Salivary levels of antibacterial peptide (LL-37/hCAP-18) and cotinine in patients with chronic periodontitis

Background: The purpose of this study is to examine the relationship between salivary LL‐37 levels and clinical severity in patients with chronic periodontitis (CP). The presence/absence of four periodontopathic bacteria and salivary cotinine levels were also examined to assess the impact of these factors on LL‐37 production. Methods: Unstimulated salivary samples were collected from 69 patients with CP. Salivary concentrations of LL‐37 and cotinine were measured by enzyme‐linked immunosorbent assay. Aggregatibacter actinomycetemcomitans, Porphyromonas gingivalis, Tannerella forsythia, and Treponema denticola in saliva were detected by polymerase chain reaction. Periodontal examination included determination of probing depth (PD), clinical attachment level, bleeding on probing, and plaque control record. Results: Mean salivary LL‐37 concentration was 225.0 ± 227.2 ng/mL, and a high prevalence of periodontopathic bacteria was observed. The stepwise ordinal logistic regression model showed that high salivary LL‐37 levels were significantly associated with the presence of T. denticola and higher percentage of teeth with PD ≥5 mm. In addition, higher salivary cotinine levels (≥8 ng/mL) were negatively associated with salivary LL‐37 levels. Conclusions: Salivary LL‐37 level was positively correlated with severe periodontal destruction, and production was apparently associated with periodontopathic bacterial infection. The negative correlations between salivary LL‐37 and cotinine levels also suggest that smoking or long‐term exposure to environmental tobacco smoke can lead to lower LL‐37 levels in the oral cavity and increased risk of periodontitis.     

Cigarette smoking, salivary/gingival crevicular fluid cotinine and periodontal status. A 10-year longitudinal study

BACKGROUND, AIMS: The primary purpose of this study was to determine the association of salivary and gingival crevicular fluid (GCF) cotinine levels with periodontal disease status in smokers and non-smokers. METHODS: 147 male smokers and 30 male non-smokers were included in the current longitudinal study. The 177 individuals were part of a group of 200 subjects (89%) seen 10 years previously for a baseline survey. Oral hygiene indices, probing depth and attachment loss were recorded. Salivary and GCF cotinine levels of 58 smokers were determined by means of ELISA. RESULTS: Results indicated that no significant difference was found in subjects who smoked, when compared to subjects who did not smoke with respect to plaque accumulation and calculus deposits. Smokers, however, had fewer gingival bleeding sites. Cigarette smoking was associated with a greater increase in probing depth and attachment loss, as well as greater tooth loss at an earlier age. There was greater tooth loss in smokers than non-smokers (p < 0.001). 11 smokers became edentulous, while only 1 non-smoker lost all his teeth within 10 years. The degree of periodontal tissue breakdown was different in each age group with greater periodontal deterioration as age increased. All smokers had detectable salivary and GCF cotinine. Mean GCF cotinine was about 4x higher than mean salivary cotinine levels. Individuals who smoked > or = 20 pack years when compared to <20 pack years, had significantly higher saliva and GCF cotinine levels (p < or = 0.05). CONCLUSION: Neither salivary cotinine nor GCF cotinine was significantly correlated with probing depth, attachment loss and tooth loss (p > 0.05).     

Smoking influences salivary histamine levels in periodontal disease

Oral Diseases (2012) 18 , 410–416 Objectives: Histamine, a potent vasoactive amine, is increased in saliva of periodontitis patients. The present study aimed to further investigate the diagnostic potential of histamine for periodontal disease and assessed smoking, a major risk factor of periodontitis, as a possible influencing factor. Methods: Salivary and serum samples of 106 participants (60 periodontitis patients, 46 controls) were collected. Salivary histamine was determined by a commercially available ELISA kit, and serum C‐reactive protein was measured by a routine laboratory test. Cigarettes per day and packyears were assessed as smoking exposure parameters. Results: Statistically significantly increased levels of salivary histamine and serum C‐reactive protein were detected between the patient and control group (P = 0.022 and P = 0.001). Salivary histamine levels were significantly higher in smoking compared with non‐smoking patients (P < 0.001), and salivary histamine as well as serum C‐reactive protein correlated significantly positively with smoking exposure parameters (P < 0.05). Conclusions: Smoking, an established and common risk factor of periodontitis, was assessed as a possible influencing factor for salivary histamine. Most interestingly, salivary histamine differed highly significantly between smoking and non‐smoking periodontitis patients. Our results suggest a possible involvement of histamine in tobacco‐exacerbated periodontal disease, but do not suggest salivary histamine as a reliable diagnostic marker for periodontitis.     

