Risk Factor For Periodontitis Research Articles

Oxidative Stress Inhibits Endotoxin Tolerance and May Affect Periodontitis

Periodontal disease is caused by dysbiosis of the dental biofilm and the host inflammatory response. Various pathogenic factors, such as proteases and lipopolysaccharides (LPSs) produced by bacteria, are involved in disease progression. Endotoxin tolerance is a function of myeloid cells, which sustain inflammation and promote tissue regeneration upon prolonged stimulation by endotoxins such as LPS. The role of endotoxin tolerance is gaining attention in various chronic inflammatory diseases, but its role in periodontal disease remains elusive. Oxidative stress, one of the major risk factors for periodontal disease, promotes disease progression through various mechanisms, of which only some are known. The effect of oxidative stress on endotoxin tolerance has not yet been studied, and we postulated that endotoxin tolerance regulation may be an additional mechanism through which oxidative stress influences periodontal disease. This study aimed to reveal the effect of oxidative stress on endotoxin tolerance and that of endotoxin tolerance on periodontitis progression. The effect of oxidative stress on endotoxin tolerance was analyzed in vitro using peritoneal macrophages of mice and hydrogen peroxide (H2O2). The results showed that oxidative stress inhibits endotoxin tolerance induced by Porphyromonas gingivalis LPS in macrophages, at least partially, by downregulating LPS-elicited negative regulators of Toll-like receptor (TLR) signaling. A novel oxidative stress mouse model was established using SMP30KO mice incapable of ascorbate biosynthesis. Using this model, we revealed that oxidative stress impairs endotoxin tolerance potential in macrophages in vivo. Furthermore, gingival expression of endotoxin tolerance-related genes and TLR signaling negative regulators was decreased, and symptoms of ligature-induced periodontitis were aggravated in the oxidative stress mouse model. Our findings suggest that oxidative stress may contribute to periodontitis progression through endotoxin tolerance inhibition.

Psychological stress: neuroimmune roles in periodontal disease.

Periodontitis is a chronic inflammatory disease that starts with pathogenic bacteria and is mediated by a combination of multiple factors. Psychosomatic factors are considered to be one of the most critical risk factors for periodontal disease. Psychological stress may threaten periodontal immune homeostasis in multiple ways by affecting the hypothalamic-pituitary-adrenal cortex system, the locus ceruleus-sympathetic-adrenal medulla system, and the peptidergic nervous system. In this review, we outline the complex role of psychological stress in promoting the development of periodontal disease, focusing on the effects of stress on flora metabolism, tissue inflammation, and alveolar bone homeostasis. At the same time, we broadly and deeply summarize the potential mechanisms of psychological stress-induced periodontal disease, emphasize the importance of neuroimmune modulation for periodontal health, and expect to provide a new perspective for periodontal science based on psychoneuroimmunology.

A longitudinal assessment of chronic periodontitis in Australian adults.

The study aimed to estimate the incidence/progression and reversal of chronic periodontitis and to identify factors associated with chronic periodontitis in Australian adults over a 12-year period. Data were obtained from the longitudinal component of the National Study of Adult Oral Health (NSAOH) in 2004-2006, and repeated data, among the same adults, in 2017-2018. NSAOH 2004-2006 was a population-based study of Australian adults aged 15+ years. The American Academy of Periodontology/European Federation of Periodontology case definitions were used, and then compared with two other case definitions. Multivariable Poisson regression models were used to estimate incidence rate ratios (IRRs) and reversal rate ratio (RRRs) of periodontitis. A total of 775 dentate Australian adults had dental examinations at both times. The proportion of incidence/progression and reversal among Australian adults was 56.4% and 11.0%, respectively. Tobacco smokers presented with more than three times higher incidence (IRR: 3.32, 95% CI: 1.50-7.60) and lower reversals (RRR: 0.94, 95% CI: 0.39-0.98) than those who had never smoked. Cessation of smoking was positively associated with periodontitis reversal. The total incidence/progression was 471.7/10,000 person-years, with reversal being 107.5/10,000 person-years. The average number of teeth lost due to periodontal disease was 1.9 in 2017-2018. Being male and not having periodontal treatment were significant risk markers for the incidence/progression of periodontitis. Smoking is a risk factor for periodontitis. Cessation of smoking is an effective means of reducing the incidence and progression of chronic periodontitis, to reduce the risk of tooth loss, and to improve overall periodontal health.

