Periodontitis and COVID-19: Immunological Characteristics, Related Pathways, and Association.

Both periodontitis and Coronavirus disease 2019 (COVID-19) pose grave threats to public health and social order, endanger human life, and place a significant financial strain on the global healthcare system. Since the COVID-19 pandemic, mounting research has revealed a link between COVID-19 and periodontitis. It is critical to comprehend the immunological mechanisms of the two illnesses as well as their immunological interaction. Much evidence showed that there are many similar inflammatory pathways between periodontitis and COVID-19, such as NF-κB pathway, NLRP3/IL-1ß pathway, and IL-6 signaling pathway. Common risk factors such as gender, lifestyle, and comorbidities contribute to the severity of both diseases. Revealing the internal relationship between the two diseases is conducive to the treatment of the two diseases in an emergency period. It is also critical to maintain good oral hygiene and a positive attitude during treatment. This review covers four main areas: immunological mechanisms, common risk factors, evidence of the association between the two diseases, and possible interventions and potential targets. These will provide potential ideas for drug development and clinical treatment of the two diseases.

Association between periodontitis and COVID-19 infection: a two-sample Mendelian randomization study.

Background and Objective: Epidemiological studies report associations between coronavirus disease 2019 (COVID-19) and periodontitis; however, causality has not been proven. The aim of this study is to assess the associations between COVID-19 susceptibility and periodontitis with two-sample Mendelian randomization (MR) analyses. Methods: A two-sample summary MR analysis was performed using data for outcome and exposure from the OpenGWAS database on people of European descent. Periodontal complex traits (PCTs) were chosen as a proxy for the periodontitis phenotype. The causal association between PCT3 (Aggregatibacter actinomycetemcomitans), PCT5 (Porphyromonas gingivalis), and gingival crevicular fluid (GCF) interleukin-1ß (IL-1ß) and COVID-19 were considered. Genome-wide association study (GWAS) data with the two largest sample sizes were selected as COVID-19 outcomes (datasets ebi-a-GCST010776 and ebi-a-GCST010777). Single-nucleotide polymorphisms (SNPs) associated with PCT3, PCT5, and GCF IL-1ß at statistical significance at genome-wide level (P < 5 × 10-8) were identified as genetic instruments. We used two-sample summary MR methods and tested the existence of a pleiotropic effect with MR-Egger. Results: Inverse-variance weighted (IVW) estimates showed that there was a positive association between COVID-19 risk and periodontitis (ebi-a-GCST010776: odds ratio [OR] = 1.02 (95% confidence interval (CI), 1.00-1.05), P = 0.0171; ebi-a-GCST010777: OR = 1.03 (95% CI, 1.00-1.05), P = 0.0397). The weighted median also showed directionally similar estimates. Exploration of the causal associations between other PCTs and COVID-19 identified a slight effect of local inflammatory response (GCF IL-1ß) on COVID-19 risk across the two datasets (ebi-a-GCST010776: IVW OR = 1.02 (95% CI, [1.01-1.03]), P < 0.001; ebi-a-GCST010777: IVW OR = 1.03 (95% CI, [1.02-1.04]), P < 0.001). The intercepts of MR-Egger yielded no proof for significant directional pleiotropy for either dataset (ebi-a-GCST010776: P = 0.7660; ebi-a-GCST010777: P = 0.6017). Conclusions: The findings suggests that periodontitis and the higher GCF IL-1ß levels is causally related to increase susceptibility of COVID-19. However, given the limitations of our study, the well-designed randomized controlled trials are needed to confirm its findings, which may represent a new non-pharmaceutical intervention for preventing COVID-19.

Correlation of COVID-19 with severity of periodontitis-A clinical and biochemical study.

Background: Various conceptual hypotheses have been put forth to link association of COVID-19 with various chronic diseases such as periodontitis. Empirical evidence is still lacking to correlate the severity of COVID-19 with periodontal diseases. Objectives: This study was undertaken with an objective to correlate COVID severity in systemically healthy patients suffering from periodontal diseases. Materials and Methods: 44 systemically healthy patients of both genders with minimum of 20 teeth in their oral cavity in age range of 20 to 50 years suffering from periodontitis were recruited and categorised into four stages as per American Academy of Periodontology (AAP) 2017 classification for periodontitis. Serum C-reactive protein (CRP) levels and periodontal disease parameters of all the patients were measured. Because of COVID-19 and the nationwide lockdown, the dental practice was highly affected. With the help of self-designed online questionnaire information regarding COVID-19 infection and associated symptoms were recorded. Cases were categorized into five groups based on the World Health Organization clinical progression scale of COVID severity. Results: All the patients suffering from COVID disease in moderate and severe forms had increased probing pocket depth, clinical attachment level, and raised serum C-reactive protein levels as compared to patients who were uninfected or suffering from mild COVID disease and the results were statistically significant. Conclusion: Prioritisation and Implementation of periodontal treatment as a preventive measure for COVID-19 should be done. A positive correlation is observed between the severity of periodontitis and COVID-19.

