Risk Factor For Periodontitis Research Articles

Disruption of cholesterol homeostasis triggers periodontal inflammation and alveolar bone loss

Oral diseases exhibit a significant association with metabolic syndrome, including dyslipidemia. However, direct evidence supporting this relationship is lacking, and the involvement of cholesterol metabolism in the pathogenesis of periodontitis (PD) has yet to be determined. In this study, we showed that high cholesterol caused periodontal inflammation in mice. Cholesterol homeostasis in human gingival fibroblasts was disrupted by enhanced uptake through C-X-C motif chemokine ligand 16 (CXCL16), upregulation of cholesterol hydroxylase (CH25H), and the production of 25-hydroxycholesterol (an oxysterol metabolite of CH25H). Retinoid-related orphan receptor α (RORα) mediated the transcriptional upregulation of inflammatory mediators; consequently, PD pathogenesis mechanisms, including alveolar bone loss, were stimulated. Our collective data provided direct evidence that hyperlipidemia is a risk factor for PD and supported that inhibition of the CXCL16-CH25H-RORα axis is a potential treatment mechanism for PD as a systemic disorder manifestation.

The Interrelation Between Obesity and Gingivitis in Adults

Background: Fat deposition in excess is known as obesity. It is a risk factor for many systemic diseases including cardiovascular and atherosclerotic diseases. It is also a risk factor for periodontal disease. This study was undertaken to evaluate association between obesity and gingivitis. Methods: 50 adult subjects participated in this study. Waist circumference (WC) and Body mass index (BMI) was measured. Visceral fat (VF) was measured with Bioelectrical impedance analyzer (BIA). For gingivitis, gingival index (GI) and Plaque index (PI) was measured. Statistical analysis was done using Multinomial logistic regression and Chi-square test. Results: There was significant correlation between BMI and gingivitis (P˂0.05), whereas no relationship was found between gingivitis, visceral fat and waist circumference (P˃0.05). Conclusion: Only relationship was found between BMI and gingivitis. Obese subjects may have a risk of gingivitis.

Physical activity as a modifiable risk factor for periodontal disease.

Non-communicable diseases (NCDs), which contribute significantly to global morbidity, are largely preventable through behavioral changes. As with other NCDs, periodontitis is associated with modifiable risk factors such as smoking and stress and is linked to multiple adverse health outcomes through a shared pathway of chronic systemic inflammation. While the health benefits of physical activity have been widely promoted in public health and extensively studied for other systemic conditions, its impact on periodontal health has only recently started to gain attention. This article critically evaluates the current literature on the relationship between physical activity and periodontitis. While cross-sectional studies have shown an inverse association between physical activity levels and periodontitis risk in the general population, clinical oral health surveys of elite athletes with high levels of physical activity have nonetheless revealed poor periodontal conditions. Although causality has not been determined, physical activity could positively impact periodontitis directly, by reducing inflammatory biomarkers, and indirectly, through its modulatory effects on insulin sensitivity, obesity, bone density, stress, and other health promoting behaviors. Given the importance of risk factor control during initial periodontal therapy, understanding the role of physical activity as a potential behavioral risk modifier is paramount. The findings of this review provide an evidence-based overview of how physical activity could influence periodontitis. There is a need for longitudinal cohort studies to verify the temporality of the reported associations and exclude confounders, while interventions are needed to assess the efficacy of physical activity on periodontal treatment outcomes.

Clinical Evaluation of Correlation between Periodontal Diseases and ABO Blood Grouping