Teeth and gums in diabetes

Teeth and gums in diabetes

Progression of Periodontal Disease in Individuals with Cleft Lip, Alveolus and Palate: 8-Year Longitudinal Study

Objective: To compare the progression of periodontal disease of sextants in individuals with cleft lip, alveolus and palate. Materials and Methods: This longitudinal, cross-section study was performed following the STROBE Statement. The sample included the study was conducted on 30 individuals, of both genders, aged 22 to 53 years, with cleft lip, alveolus and palate. The following clinical parameters were evaluated: measurement of probing depth of the sulcus or Periodontal pocket (PD), Clinical Attachment Level (CAL), Gingival Index (GI), plaque index (PI), buccal Gingival Recession (GR) in six sites of all teeth, except for the third molars. Analysis of the variation of clinical parameters of each tooth over the study period in relation to its sextant was performed by the Kruskal-Wallis and Dunn test. The variation of clinical parameters during the study period and the age of individuals were correlated using the Spearman correlation test. All tests considered a significance level of 5%. Results: The following means were found: PD 2.4 mm, CAL 2.6 mm, GI 0.9, PI 1.0 and BR 0.3 mm. There was increase in the mean PD and CAL (p<0.001) and reduction of mean PI and GI (p<0.001) over time, yet the variation between sextants was not statistically significant. Conclusion: During the study period, there was progression of periodontal disease in all sextants, without difference between the upper anterior sextant, cleft area and the others, suggesting that the cleft, per se, is not a risk factor for periodontal disease. Clinical relevance: the epidemiology and progression of periodontal disease in individuals with cleft lip and palate must be understood in order to establish effective therapeutic approaches.

Periodontal Disease Risk Factors Assessment in Association with Frequency of Tooth Brushing

Aim: To analyze the co-relation between frequencies of tooth brushing as a periodontal risk assessment tool in a population. Study design: Cross Sectional Survey Place and duration of study: Bacha Khan Medical College, Mardan from 1st January 2021 to 31st December 2021. Methodology: Four hundred and eleven participants were enrolled. Data was collected by administering the study questionnaire including 14 items assessing risk factors for periodontal disease as well as their oral hygiene habits. Descriptive statistics were used for data summarization and presentation. Results: Approximately 34.3% of study participants claimed to brush twice daily and 61.6% once daily. Mean age was 22.1 years and majority of them females constituting 66.7%. 39.33% had a history of bleeding gums while 28.2% had swollen gums. 51% of the subjects reported brushing for less than 2 minutes duration. 67% participants of population were of upper middle socioeconomic status. Conclusion: The clear correlation establish amongst risk of emerging periodontal disease and occurrence of tooth brushing. Keywords: Periodontal disease, Oral hygiene, Risk factors, Tooth brushing

Calculus as a Risk Factor for Periodontal Disease: Narrative Review on Treatment Indications When the Response to Scaling and Root Planing Is Inadequate.

Background: Based on the 2018 classification of periodontal disease, a series of articles have been published describing the decision points of periodontal therapy and how the findings collected at those decision points can be used as guidelines for periodontal therapy. The articles are reviewed with a focus on the finding of inadequate calculus removal at the decision points and how that finding impacts treatment outcomes. Methods: A narrative review of the literature discussing the influence of calculus on inflammation was performed and the effects of inadequate removal of calculus during periodontal therapy were analyzed in light of the 2018 classification of periodontal disease, the decision points of periodontal therapy, and the guidelines of periodontal therapy. Results: The published literature supports that calculus is a major risk factor for periodontal inflammation. Recent studies indicate that the pathologic risk of calculus goes beyond the retention of biofilm and may represent a different pathophysiologic pathway for periodontal disease separate from the direct action of biofilm. The inadequate removal of calculus is a factor in the failure of periodontal therapy. Conclusions: The inadequate removal of calculus plays an important role in the frequent failure of non-surgical periodontal therapy to eliminate inflammation.

Periodontal disease in people with a history of psychosis: Results from the UK biobank population-based study.

