Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola, collectively recognized as periodontopathogens within the red complex, have been extensively studied in clinical samples collected from individuals with periodontitis. A lab-on-a-chip (LOC) is a miniature mechanism that integrates various laboratory operations onto a single microchip or a small-scale platform. This systematic review evaluates the application of LOC technology in identifying microorganisms from the red complex. This study adhered to PRISMA recommendations, and the review process encompassed several databases. In the electronic search, a total of 58 reports were found, and ultimately, 10 studies were considered relevant for inclusion. All these studies described effective, rapid, and reliable LOC systems for detecting and amplifying P. gingivalis, T. forsythia, and T. denticola. Compared to traditional methods, the LOC approach demonstrated minimal reagent requirements. Additionally, the results indicated that the amplification process took approximately 2 to 8 min, while detection could be completed in as little as 2 min and 40 s, resulting in a total experimental duration of around 11 min. Integrating miniaturization, speed, accuracy, and automation within microchip platforms makes them promising tools for detecting and amplifying microorganisms associated with the red complex in periodontal diseases.

Alzheimer\'s disease (AD) is a neurodegenerative disease and the most common example of dementia. The neuropathological features of AD are the abnormal deposition of extracellular amyloid-β (Aβ) and intraneuronal neurofibrillary tangles with hyperphosphorylated tau protein. It is recognized that AD starts in the frontal cerebral cortex, and then it progresses to the entorhinal cortex, the hippocampus, and the rest of the brain. However, some studies on animals suggest that AD could also progress in the reverse order starting from the midbrain and then spreading to the frontal cortex. Spirochetes are neurotrophic: From a peripheral route of infection, they can reach the brain via the midbrain. Their direct and indirect effect via the interaction of their virulence factors and the microglia potentially leads to the host peripheral nerve, the midbrain (especially the locus coeruleus), and cortical damage. On this basis, this review aims to discuss the hypothesis of the ability of Treponema denticola to damage the peripheral axons in the periodontal ligament, to evade the complemental pathway and microglial immune response, to determine the cytoskeletal impairment and therefore causing the axonal transport disruption, an altered mitochondrial migration and the consequent neuronal apoptosis. Further insights about the central neurodegeneration mechanism and Treponema denticola\'s resistance to the immune response when aggregated in biofilm and its quorum sensing are suggested as a pathogenetic model for the advanced stages of AD.

Research has suggested 2 potential mechanisms by which the periodontal inflammatory response may communicate to distant organs: 1) direct translocation of periodontal bacteria from the oral cavity to another organ system; and 2) inflammation as a result of metastatic periodontal inflammation. The purpose of this scoping review is to explore these mechanisms as potential mediators between periodontitis and Alzheimer\'s disease.
A reiterative literature search of peer-reviewed articles was performed in the PubMed and Scopus databases using keywords or combinations such as Alzheimer\'s disease AND periodontitis OR periodontal disease AND inflammation.
A total of 777 articles were identified. After eliminating duplicates and reviewing titles and abstracts, 84 articles were selected for full-text review. Following full-text review, 19 articles met the eligibility criteria for the study.
The review of the literature highlights how periodontitis may contribute to neuroinflammation by the introduction of periodontal bacteria and/or proinflammatory cytokines locally produced at the periodontium.
Inflammation is an important mechanism in the onset and progression of both periodontitis and Alzheimer\'s disease. Nevertheless, further studies are necessary to better understand the multifactorial pathogenesis of Alzheimer\'s disease.
La recherche a suggéré 2 possibilités de mécanismes par lesquels la réponse inflammatoire parodontale peut communiquer avec des organes distants : 1) la translocation directe des bactéries parodontales de la cavité buccale vers un autre système organique; et 2) l’inflammation découlant d’une inflammation parodontale métastatique. Le but de cet examen de la portée est d’explorer ces mécanismes en tant que médiateurs potentiels entre la parodontite et la maladie d’Alzheimer.
Une recherche documentaire réitérative d’articles évalués par des pairs a été effectuée dans les bases de données PubMed et Scopus en utilisant les mots-clés ou des combinaisons de mots-clés tels que maladie d’Alzheimer ET parodontite OU maladie parodontale ET inflammation (en anglais).
Un total de 777 articles a été répertorié. Après avoir éliminé les doublons et examiné les titres et les résumés, 84 articles ont été sélectionnés pour être examinés dans leur intégralité. À la suite de l’examen du texte complet, 19 articles répondaient aux critères d’admissibilité de l’étude.
L’analyse documentaire souligne comment la parodontite peut contribuer à la neuroinflammation en introduisant des bactéries parodontales ou des cytokines pro-inflammatoires produites localement au niveau du parodonte.
L’inflammation est un mécanisme important dans l’apparition et la progression à la fois de la parodontite et de la maladie d’Alzheimer. Néanmoins, d’autres études sont nécessaires pour mieux comprendre la pathogenèse multifactorielle de la maladie d’Alzheimer.