Potential links between COVID-19 and periodontitis: a bioinformatic analysis based on GEO datasets.

BACKGROUND: 2019 Coronavirus disease (COVID-19) is an infectious disease caused by the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The COVID-19 pandemic has already had a serious influence on human existence, causing a huge public health concern for countries all around the world. Because SARS-CoV-2 infection can be spread by contact with the oral cavity, the link between oral illness and COVID-19 is gaining traction. Through bioinformatics approaches, we explored the possible molecular mechanisms linking the COVID-19 and periodontitis to provide the basis and direction for future research. METHODS: Transcriptomic data from blood samples of patients with COVID-19 and periodontitis was downloaded from the Gene Expression Omnibus database. The shared differentially expressed genes were identified. The analysis of Gene Ontology, Kyoto Encyclopedia of Genesand Genomes pathway, and protein-protein interaction network was conducted for the shared differentially expressed genes. Top 5 hub genes were selected through Maximal Clique Centrality algorithm. Then mRNA-miRNA network of the hub genes was established based on miRDB database, miRTarbase database and Targetscan database. The Least absolute shrinkage and selection operator regression analysis was used to discover possible biomarkers, which were then investigated in relation to immune-related genes. RESULTS: Fifty-six shared genes were identified through differential expression analysis in COVID-19 and periodontitis. The function of these genes was enriched in regulation of hormone secretion, regulation of secretion by cell. Myozenin 2 was identified through Least absolute shrinkage and selection operator regression Analysis, which was down-regulated in both COVID-19 and periodontitis. There was a positive correlation between Myozenin 2 and the biomarker of activated B cell, memory B cell, effector memory CD4 T cell, Type 17 helper cell, T follicular helper cell and Type 2 helper cell. CONCLUSION: By bioinformatics analysis, Myozenin 2 is predicted to correlate to the pathogenesis and immune infiltrating of COVID-19 and periodontitis. However, more clinical and experimental researches are needed to validate the function of Myozenin 2.

The bidirectional biological interplay between microbiome and viruses in periodontitis and type-2 diabetes mellitus.

Periodontitis was an inflammatory disease associated with a dysbiosis of the oral flora characterized by a chronic sustained inflammation inducing the resorption of alveolar bone and leading to tooth loss. Type 2 diabetes mellitus (T2D) was a metabolic disease caused by impaired insulin action. The oral microbiome played a crucial role in modulating both the innate and adaptive immune system during the trigger and exacerbation of periodontitis and T2D. The bidirectional relationship of T2D and periodontitis had been the focus of intensive research, but those were not well explored. In this commentary, an in-depth analysis of the changes of microbiome and bacterial metabolites in periodontitis with or without diabetes was described. The promotion of periodontitis to T2D might involve inflammatory factors/receptors, oxidative stress, microRNA and so on. The effect of diabetes on periodontitis might involve adipose factor pathway, AGE/RAGE and RANK/RANKL pathway etc. Generally, periodontitis and diabetes are closely related to the microecological-epithelial interaction, soft tissue degradation, bone coupling disorder, immune regulation and gene transcription. The viruses, including HBV, HCV, HSV-1, Coronavirus, HCMV, EBV, HIV, phageome and so on, played an important role in the development of T2D and periodontitis. An in-depth understanding of the relationship between microbiome and host was of great significance to clarify the bidirectional mechanisms, suggesting that the periodontitis or T2D remission will have a positive impact on the other.

A pilot clinical and radiographic study on the association between periodontitis and serious COVID-19 infection.