To test the hypotheses that: (1) Prevalence of periodontal disease would be higher in people with a history of psychosis when compared to the general population and (2) Demographic, life-style related factors and co-morbid medical conditions would predict periodontal disease in people experiencing psychosis. The authors performed cross-sectional analysis of baseline data from the UK Biobank study (2007-2010), identifying cases with psychosis using clinical diagnosis, antipsychotic medication, and self-report. Demographic (age, gender, ethnicity, socioeconomic status), lifestyle-related(BMI, blood pressure, smoking and alcohol intake, physical activity) and physical co-morbidities (cancer, cardiovascular, respiratory, inflammatory disease and metabolic conditions) were included as potential risk factors for periodontal disease among people with a history of psychosis using logistic regression analyses. The analysis sample included 502,505 participants. Risk of periodontal disease was higher in people with psychosis, regardless of how cases were identified. Patients with a clinical diagnosis had the highest proportion of periodontal disease compared to the general population (21.3% vs. 14.8%, prevalence ratio 1.40, 95% CI: 1.26-1.56). Older and female cases were more likely to experience periodontal disease. Lifestyle factors (smoking) and comorbidities (cardiovascular, cancer or respiratory disease) were associated with periodontal disease among people with a history of psychosis. The findings suggest that periodontal disease is more common in people with a history of psychosis, compared to the general population. Prevention and early diagnosis of periodontal disease should be a priority for oral health promotion programmes, which should also address modifiable risk factors like smoking which also contribute to co-morbid systemic disease.

Income-related inequalities in the association of smoking with periodontitis: a cross-sectional analysis in Tokyo Metropolitan Districts.

Socio-economic status (SES) and smoking are risk factors for periodontitis; however, their interaction has not been determined. We investigated the effect of modification of SES and smoking with periodontal conditions. Data on the social background, smoking status, and dental examination of 1033 individuals residing in the Tokyo Metropolitan District were analyzed. The outcomes were the number of remaining teeth and the proportion of teeth with probing pocket depth (PPD) ≥ 4mm and ≥ 6mm. Multilevel linear and Poisson regression analyses were performed after adjusting for possible confounding factors, including SES, assessed by the average income of the residential area. The mean number of remaining teeth was 24.6 ± 4.8, and the proportion of teeth with PPD ≥ 4mm and ≥ 6mm was 31.2 ± 28.5% and 12.2 ± 18.1%, respectively. After adjusting for confounding factors, the lowest-income population had significantly lesser teeth (coefficient: - 0.46, 95% CI - 0.89, 0.02, p = 0.039) and a higher proportion of teeth with PPD ≥ 4mm than the highest-income population (ratio of means: 1.22, 95% CI 1.03-1.44, p = 0.013). Significant interactions were observed; income inequalities in periodontitis were significant only among current smokers. Inequality in socio-economic status is associated with oral health inequalities. The adverse effects of smoking on periodontitis might be greater in the low-income population. The low-income population, especially current smokers, had significantly more compromised oral health than the high-income population. In addition to the emphasis on smoking cessation, the promotion of universal health coverage for dental care is necessary to reduce oral health inequalities.

Effect Of Dental Proximal Restorations On Periodontal Health In Patients.

The oral cavity is colonized by more than 700 species of bacteria and hundreds of those can be present within oral biofilms. Objective was to determine the frequency of periodontal attachment loss in patients with dental proximal restorations. This cross-sectional study included 100 patients with Class II (mesial /distal or mesio-occluso-distal composite and amalgam restorations. The minimum duration of pre-existing restoration for which periodontal attachment loss was assessed was more than 3 months. Patients wearing orthodontic appliances, pregnant women, patients having systemic health problems with well-established links to periodontal diseases such as diabetes mellitus and patients who had received periodontal treatment within the last 3 months were excluded. Periodontal Pocket depth and bleeding on probing was recorded using WHO periodontal probe. Pocket depth greater than 3 mm was considered pathologic. The data were analyzed using the SPSS, version 20. Descriptive statistics were computed. Chi square test was applied to compare the effects of duration of restoration and type of teeth on periodontal attachment loss. Of total 100 participants 65 (65%) were males and 35 (35%) were females. The mean age was 30.74±9.21 years. In 14% cases having class II or Mesio occluso distal restorations normal pocket depth was recorded while 86% had pathologic pockets. Teeth where proximal restorations were present for more than one year were most commonly associated (29%) with pathologic pockets followed by proximal restorations which were present for three months (25%). As the duration of proximal restoration increased, the frequency of periodontal pathologic pockets increased (p<0.001). The prevalence of periodontal pocket was more in molars than premolars (p<0.001). Proximal restoration can be a significant risk factor for periodontal disease. Strict oral hygiene, proper design of restoration margin and supportive periodontal therapy is the utmost responsibility of the clinician.