Association between passive smoking and salivary markers related to periodontitis

OBJECTIVES: The mechanism of passive smoking in terms of development of periodontitis has not been investigated. This study examined the effect of passive smoking on salivary markers related to periodontitis. METHODS: Periodontal status was evaluated on the basis of probing pocket depth and clinical attachment level in 273 workers. Salivary marker levels were determined by enzyme assay including enzyme-linked immunosorbent assay. Six periodontal pathogens in saliva were assessed using real-time PCR methodology. Non-, passive and active smokers were defined as subjects exhibiting salivary cotinine levels of 0 (53 subjects), 1-7 (118) and > or = 8 ng/ml (102). RESULTS: Levels of salivary markers, including IL-1beta, lactoferrin, albumin and aspartate aminotransferase (AST), were elevated significantly in passive smokers relative to non-smokers. Additionally, these marker levels, with the exception of IL-1beta, decreased significantly in active smokers in comparison with passive smokers. However, no meaningful differences in percentages of periodontal pathogens were observed between non- and passive smokers. Multiple linear regression analyses were performed for each marker utilizing age, gender, cotinine level and periodontal status as independent variables. IL-1beta, albumin and AST were independently associated with cotinine level. CONCLUSION: Passive smoke exposure leads to elevation of IL-1beta, albumin and AST levels in saliva.     

Saliva concentrations of RANKL and osteoprotegerin in smoker versus non-smoker chronic periodontitis patients

Objectives: To compare the salivary receptor activator of NF‐κB ligand (RANKL) and osteoprotegerin (OPG) concentrations in smokers versus non‐smokers with chronic periodontitis. Material and Methods: Whole saliva samples were obtained from 67 untreated chronic periodontitis patients, of whom 34 were smokers, and from 44 maintenance patients, of whom 22 were smokers. Full‐mouth clinical periodontal measurements were recorded. Saliva cotinine, sRANKL and OPG concentrations were determined by ELISA. Statistical analysis was performed using the Mann–Whitney U test, Bonferroni's correction for multiple comparisons and Spearman's correlations. Results: Untreated smokers exhibited significantly higher values of clinical periodontal recordings than untreated non‐smokers (all p<0.05). Salivary cotinine level correlated with clinical attachment level (p=0.023). Smoker versus non‐smoker maintenance groups showed no significant differences in clinical parameters. There were significant differences in sRANKL and OPG concentrations between untreated and maintenance groups (all p<0.01). Salivary OPG concentration was significantly lower (all p<0.01) and the sRANKL/OPG ratio was higher (all p<0.01) in smokers than in non‐smokers. OPG concentration correlated positively with probing depth, clinical attachment level and bleeding on probing (all p<0.005) and negatively with pack‐year, and cotinine level (p<0.05). Conclusion: Salivary RANKL and OPG concentrations are suggested to be affected by smoking as not only the untreated but also the treated smokers exhibited higher RANKL and lower OPG concentrations than non‐smokers.     

Effects of smoking and gingival inflammation on salivary antioxidant capacity

AIM: This study evaluated possible effects of smoking and gingival inflammation on salivary antioxidants in gingivitis patients. METHODS: Twenty otherwise healthy gingivitis patients (10 self-reported smokers) and 20 periodontally and systemically healthy volunteer subjects were enrolled in the study. Whole saliva samples and full-mouth clinical periodontal recordings were obtained at baseline and one month following initial phase of treatment in gingivitis patients. Salivary cotinine, glutathione and ascorbic acid concentrations, and total antioxidant capacity were determined, and the data generated were tested by non-parametric tests. RESULTS: Salivary cotinine measurements resulted in re-classification of three self-reported non-smokers as smokers. Smoker patients revealed significantly higher probing depths but lower bleeding values than non-smoker patients (p=0.044 and 0.001, respectively). Significant reductions in clinical recordings were obtained in non-smoker (all p<0.05) and smoker (all p<0.01) patients following periodontal treatment. Salivary total glutathione concentrations were reduced following therapy in gingivitis patients who smoke (p<0.01). Otherwise, no statistically significant differences were found between the groups in biochemical parameters at baseline or following treatment (p>0.05). CONCLUSIONS: Within the limits of this study, neither smoking nor gingival inflammation compromised the antioxidant capacity of saliva in systemically healthy gingivitis patients.     