BACKGROUND: During the pandemic of COVID-19, the scientific community tried to identify the risk factors that aggravate the viral infection. Oral health and specifically periodontitis have been shown to have a significant impact on overall health. Current, yet limited, evidence suggests a link between periodontal status and severity of COVID-19 infection. OBJECTIVES: The present pilot study aimed to assess whether younger patients (≤60 years) that have been hospitalized in the intensive care unit (ICU) for severe COVID-19 infection were susceptible to severe periodontitis. MATERIAL AND METHODS: All dentate patients ≤60 years of age diagnosed with COVID-19 and surviving hospitalization in the ICU were considered for inclusion. Susceptibility to periodontitis was determined by assessing radiographic bone loss (RBL) in recent dental radiographs (posterior bitewings, periapical, and panoramic X-rays). RBL in % was obtained from the most affected tooth and patients were classified into: Stage I, RBL ≤ 15%; Stage II, RBL = 15%-33% and Stage III/IV, RBL ≥ 33%. The grade was defined using the RBL to age ratio on the most severely affected tooth. Patients were attributed to: Grade A, ratio <0.25; Grade B, ratio 0.25-1 and Grade C, ratio >1. Patients classified into Stage III/IV and Grade C were considered highly susceptible to periodontitis. RESULTS: Of 87 eligible patients, 30 patients were finally assessed radiographically and/or clinically; from the remaining 57 patients, 16 refused participation for various reasons and 41 could not be reached. Based on the radiographic assessment, all patients were periodontally compromised. Half of them were classified with Stage III/IV and Grade B or C; 26.7% were classified with Stage III/IV and Grade C. CONCLUSIONS: The present pilot study showed that about half of the patients suffering from severe forms of COVID-19 infection in need of ICU admission suffered also from severe periodontitis, and about one-fourth of them were highly susceptible to it.

Association of periodontal therapy, with inflammatory biomarkers and complications in COVID-19 patients: a case control study.

BACKGROUND: In previous studies, COVID-19 complications were reported to be associated with periodontitis. Accordingly, this study was designed to test the hypothesis that a history of periodontal therapy could be associated with lower risk of COVID-19 complications. METHODS: A case-control study was performed using the medical health records of COVID-19 patients in the State of Qatar between March 2020 and February 2021 and dental records between January 2017 and December 2021. Cases were defined as COVID-19 patients who suffered complications (death, ICU admissions and/or mechanical ventilation); controls were COVID-19 patients who recovered without major complications. Associations between a history of periodontal therapy and COVID-19 complications were analysed using logistic regression models adjusted for demographic and medical factors. Blood parameters were compared using Kruskal-Wallis test. RESULTS: In total, 1,325 patients were included. Adjusted odds ratio (AOR) analysis revealed that non-treated periodontitis was associated with significant risk of need for mechanical ventilation (AOR = 3.91, 95% CI 1.21-12.57, p = 0.022) compared to periodontally healthy patients, while treated periodontitis was not (AOR = 1.28, 95% CI 0.25-6.58, p = 0.768). Blood analyses revealed that periodontitis patients with a history of periodontal therapy had significantly lower levels of D-dimer and Ferritin than non-treated periodontitis patients. CONCLUSION: Among COVID-19 patients with periodontal bone loss, only those that have not received periodontal therapy had higher risk of need for assisted ventilation. COVID-19 patients with a history of periodontal therapy were associated with significantly lower D-dimer levels than those without recent records of periodontal therapy. CLINICAL RELEVANCE: The fact that patients with treated periodontitis were less likely to suffer COVID-19 complications than non-treated ones further strengthen the hypothesis linking periodontitis to COVID-19 complications and suggests that managing periodontitis could help reduce the risk for COVID-19 complications, although future research is needed to verify this.

Periodontitis-Derived Dark-NETs in Severe Covid-19.

The frequent severe COVID-19 course in patients with periodontitis suggests a link of the aetiopathogenesis of both diseases. The formation of intravascular neutrophil extracellular traps (NETs) is crucial to the pathogenesis of severe COVID-19. Periodontitis is characterised by an increased level of circulating NETs, a propensity for increased NET formation, delayed NET clearance and low-grade endotoxemia (LGE). The latter has an enormous impact on innate immunity and susceptibility to infection with SARS-CoV-2. LPS binds the SARS-CoV-2 spike protein and this complex, which is more active than unbound LPS, precipitates massive NET formation. Thus, circulating NET formation is the common denominator in both COVID-19 and periodontitis and other diseases with low-grade endotoxemia like diabetes, obesity and cardiovascular diseases (CVD) also increase the risk to develop severe COVID-19. Here we discuss the role of propensity for increased NET formation, DNase I deficiency and low-grade endotoxaemia in periodontitis as aggravating factors for the severe course of COVID-19 and possible strategies for the diminution of increased levels of circulating periodontitis-derived NETs in COVID-19 with periodontitis comorbidity.