Effects of nicotine and lipopolysaccharide stimulation on adhesion molecules in human gingival endothelial cells.

Smoking is a risk factor for periodontitis, and the immune response of periodontal tissues in patients with periodontitis may be strongly affected by smoking. The purpose of this study was to elucidate the bioactivity and signal transduction of human gingival endothelial cells (HGECs) due to nicotinic stimulation using a cultured medium supplemented with lipopolysaccharide (LPS) as a model of periodontitis. HGECs were cultured in medium supplemented with LPS, nicotine, nicotine + LPS, and medium supplemented without nicotine or LPS (control). Cell proliferation was assessed using Alamar blue. Cytotoxicity was assessed by lactate dehydrogenase leakage. The expression of adhesion molecule-1 (ICAM-1, VCAM-1) was assessed by reverse transcription quantitative polymerase chain reaction (RT-qPCR) and enzyme-linked immunosorbent assay. The expression of nicotinic acetylcholine receptor (nAChR) subunits (α3, α5, α7, β2 and β4) was evaluated by RT-PCR. The involvement of p38 mitogen-activated protein kinase (p38MAPK) and protein kinase C (PKC) cell signaling pathways in ICAM-1 and VCAM-1 expression was investigated by RT-qPCR with specific inhibitors. HGECs stimulated with LPS, nicotine and nicotine + LPS showed inhibition of cell proliferation, increase of cell death, and increase of gene and protein expression of ICAM-1. Moreover, HGECs showed the presence of α5 and α7 nAChR subunits. The expression of ICAM-1 in HGECs stimulated with LPS, nicotine, and nicotine + LPS was significantly suppressed by p38MAPK inhibitor, but not by a PKC inhibitor. The nAChR subunits of HGECs are α5 and α7, and that HGECs stimulated with nicotine and LPS express ICAM-1 via p38MAPK pathway.

Periodontal Disease in the Brazilian Population: A Retrospective Analysis on the 2013 National Health Survey to Identifying Risk Profiles.

Periodontal disease (PD) is a global public health problem with prevalence varying according to social and economic contexts; however, few studies have investigated the distribution of PD worldwide. PD is the host response to an infection or progression of a clinical condition, and the identification of modifiable risk factors for adequate clinical management of patients should be a priority in health policies directed to vulnerable population groups. In this context, we investigated the characteristics and risk factors for PD using the Brazilian National Health Survey 2013 (PNS-2013). A cluster analysis using the interdependence technique was applied to explore data on the risk of periodontitis. The presence or absence of a risk factor was analyzed using five variables (ten categories), while ordinal regression assessed risk profiles based on sociodemographic aspects of the Brazilian population. Individuals were classified as low (26.33%), medium (23.34%), or high risk (50.32%) for PD. Age, educational level, ethnicity, and Brazilian regions (except the North region) were significantly associated with risk for PD in the adjusted final regression model. Individual and social contexts were factors related to the high risk of PD in the Brazilian population. Our results highlight the need for public policies on healthy habits to prevent systemic diseases affecting oral health.

Is Obesity a Risk Factor for Periodontal Disease in Adults? A Systematic Review.

There is inconclusive evidence about the link between the severity and prevalence of periodontitis in obese adults. Therefore, this systematic review aims to explore the possibility of significant evidence on the association between obesity and periodontitis and to determine the necessity to consider obesity as a risk factor for periodontitis. We followed the PRISMA protocol, and studies that met the eligibility criteria were included in this review. The risk of bias in individual studies was also evaluated. This review included 15 observational studies (9 cross-sectional studies, 2 case-control, and 4 cohort studies). The total study subjects from these studies were 6603 (males = 3432; females = 3171). Most studies showed a significant association between obesity and periodontitis. Among these studies, a few showed obese females to be at a higher risk, and one study found no association between obesity and periodontal disease at all. Based on the evidence obtained from this review, the body mass index (BMI) should be routinely assessed in patients to assess the risk for periodontal disease and to offer personalized management of periodontitis. Based on the findings of this review, we recommend the need to initiate awareness among clinicians and implement dental hygiene care prevention measures for obese patients.