Periodontal disease, is a set of inflammatory conditions affecting the tissues surrounding the teeth. Several studies have focused on the relationship between ABO blood and RH factor groups and periodontal diseases. However, the results showed a lot of discrepancies Aim of the study: to evaluate the relationship between ABO, Rh blood groups and distribution of periodontal diseases. Material And Method: This study involved 560 subjects aged between 20 to 55 years; selected on random basis from the outpatient department of Periodontology at AL -mammon specialized dental center in Baghdad. The patients sample have been classified in a 3 groups in relation to their clinical presentation and the periodontal scores on a basis of Ramfjord’s Periodontal index. Result: out of 560 patients there were 312 male, 248 female patients. According to sample classification in relation to clinical condition and periodontal score, Group I 115 patients with healthy gingiva; group II 225 patients with gingivitis; and group III 220 patients with periodontitis ,the highest prevalence of periodontitis are among blood group O(34.1%), while higher gingivitis percentage are associated with blood group A (34.2%). The prevalence of gingivitis was higher in Rh positive group 43.1%, while periodontitis show higher prevalence in Rh negative group 40%. Discussion and conclusion: We concluded that there was significant relationship between ABO, Rh blood group system and periodontal disease. Blood group ‘A’ could be a factor of risk for gingivitis and blood group ‘O’ could be a factor of risk for the developing of periodontitis. Similarly Rh positive group considered a risk factor for gingivitis, while Rh negative group is a risk factor for periodontitis.

The effect of antipsychotic medication and the associated hyperprolactinemia as a risk factor for periodontal diseases in schizophrenic patients: a cohort retrospective study

BackgroundPeriodontal disease is a major health problem that results in tooth loss and thus affects oral health, which affects quality of life. In particular, schizophrenic patients are at higher risk for periodontal disease due to several factors, including the effect of antipsychotic medications received by those patients. Accordingly, the aim of the present cohort retrospective study is to explore the effect of antipsychotics on periodontal health and the possible effect of antipsychotic-induced hyperprolactinemia as a risk factor for periodontal disease progression in schizophrenic patients.Methods and outcomesThe study population consisted of three groups: Group A (n = 21): schizophrenic patients that have been taking “prolactin-inducing” antipsychotics for at least 1 year; Group B (n = 21): schizophrenic patients who have been taking “prolactin-sparing” antipsychotics for at least 1 year; and Group C (n = 22): newly diagnosed schizophrenic patients and/or patients who did not receive any psychiatric treatment for at least 1 year. The study groups underwent assessment of periodontal conditions in terms of pocket depth (PD), clinical attachment loss (CAL), gingival recession, tooth mobility, and bleeding on probing (BOP). Also, bone mineral density was evaluated using DEXA scans, and the serum prolactin level was measured by automated immunoassay.ResultsResults revealed a statistically significant difference in PD, CAL, and serum prolactin levels (P ≤ 0.001, P = 0.001, and P ≤ 0.001, respectively) among the 3 study groups. For both PD and CAL measurements, group A has shown significantly higher values than both groups B and C, whereas there was no statistically significant difference between the values of groups C and B. Concerning serum prolactin levels, group A had significantly higher values than groups B and C (P ≤ 0.001 and P ≤ 0.001 respectively). There was a statistically significant difference (P ≤ 0.001) between the 3 study groups in terms of bone mineral density. Moreover, there was a statistically significant direct relation between serum prolactin level and other parameters including clinical attachment loss, pocket depth measurements and bone mineral density.ConclusionAccording to our results, it could be concluded that all antipsychotics contribute to the progression of periodontal disease, with a higher risk for prolactin-inducing antipsychotics. However, further long term, large sampled, interventional and controlled studies are required to reach definitive guidelines to allow clinicians properly manage this group of patients.

Risk factors associated with periodontal disease and its impact on quality of life among pregnant women

Background Periodontal disease during pregnancy affects maternal oral health and increases the risk of adverse pregnancy outcomes. However, studies on the risk factors for periodontal disease and its impact on oral health-related quality of life in pregnant women in Taiwan are lacking. This present study aimed to identify the risk factors associated with periodontal disease during pregnancy and examine the relationship of periodontal disease with oral health-related quality of life among pregnant women. Methods This study was conducted in a large medical centre in northern Taiwan. Eighty-four participants completed a periodontal examination by dentists as well as structured questionnaires, including the Oral Health Impact Profile-14, demographics, obstetric history, dietary habits, and oral hygiene behaviours. Multivariate logistic regression was used to determine the risk factors associated with periodontal disease and a t-test was used to compare the difference in oral health-related quality of life between pregnant women with and without periodontal disease. Results Fifty participants (59.5%) had periodontal diseases. Risk factors for periodontal disease included eating out for lunch, consuming beverages, brushing less than three times per day, and not receiving regular professional dental cleanings. The oral health-related quality of life was significantly poorer in pregnant women with periodontal disease than in those without. Conclusions The risk factors for periodontal disease, including eating out for lunch, drinking beverages, brushing teeth less, and not regular dental cleaning, provide convincing evidence for pregnant women to maintain good oral hygiene to prevent periodontal disease and improve oral health-related quality of life.