Validation of a noninvasive aMMP-8 point-of-care diagnostic methodology in COVID-19 patients with periodontal disease.

OBJECTIVES: The aim of this study was to validate an active matrix metalloproteinase (MMP-8) point-of-care diagnostic tool in COVID-19 patients with periodontal disease. SUBJECTS, MATERIALS, AND METHODS: Seventy-two COVID-19-positive and 30 COVID-19-negative subjects were enrolled in the study. Demographic data were recorded, periodontal examination carried out, and chairside tests run for evaluating the expression of active MMP-8 (aMMP-8) in the site with maximum periodontal breakdown via gingival crevicular fluid sampling as well as via a mouth rinse-based kit for general disease activity. In COVID-19-positive patients, the kits were run again once the patients turned COVID-19 negative. RESULTS: The overall (n = 102) sensitivity/specificity of the mouthrinse-based kits to detect periodontal disease was 79.41%/36.76% and that of site-specific kits was 64.71%/55.88% while adjusting for age, gender, and smoking status increased the sensitivity and specificity (82.35%/76.47% and 73.53%/88.24, respectively). Receiver operating characteristic (ROC) analysis for the adjusted model revealed very good area under the ROC curve 0.746-0.869 (p < .001) and 0.740-0.872 (p < .001) (the aMMP-8 mouth rinse and site-specific kits, respectively). No statistically significant difference was observed in the distribution of results of aMMP-8 mouth rinse test (p = .302) and aMMP-8 site-specific test (p = .189) once the subjects recovered from COVID-19. CONCLUSIONS: The findings of the present study support the aMMP-8 point-of-care testing (PoCT) kits as screening tools for periodontitis in COVID-19 patients. The overall screening accuracy can be further increased by utilizing adjunctively risk factors of periodontitis. The reported noninvasive, user-friendly, and objective PoCT diagnostic methodology may provide a way of stratifying risk groups, deciding upon referrals, and in the institution of diligent oral hygiene regimens.

Periodontitis and COVID-19: Biological Mechanisms and Meta-analyses of Epidemiological Evidence.

Since the beginning of 2020, the entire global health care system has been severely challenged by the outbreak of coronavirus 2019 disease (COVID-19). Robust evidence has demonstrated a more severe course of COVID-19 in the presence of several comorbidities, such as cardiovascular diseases, diabetes mellitus, and obesity. Here, we critically appraise the recent research discoveries linking periodontitis to severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and to severe COVID-19, with a special focus on the associated biological mechanisms and the available epidemiological evidence. SARS-CoV-2 main receptors and coreceptors (ACE2, TMPRSS2, furin, CD147) are overexpressed in periodontal tissues of periodontitis patients, with inflammation, periodontal pathogens, and damage-induced pyroptosis triggering a positive feedback loop. However, meta-analyses of epidemiological studies only indicated a nonstatistically significant tendency for an increased risk of SARS-CoV-2 infection in subjects with periodontitis (odds ratio [OR] = 1.69; 95% CI, 0.91-3.13, P = 0.09). Furthermore, periodontitis may worsen clinical COVID-19 courses through multiple direct and indirect pathways, including damage to lower airways due to aspiration of periodontal pathogens, exacerbation of the cytokine storm via the low-grade chronic systemic inflammation, and SARS-CoV-2 dissemination through the ulcerated gingival epithelium with consequent induced pulmonary vessels vasculopathy. Indeed, meta-analyses of epidemiological studies indicated that periodontitis subjects are more likely to experience a more severe course of COVID-19. Specifically, periodontitis was associated with a 4-fold increased odds of hospitalization (OR = 4.72; 95% CI, 1.11-20.03, P = 0.04), 6-fold of requiring assisted ventilation (OR = 6.24; 95% CI, 2.78-14.02, P = 0.00), and more than 7-fold of death due to COVID-19 complications (OR = 7.51; 95% CI, 2.16-26.10, P = 0.00). The breakthrough analyzed here emphasizes the relevance of the mouth-systemic connection as a target to mitigate the current COVID-19 emergency and the future predicted coronavirus pandemics.