Effects of smoking on salivary C-telopeptide pyridinoline cross-links of type I collagen and osteocalcin levels

Aim

This study was planned to investigate whether smoker patients with inflammatory periodontal disease exhibit different salivary concentrations of C-telopeptide pyridinoline cross-links of type I collagen (ICTP) and osteocalcin (OC) compared to the non-smoker and/or ex-smoker counterparts.

Methods

Whole saliva samples, full-mouth clinical periodontal recordings were obtained from 67 otherwise healthy patients with inflammatory periodontal disease. According to self-reports there were 34 smokers, 22 non-smokers and 11 ex-smokers. Salivary cotinine, ICTP and OC levels were determined by enzyme-linked immunoassays.

Results

Salivary cotinine measurements confirmed self-reports about smoking. Smoker patients revealed significantly higher plaque index values than non-smokers (p < 0.05). Bleeding on probing values were significantly lower in smoker group than ex-smoker group (p < 0.05). There was no significant difference between the study groups in salivary ICTP levels (p > 0.05). OC levels in smoker group was significantly lower than the other groups (p < 0.001). Salivary ICTP levels correlated negatively with number of teeth present (p < 0.05), positively with bleeding on probing (p < 0.01). Salivary OC levels correlated negatively with years smoked (p < 0.01).

Conclusions

Within the limits of this study, smoking seems to suppress salivary osteocalcin level but ICTP levels seem not to be affected by smoking status. This suppression in OC levels may be one mechanism of deteriorating effects of smoking on periodontal health.     

Effect of Tobacco Smoke on the Oral Health of US Women of Childbearing Age

Objectives: To determine the oral health status of US women of childbearing age and to analyze the effect of tobacco smoke on their oral health. Methods: Data from the 1999‐2004 National Health and Nutrition Examination Survey were evaluated for women 15‐44 years of age. The association of exposure to tobacco smoke with untreated caries, mean DMFS, gingivitis, and periodontitis were examined in bivariate and regression analyses controlling for potential confounders. Results: The prevalence of untreated caries was 25%, for gingivitis 49%, and for periodontitis 6%. After adjusting for potential confounders, self‐reported current smoking was a strong independent risk indicator for untreated caries, periodontitis, and to a lesser extent for greater DMFS count. Women with detectable cotinine levels below 15 ng/mL presented with an increased risk for gingivitis. Independent factors associated with increased risk for untreated caries were being Black, having less than a high school education, Medicaid or no health insurance, previous live births, and infrequent and episodic dental visits. Characteristics associated with gingivitis were being Mexican‐American, obese, pregnant, and having infrequent dental visits. Older age, no insurance, and the last dental visit for treatment were independently associated with periodontitis. Conclusions: Dental caries and periodontitis were prevalent among certain subgroups of women of reproductive age. Smoking was found to be a significant risk indicator for various negative oral health outcomes. Barriers to accessing to dental care that were manifested by untreated caries among Black women, mothers, and Medicaid beneficiaries must be better understood.     

Associations Between Salivary Bone Metabolism Markers and Periodontal Breakdown

Background: A dual relationship between glycemic status and bone remodeling was suggested recently. The present study aimed to 1) analyze salivary levels of receptor activator for nuclear factor κ‐B ligand (RANKL), osteoprotegerin, osteocalcin, and osteopontin as potential biomarkers of alveolar bone loss and 2) determine whether the glycemic status affects the relationship between bone remodeling markers and periodontal status. Methods: Salivary levels of RANKL, osteoprotegerin, osteocalcin, osteopontin, and serum glycosylated hemoglobin A1c, insulin, and glucose were analyzed in 220 participants divided into four groups according to their periodontal health status: 1) 79 participants had at least 14 teeth with probing depth (PD) ≥4 mm (generalized periodontitis [GP]); 2) 65 participants had either two or seven teeth with PD ≥4 mm (two groups of localized periodontitis [LP1 and LP2, respectively]); and 3) 76 participants had no teeth with PD ≥4 mm (non‐periodontitis control group). Results: Salivary concentrations of RANKL, osteocalcin, and osteopontin were higher, and osteoprotegerin was lower in females than in males. Salivary osteoprotegerin concentrations were higher in the GP and LP2 groups than in the control group, whereas RANKL, osteocalcin, and osteopontin were not related with periodontal status. Salivary osteopontin correlated positively with serum and salivary insulin. The association observed between increased osteoprotegerin concentrations and periodontitis was lost after salivary insulin was included into the analyses as a confounding factor. Conclusions: Salivary concentrations of bone markers are either affected by glycemic status or detected at very low levels. These factors hinder their use as salivary biomarkers of periodontitis.     