Validation of a physiological type 2 diabetes model in human periodontal ligament stem cells.

Type 2 diabetes (T2DM), a recognized risk factor for periodontitis, is characterized by insulin resistance. However, the molecular mechanisms concerning the role of insulin resistance in linking T2DM and periodontitis remain poorly elucidated due to the absence of an appropriate T2DM cell model. We aimed to explore an appropriate model of T2DM in human periodontal ligament stem cells (hPDLSCs) and uncover the involved mechanisms. hPDLSCs were incubated with common reagents for recapitulating insulin resistance state including high glucose (HG) (15, 25, 35, 45 mM), glucosamine (0.8, 8, 18, 28, 38 mM), or palmitic acid (PA; 100, 200, 400, 800 μM), combined with LPS for 48 h. The insulin signaling pathway, inflammation, and pyroptosis were detected by western blots and quantitative real-time polymerase chain reaction (RT-qPCR). The effects on osteogenesis were evaluated by alkaline phosphatase staining, alizarin red S staining, RT-qPCR, and western blots. HG failed to recapitulate insulin resistance. Glucosamine was sufficient to induce insulin resistance but failed to trigger inflammation. In total, 100 and 200 μM PA exhibited the most proinflammatory, insulin resistance, and pyroptosis induced role, and inhibited the osteogenic differentiation of hPDLSCs. Palmitic acid is a promising candidate for developing T2DM model in hPDLSCs.

Diabetes mellitus promotes susceptibility to periodontitis-novel insight into the molecular mechanisms.

Diabetes mellitus is a main risk factor for periodontitis, but until now, the underlying molecular mechanisms remain unclear. Diabetes can increase the pathogenicity of the periodontal microbiota and the inflammatory/host immune response of the periodontium. Hyperglycemia induces reactive oxygen species (ROS) production and enhances oxidative stress (OS), exacerbating periodontal tissue destruction. Furthermore, the alveolar bone resorption damage and the epigenetic changes in periodontal tissue induced by diabetes may also contribute to periodontitis. We will review the latest clinical data on the evidence of diabetes promoting the susceptibility of periodontitis from epidemiological, molecular mechanistic, and potential therapeutic targets and discuss the possible molecular mechanistic targets, focusing in particular on novel data on inflammatory/host immune response and OS. Understanding the intertwined pathogenesis of diabetes mellitus and periodontitis can explain the cross-interference between endocrine metabolic and inflammatory diseases better, provide a theoretical basis for new systemic holistic treatment, and promote interprofessional collaboration between endocrine physicians and dentists.

Quercetin promotes autophagy to alleviate cigarette smoke-related periodontitis.

Cigarette smoking has been reported as an independent risk factor for periodontitis. Tobacco toxins affect periodontal tissue not only locally but also systemically, leading to the deterioration and recurrence of periodontitis. However, the mechanism of cigarette smoke-related periodontitis (CSRP) is unclear and thus lacks targeted treatment strategies. Quercetin, a plant-derived polyphenolic flavonoid, has been reported to have therapeutic effects on periodontitis due to its documented antioxidant activity. This study aimed to evaluate the effects of quercetin on CSRP and elucidated the underlying mechanism. The cigarette smoke-related ligature-induced periodontitis mouse model was established by intraperitoneal injection of cigarette smoke extract (CSE) and silk ligation of bilateral maxillary second molars. Quercetin was adopted by gavage as a therapeutic strategy. Micro-computed tomography was used to evaluate the alveolar bone resorption. Immunohistochemistry detected the oxidative stress and autophagy markers in vivo. Cell viability was determined by Cell Counting Kit-8, and oxidative stress levels were tested by 2,7-dichlorodihydrofluorescein diacetate probe and lipid peroxidation malondialdehyde assay kit. Alkaline phosphatase and alizarin red staining were used to determine osteogenic differentiation. Network pharmacology analysis, molecular docking, and western blot were utilized to elucidate the underlying molecular mechanism. Alveolar bone resorption was exacerbated and oxidative stress products were accumulated during CSE exposure in vivo. Oxidative stress damage induced by CSE caused inhibition of osteogenic differentiation in vitro. Quercetin effectively protected the osteogenic differentiation of human periodontal ligament cells (hPDLCs) and periodontal tissue by upregulating the expression of Beclin-1 thus to promote autophagy and reduce oxidative stress damage. Our results established a role of oxidative stress damage and autophagy dysfunction in the mechanism of CSE-induced destruction of periodontal tissue and hPDLCs, and provided a potential application value of quercetin to ameliorate CSRP.