Illegal drugs and periodontal conditions.

In recent years, the practice of dentistry and periodontology has become complicated by several risk factors, including the treatment of an increasing number of patients with substance use disorder. This review presents an update in the current literature of the impact of illegal drug use on periodontal conditions and their possible effect as risk factors or indicators. The main illegal drugs that may have an impact on periodontal health and conditions are described, including their effect, medical manifestations, risks, and the overall effect on oral health and on the periodontium. Where available, data from epidemiologic studies are analyzed and summarized. The clinical management of periodontal patients using illegal drugs is reported in a comprehensive approach inclusive of the detection of illicit drug users, screening, interviewing and counseling, the referral to treatment, and the dental and periodontal management. With regard to the impact of illegal substance use on periodontal conditions, there is moderate evidence that regular long-term use of cannabis is a risk factor for periodontal disease, manifesting as a loss of periodontal attachment, deep pockets, recessions, and gingival enlargements. Limited evidence also shows that the use of cocaine can cause a series of gingival conditions that mostly presents as chemical induced-traumatic lesions (application of cocaine on the gingiva) or necrotizing ulcerative lesions. There is a scarcity of data regarding the impact of other drug use on periodontal health. There is evidence to suggest that regular long-term use of cannabis is a risk factor for periodontal disease and that the use of cocaine can cause a series of periodontal conditions. The dental treatment of subjects that use illegal substances is becoming more common in the daily clinical practice of periodontists and other dental clinicians. When the clinicians encounter such patients, it is essential to manage their addiction properly taking into consideration the impact of it on comprehensive dental treatment. Further studies and clinical observations are required to obtain sound and definitive information.

Cellular Senescence and Periodontitis: Mechanisms and Therapeutics.

Simple SummaryOral health is increasingly recognized as an important part of overall health. Tooth loss is a contributor to overall musculoskeletal frailty and is closely associated with increased morbidity in the elderly population. Limited intervention exists to alleviate tooth loss associated with periodontitis, other than antibiotics. Mounting evidence suggests that targeting cellular senescence could slow down the fundamental aging process, and thus alleviate a wide range of age-related tissue dysfunctions, likely including tooth loss. Therefore, we feel it might be valuable to review the current understanding of the role and potential mechanisms of senescent cells in oral health with aging.Periodontitis is a chronic inflammatory disease which increases in prevalence and severity in the older population. Aging is a leading risk factor for periodontitis, which exacerbates alveolar bone loss and results in tooth loss in the elderly. However, the mechanism by which aging affects periodontitis is not well understood. There is considerable evidence to suggest that targeting cellular senescence could slow down the fundamental aging process, and thus alleviate a series of age-related pathological conditions, likely including alveolar bone loss. Recently, it has been discovered that the senescent cells accumulate in the alveolar bone and promote a senescence-associated secretory phenotype (SASP). Senescent cells interacting with bacteria, together with secreted SASP components altering the local microenvironment and inducing paracrine effects in neighboring cells, exacerbate the chronic inflammation in periodontal tissue and lead to more alveolar bone loss. This review will probe into mechanisms underlying excessive alveolar bone loss in periodontitis with aging and discuss potential therapeutics for the treatment of alveolar bone loss targeting cellular senescence and the SASP. Inspecting the relationship between cellular senescence and periodontitis will lead to new avenues of research in this field and contribute to developing potential translatable clinical interventions to mitigate or even reverse the harmful effects of aging on oral health.

Identification of Key Genes and Pathways Associated with Oxidative Stress in Periodontitis.

Methods The differentially expressed genes (DEGs) were identified using periodontitis-related microarray from the GEO database, and OS-genes were extracted from GeneCards database. The intersection of the OS-genes and the DEGs was considered as oxidative stress-related DEGs (OS-DEGs) in periodontitis. The Pearson correlation and protein-protein interaction analyses were used to screen key OS-genes. Gene set enrichment, functional enrichment, and pathway enrichment analyses were performed in OS-genes. Based on key OS-genes, a risk score model was constructed through logistic regression, receiver operating characteristic curve, and stratified analyses. Results In total, 74 OS-DEGs were found in periodontitis, including 65 upregulated genes and 9 downregulated genes. Six of them were identified as key OS-genes (CXCR4, SELL, FCGR3B, FCGR2B, PECAM1, and ITGAL) in periodontitis. All the key OS-genes were significantly upregulated and associated with the increased risk of periodontitis. Functional enrichment analysis showed that these genes were mainly associated with leukocyte cell-cell adhesion, phagocytosis, and cellular extravasation. Pathway analysis revealed that these genes were involved in several signaling pathways, such as leukocyte transendothelial migration and osteoclast differentiation. Conclusion In this study, we screened six key OS-genes that were screened as risk factors of periodontitis. We also identified multiple signaling pathways that might play crucial roles in regulating oxidative stress damage in periodontitis. In the future, more experiments need to be carried out to validate our current findings.