Effects of smoking on trace metal levels in saliva

Oral Diseases (2010) 16 , 823–830 Objectives: To compare the salivary levels of trace metals between non‐smokers and smokers using inductively coupled plasma mass spectroscopy (ICP‐MS). The effect of pretreatment methods on the accuracy of ICP‐MS analysis and daily variations in trace metal levels in saliva were also investigated. Subjects and methods: The participants were 10 male non‐smokers (mean age: 27.4 ± 3.4 years) and 30 male smokers (mean age: 26.5 ± 4.1 years). Unstimulated whole saliva was collected. Salivary flow rate, the number of metal restorations in the oral cavity, the level of blood contamination in the saliva and the levels of cotinine and trace metals in the saliva of each participant were determined. Results: Direct dilution of saliva samples with nitric acid showed the most accurate ICP‐MS results. Trace metal levels in saliva showed wide daily variations. They were not affected by the number of metal restorations. Trace metal concentrations of saliva samples without blood contamination were much lower than the previously reported values. Salivary levels of cotinine and aluminum were significantly increased in smokers. Conclusions: Saliva can be a medium for trace metal analysis. Salivary levels of cotinine and aluminum can be useful markers to evaluate smoking status.     

Relationship between salivary melatonin and severity of periodontal disease

BACKGROUND: Melatonin possesses antioxidant, free-radical scavenging, and immunoenhancing properties that promote fibroblast activity and bone regeneration. The aim of this study was to examine the possible links between salivary melatonin levels and the severity of periodontal disease using the community periodontal index (CPI). METHODS: Thirty-seven patients with different degrees of periodontal disease were studied. Salivary and plasma melatonin levels (by radioimmunoassay), salivary/plasma melatonin ratio, and CPI status were collected for each patient. The Spearman correlation coefficient was used to analyze relationships among variables. RESULTS: Data showed a significant correlation between CPI and salivary/plasma melatonin ratios. When saliva volume was controlled for, a significant correlation (P<0.05) was found between lower salivary melatonin and a worse CPI. This finding suggests that melatonin may act as a protector against free radicals produced by inflammatory periodontal diseases. CONCLUSIONS: Salivary melatonin levels varied according to the degree of periodontal disease. As the degree of periodontal disease increased, the salivary melatonin level decreased, indicating that melatonin may act to protect the body from external bacterial insults. Therefore, melatonin may be potentially valuable in the treatment of periodontal diseases, although further research is required to validate this hypothesis.     

Salivary Lipid Peroxidation in Patients With Generalized Chronic Periodontitis and Acute Coronary Syndrome

Background: Lipid peroxidation is a major consequence of oxidative stress and can be evaluated via malondialdehyde (MDA) levels. The present study aims to assess MDA levels in the saliva of patients with chronic periodontitis (CP) and acute coronary syndrome (ACS) and establish their correlation with periodontal clinical parameters, serum high‐sensitivity C‐reactive protein (hsCRP), and plasma fibrinogen. Methods: The study enrolled 64 patients stratified into four age‐ and sex‐matched groups: both ACS and CP, ACS only, CP only, and healthy controls. All patients were examined, periodontal clinical parameters were recorded, and saliva and blood samples were collected. Salivary MDA levels were measured using a spectrophotometric assay. A quantitative turbidimetric test was used for the measurement of serum hsCRP levels, and plasma fibrinogen levels were determined using an automated analyzer. Results: Salivary MDA levels were significantly higher in patients with both ACS and CP than in those with only ACS or only CP and healthy controls (P <0.05). There were significant positive correlations between salivary MDA levels and periodontal clinical parameters as well as biomarkers for cardiovascular events (P <0.001). Conclusions: To our knowledge, this study is the first to investigate salivary MDA levels in patients with ACS and their correlations with serum hsCRP and plasma fibrinogen levels. The results indicate that salivary MDA levels could be a biomarker for cardiovascular and/or periodontal disease.     