Effect of Psychological Stress on Salivary Cortisol and Periodontitis

Objective: The progression of periodontitis, induced by polymicrobial dysbiosis, can be modified by systemic or environmental factorssuch as stress or anxiety that affect host response. This study evaluates the potential associations between psychosocial stress, salivary cortisol and periodontitis.Methods: In this cross-sectional study, 80 adult participants (41 males and 39 females) aged 20-45 years were included. Participantscompleted a stress self-assessment using a PSS scale questionnaire. Samples of saliva were collected for testing cortisol levels byELISA. The participants were then divided into four groups established on periodontal parameters (plaque index (PI), bleeding onprobing (BOP), probing pocket depth, and clinical attachment level), and stress levels: Group 1 (healthy periodontium without stress),Group 2 (periodontitis without stress), Group 3 (healthy periodontium with stress), and Group 4 (periodontitis with stress).Results: Statistically significant differences were observed between the values detected in the four experimental groups for PI, BI, PD,and CAL (p≤0.05). The highest means of cortisol level were revealed in the stressed healthy group and stressed with periodontitisgroup, at 39.7 and 40.5, respectively. Hence there were statistically significant differences overall across the four groups (p≤0.05).Conclusions: This study demonstrates that psychosocial stress is a risk factor for periodontal diseases, and in cortisol, as one of theelements that enhance periodontal damage, increases were recorded for all four clinical parameters, BI, PI, PD, CAL, which are usedas diagnostic tools for periodontitis.

Altered homeostatic factor of db/db mice’s periodontal ligament: A pilot study

Purpose: Diabetes is a risk factor for periodontal disease and can cause alveolar bone loss. The purpose of this study was to explore the effect of diabetes on homeostatic factor of periodontal tissue using leptin receptor (db/db) mice.Materials and Methods: The db/db mice(experimental group) were compared with the wild type mice (control group) using histology and immunohistochemical analyses. Collagen fibers were evaluated using H&E, picrosirius red, fibromodu-lin staining and osteogenic factors (periostin, osteopontin, osteocalcin, osterix), and factors related to osteoclasts (OPG, RANKL) in the PDL were investigated.Results: Collagen fibers and osteogenic factors in the PDL showed no differences between a control and an experimental group. In an experimental group, expression of receptor activator of nuclear factor kappa-Β ligand (RANKL) was similar compared with a control group, while expression of osteoprotegerin (OPG) was decreased.Conclusions: RANKL/OPG ratio may be one of homeostatic factors related to bone remodeling in diabetic mice.

Plasmin-Mediated Fibrinolysis in Periodontitis Pathogenesis.

The hemostatic and inflammatory systems work hand in hand to maintain homeostasis at mucosal barrier sites. Among the factors of the hemostatic system, fibrin is well recognized for its role in mucosal homeostasis, wound healing, and inflammation. Here, we present a basic overview of the fibrinolytic system, discuss fibrin as an innate immune regulator, and provide recent work uncovering the role of fibrin-neutrophil activation as a regulator of mucosal/periodontal homeostasis. We reason that the role of fibrin in periodontitis becomes most evident in individuals with the Mendelian genetic defect, congenital plasminogen (PLG) deficiency, who are predisposed to severe periodontitis in childhood due to a defect in fibrinolysis. Consistent with plasminogen deficiency being a risk factor for periodontitis, recent genomics studies uncover genetic polymorphisms in PLG, encoding plasminogen, being significantly associated with periodontal disease, and suggesting PLG variants as candidate risk indicators for common forms of periodontitis.