Does periodontitis influence the risk of COVID-19? A scoping review.

OBJECTIVE: Research has shown that the novel severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) significantly influences the oral microbiome to expedite systemic diseases by invading harmful oral pathogens near and distant organs. To identify, explore, and map the possible mechanisms underlying periodontitis in severe coronavirus disease 2019 (COVID-19) cases. MATERIAL AND METHODS: Relevant articles published from December 2019 to February 2022 were identified and screened using keywords and inclusion criteria from various databases. RESULTS: This review sheds light on multiple pathways of periodontitis, the spread of periodontal infection and microbial metabolites to the lungs, and the dysregulated immune system with elevated cytokines, reactive oxygen species generation, nuclear DNA damage, and senescence, which have the potential to promote stronger viral attachment to host cells and the onset of COVID-19 manifestation with increased severity and risk of mortality. In addition, the cytokine connection to SARS-CoV-2, T-cell responses against periodontitis, its connection with COVID-19, the role of host factors, and periodontal therapy have been discussed. CONCLUSIONS: The relationship between COVID-19 and periodontitis needs further investigation along with the development of alternative therapies to prevent periodontitis for better management and control of COVID-19.

Periodontitis promotes the expression of gingival transmembrane serine protease 2 (TMPRSS2), a priming protease for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2).

OBJECTIVES: The oral cavity is one of the main entry sites for SARS-CoV-2. Gingival keratinocytes express transmembrane serine protease 2 (TMPRSS2), responsible for priming the SARS-CoV-2 spike protein. We investigated whether periodontitis increased the expression of TMPRSS2. METHODS: To investigate gene expression in periodontitis, we analyzed the expression of specific genes from (1) the Gene Expression Omnibus (GEO) dataset of 247 human gingival tissues and (2) an experimentally-induced periodontitis mouse model. Human gingival tissues with or without periodontitis were immunohistochemically stained using an anti-TMPRSS2 antibody. Analysis of the TMPRSS2 promoter was performed using a ChIP-Atlas dataset. TMPRSS2 expression was detected in cultured human keratinocytes using quantitative reverse transcription (qRT)-PCR and Western blot analysis. RESULTS: GEO dataset analysis and an experimentally-induced periodontitis model revealed increased expression of TMPRSS2 in periodontitis gingiva. The keratinocyte cell membrane in periodontitis gingiva was strongly immunohistochemically stained for TMPRSS2. Using ChIP-Atlas and GEO datasets, we screened for transcription factors that bind to the TMPRSS2 promoter region. We found one candidate, estrogen receptor 1 (ESR1), highly expressed in periodontitis gingiva. Analysis of the GEO dataset revealed a correlation between ESR1 and TMPRSS2 expression in gingival tissues. An ESR1 ligand induced TMPRSS2 expression in cultured keratinocytes. CONCLUSIONS: Periodontitis increases TMPRSS2 expression in the cell membrane of gingival keratinocytes.

Interconnection of periodontal disease and comorbidities: Evidence, mechanisms, and implications.

Periodontitis, a microbiome-driven inflammatory disease of the tooth-attachment apparatus, is epidemiologically linked with other disorders, including cardio-metabolic, cognitive neurodegenerative and autoimmune diseases, respiratory infections, and certain cancers. These associations may, in part, be causal, as suggested by interventional studies showing that local treatment of periodontitis reduces systemic inflammation and surrogate markers of comorbid diseases. The potential cause-and-effect connection between periodontitis and comorbidities is corroborated by studies in preclinical models of disease, which additionally provided mechanistic insights into these associations. This overview discusses recent advances in our understanding of the periodontitis-systemic disease connection, which may potentially lead to innovative therapeutic options to reduce the risk of periodontitis-linked comorbidities.

Periodontitis and coronavirus disease 2019.

The coronavirus disease 2019 caused by severe acute respiratory syndrome coronavirus 2 is usually a mild condition; however, in some cases it can result in severe sickness and even death. Thus, understanding the reasons behind these grave outcomes is of great importance. Coronavirus disease 2019 and periodontitis share some intriguing characteristics. They can both lead to systemic inflammation and alterations of coagulation pathways, and both share confounding factors, such as diabetes, hypertension, and obesity. Accordingly, a possible association between these conditions has been hypothesized in the literature. The objective of this review was to evaluate the scientific evidence linking these diseases and the possible underlying mechanisms. Evidence has shown that coronavirus disease 2019 presents oral manifestations and can even affect periodontal tissues. Moreover, some studies have shown a possible association between coronavirus disease 2019 severity and the presence of periodontitis. Current evidence suggests that this association could be explained through the direct role of periodontal bacteria in aggravating lung infections, as well as through the indirect effect of periodontitis in inducing systemic inflammation and priming of the immune system to an exacerbated reaction to severe acute respiratory syndrome coronavirus 2 infection. Future research is needed to confirm these observations and explore the possible role that periodontal care might play in the coronavirus disease 2019 pandemic.

