Stress In Periodontal Diseases Research Articles

Role of Oxidative Stress in Periodontal Diseases.

Periodontal disease, a significant worldwide health burden, is characterized by chronic inflammation and destruction of periodontal tissues, including the cementum, periodontal ligament(PDL), alveolar bone, and gingival tissue. Recent research has linked the development and progression of periodontal disease to oxidative stress. This study provides comprehensive explanations of the mechanisms behind oxidative stress in periodontal disease, with a focus on the generation of reactive oxygen species (ROS) and their effects on periodontal tissues. Oxidative stress triggers a number of detrimental reactions, including lipid peroxidation, protein oxidation, and damage to deoxyribonucleic acid (DNA). Alveolar bone resorption, connective tissue degradation, and periodontal inflammation are further conditions exacerbated by these processes. In addition, the delicate balance between antioxidants and oxidants is upset by oxidative stress, which impairs antioxidant defense systems and exacerbates periodontal tissue damage. This review highlights the negative effects of oxidative stress and enhancesperiodontal health outcomes.

Role of oxidative stress in the relationship between periodontitis and systemic diseases.

Periodontitis is a common inflammatory disease. It is characterized by destruction of the supporting structures of the teeth and could lead to tooth loss and systemic inflammation. Bacteria in inflamed gingival tissue and virulence factors are capable of entering the bloodstream to induce systemic inflammatory response, thus influencing the pathological process of many diseases, such as cardiovascular diseases, diabetes, chronic kidney disease, as well as liver injury. An increasing body of evidence show the complex interplay between oxidative stress and inflammation in disease pathogenesis. When periodontitis occurs, increased reactive oxygen species accumulation leads to oxidative stress. Oxidative stress contributes to major cellular components damage, including DNA, proteins, and lipids. In this article, the focus will be on oxidative stress in periodontal disease, the relationship between periodontitis and systemic inflammation, and the impact of periodontal therapy on oxidative stress parameters.

Assessment of the Salivary Level of Malondialdehyde in Localized Periodontitis Versus Generalized Periodontitis: An Analytical Cross-Sectional Study

Introduction: We aimed to compare the salivary level of malondialdehyde (MDA) in localized periodontitis versus generalized periodontitis. Methods: Nineteen healthy participants, 35 cases of generalized periodontitis, and 36 cases of localized periodontitis included in the study. The enzyme-linked immunosorbent (ELISA) assay was used to blindly quantify the amounts of MDA in saliva. Data analyzed using one-way ANOVA and Tukey’s post hoc test via R software. Results: Ninety subjects completed the study. There was a statistically significant difference among study groups (P < 0.001). The Tukey’s post hoc test showed a statistically significant difference for all pairwise compressions (P < 0.001) Conclusion: The salivary levels of MDA increase in periodontitis patients. Within limitations of this cross-sectional study, it could be concluded that salivary MDA levels may possibly be a potential biomarker to examine oxidative stress in periodontal disease.

Role of stress in periodontal disease in a population of Al-Qassim region, Saudi Arabia

Introduction: Periodontitis is a plaque-induced inflammatory disease affecting the alveolar bone in the jaw and supporting soft tissues, it is a multifactorial disease, initiated by bacteria but modulated by several other factors, including stress. Stress is an equated response to constant adverse stimuli. Aim: The purpose of the present clinical study was to identify a possible relationship between life stress and periodontal condition. Materials and Methods: Sixty patients were given a predesigned questionnaire (Perceived Stress Scale) to measure their stress levels, and clinical examination was carried out using Community Periodontal Index for periodontal status. Results and Discussion: High stress was observed among males, obese, married individuals, people engaged in fieldwork, individuals having monthly work time >40 h, daily sleep <8 h, smokers, participants with irregular brushing habits, and participants who did not undergo regular dental checkups. The present study showed a statistically significant relationship between the regular dental checkup and Russell's periodontal index. Conclusion: Stress is a prominent factor that deteriorates periodontal conditions among normal healthy individuals. The several factors leading to a stressful condition include regular lifestyle practices such as altered sleep hours, working conditions, and social and economic status. Thus, it is important to recognize the plausible relationship of stress and periodontal diseases. Hence, stress should be identified in patients and considered an important component during treatment planning.