Serum levels of various vitamins in periodontal health and disease- a cross sectional study.

Vitamins are micronutrients that are required in small or trace amounts. They play an essential role in the metabolism and maintenance of tissue function. This investigation aimed to assess if a deficiency of certain essential vitamins is a risk factor for developing periodontitis. The subject population consisted of 100 subjects, 50 with generalized chronic periodontitis and 50 periodontally healthy volunteers. The following clinical parameters were measured: Gingival Index, pocket depth (mm); Clinical Attachment Loss (mm). Serum samples were collected and analyzed for levels of cis-β-carotene, β-cryptoxanthin, vitamin B 12, folate, vitamin D, and vitamin E. Individual data collected was summarized and analyzed using statistical software. All the clinical parameters for periodontal status in the periodontitis group compared to healthy volunteers were highly significant (p<0.0001). The mean levels of all the micronutrients, vitamin A precursors cis-β-carotene and β-cryptoxanthin, folate, vitamin B 12, D & E were lower in the periodontitis group than the healthy volunteers, although the difference was statistically significant only in case of β-cryptoxanthin, Vitamin B12 and Vitamin D (p<0.05). The findings of our study suggest that serum micronutrient levels especially Vitamin A, Vitamin B 12, and Vitamin D may be modifiable risk factors for periodontal disease. Providing an optimized combination of various vitamins in each meal in combination with sufficient measures of standard oral hygiene care may provide an important role in the prevention of periodontitis.

Mechanism of obesity affecting periodontal tissue regeneration and therapeutic strategies

Obesity is an important health problem in our society today, which can lead to the chronic low-grade inflammation state, to be an inducement for many chronic diseases such as hypertension, type 2 diabetes and non-alcoholic fatty liver disease. As a common oral chronic infectious disease, periodontitis is mainly characterized by gingival inflammation, periodontal pocket formation, alveolar bone resorption and tooth mobility. The ultimate goal of periodontitis treatment is to achieve periodontal tissue regeneration in the defect area. As a major risk factor for periodontitis, obesity can alter the periodontal inflammatory microenvironment in multiple ways, affecting the effects of periodontal tissue regeneration ultimately. Therefore, this paper will review the relationship between obesity and periodontal tissue regeneration, mechanism of obesity affecting periodontal tissue regeneration and the therapeutic strategies of periodontal tissue regeneration, providing new ideas for periodontal tissue regeneration treatment in obesity.

Periodontal Disease and Other Adverse Health Outcomes Share Risk Factors, including Dietary Factors and Vitamin D Status.

For nearly a century, researchers have associated periodontal disease (PD) with risks of other adverse health outcomes such as cardiovascular disease, diabetes mellitus, and respiratory diseases, as well as adverse pregnancy outcomes. Those findings have led to the hypothesis that PD causes those adverse health outcomes either by increasing systemic inflammation or by the action of periodontopathic bacteria. However, experiments largely failed to support that hypothesis. Instead, the association is casual, not causal, and is due to shared underlying modifiable risk factors, including smoking, diet, obesity, low levels of physical activity, and low vitamin D status. Diabetes mellitus is also considered a risk factor for PD, whereas red and processed meat are the most important dietary risk factors for diabetes. Because PD generally develops before other adverse health outcomes, a diagnosis of PD can alert patients that they could reduce the risk of adverse health outcomes with lifestyle changes. In addition, type 2 diabetes mellitus can often be reversed rapidly by adopting an anti-inflammatory, nonhyperinsulinemic diet that emphasizes healthful, whole plant-based foods. This review describes the evidence that proinflammatory and prohyperinsulinemia diets and low vitamin D status are important risk factors for PD and other adverse health outcomes. We also make recommendations regarding dietary patterns, food groups, and serum 25-hydroxyvitamin D concentrations. Oral health professionals should routinely inform patients with PD that they could reduce their risk of severe PD as well as the risks of many other adverse health outcomes by making appropriate lifestyle changes.