Salivary Cytokines and the Association Between Obstructive Sleep Apnea Syndrome and Periodontal Disease

Background: A higher prevalence of periodontal disease has been reported in patients with obstructive sleep apnea syndrome (OSAS), and these two chronic conditions may be linked via inflammatory pathways. The aim of the present study is to evaluate the salivary interleukin (IL)‐1β, IL‐6, IL‐21, IL‐33, and pentraxin‐3 (PTX3) concentrations in patients with and without OSAS. Methods: A total of 52 patients were included in the study. Thirteen individuals were in the control (non‐OSAS) group, 17 were in the mild/moderate OSAS group, and 22 were in the severe OSAS group. Clinical periodontal measurements were recorded, and saliva samples were obtained before initiation of periodontal intervention. Enzyme‐linked immunosorbent assay was used to determine salivary cytokine concentrations. Data were statistically analyzed using D'Agostino‐Pearson omnibus normality, Spearman ρ rank, Kruskal‐Wallis, and Dunn tests. Results: Salivary IL‐6 and IL‐33 concentrations were similar in the two OSAS groups (P >0.05), which were statistically higher than the control group (P <0.05). IL‐1β, IL‐21, and PTX3 concentrations were similar in the study groups. The only significant correlation between clinical periodontal parameters and salivary cytokines was found between clinical attachment level (CAL) and IL‐21 (P = 0.02). Highly significant correlations were found between probing depth, CAL measures, and indicators of OSAS severity (P <0.01). Conclusions: The present findings suggest that OSAS may have an increasing effect on salivary IL‐6 and IL‐33 concentrations regardless of OSAS severity. Additional investigation is required to elucidate a potential bidirectional relationship between OSAS and periodontal disease.     

Salivary nitric oxide levels in inflammatory periodontal disease - a case-control and interventional study

To cite this article: Int J Dent Hygiene 10 , 2012; 67–73
DOI: 10.1111/j.1601‐5037.2011.00508.x
Parwani SR, Chitnis PJ, Parwani RN. Salivary nitric oxide levels in inflammatory periodontal disease – A case‐control and interventional study. Abstract: Background: Biochemical markers of inflammatory periodontal disease present in saliva can partially determine the extent of periodontal disease. Furthermore, collection of salivary constituents is a simple and non‐invasive procedure. Nitric oxide (NO) has been linked to etiopathogenesis of inflammatory periodontal disease and is expressed in saliva. This study was conducted with the objective of estimating salivary NO levels in inflammatory periodontal diseases (gingivitis and periodontitis) and comparing these levels with control subjects. A re‐assessment of these levels was also made after providing appropriate treatment with a view to ascertain its diagnostic and prognostic values. Methods: This was a case–control as well as an interventional study including a total of 90 (30 control, 30 gingivitis and 30 periodontitis) subjects. Saliva samples were collected from each subject, and NO levels were assayed by Griess reaction. Results: NO levels were increased significantly in gingivitis and periodontitis subjects as compared with controls. There was a statistically significant decrease in the NO levels in each study group after the healing period (corresponding to the reduced clinical signs of inflammation). Our study also correlated probing pocket depths with salivary NO levels in periodontitis group where we found a positive correlation between the two. Conclusion: Salivary NO levels can be utilized as a good indicator of the inflammatory status of the periodontium, and evaluating its levels in saliva by Griess reaction on a photoelectric colorimeter is a reliable, accurate and faster method to estimate the level of inflammation in periodontal tissues.     