OBJECTIVE: The objective of this systematic review and meta-analysis was to evaluate the effect of periodontal surgery on the subgingival microbiome.
BACKGROUND: Periodontitis is a chronic inflammation of the tooth supporting tissues caused by the dysbiosis of the subgingival biofilm. It is managed through different non-surgical and surgical treatment modalities. Recent EFP S3 guidelines recommended performing periodontal surgery as part of Step 3 periodontitis treatment after Step 1 and Step 2 periodontal therapy, with the aim to achieve pocket closure of persisting sites. Changes in the sub-gingival microbiome may explain the treatment outcomes observed at different time points. Various microbiological detection techniques for disease-associated pathogens have been evolved over time and have been described in the literature. However, the impact of different types of periodontal surgery on the subgingival microbiome remains unclear.
METHODS: A systematic literature search was conducted in Medline, Embase, LILACS and Cochrane Library supplemented by manual search (23DEC2019, updated 21APR2022).
RESULTS: From an initial search of 3046 studies, 28 were included according to our specific inclusion criteria. Seven microbiological detection techniques were used to analyse disease-associated species in subgingival plaque samples: optical microscope, culture, polymerase chain reaction (PCR), checkerboard, enzymatic reactions, immunofluorescence and 16S gene sequencing. The included studies exhibited differences in various aspects of their methodologies such as subgingival plaque sample collection or treatment modalities. Clinical data showed a significant decrease in probing pocket depths (PPD) and clinical attachment loss (CAL) after periodontal surgery. Microbiological findings were overall heterogeneous. Meta-analysis was performed on a sub-cohort of studies all using checkerboard as a microbiological detection technique. Random effect models for Treponema denticola (T. denticola), Porphyromonas gingivalis (P. gingivalis) and Tannerella forsythia (T. forsythia) did not show a significant effect on mean counts 3 months after periodontal surgery. Notably, Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans) showed a significant increase 3 months after periodontal surgery. 16S gene sequencing was used in one included study and reported a decrease in disease-associated species with an increase in health-associated species after periodontal surgery at 3 and 6 months.
CONCLUSIONS: This systematic review has shown that the effect of periodontal surgery on the changes in subgingival microbiome is heterogeneous and may not always be associated with a decrease in disease-associated species. The variability could be attributed to the microbiological techniques employed for the analysis. Therefore, there is a need for well-designed and adequately powered studies to understand how periodontal surgery influences the subgingival microbiome and how the individual\'s microbiome affects treatment outcomes after periodontal surgery.

Periodontitis is a diseased condition of the gum which imposes considerable costs on healthcare systems. It progresses further beyond the inflammation of supportive tissues of the teeth, and the collateral damages are closely associated with Alzheimer\'s disease, cardiovascular disease, and diabetes mellitus.
A comprehensive literature review was performed to summarize published studies in English during the period of 1990-2021 to discuss the rationales for developing periodontal vaccine, cost-effectiveness analyses on the prevention of periodontitis, Treponema denticola-based vaccine candidates, as well as immunological mechanisms in animal models.
Preventive strategies against periodontitis may halt the onset of gum inflammation and the consequent chronic diseases. Considering the multi-microbial condition of periodontitis, an ideal periodontal vaccine should target multiple pathological pathways. Preventive approaches compared to surgical treatments evidently have significant impact on the healthcare budget and long-term health of the individuals in different communities. Despite many advances in periodontal vaccine research, there are still significant hurdles to overcome in developing a vaccine. Investment in research and development activities on key periodontal pathogens including Treponema denticola and Porphyromonas gingivalis in the foreseeable future is a worthy and cost-effective approach for the policymakers to prevent deleterious impacts of periodontitis.