NADPH-dependent ROS accumulation contributes to the impaired osteogenic differentiation of periodontal ligament stem cells under high glucose conditions.

Diabetes mellitus is an established risk factor for periodontal disease that can aggravate the severity of periodontal inflammation and accelerate periodontal destruction. The chronic high glucose condition is a hallmark of diabetes-related pathogenesis, and has been demonstrated to impair the osteogenic differentiation of periodontal ligament stem cells (PDLSCs), leading to delayed recovery of periodontal defects in diabetic patients. Reactive oxygen species (ROS) are small molecules that can influence cell fate determination and the direction of cell differentiation. Although excessive accumulation of ROS has been found to be associated with high glucose-induced cell damage, the underlying mechanisms remain unclear. Nicotinamide adenine dinucleotide phosphate (NADPH) is an important electron donor and functions as a critical ROS scavenger in antioxidant systems. It has been identified as a key mediator of various biological processes, including energy metabolism and cell differentiation. However, whether NADPH is involved in the dysregulation of ROS and further compromise of PDLSC osteogenic differentiation under high glucose conditions is still not known. In the present study, we found that PDLSCs incubated under high glucose conditions showed impaired osteogenic differentiation, excessive ROS accumulation and increased NADPH production. Furthermore, after inhibiting the synthesis of NADPH, the osteogenic differentiation of PDLSCs was significantly enhanced, accompanied by reduced cellular ROS accumulation. Our findings demonstrated the crucial role of NADPH in regulating cellular osteogenic differentiation under high glucose conditions and suggested a new target for rescuing high glucose-induced cell dysfunction and promoting tissue regeneration in the future.

Cigarette smoke extract impairs gingival epithelial barrier function

We previously showed that junctional adhesion molecule 1 (JAM1) and coxsackievirus and adenovirus receptor (CXADR), tight junction-associated proteins, have important roles to maintain epithelial barrier function in gingival tissues. Smoking is considered to be a significant risk factor for periodontal disease. The present study was conducted to examine the effects of cigarette smoke extract (CSE) on JAM1 and CXADR in human gingival epithelial cells. CSE was found to cause translocation of JAM1 from the cellular surface to EGFR-positive endosomes, whereas CXADR did not. Using a three-dimensional multilayered gingival epithelial tissue model, CSE administration was found to increase permeability to lipopolysaccharide and peptidoglycan, whereas overexpression of JAM1 in the tissue model prevented penetration by those substrates. Furthermore, vitamin C increased JAM1 expression, and inhibited penetration of LPS and PGN induced by CSE. These findings strongly suggest that CSE disrupts gingival barrier function via dislocation of JAM1, thus allowing bacterial virulence factors to penetrate into subepithelial tissues. Furthermore, they indicate that vitamin C increases JAM1 expression and prevents disruption of gingival barrier function by CSE.

Optimizing a Diagnostic Model of Periodontitis by Using Targeted Proteomics.

Periodontitis (PD), a widespread chronic infectious disease, compromises oral health and is associated with various systemic conditions and hematological alterations. Yet, to date, it is not clear whether serum protein profiling improves the assessment of PD. We collected general health data, performed dental examinations, and generated serum protein profiles using novel Proximity Extension Assay technology for 654 participants of the Bialystok PLUS study. To evaluate the incremental benefit of proteomics, we constructed two logistic regression models assessing the risk of having PD according to the CDC/AAP definition; the first one contained established PD predictors, and in addition, the second one was enhanced by extensive protein information. We then compared both models in terms of overall fit, discrimination, and calibration. For internal model validation, we performed bootstrap resampling (n = 2000). We identified 14 proteins, which improved the global fit and discrimination of a model of established PD risk factors, while maintaining reasonable calibration (area under the curve 0.82 vs 0.86; P < 0.001). Our results suggest that proteomic technologies offer an interesting advancement in the goal of finding easy-to-use and scalable diagnostic applications for PD that do not require direct examination of the periodontium.

