. Five streptozotocin-induced diabetic rhesus monkeys were chosen as the experimental group. Ligature placement was used to induce periodontitis. The changes in the levels of advanced glycation end products (AGEs), beta-defensin-3 (BD-3), and interleukin-17 (IL-17) were measured using enzyme-linked immunosorbent assays (ELISA) and real-time reverse transcription polymerase chain reaction (RT-PCR) at different stages during disease progression. Periodontitis was confirmed by clinical assessment, radiographic images, and histological examination. Significant changes in the levels of AGEs and BD-3 in serum were observed at the periodontitis stage in diabetic rhesus monkeys ( P < 0.05). The expression of BD-3 mRNA in the gingiva of diabetic group at baseline was significantly high ( P < 0.05). Diabetic monkeys exhibited significantly enhanced IL-17 mRNA expression at the periodontitis stage ( P < 0.05). Our findings indicated that the rhesus monkey can serve as an ideal model for exploring the pathogenesis of diabetic periodontitis, and the hyperglycemic environment may accelerate inflammatory response and weaken the defense system in periodontal tissues. Impact statement The mechanism underlying the association between diabetes mellitus (DM) and periodontal disease is not yet fully understood. Hence, there is a need to establish animal models to reveal the effect of DM on the pathogenesis of periodontitis. In this study, we explored the appropriate methods for inducing periodontitis and shortening the modeling time in rhesus monkeys, to investigate the pathogenesis of diabetic periodontitis and develop innovative therapies. Our results suggest that a hyperglycemic environment might lead to the destruction of periodontal tissues by accelerating inflammatory response and weakening the defense system in periodontal tissues. Therefore, this study has significant treatment implications regarding the regulation of the immune response against periodontal diseases in patients with DM.

Infection with P. gingivalis and the antibody response to SIRVYK might be associated with TPL and PB.

Current evidence suggests that oral microbial dysbiosis is a primary etiological factor in oral diseases, such as dental caries and chronic periodontitis. 1,2 Oral microbial dysbiosis is also associated with the pathogenesis of systemic diseases, such as cardiovascular disease, 3 diabetes mellitus, 4 and adverse pregnancy outcomes.Previously, studies relying on traditional culture-based and PCR-based methods identified a limited number of gram-negative anaerobia bacteria as keystone periodontal pathogens, in particular, Porphyromonas gingivalis, Tannerella forsythia, Treponema denticola, Aggregatibacter actinomycetemcomitans, Fusobacterium nucleatum, and Prevotella intermedia. 1,5 They have been used as diagnostic markers of periodontitis. 6 Evidence shows that these periodontal pathogens have been associated with adverse pregnancy outcomes. [7][8][9] However, the oral cavity is comprised of a prodigious microbiome, including hundreds of "not-yet-cultivable" bacterial species whose functions remain unknown. 10 This is an open access article under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.