The Influence of Diet on Oxidative Stress and Inflammation Induced by Bacterial Biofilms in the Human Oral Cavity.

The article is a concise compendium of knowledge on the etiology of pathogenic microorganisms of all complexes causing oral diseases. The influence of particular components of the diet and the role of oxidative stress in periodontal diseases were described. The study investigated the bacteriostatic effect of the diet of adults in in vivo and in vitro tests on the formation of bacterial biofilms living in the subgingival plaque, causing diseases called periodontitis. If left untreated, periodontitis can damage the gums and alveolar bones. Anaerobic bacteria, called periopathogens or periodontopathogens, play a key role in the etiopathogenesis of periodontitis. The most important periopathogens of the oral microbiota are bacteria of all complexes, including the red complex. The obtained results suggest the possibility of using a specific diet in the prevention and treatment of periodontal diseases-already treated as a disease of civilization. The quoted article is an innovative compilation of knowledge on this subject and it can be a valuable source of knowledge for professional hygienists, dentists, peridontologists, dentistry students and anyone who cares about proper oral hygiene. The obtained results suggest the possibility of using this type of diet in the prophylaxis of the oral cavity in order to avoid periodontitis.

Salivary antioxidant enzymes and lipid peroxidation product malondialdehyde and sialic acid levels among smokers and non-smokers with chronic periodontitis-A clinico-biochemical study.

Background:Pathogenesis of most of the inflammatory process are associated with reactive oxygen species (ROS), derived from various metabolic sources and which may lead to direct or indirect tissue damage due to oxidative stress, resulting in periodontal diseases. Usually antioxidant systems are capable of removing free radicals, thereby preventing tissue damage from free radical. ROS can result in tissue damage, involving lipid peroxidation. The aim of this study was to evaluate and compare the levels of superoxide dismutase (SOD), glutathione peroxidase (GPx), malondialdehyde (MDA), and sialic acid (SA) in periodontally healthy and chronic periodontitis among nonsmokers and smokers and to determine their value as diagnostic markers for chronic periodontitis.Materials and Methods:A total of 90 male patients aged 20--60 years were recruited and grouped as Group 1: 30 Healthy nonsmokers, who had never smoked. Group 2: 30 nonsmokers with chronic periodontitis. Group 3: 30 smokers with chronic periodontitis. Unstimulated saliva was collected for at least 5 min and clinical measurements; SOD, GPx, MDA and SA were assessed using a spectrophotometric method.Results:Data showed a significant correlation between salivary SOD, GPx, MDA, and SA in group 1, group 2, and group 3. SOD and GPx were found to be lower and MDA and SA levels were found to be higher among smokers with chronic periodontitis.Conclusion:Reduced levels of antioxidant enzymes SOD and GPx and elevated levels of lipid peroxidation product MDA as well as increased levels of SA could be used as diagnostic markers to measure oxidative stress in periodontal disease associated with risk factor such as smoking.

8-Isoprostane in chronic periodontitis and type II diabetes: Exploring the link.

