Serum IgG titers to periodontal pathogens predict 3-month outcome in ischemic stroke patients.

Several cohort studies have shown that periodontal disease is associated with an increased risk for stroke. However, it remains unclear whether serum antibody titers for a specific periodontal pathogen are associated with outcome after ischemic stroke, and which kinds of pathogens are associated with ischemic stroke. We examined the relationship between serum IgG titers to periodontal pathogens and outcome in ischemic stroke patients. A total of 445 patients with acute ischemic stroke (194 female [44.0%], mean age 71.9±12.3 years) were registered in this study. Serum IgG titers to 9 periodontal pathogens (Porphyromonas gingivalis, Aggregatibacter actinomycetemcomitans, Prevotella intermedia, Prevotella nigrescens, Fusobacterium nucleatum, Treponema denticola, Tannerella forsythensis, Campylobacter rectus, Eikenella corrodens) were evaluated using the enzyme-linked immunosorbent assay (ELISA) method. An unfavorable outcome was defined as a 3 or higher on the modified Rankin Scale. The proportion of patients with unfavorable outcome was 25.4% (113 patients). Based on multivariate logistic regression analysis, numbers of IgG antibodies positive for periodontal pathogens (odds ratio 1.20, 95% CI 1.02-1.41, p = 0.03) were independent predictors of unfavorable outcome in ischemic stroke patients.

Is sialic acid a promising marker for periodontal diseases?

OBJECTIVE: Periodontal diseases are inflammatory chronic infections. Sialic acid (SA) is an acute phase reactant by itself. The aim of this study is to investigate the relationship between salivary and serum SA levels and clinical parameters in different forms of periodontal diseases. SUBJECT AND METHODS: Systemically healthy subjects were included in the study; patients with chronic gingivitis (CG) (n = 10), chronic periodontitis (CP) (n = 10), and aggressive periodontitis (AgP) (n = 10), and ten volunteers with healthy periodontium as the control group. Total SA levels were determined by Warren's thiobarbituric acid method in whole saliva, parotis saliva, and serum samples of subjects before and 3 months after nonsurgical periodontal treatment. Full mouth clinical parameters including plaque index, gingival index, probing depth, and bleeding on probing were also recorded. RESULTS: Before treatment, in both periodontitis groups salivary and serum SA levels were higher than those of controls (P = 0.001). Both salivary and serum SA levels decreased significantly in the patient groups after treatment (P < 0.001). Multiple comparisons of baseline clinical parameters in all groups revealed significant differences (P = 0.001) and these parameters decreased significantly on the 90th day (P < 0.01). There were positive correlations between SA levels and periodontal indices of the CG, CP, and AgP groups (P < 0.05). CONCLUSION: Our results suggest that SA level in both saliva and serum may be a potentially useful marker to determine inflammatory changes and investigate different forms of periodontal diseases.

Effect of periodontal treatment on Aggregatibacter actinomycetemcomitans colonization and serum IgG levels against A. actinomycetemcomitans serotypes and Omp29 of aggressive periodontitis patients.

OBJECTIVE: To evaluate the effect of the periodontal treatment on Aggregatibacter actinomycetemcomitans JP2 clone, and the IgG serum levels against its outer membrane protein (Omp29) and A. actinomycetemcomitans serotypes in aggressive periodontitis (AgP). SUBJECTS AND METHODS: Seventeen patients with generalized (GAgP), 10 with localized (LAgP), and 10 healthy controls were included. AgP participants were submitted to periodontal treatment-scaling and root planing plus antibiotics (SRP+A). Periodontal parameters, for example, probing depth (PD) and clinical attachment loss (CAL), were evaluated at baseline and at 1-year. Serum IgG against Omp29 and serotypes a, b, and c were determined by ELISA. The levels of A. actinomycetemcomitans JP2 clone were determined in subgingival biofilm samples by qPCR. RESULTS: Periodontal treatment resulted in significant reductions of PD, CAL, and IgG levels against Omp29, serotypes b, and c. After therapy, IgG levels against A. actinomycetemcomitans serotypes, as well as the levels of the JP2 clone in AgP, became similar to controls. The reduction in JP2 clone count was correlated with a reduction of PD and IgG response against Omp29. CONCLUSION: Scaling and root planing plus antibiotics decreased IgG levels response against Omp29 and A. actinomycetemcomitans serotypes involved in the disease (b and c), while the serum response increased against tne commensal serotype (a), similar to what occurs in periodontally healthy individuals.