The development of periodontitis is associated with an imbalanced subgingival microbial community enriched with species such as the traditionally classified red-complex bacteria (Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola). Saliva has been suggested as an alternative to subgingival plaque for the microbial analysis due to its easy and non-invasive collection. This systematic review aims to determine whether the levels of red-complex bacteria assessed using saliva reflect those in subgingival plaque from periodontitis patients. The MEDLINE, EMBASE, and Cochrane Library databases were searched up to April 30, 2021. Studies were considered eligible if microbial data of at least one of the red-complex species were reported in both saliva and subgingival plaque from periodontitis patients, based on DNA-based methods. Of the 17 included studies, 4 studies used 16S rRNA gene sequencing techniques, and the rest used PCR-based approaches. The detection frequency of each red-complex species in periodontitis patients was reported to be > 60% in most studies, irrespective of samples types. Meta-analyses revealed that both detection frequencies and relative abundances of red-complex bacteria in saliva were significantly lower than those in subgingival plaque. Moreover, the relative abundances of all 3 bacterial species in saliva showed significantly positive correlation with those in subgingival plaque. In conclusion, current evidence suggests that one-time saliva sampling cannot replace subgingival plaque for microbial analysis of the red-complex bacteria in periodontitis patients. Given the positive microbial associations between saliva and subgingival plaque, a thorough review of longitudinal clinical studies is needed to further assess the role of saliva.

BACKGROUND: Periodontal bacteria is the major pathogens in the oral cavity and the main cause of adult chronic periodontitis, but their association with incidence and prognosis in cancer is controversial. The aim of this study was to evaluate the effect of periodontal bacteria infection on incidence and prognosis of cancer.
METHODS: A systematic literature search of PubMed, Embase, Web of Science, and Cochrane Library databases was performed to obtain 39 studies comprising 7184 participants. The incidence of cancer was evaluated as odd ratios (OR) with a 95% confidence interval (95% CI) using Review Manager 5.2 software. Overall survival, cancer-specific survival and disease-free survival, which were measured as hazard ratios (HR) with a 95% CI using Review Manager 5.2 software.
RESULTS: Our results indicated that periodontal bacteria infection increased the incidence of cancer (OR = 1.25; 95%CI: 1.03-1.52) and was associated with poor overall survival (HR = 1.75; 95% CI: 1.40-2.20), disease-free survival (HR = 2.18; 95%CI: 1.24-3.84) and cancer-specific survival (HR = 1.85, 95%CI: 1.44-2.39). Subgroup analysis indicted that the risk of cancer was associated with Porphyromonas gingivalis (Pg) infection (OR = 2.16; 95%CI: 1.34-3.47) and Prevotella intermedia (Pi) infection (OR = 1.28; 95%CI: 1.01-1.63) but not Tannerella forsythia (Tf) (OR = 1.06; 95%CI: 0.8-1.41), Treponema denticola (Td) (OR = 1.30; 95%CI: 0.99-1.72), Aggregatibacter actinomycetemcomitans (Aa) (OR = 1.00; 95%CI: 0.48-2.08) and Fusobacterium nucleatum (Fn) (OR = 0.61; 95%CI: 0.32-1.16).
CONCLUSIONS: This meta-analysis revealed periodontal bacteria infection increased the incidence of cancer and predicted poor prognosis of cancer.

There is currently no consensus regarding microorganisms that may be considered true peri-implant pathogens. Therefore, the aim of this systematic review is to determine the weight of evidence for microorganisms related to peri-implantitis based on results of association studies.
This review was performed following the Preferred Reporting Items for Systematic Reviews and MetaAnalyses (PRISMA). Two independent researchers searched PubMed/Medline, Embase, and Cochrane Library databases up to August 4, 2015, for studies comparing microbiologic outcomes of subgingival biofilm samples from healthy implants and implants with peri-implantitis.
A total of 799 titles was identified and 11 studies were included in this review. All data were extracted using a predefined form. Microorganisms found in increased count/abundance/frequency in peri-implantitis belonged to Bacteria domain and viruses, and included a total of six bacterial phyla, 17 bacterial genera, 23 bacterial species, and two genera of viruses. The main bacterial species associated with peri-implantitis are recognized as periodontal pathogens.
Results of this systematic review suggest moderate evidence supporting association of Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia and some evidence supporting association of Prevotella intermedia and Campylobacter rectus with the etiology of peri-implantitis.