Background. Reactive oxygen species (ROS) are associated with the pathogenesis of inflammatory diseases and have a direct or indirect role in tissue damage constituting oxidative stress. ROS are also involved in impairment of β-cell function during development of diabetes, which leads to genetic ablation of KATP channels, triggering up-regulation of antioxidant enzymes. Several markers of lipid peroxidation, protein oxidation and DNA damage induced by ROS can be measured. Over the last decade, isoprostanes have been considered as the best markers of lipid peroxidation. The aim of this study was to determine the presence of 8-isoprostane in healthy, chronic periodontitis and chronic periodontitis subjects with type II diabetes and to find the correlation between 8-isoprostane levels among groups and with clinical parameters like gingival index, probing depth and clinical attachment levels. Methods. Ninety subjects were selected and divided into 3 groups: healthy, chronic periodontitis and chronic periodontitis subjects with type II diabetes (n=30 each). Saliva was collected from these subjects after obtaining consent and analyzed for 8-isoprostane levels using ELISA kit. Statistical analysis was performed using Kruskal-Wallis test, Mann-Whitney U test and Spearman’s correlation coefficient (P<0.001). Results. Statistically significant difference was found in the levels of 8-isoprostane between healthy, chronic periodontitis and chronic periodontitis subjects with type II diabetes and with all clinical parameters. Conclusion. 8-isoprostane can be considered as a pathophysiological marker to measure oxidative stress in periodontal diseases.

Oxidative Stress and Antioxidant System in Periodontitis.

Periodontitis is a common inflammatory disease, which is initiated by bacterial infection and subsequently progressed by aberrant host response. It can result in the destruction of teeth supporting tissues and have an influence on systemic health. When periodontitis occurs, reactive oxygen species, which are overproduced mostly by hyperactive neutrophils, could not be balanced by antioxidant defense system and cause tissues damage. This is characterized by increased metabolites of lipid peroxidation, DNA damage and protein damage. Local and systemic activities of antioxidants can also be influenced by periodontitis. Total antioxidant capacity, total oxidant status and oxidative stress index have been used to evaluate the oxidative stress associated with periodontitis. Studies have confirmed that inflammatory response in periodontitis is associated with an increased local and systemic oxidative stress and compromised antioxidant capacity. Our review focuses on increased oxidative stress in periodontal disease, specifically, on the relationship between the local and systemic biomarkers of oxidative stress and periodontitis and their association with the pathogenesis of periodontitis. Also, the relationship between periodontitis and systemic inflammation, and the effects of periodontal therapy on oxidative stress parameters will be discussed.

Malondialdehyde, superoxide dismutase and melatonin levels in gingival crevicular fluid of aggressive and chronic periodontitis patients.

The aim of this study was to investigate malondialdehyde (MDA), superoxide dismutase (SOD) and melatonin levels in the gingival crevicular fluid (GCF) of patients with chronic periodontitis (CP) and generalized aggressive periodontitis (GAgP) as biomarkers for oxidative stress. The study comprised 65 subjects: 15 healthy individuals, 25 CP patients and 25 GAgP patients. Plaque index, gingival index, pocket depth, clinical attachment level measurements and GCF samples were obtained from all subjects. MDA, SOD and melatonin levels were determined utilizing enzyme-linked immunosorbent assay. GCF-MDA levels were significantly higher in the GAgP group compared to the CP and control groups (p < 0.001) and significantly higher in the CP group than the C group (p < 0.001). SOD and melatonin GCF levels were significantly higher in the control than the GAgP and CP groups (p < 0.05), and significantly lower in the GAgP than the CP group (p < 0.05). The CP group demonstrated a significant negative correlation between GCF-MDA and melatonin concentrations. A positive correlation was observed between SOD and CAL in the CP group and PD in the GAgP group. MDA, melatonin and SOD could be considered as biomarkers for oxidative stress in periodontal diseases and might be useful diagnostic aids in distinguishing CP and GAgP patients.

The role of oxidative stress in the interaction of periodontal disease with systemic diseases or conditions

Periodontal diseases are among the most common chronic infectious and inflammatory diseases in the world. Bacteria in the dental biofilm trigger host response and the activated inflammatory system plays a major role in periodontal tissue destruction. Alterations in the oxidative stress-mediated inflammatory pathways could be one of the possible potential mechanisms in periodontal tissue breakdown. Local or systemic infectious diseases, inflammatory diseases, such as periodontitis, obesity, type II diabetes, vascular diseases and other inflammatory conditions are associated with an increased risk of oxidative stress. A linear relationship between oxidative stress, periodontal disease and systemic disease is likely to exist. The available literature clearly highlights the increased oxidative stress in periodontal disease that is associated with different systemic diseases and/or conditions. Further studies are needed to elucidate the role of oxidative balance in periodontal diseases and systemic disease interactions.

