Periodontal pathologies are highly widespread throughout the world. Epidemiological studies have shown that as much as 1% of the population is suffering from periodontal disease. In recent years, there has been a growing number of studies linking these diseases with autoimmune diseases, especially with rheumatoid arthritis. This literature review evaluates changes in the relationship between periodontal pathologies caused by the bacterium Porphyromonas gingivalis and rheumatoid arthritis. The systematic review of the literature was performed according to the PRISMA analysis protocol. The review was performed with articles from the PubMed database. Searched articles were not older than 5 years. Only full texts and research performed with people were selected. A total of 56 results were received. A review and analysis of their full texts have been carried out and 10 articles were selected according to the established criteria. They were analyzed and results were presented. The results obtained from the literature were based on the influence of Porphyromonas gingivalis on the pathogenesis of rheumatoid arthritis. In the literature, the activity of this bacterium is explained by the analysis of its enzyme peptidylarginine deiminase and its principle of action. Studies have also been found to prove the presence of Porphyromonas gingivalis not only in the oral cavity but its DNA is also found in synovial fluid and plasma. In the researched articles, direct links between Porphyromonas gingivalis and rheumatoid arthritis have led doctors to draw attention to patients' oral hygiene and the condition of parodentium, as this may be the cause of autoimmune lesions. Treatment of periodontal disease will not only help maintain a healthy oral cavity but prevent the spread of bacteria to the surrounding tissues.

IL-8 and its polymorphisms are involved in multiple acute and chronic inflammatory processes including pathological changes to surrounding structures of the teeth called periodontal diseases or periodontitis. The aim of this manuscript was to systematically review studies from 2006 to 2021 on IL-8 polymorphisms and their association with periodontitis. Literature analysis was done following the PRISMA protocol guidance using articles not older than 15 years (2006)(2007)(2008)(2009)(2010)(2011)(2012)(2013)(2014)(2015)(2016)(2017)(2018)(2019)(2020)(2021). The search was carried out using PubMed (MEDLINE), ScienceDirect and Wiley Online Library databases. For the focus question, the PICO (population (P), intervention (I), control (C), and outcome (O)) study design protocol was used, and the following question was formulated: are IL-8 gene polymorphisms associated with periodontitis? A total of 2422 articles were found at the beginning of the search. After applying the inclusion and exclusion criteria, screening, and full-text article exclusion with reasons, 31 studies were included in the analysis. In conclusion, IL-8 and its gene polymorphisms are associated with an increased risk of periodontal diseases.

Background The present study aimed to evaluate whether non-surgical treatment interferes with clinical parameters and local patterns of osteo-immunoinflammatory mediators (IL-17 and TNF-α) and matrix metalloproteinase-8 (MMP-8) that are found in peri-implant crevicular fluid (PICF) and biofilms during the progression of peri-implant mucositis. Material/Methods We selected 30 patients with peri-implant caused mucositis before (MP) and after treatment (TP) and 30 healthy people (HP) for the analysis of IL-17, TNF-α cytokine, and MMP-8 production in PICF and for analysis of colonization dynamics of periodontopathogenic bacteria in supra- and subgingival plaque samples. The levels of IL-17 and MMP-8 concentrations in samples were assayed by enzymatic immunosorbent assay (ELISA) and TNF-α levels were determined by enzyme amplified sensitivity immunoassay (EASIA) method in PICF. The micro-IDent test was used to detect 11 species of periodontopathogenic bacteria in subgingival biofilm. Results We found significantly ( P <0.001) higher levels of IL-17, TNF-α, and MMP-8 in the PICF of the MP and TP groups in comparison to the HP group. A significant association was found in MP associated with Parvimonas micra , as TNF-α in PICF was significantly higher ( P =0.034) than in patients without Parvimonas micra . TNF-α levels in the samples of PICF showed a moderate correlation with clinical parameters, including plaque index (PI) ( P =0.007) and MMP-8 levels ( P =0.001), in the MP group. Conclusions Assessment of levels of inflammatory cytokines in PICF can aid in the identification of peri-implant mucositis, which can assist in early diagnosis, prevention, and treatment.

Background and Objectives: Periodontitis is a multifactorial inflammatory disease associated with biofilm dysbiosis and is defined by progressive periodontium destruction. Genes largely regulate this entire process. SIRTs are a group of histone deacetylases (HDACs) intimately involved in cell metabolism and are responsible for altering and regulating numerous cell functions. Understanding SIRTs and their functions in periodontitis may be useful for therapeutic treatment strategies in the future. The aim of our study was to investigate the associations amid SIRT1 single-gene nucleotide polymorphisms (rs3818292, rs3758391, and rs7895833) and SIRT1 serum levels for patients affected by periodontitis in the Caucasian population. Materials and Methods: The study included 201 patients affected by periodontitis and 500 healthy controls. DNA extraction from peripheral leukocytes was carried out using commercial kits. The real-time PCR method was selected for the determination of the genotype of the periodontitis patients and the control group. The ELISA method was used to measure the SIRT1 concentration. A statistical data analysis was performed using “BM SPSS Statistics 27.0” software. Results: The SIRT1 rs3818292 AG genotype was associated with a 2-fold and 1.9-fold increase in the development of periodontitis under the codominant and overdominant models (OR = 1.959; CI = 1.239–3.098; p = 0.004; and OR = 1.944; CI = 1.230–3.073; p = 0.004, respectively). The serum SIRT1 levels were not statistically significantly different between subjects in the periodontitis and control groups (0.984 (5.159) ng/mL vs. 0.514 (7.705) ng/mL, p = 0.792). Conclusions: in our study, the genotypes and alleles of SIRT1 rs3818292, rs3758391, and rs7895833 statistically significantly differed between the periodontitis and control groups, exclusively in the male population and subjects older than 60 years.

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