Salivary calcium reflects skeletal bone density of heavy smokers

OBJECTIVE: Our recent studies suggest, that elevated calcium concentration of saliva is characteristic of periodontitis. In this study we analyzed the effect of smoking on salivary calcium and bone density by comparing the level of salivary calcium and the ultrasound scale of bone density of heavy smokers to those of non-smokers. DESIGN: Salivary samples were collected from 603 women (50-62 years) participating in a pre-screen referral program for osteoporosis. Out of this group a total of 577 were accepted for the present study. General health, medications and tobacco smoking were recorded. The group included 487 non-smokers, 37 moderate smokers (1-10 cigarettes per day) and 53 heavy smokers (>10 cigarettes per day). Bone density was measured at the right heel by the quantitative ultrasound technique. Calcium and phosphate concentrations of saliva were measured and expressed as microg/ml of saliva. RESULTS: The ultrasonographic variables of the heel, broadband ultrasound attenuation (BUA), speed of sound (SOS) and T-score (a standard deviation unit from mean values of healthy young adults) of heavy smokers were significantly lower than those of women who did not smoke (P = 0.007, 0.014 and 0.011, respectively). Salivary calcium concentration of heavy smokers 70.5 (14.6) microg/ml was higher than that of non-smokers 64.0 (14.1) microg/ml (P = 0.001). There were no significant differences in salivary phosphate level or in the salivary flow rate between heavy smokers and non-smokers. Conclusions: Heavy smokers seem to have lower bone mineral density and higher salivary calcium than their non-smoking counterparts. We suggest that the high salivary calcium concentration of smokers is in connection with skeletal calcium disturbances.     

Association between passive and active smoking evaluated by salivary cotinine and periodontitis

AIM: This study attempted to determine the relationship between passive and active smoking on the basis of salivary cotinine levels and periodontitis severity. METHODS: Japanese workers (n=273) were surveyed via an oral examination, a self-administered questionnaire and collection of whole saliva. Probing pocket depth (PPD) and clinical attachment level (CAL) served as periodontal parameters. Periodontitis was defined as the presence of two or more teeth with PPD > or =3.5 mm and CAL > or =3.5 mm. Salivary cotinine was determined using ELISA. Statistical methods included Wilcoxon's rank-sum test and multiple logistic regression analysis. RESULTS: Based on the results of receiver-operating characteristic plots for cotinine-level classification derived from self-reported smoking status, non-, passive and active smokers were defined as those subjects exhibiting cotinine levels of 0, 1-7 and > or =8 ng/ml, respectively. Numbers of teeth displaying CAL > or =3.5 mm in passive and active smokers were significantly higher than those in non-smokers. Multiple logistic regression analysis revealed significantly higher periodontitis odds ratios in passive and active smokers relative to non-smokers following adjustment for other lifestyle factors; odds ratios were 2.87 [95% confidence interval (CI); 1.05-7.82] and 4.91 (95% CI; 1.80-13.35), respectively. CONCLUSION: These findings suggest that passive smoking classified in terms of salivary cotinine level may be an independent periodontitis risk indicator.     

Environmental Tobacco Smoke and Periodontitis in United States Non‐Smokers, 2009 to 2012

Background: Epidemiologic studies using half‐mouth designs for assessment of periodontal disease prevalence have reported that environmental tobacco smoke (ETS) exposure of non‐smokers is associated with a two‐ to three‐fold increase in the odds of developing periodontitis. In response to the possibility of under‐reporting of periodontitis, the Centers for Disease Control updated periodontal examination procedures in 2009 for the National Health and Nutritional Examination Survey (NHANES), including full‐mouth, six‐site periodontal probing, and attachment loss assessment. Aims of this study are to estimate prevalence of periodontitis among United States non‐smoking adults exposed to ETS, report the values of the improved methods for estimating disease prevalence, and evaluate the predictive contribution of ETS exposure to periodontitis. Methods: A cross‐sectional study was conducted using NHANES data from the 2009 to 2012 examination cycle. To address these aims, oral examination data were used to determine prevalence of periodontitis among United States non‐smoking adults and to test the influence of ETS exposure on occurrence of periodontitis. Results: There was a 28% increase in the odds of periodontitis for those with any ETS exposure compared with those with no measurable exposure (Wald χ² test statistic [df] = 6.58 [1], P = 0.01; 95% confidence interval = 1.06 to 1.55). Conclusion: ETS exposure increases the risk of an individual developing periodontitis.     