Detection of Oxidative Stress in Periodontal Disease and Oral Cancer

Introduction Oxidative stress is the systemic disturbance caused by the increased Reactive oxygen species a biological system's ability to readily detoxify the reactive intermediates or to repair the resulting damage. Disturbances in the normal redox state of cells can cause toxic effects

Gingival fibroblasts resist apoptosis in response to oxidative stress in a model of periodontal diseases.

Periodontal diseases are classified as inflammation affecting the supporting tissue of teeth, which eventually leads to tooth loss. Mild reversible gingivitis and severe irreversible periodontitis are the most common periodontal diseases. Periodontal pathogens initiate the diseases. The bacterial toxin, lipopolysaccharide (LPS), triggers the inflammatory response and leads to oxidative stress. However, the progress of oxidative stress in periodontal diseases is unknown. The purpose of this study is to examine oxidative stress and cell damage in gingivitis and periodontitis. Our results showed that LPS increases reactive oxygen species (ROS) accumulation in gingival fibroblast (GF). However, oxidative stress resulting from excessive ROS did not influence DNA damage and cell apoptosis within 24 h. The mechanism may be related to the increased expression of DNA repair genes, Ogg1, Neil1 and Rad50. Detection of apoptosis-related proteins also showed anti-apoptotic effects and pro-apoptotic effects were balanced. The earliest damage appeared in DNA when increased γH2AX, an early biomarker for DNA damage, was detected in the LPS group after 48 h. Later, when recurrent inflammation persisted, 8-OHdG, a biomarker for oxidative stress was much higher in periodontitis model compared to the control in vivo. Staining of 8-OHdG in human periodontitis specimens confirmed the results. Furthermore, TUNEL staining of apoptotic cells indicated that the periodontitis model induced more cell apoptosis in gingival tissue. This suggested GF could resist early and acute inflammation (gingivitis), which was regarded as reversible, but recurrent and chronic inflammation (periodontitis) led to permanent cell damage and death.

PTU-247 Does enhanced recovery after colorectal surgery increase the incidence of parastomal hernias?

<h3>Introduction</h3> Evidence supporting the benefits of enhanced recovery after surgery (ERAS) protocols is abundant; however there is no published data on how ERAS may affect the incidence of parastomal hernias. <h3>Method</h3> Retrospective, observational, single centre cohort study of patients who underwent elective or emergency operations with stoma formation from January 2006 until March 2013. The cohort was split into ERAS and traditional recovery, and a review of case-notes and stoma nurse records allowed identification of those who developed parastomal hernias at any time point post-operatively. <h3>Results</h3> 208 patients were included; 95 underwent a traditional recovery, and 113 underwent ERAS. The demographics of these 2 groups were comparable. 14.74% non-ERAS patients (n = 14) developed parastomal hernias compared to 34.51% (n = 39) in the Enhanced Recovery group (p = 0.0011). <h3>Conclusion</h3> This study demonstrated a significantly increased incidence of parastomal hernias in those undergoing enhanced recovery, consistent with the earlier postoperative mobilisation. While the other benefits of ERAS outweigh this risk, this reality of modern post-operative care should reinvigorate the use of scrupulous surgical technique, and consideration of stoma site reinforcement options. <h3>Disclosure of interest</h3> None Declared. <h3>References</h3> Gravante G, Elmussareh M. Enhanced recovery for colorectal surgery: practical hints, results and future challenges. World J Gastrointest Surg. 2012;4(8):190–8 Chestovich PJ, Lin AY, Yoo J. Fast-track pathways in colorectal surgery. Surg Clin North Am. 2013;93(1):21–32 Lv L, Shao YF, Zhou YB. The enhanced recovery after surgery (ERAS) pathway for patients undergoing colorectal surgery: an update of meta-analysis of randomized controlled trials. Int J Colorectal Dis. 2012;27(12):1549–54 Abraham N, Albayati S. Enhanced recovery after surgery programs hastens recovery after colorectal resections. World J Gastrointest Surg. 2011;3(1):1–6 Godbout JP. Glaser R. Review Stress-induced immune dysregulation: implications for wound healing, infectious disease and cancer. J Neuroimmune Pharmacol. 2006;1(4):421–7 Boyapati L, Wang H. Review the role of stress in periodontal disease and wound healing. Periodontol 2000. 2007;44:195–210 Hotouras A, Murphy J, Thaha M, Chan CL. The persistent challenge of parastomal herniation: a review of the literature and future developments. Colorectal Dis 2013;15(5):e202–14 Sohn YJ, Moon SM, Shin US, Jee SH. Incidence and risk factors of parastomal hernia. J Korean Soc Coloproctol 2012;28(5):241–6