Association between Handgrip Strength and Periodontitis in Korean Adults Aged ≥30 Years: Data from the Korea National Health and Nutrition Examination Survey (2014-2015).

This study used data from the Korea National Health and Nutrition Examination Survey 2014–2015 database to analyze the association between periodontitis and handgrip strength, a representative measure of hand impairment and function, in adults aged ≥30 years. The data of 5926 adults (male: 2766, females: 3160) who underwent handgrip strength and periodontal tissue examination and had neither rheumatoid arthritis nor osteoarthritis were analyzed. Handgrip strength was assessed using a digital grip strength dynamometer. The average values of the right handgrip strength, calculated separately by sex and age group (five 10-year age groups), were used as the cut-off for reduced handgrip strength. Periodontal status was evaluated using the Community Periodontal Index, defining scores ≥ 3 as periodontitis. Chi-square test and multivariate logistic regression analyses were performed to compare the differences in the prevalence of periodontitis according to handgrip strength. In the final regression model adjusted for risk factors for periodontitis, the likelihood of periodontitis decreased as the level of handgrip strength increased (p < 0.05). Therefore, this study suggests that handgrip strength may be a valuable indicator of periodontal health.

Dental and Periodontal Health in Acute Intermittent Porphyria.

In the inherited metabolic disorder acute intermittent porphyria (AIP), high sugar intake prevents porphyric attacks due to the glucose effect and the following high insulin levels that may lower AIP disease activity. Insulin resistance is a known risk factor for periodontitis and sugar changes diabetogenic hormones and affects dental health. We hypothesized differences in homeostasis model assessment (HOMA) scores for insulin resistance in AIP cases vs. controls and in those with periodontitis. Our aim was to systematically study dental health in AIP as poor dental health was previously only described in case reports. Further, we aimed to examine if poor dental health and kidney failure might worsen AIP as chronic inflammation and kidney failure might increase disease activity. In 47 AIP cases and 47 matched controls, X-rays and physical examination of clinical attachment loss (CAL), probing pocket depth (PPD), and decayed missing filled teeth (DMFT) were performed. Dietary intake was evaluated through a diet logbook. Plasma cytokines and diabetogenic hormones were measured using multiplex technology and urine porphobilinogen and kidney and liver function by routine methods. An excel spreadsheet from the University of Oxford was used to estimate HOMA scores; beta cell function, HOMA%B (%B), insulin sensitivity, HOMA%S (%S), and insulin resistance HOMA-IR (IR), based on glucose and plasma (P) C-peptide. The Wilcoxon matched-pairs signed rank test, the Mann–Whitney U-test, and Spearman’s non-parametric correlation were used. Insulin (p = 0.007) and C-peptide (p = 0.006) were higher in the AIP cases with periodontitis versus those without. In AIP patients, the liver fibrosis index 4 correlated with DMFT (p < 0.001) and CAL ≥4 mm (p = 0.006); the estimated glomerular filtration rate correlated with DMFT (p < 0.001) and CAL ≥4 mm (p = 0.02). CAL ≥4 mm was correlated with chemokine ligand 11 and interleukin (IL)-13 (p = 0.04 for both), and PPD >5 mm was correlated with plasminogen activator inhibitor-1 (p = 0.003) and complement component 3 (p = 0.02). In conclusion, dental health in AIP cases was correlated with insulin resistance, inflammatory markers, and biomarkers of kidney and liver function, demonstrating that organ damage in the kidney and liver are associated with poorer dental health.