ACE2 gene expression and inflammatory conditions in periodontal microenvironment of COVID-19 patients with and without diabetes evaluated by qPCR (preprint)

Objective Chronic periodontitis has been proposed to be linked to coronavirus disease (COVID-19) on the basis of itsinflammation mechanism. We aimed to evaluate this association by investigating the expression of Angiotensin Converting Enzyme-2 (ACE2) in periodontal compartments, which contain dysbiosis-associated pathogenic bacteria, and how it can be directly or indirectly involved in exacerbating inflammation in periodontal tissue. Material and Methods This observational clinical study included 23 adult hospitalized patients admitted to Universitas Indonesia Hospital with PCR-confirmed COVID-19, while 6 non-COVID-19 participants come to periodontal clinic were included as control. Using real time-PCR (qPCR) and gingival crevicular fluids (GCF) samples from COVID-19 patients with and without diabetes and periodontitis, we assessed the mRNA expression of angiotensin-converting enzyme 2 (ACE2), IL-6, IL8, complement C3, and LL37 as well as the relative proportion of Porphyromonas gingivalis , Fusobacterium nucleatum , and Veillonella parvula to represent the dysbiosis condition in periodontal microenvironment. All analyses were performed to determine their relationship. Results ACE2 mRNA expression was detected in the GCF of periodontitis-COVID-19 patients with and without diabetes. However, only periodontitis-COVID-19 patients with diabetes showed a positive relationship between ACE2 expression and inflammatory conditions in the periodontal microenvironment. In addition, the interplay between pro-inflammatory cytokine (Il-6) and complement C3 could be used as a predictor of the severity of periodontal inflammation in COVID-19 patients with diabetes. Conclusion The study data show that the SARS-CoV-2 entry gene is expressed in the GCF of patients with COVID-19, and its expression correlates with inflammatory markers.

The effect of the COVID-19 outbreak on the periodontal status of patients with periodontitis in supportive therapy: a retrospective study.

OBJECTIVE: The aim of this study was to assess the impact of lockdown due to the coronavirus COVID-19 pandemic on the periodontal status of patients with periodontitis in supportive periodontal therapy. METHOD AND MATERIALS: A retrospective analysis of patients affected by periodontitis stage III-IV-grade A, B, and C, who had their supportive periodontal therapy to September 2020, after a period of 6 months from the planned maintenance recall (March 2020) was performed. Clinical parameters full-mouth plaque score (FMPS), full-mouth bleeding score (FMBS), and probing depth (PD) were evaluated. Patients were assigned to three groups: A (nonsmokers); B (< 10 cigarettes/day); and C (> 10 cigarettes/day). Statistical analysis was used to compare intra-group and inter-group differences. RESULTS: In total, 55 subjects with the mean age of 47.7 ± 7.0 years were enrolled. The number of participants in group A and group B decreased, respectively, from 25 (45.5%) to 20 (36.4%) and from 17 (30.9%) to 13 (23.6%). The C group increased from 13 (23.6%) to 22 (40.0%). A statistically significant increase in mean FMPS was recorded in group A (from 22.5 ± 3.5 to 30.0 ± 28.3; P < .0001); group B (from 22.5 ± 12.7 to 42.5 ± 3.5; P < .0001); and group C (from 22.5 ± 25.5 to 42.5 ± 10.6; P < .0001). A statistically significant increase in mean FMBS was recorded in group A (from 15.0 ± 7.1 to 25.0 ± 21.2; P < .0001); group B (from 15.0 ± 0.0 to 37.5 ± 3.5; P < .001); and group C (from 12.5 ± 3.5 to 30.0 ± 7.1; P < .0001). A statistically significant increase in mean PD was recorded in group A (from 4.48 ± 0.5 to 5.25 ± 1.2; P < .001); in group B (from 4.71 ± 0.7 to 5.38 ± 1.31; P < .0001); and group C (from 6.00 ± 0.0 to 7.09 ± 1.1; P < .0001). CONCLUSIONS: Within the limitations of this study the results showed that the pandemic period resulted in an increase in probing depth for the patients in regular SPT, possibly due to increased tobacco consumption.