Mass spectrometry-based metabolomic profiling identifies alterations in salivary redox status and fatty acid metabolism in response to inflammation and oxidative stress in periodontal disease

Periodontal diseases represent the most common chronic inflammatory diseases in humans and a major cause of tooth loss. Combining mass spectrometry-based ionomics and targeted lipidomics on fatty acid metabolites, we identified significant alterations in redox status and fatty acid metabolism in saliva in response to chronic inflammation and oxidative stress in periodontal disease in a cohort of nonsmoker subjects with chronic periodontitis. For the first time, ionomic profiling of around 30 ions in saliva revealed significantly decreased levels of redox-active metal ions including Mn, Cu, and Zn in the periodontal group, which is consistent with decreased levels of superoxide dismutases in saliva and serum. A targeted lipidomic approach was employed to monitor the major metabolites of arachidonic acid and linoleic acid in saliva. We observed increased levels of cyclooxygenase products including PGE2, PGD2, and PGF2α and TXB2, but decreased level of PGI2 in the periodontal group. A unique pattern of the lipoxygenase products of arachidonic acid and linoleic acid was observed with increased level of 5-HETE but decreased levels of 13-HODE and 9-HODE. Levels of salivary F2-isoprostanes, free radical lipid peroxidation products, and a gold standard for oxidative stress in vivo were also significantly elevated. Taking these data together, our study using multiple powerful omics techniques demonstrates that local redox alteration contributes significantly to periodontitis through the modulation of fatty acid metabolism in response to inflammation and oxidative stress. This study highlights the importance of redox status in periodontitis and provides a rationale for preventing periodontal disease by dietary interventions aiming to restore redox balance.

Effect of nonsurgical periodontal therapy on crevicular fluid and serum glutathione peroxidase levels.

Background: Plasma glutathione peroxidase (eGPx) is an important selenium containing antioxidant in human defense against oxidative stress. While crevicular fluid (GCF) eGPx levels and its association with periodontal disease is well documented, there is no data on correlation of GCF and serum eGPx levels in chronic periodontitis. Hence this study was undertaken to further probe into the role of oxidative stress in periodontal diseases and effect of nonsurgical periodontal therapy (NSPT) by correlating GCF and serum levels of eGPx. Materials and methods: Thirty subjects (16-Males and 14-Females; age: 30–38 years) participated in the study. The subjects were divided, based on gingival index, probing pocket depth and clinical attachment level into: Healthy (group-1, n=10), Gingivitis (group-2, n=10) and Periodontitis (group-3, n=10). Chronic periodontitis patients after NSPT constituted group 4. GCF and serum samples collected from each subject were quantified for eGPx levels using Enzyme linked Immunosorbent Assay. Results: The mean eGPx concentrations increased from health (14.01 ng/μl and 78.26 ng/ml) to gingivitis (22.86 ng/μl and 90.44 ng/ml) and then to periodontitis (29.89 ng/μl and 103.43 ng/ml), in GCF and serum respectively. After NSPT, there was statistically significant reduction in eGPx concentration in GCF and serum (19.41 ng/μl and 85.21 ng/ml). Further, all the GCF eGPx values showed a positive correlation to that of serum eGPx level. Conclusion: Thus, increased eGPx concentration in GCF can be considered as an indicator of local increase in oxidative stress. While, increase in serum eGPx levels indicates that periodontal disease can also lead to increased oxidative stress at the systemic level.