RESPONSE OF THE PERIODONTAL TISSUES TO β-ADRENERGIC STIMULATION

Objectives Stress is a risk factor for periodontitis, and β-adrenergic receptor (βAR) stimulation increases angiogenesis on long bones. Enhanced periodontal vascularization could act as a potential host susceptibility factor. The aim was to investigate the mandibular angiogenic response to βAR stimulation. Study Design Twenty C57BL6 female mice received daily intraperitoneal injections of isoproterenol (ISO) or phosphate-buffered saline (PBS) for 6 weeks. Hemimandibles and tibias were collected for immunolocalization of endomucin, tyrosine hydroxylase, neuropeptide Y, and norepinephrine transporter (NET). Vascular Endothelial Growth Factor A, IL-1β, IL-6, Adrb2, and Rankl mRNA expression were assessed 2 hours after PBS or ISO treatment. Results Despite similar sympathetic innervation and Adrb2 expression in mandibular tissues and tibias, ISO treatment did not increase endomucin+ vessel area or the total number of endomucin+ vessels in the mandible. Moreover, the expression of VEGFa, IL-6, IL-1β, and Rankl in the molar region did not change following ISO administration. We also detected high expression of NET by immunofluorescence in mandibular alveolar osteoblasts, osteocytes, and periodontal ligament fibroblasts, which was confirmed by quantitative polymerase chain reaction, compared to the tibia from the same animals. Conclusions Stress and sympathetic nervous system activation increase the risk of periodontitis via mechanisms other than change in microvascular density and possibly requiring inflammatory cells. Stress is a risk factor for periodontitis, and β-adrenergic receptor (βAR) stimulation increases angiogenesis on long bones. Enhanced periodontal vascularization could act as a potential host susceptibility factor. The aim was to investigate the mandibular angiogenic response to βAR stimulation. Twenty C57BL6 female mice received daily intraperitoneal injections of isoproterenol (ISO) or phosphate-buffered saline (PBS) for 6 weeks. Hemimandibles and tibias were collected for immunolocalization of endomucin, tyrosine hydroxylase, neuropeptide Y, and norepinephrine transporter (NET). Vascular Endothelial Growth Factor A, IL-1β, IL-6, Adrb2, and Rankl mRNA expression were assessed 2 hours after PBS or ISO treatment. Despite similar sympathetic innervation and Adrb2 expression in mandibular tissues and tibias, ISO treatment did not increase endomucin+ vessel area or the total number of endomucin+ vessels in the mandible. Moreover, the expression of VEGFa, IL-6, IL-1β, and Rankl in the molar region did not change following ISO administration. We also detected high expression of NET by immunofluorescence in mandibular alveolar osteoblasts, osteocytes, and periodontal ligament fibroblasts, which was confirmed by quantitative polymerase chain reaction, compared to the tibia from the same animals. Stress and sympathetic nervous system activation increase the risk of periodontitis via mechanisms other than change in microvascular density and possibly requiring inflammatory cells.

Mental health and periodontal and peri-implant diseases.

Mental health disorders, particularly depression and anxiety, affect a significant number of the global population. Several pathophysiological pathways for these disorders have been identified, including the hypothalamic-pituitary-adrenal axis, autonomic nervous system, and the immune system. In addition, life events, environmental factors, and lifestyle affect the onset, progression, and recurrence of mental health disorders. These may all overlap with periodontal and/or peri-implant disease. Mental health disorders are associated with more severe periodontal disease and, in some cases, poorer healing outcomes to nonsurgical periodontal therapy. They can result in behavior modification, such as poor oral hygiene practices, tobacco smoking, and alcohol abuse, which are also risk factors for periodontal disease and, therefore, may have a contributory effect. Stress has immunomodulatory effects regulating immune cell numbers and function, as well as proinflammatory cytokine production. Stress markers such as cortisol and catecholamines may modulate periodontal bacterial growth and the expression of virulence factors. Stress and some mental health disorders are accompanied by a low-grade chronic inflammation that may be involved in their relationship with periodontal disease and vice versa. Although the gut microbiome interacting with the central nervous system (gut-brain axis) is thought to play a significant role in mental illness, less is understood about the role of the oral microbiome. The evidence for mental health disorders on implant outcomes is lacking, but may mainly be through behaviourial changes. Through lack of compliance withoral hygiene and maintenance visits, peri-implant health can be affected. Increased smoking and risk of periodontal disease may also affect implant outcomes. Selective serotonin reuptake inhibitors have been linked with higher implant failure. They have an anabolic effect on bone, reducing turnover, which could account for the increased loss.