Impact of Stress on Periodontal Health: Literature Revision.

Stress is a physiological response of the body to stressful life events but may not be when the individual is persistently exposed to the stress trigger, and it negatively affects certain physiological functions, thus triggering psychosomatic diseases. In literature, chronic stress and inadequate coping strategies are found to mediate the risk and development of periodontitis; mechanisms have therefore been proposed to explain the effects of stress on the periodontium. Since stress is a prevalent problem in modern life and given the importance of maintaining oral health, the present literature review aimed to estimate the association between stress and periodontal disease. The research question adopted is the following: "Are psychological stress and periodontal disease related?" The search was conducted in August 2022 and limited to articles in electronic databases from 2017 to 2022 in English, excluding reviews and literature reviews. From the electronic databases, a total of 532 articles were identified and became 306 after reviews and duplicates were removed. An additional bibliographic search was conducted through the same electronic databases, controlled terms and keywords including only systematic reviews, which were previously excluded. Through the bibliography cited in the systematic reviews, an additional 18 articles were identified, with a new total of 324. As a result of reading the title and abstract of these 324 articles, an additional 295 were excluded. Reading the full text of the remaining 29 studies, 2 articles were excluded due to non-adherence to the eligibility criteria. The remaining 27 results were included in our literature review. It has been suggested in the literature that adverse socioeconomic conditions elicit a stress response, which can trigger periodontal inflammation. Most of the 27 articles included in the study confirm and demonstrate a positive association between psychological stress and periodontal disease. Numerous studies have shown the mechanisms through which chronic stress negatively affects periodontal tissues. Therefore, in the light of the results obtained from this review, it is important that oral health professionals, also for general health purposes, consider stress factors among the risk factors of periodontal disease, its severity and decreased efficacy of treatments. It is therefore advisable to act preventively through the interception of chronic stress.

Circular RNA hsa_circ_0084054 promotes the progression of periodontitis with diabetes via the miR-508-3p/PTEN axis.

Diabetes is an important risk factor for periodontitis, and circular RNA (circRNA) may play an important role in aggravating inflammation and accelerating disease progression by regulating miRNA/mRNA. This study aimed to investigate the role and mechanism of the hsa_circ_0084054/miR-508-3p/PTEN axis in the progression of periodontitis with diabetes. First, circRNA sequencing was used to screen the differentially expressed circRNAs of periodontal ligament cells (PDLCs) treated with high glucose and/or Porphyromonas gingivalis lipopolysaccharide (LPS) in vitro, and the overtly differentially expressed hsa_circ_0084054 was selected and was also verified in periodontal ligament (PDL) tissue from periodontitis patients with diabetes. Then, its ring structure was tested by Sanger sequencing, RNase R, and actinomycin D assays. The bioinformatics analysis, dual luciferase reporter assay, and RIP assay were used to explore the interaction of hsa_circ_0084054/miR-508-3p/PTEN axis, whose effects on inflammation, oxidative stress, and apoptosis of PDLCs were evaluated through the measurement of inflammatory factors, reactive oxygen species (ROS), total superoxide dismutase (SOD), malondialdehyde (MDA), and Annexin V/PI assay. By high-throughput sequencing, it was found that hsa_circ_0084054 was significantly increased in HG + LPS group compared with control group and LPS group, which was also verified in periodontal ligament (PDL) tissue from periodontitis patients with diabetes. Silencing hsa_circ_0084054 in PDLCs decreased the expression of inflammatory factors (IL-1β, IL-6, TNF-α), the levels of ROS and MDA, and the proportion of apoptotic cells; conversely, SOD activity was enhanced. In addition, we found that hsa_circ_0084054 could up-regulate the expression of PTEN through sponge miR-508-3p to inhibit AKT phosphorylation, finally trigger the aggravation of oxidative stress and inflammation in periodontitis patients with diabetes. hsa_circ_0084054 can aggravate inflammation and promote the progression of periodontitis with diabetes by regulating miR-508-3p/PTEN signaling axis, which may serve as a new target for the intervention of periodontitis with diabetes.