Periodontitis as an inflammatory trigger in hypertension: From basic immunology to clinical implications.

Hypertension and periodontitis are both highly prevalent co-morbidities worldwide, and their occurrence increases with age. Multiple observational epidemiological studies have shown that periodontitis is associated with an increased cardiovascular disease (CVD) occurrence. Large systematic reviews and metanalyses further show that periodontitis increases the risk of hypertension and is associated with increased systolic and diastolic blood pressure. Genetic and clinical evidence, utilizing mendelian randomization and randomized clinical trials, support the causal role of periodontitis in hypertension. The mechanisms of this link remain unclear. Critical components of immune and inflammatory pathogenesis of periodontitis considerably overlap with immune mechanisms of hypertension. Clinical studies support that both C-reactive protein (CRP) levels and white blood cell counts (WBC) mediate the relationship between periodontal disease and high blood pressure. In particular, activation of Th1, Th17, T regulatory cells, and proinflammatory monocytes has been shown to be essential in both conditions. Immunosenescent dysregulated CD28null T cells have been implicated, along with key effector cytokines such as interleukin 6 (IL-6), TNF-alpha (TNF-α), interferon-gamma (IFN-γ), and interleukin 17 (IL-17). A better understanding of the relationships between hypertension and periodontitis is essential not only for possible utilization of this knowledge for a non-pharmacological approach to improving blood pressure control. It may also provide valuable pathogenetic clues linking inflammation and hypertension, which has become particularly relevant in the light of links between hypertension and autoimmune disorders or, more recently, COVID-19.

A Misleading Apical Periodontitis Like Symptoms Post COVID-19 Vaccine (preprint)

Background: Adverse effects of vaccines are common, yet the reaction to vaccines widely varies between people. Companies provide an adverse effects list of their products. Adverse reactions might indicate the effectiveness of vaccines and that the immune system is responding. Case presentationIn this study, we present unusual side effects of the Pfizer/BioN-Tech vaccine. The patient had severe continuous pain related to the lower left first molar after the second dose of the Pfizer/BioN-Tech vaccine. The symptoms are typically resembling symptomatic apical periodontitis cases.ConclusionPfizer/BioN-Tech vaccine might lead to symptoms that mimic symptomatic apical periodontitis. The patient who develops such symptoms shortly after the covid -19 vaccine without an apparent cause should be assured and kept under observation for one to two weeks. A tentative diagnosis and treatment plan should be considered in the follow-up visit.

A case-control study on the association between periodontitis and coronavirus disease (COVID-19).

BACKGROUND: Coronavirus disease (COVID-19) and periodontitis share common characteristics, such as an exaggerated inflammatory response. As periodontal diseases were shown to be associated with respiratory diseases, such as pneumonia, it is quite possible that a relationship may exist between periodontitis and COVID-19. Hence, the aim of the present study was to determine whether periodontitis and poor oral hygiene are associated with COVID-19. METHODS: A case-control study was conducted. Patients who had positive real-time reverse transcription polymerase chain reaction results for severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection were included in the case group (n = 79), and patients with negative results were included in the control group (n = 71). The periodontal examination involved recording the plaque scores, calculus scores, tooth mobility, gingival bleeding, probing depth, recession, and clinical attachment level (CAL). RESULTS: Logistic regression analysis showed significant associations of mean plaque scores ≥ 1 (odds ratio (OR), 7.01; 95% confidence interval (CI), 1.83 to 26.94), gingivitis (OR, 17.65; 95% CI, 5.95 to 52.37), mean CAL ≥ 2 mm (OR, 8.46; 95% CI, 3.47 to 20.63), and severe periodontitis (OR, 11.75; 95% CI, 3.89 to 35.49) with COVID-19; these findings were more prevalent in the case group. CONCLUSION: Based on the above mentioned observations, it can be concluded that there is an association between periodontitis severity and COVID-19. Gingival bleeding and dental plaque accumulation are also more frequent among COVID-19 patients. Hence, it is essential to maintain periodontal health and good oral hygiene as an important measure for COVID-19 prevention and management.