Effect of Nonsurgical Periodontal Therapy on Crevicular Fluid and Serum Glutathione Peroxidase Levels

Background: Plasma glutathione peroxidase (eGPx) is an important selenium containing antioxidant in human defense against oxidative stress. While crevicular fluid (GCF) eGPx levels and its association with periodontal disease is well documented, there is no data on correlation of GCF and serum eGPx levels in chronic periodontitis. Hence this study was undertaken to further probe into the role of oxidative stress in periodontal diseases and effect of nonsurgical periodontal therapy (NSPT) by correlating GCF and serum levels of eGPx.Materials and methods: Thirty subjects (16-Males and 14-Females; age: 30–38 years) participated in the study. The subjects were divided, based on gingival index, probing pocket depth and clinical attachment level into: Healthy (group-1,n=10), Gingivitis (group-2,n=10) and Periodontitis (group-3,n=10). Chronic periodontitis patients after NSPT constituted group 4. GCF and serum samples collected from each subject were quantified for eGPx levels using Enzyme linked Immunosorbent Assay.Results: The mean eGPx concentrations increased from health (14.01 ng/μl and 78.26 ng/ml) to gingivitis (22.86 ng/μl and 90.44 ng/ml) and then to periodontitis (29.89 ng/μl and 103.43 ng/ml), in GCF and serum respectively. After NSPT, there was statistically significant reduction in eGPx concentration in GCF and serum (19.41 ng/μl and 85.21 ng/ml). Further, all the GCF eGPx values showed a positive correlation to that of serum eGPx level.Conclusion: Thus, increased eGPx concentration in GCF can be considered as an indicator of local increase in oxidative stress. While, increase in serum eGPx levels indicates that periodontal disease can also lead to increased oxidative stress at the systemic level.

Crevicular fluid levels of plasma glutathione peroxidase (eGPx) in periodontal health and disease

Background & objectives Reactive oxygen species (ROS) have been implicated in numerous human diseases, including periodontal diseases. Plasma glutathione peroxidase (eGPx) as an important antioxidant, has a protective role against ROS and is an established marker of oxidative stress. The present study evaluated the levels of eGPx in GCF to further probe into the role of oxidants and antioxidants in periodontal disease. Methods 60 subjects were divided into three groups consisting of 20 subjects in each group based on gingival index, pocket probing depth, clinical attachment loss and radiological parameters (bone loss): healthy (group 1), gingivitis (group 2) and periodontitis (group 3), whilst, group 3 patients after the treatment constituted group 4. GCF samples were collected from all groups to estimate the levels of eGPx using ELISA. Results The mean eGPx concentration in GCF were observed to be the highest in group 3 i.e., 30.89 ± 4.93 ng/μl and lowest in group 1 i.e., 15.32 ± 3.06 ng/μl. The mean eGPx concentration in group 2 (23.77 ± 2.91 ng/μl) and group 4 (18.92 ± 3.53 ng/μl) fell between the highest and the lowest values. Conclusion This suggests that eGPx levels in GCF increase proportionally with the severity of periodontal diseases. eGPx can be considered as a marker of oxidative stress in periodontal diseases. However, controlled, longitudinal studies with larger samples have to be carried out to confirm this possibility.