Salivary Levels of NLRP3 Inflammasome‐Related Proteins as Potential Biomarkers of Periodontal Clinical Status

Background: Emerging evidence suggests that activation of inflammasomes plays a central mechanism in pathogenesis of periodontitis. This study aims to compare salivary levels of nod‐like receptor family pyrin domain containing protein (NLRP) 3, apoptosis‐associated speck‐like protein containing a caspase recruitment domain (ASC), cysteine aspartase (caspase)‐1, and interleukin (IL)‐1β from individuals with aggressive (AgP) or chronic periodontitis (CP) and healthy controls (HC), as well as elucidate its association with periodontal clinical status. Methods: Saliva samples from individuals with CP (n = 75), AgP (n = 20), and HC (n = 69) were collected. Periodontal status was assessed by measurement of probing depth, clinical attachment level, and extent and severity of disease. Salivary levels of analytes were analyzed by enzyme‐linked immunosorbent assay. Association between biomarkers with CP or AgP was analyzed using multivariate binary logistic regression models. Results: Significantly higher levels of NLRP3, ASC, and IL‐1β were detected in periodontitis groups in comparison to the periodontally HC group. However, no significant differences were observed for caspase‐1 levels between clinical groups, and only NLRP3 salivary concentration was significantly higher in AgP compared with CP patients. Also, positive significant correlations among NLRP3, ASC, and IL‐1β salivary concentrations and clinical parameters were observed. Logistic regression analyses revealed a strong/independent association of NLRP3, ASC, and IL‐1β salivary levels with CP and AgP. Conclusion: Although the concentration of caspase‐1 in saliva samples makes its determination useless for detection of periodontal disease and/or its severity, salivary levels of NLRP3, ASC, and IL‐1β may act as strong/independent indicators of amount and extent of periodontal breakdown in both CP and AgP and could potentially be used for prevention and therapy of this group of diseases.     

Salivary variables in relation to tobacco smoking and female sex steroid hormone-use in 30 to 59-year-old women

Several systemic conditions may have an influence on oral health. Hormone replacement therapy (HRT) has a positive effect on alveolar bone of menopausal women and smoking a negative effect. However, little is known about their effect on saliva. The purpose of this study was to examine the effect of hormone-use and tobacco smoking on the composition of saliva, in particular on the inorganic constituents. Salivary samples were collected from a representative study group comprising 1013 women (30-59 years) participating in a pre-screen referral program for osteoporosis. The participants were divided into 2 subgroups according to age. The younger group ( &#104 45 years) comprised 413 women and the older group ( &#83 50 years) 600 women. Salivary calcium, magnesium, sodium, potassium, inorganic phosphate, total protein, and flow rate of paraffin-stimulated saliva were measured. In the older age group, female sex steroid users (hormone users) had lower salivary protein concentrations than non-users. Smoking was associated with high salivary calcium, magnesium, and potassium levels in the group of older participants. Neither tobacco smoking nor female sex steroid hormones had any significant effect on the salivary composition in the younger age group. In conclusion, smoking was reflected more clearly than female sex steroid hormone-use in the inorganic composition of saliva in the older age group. The salivary composition was not affected by hormone-use or by smoking among the younger age group.     

Salivary variables in relation to tobacco smoking and female sex steroid hormone-use in 30 to 59-year-old women

Several systemic conditions may have an influence on oral health. Hormone replacement therapy (HRT) has a positive effect on alveolar bone of menopausal women and smoking a negative effect. However, little is known about their effect on saliva. The purpose of this study was to examine the effect of hormone-use and tobacco smoking on the composition of saliva, in particular on the inorganic constituents. Salivary samples were collected from a representative study group comprising 1,013 women (30-59 years) participating in a pre-screen referral program for osteoporosis. The participants were divided into 2 subgroups according to age. The younger group (< or = 45 years) comprised 413 women and the older group (> or = 50 years) 600 women. Salivary calcium, magnesium, sodium, potassium, inorganic phosphate, total protein, and flow rate of paraffin-stimulated saliva were measured. In the older age group, female sex steroid users (hormone users) had lower salivary protein concentrations than non-users. Smoking was associated with high salivary calcium, magnesium, and potassium levels in the group of older participants. Neither tobacco smoking nor female sex steroid hormones had any significant effect on the salivary composition in the younger age group. In conclusion, smoking was reflected more clearly than female sex steroid hormone-use in the inorganic composition of saliva in the older age group. The salivary composition was not affected by hormone-use or by smoking among the younger age group.