Analysis of metabolic profiles of generalized aggressive periodontitis.

BACKGROUND AND OBJECTIVE: The specific pathogenesis of generalized aggressive periodontitis (GAgP) has not yet been clarified, and few studies have focused on the association between GAgP and metabolomics. To elucidate the roles of metabolic profiles in the status of GAgP, this study aimed to identify the differential metabolic profiles between patients with GAgP and healthy controls using an untargeted metabolomic profiling method. MATERIAL AND METHODS: Serum and gingival crevicular fluid samples were collected from healthy controls (n = 20) and patients with GAgP (n = 20) in this cross-sectional study. The relative levels of biomarkers in the samples were measured by gas chromatography-mass spectrometry. Principal components analysis and orthogonal partial least-squares discriminant analysis were used for statistical analysis. Metabolites were analysed qualitatively using the FiehnLib and NIST databases. Full-mouth probing depth and clinical attachment loss were recorded as indexes of periodontal disease. RESULTS: A total of 349 metabolites were qualitatively detected in the gingival crevicular fluid samples, and 200 metabolites were detected in the serum samples. Compared with healthy controls, patients with GAgP showed significant increases in serum urea and allo-inositol levels. In contrast, glutathione, 2,5-dihydroxybenzaldehyde, adipic acid and 2-deoxyguanosine levels were decreased in patients with GAgP. In the gingival crevicular fluid samples, noradrenaline, uridine, α-tocopherol, dehydroascorbic acid, xanthine, galactose, glucose-1-phosphate and ribulose-5-phosphate levels were increased in patients with GAgP, while thymidine, glutathione and ribose-5-phosphate levels were decreased. CONCLUSION: The metabolomics analysis by gas chromatography-mass spectrometry is an effective and minimally non-invasive way to differentiate the metabolites characteristic of patients with GAgP. Both serum and gingival crevicular fluid metabolomics are significantly different between patients with GAgP and healthy controls. These metabolic profiles have great potential in detecting GAgP and helping to understand its underlying mechanisms.

Association between circulating levels of heat-shock protein 27 and aggressive periodontitis.

Heat-shock protein (Hsp) 27 is a major intracellular molecular chaperone and controller of intracellular responses to inflammatory signals. In the extracellular space, recombinant Hsp27 has been described to exert anti-inflammatory activities. The aim of this study was to assess the association between circulating levels of Hsp27 and different types of periodontitis. Pro- and anti-inflammatory cytokines and the stress proteins Hsp27 and Hsp60 with proposed anti- and pro-inflammatory properties, respectively, were measured by two-site ELISA in the serum of patients with aggressive periodontitis (AgP, n = 30), chronic periodontitis (CP, n = 29) and periodontally healthy controls (H, n = 28). Furthermore, Hsp27 and Hsp60 levels were also measured longitudinally in 12 AgP patients at 6 time points up to 3 months after treatment. AgP patients had lower levels of Hsp27 compared to CP patients and healthy subjects (adjusted one-way ANOVA, p < 0.001, followed by post hoc Tukey HSD comparisons), while no differences in levels of Hsp60 or cytokines between the three groups were detected. In CP patients and H subjects, the systemic Hsp27 levels correlated with Hsp60 (r = 0.43, p < 0.001; r = 0.59, p < 0.001, respectively) and with pro-inflammatory cytokines TNF-α (r = 0.48, p < 0.001; r = 0.55, p < 0.001, respectively) and IL-6 (r = 0.44, p < 0.01). However, no such correlations were detected in AgP cases. No consistent temporal patterns of changes of Hsp27 concentration were detected across AgP patients following periodontal treatment. This study provides the first evidence that Hsp27 may be differentially expressed and regulated in AgP patients as compared with CP patients and healthy individuals.