The NADPH oxidase NOX2 plays a role in periodontal pathologies

Oxidative stress plays an important role in periodontal health and disease. The phagocyte nicotinamide adenine dinucleotide phosphate oxidase NOX2 is most likely one of the key sources of reactive oxygen species (ROS) in periodontal tissues. This review will discuss three clinical aspects of NOX2 function. We will first focus on oral pathology in NOX2 deficiency such as chronic granulomatous disease (CGD). CGD patients are thought to suffer from infections and sterile hyperinflammation in the oral cavity. Indeed, the periodontium appears to be the most common site of infection in CGD patients; however, as periodontitis is also common in the general population, it is not clear to which extent these infections can be attributed to the disease. Secondly, the role of oxidative stress in periodontal disease of diabetic patients will be reviewed. Diabetes is indeed a major risk factor to develop periodontal disease, and increased activity of leukocytes is commonly observed. Enhanced NOX2 activity is likely to be involved in the pathomechanism, but data remains somewhat preliminary. The strongest case for involvement of NOX2 in periodontal diseases is aggressive periodontitis. Increased ROS generation by leukocytes from patients with aggressive periodontitis has clearly been documented. This increased ROS generation is to be caused by two factors: (1) genetically enhanced ROS generation and (2) oral pathogens that enhance NOX function. NOX enzymes in the oral cavity have so far received little attention but are likely to be important players in this setting. New therapies could be derived from these new concepts.

The role of stress in periodontal disease and wound healing

The role of stress in periodontal disease and wound healing

Models to evaluate the role of stress in periodontal disease.

We evaluated the association of stress,distress, and coping behaviors with periodontal disease in 1,426 subjects, aged 25 to 74, in Erie County, NY, Demographic characteristics, medical and dental history, and tobacco and alcohol consumption, as well as clinical assessments of supragingival plaque, subgingival flora, gingival bleeding, calculus, probing depth, clinical attachment level (CAL), and radiographic alveolar bone loss (ABL) were obtained for each subject. Subjects also completed a set of 5 psychosocial instruments that measured life events, daily strains, hassles and uplifts, distress, and coping behaviors. Internal consistencies of all subscales on the instruments were high, with Cronbach's alpha ranging from 0.88 to 0.99. Logistic regression indicated that financial strain was significantly associated with greater attachment and alveolar bone loss (OR 1.70; 95% CI, 1.09-2.65; and 1.68; 95% CI, 1.20-2.37, respectively) after adjusting for age, gender, and smoking. When those with financial strain were stratified with respect to coping behaviors, it was found that those who exhibited high emotion-focused coping (inadequate coping) had and even higher risk of having more severe attachment loss (OR 2.24; 95% CI, 1.15-4.38) and alveolar bone loss (OR 1.91; 95% CI, 1.15-3.17) than those with low levels of financial strain within the same coping group, after adjustment for age, gender, and cigarette smoking. After further adjusting for number of visits to the dentist, those with financial strain who were high emotion-focused copers still had higher levels of periodontal disease based on CAL (OR 2.12; 95% CI, 1.07-4.18). In contrast, subjects with high levels of financial strain who reported high levels of problem-based coping (good coping) had no more periodontal disease than those with low levels of financial strain. Salivary cortisol levels were higher in a test group exhibiting severe periodontitis, a high level of financial strain, and high emotion-focused coping, as compared to a control group consisting of those with little or no periodontal disease, low financial strain, and low levels of emotion-focused coping (11.04 +/-4.4 vs/ 8.6 +/- 4.1 nmol/L salivary cortisol, respectively). These findings suggest that psychosocial measures of stress associated with financial strain are significant risk indicators for periodontal disease in adults. Further prospective studies are needed to help establish the time course of stress, distress, and inadequate coping on the onset and progression of periodontal disease, as well as to evaluate the mechanisms by which stress exerts its effects on periodontal infections.