Inflammatory serum markers up to 5 years after comprehensive periodontal therapy of aggressive and chronic periodontitis.

AIM: The aim of the study is to assess the long-term effect of active periodontal therapy on serum inflammatory parameters in patients with aggressive (AgP) and chronic (ChP) periodontitis in a non-randomised clinical study. METHODS: Twenty-five ChP and 17 AgP were examined clinically prior to (baseline), 12 weeks and 60 months after subgingival debridement of all pockets within 2 days. Systemic antibiotics were prescribed if Aggregatibacter actinomycetemcomitans was detected (10 AgP, 8 ChP), flap surgery was rendered if required. Neutrophil elastase (NE), C-reactive protein (CRP), lipopolysaccharide binding protein, interleukin 6, 8, and leukocyte counts were assessed at baseline, 12 weeks and 60 months. RESULTS: Clinical parameters improved significantly in both groups from 12 weeks to 60 months. Eleven AgP and 18 ChP patients received surgical treatment after the 12 weeks examination. Only 3 patients in each group attended ≥ 2 supportive maintenance visits per year. NE and CRP were significantly higher in AgP than ChP at baseline and 60 months (p < 0.01). For leukocyte counts in ChP, significant changes were observed (baseline: 6.11 ± 1.44 nl-1; 12 weeks: 5.34 ± 1.40 nl-1; 60 months: 7.73 ± 2.89 nl-1; p < 0.05). Multiple regression analysis identified African origin, surgical treatment and female sex to correlate with better clinical improvement. CONCLUSION: Despite comprehensive periodontal treatment, AgP patients exhibit higher NE and CRP levels than ChP patients up to 5 years after therapy. CLINICAL RELEVANCE: Systemic inflammatory burden in AgP patients is higher than in ChP patients even 5 years after periodontal treatment.

Saliva, Serum Levels of Interleukin-21, -33 and Prostaglandin E2 in Patients with Generalised Aggressive or Chronic Periodontitis.

PURPOSE: This cross-sectional study aims to evaluate saliva, serum levels of interleukin-21 (IL-21), IL-33, and prostaglandin E2 (PGE2) in patients with generalised chronic periodontitis or aggressive periodontitis. MATERIALS AND METHODS: Before initiation of any periodontal treatment, saliva and serum samples were collected and clinical periodontal measurements were recorded from 94 participants (25 aggressive periodontitis patients, 25 chronic periodontitis patients, 44 periodontally healthy individuals). IL-21, IL-33 and PGE2 levels in serum and saliva samples were determined by ELISA. Data were tested statistically using Kruskal-Wallis, Mann-Whitney U-, and Spearman-rho rank tests. RESULTS: Saliva IL-33 levels were statistically significantly higher in the chronic than the aggressive group (p < 0.05). Serum IL-33, saliva and serum IL-21 and PGE2 levels were similar in the two periodontitis groups. Saliva IL-33 levels correlated with age in the chronic periodontitis group (p < 0.05). Statistically significant positive correlations were found between serum, saliva PGE2 levels and plaque index (p < 0.05). IL-33 and IL-21 levels in serum samples positively correlated in the periodontitis groups (p < 0.05). CONCLUSION: IL-21 and PGE2 analysis did not exhibit discriminating data between generalised chronic and aggressive periodontitis, but the present findings support the role of these cytokines in periodontitis. Statistically significantly higher saliva IL-33 levels in the chronic periodontitis group warrant further research.

Salivary and Serum Markers Related to Innate Immunity in Generalized Aggressive Periodontitis.

BACKGROUND: Host inflammatory and immune responses play an important role in aggressive periodontitis (AgP). Thus, this study aims to evaluate levels of the innate immunity-related markers calprotectin, colony-stimulating factor (CSF)-1, macrophage migration inhibitory factor (MIF), monokine induced by interferon-γ (MIG), and matrix metalloproteinase (MMP)-8 in serum and saliva from patients with generalized AgP and those with gingivitis or a healthy periodontium. METHODS: This study enrolled 40 individuals (17 males and 23 females; mean age 33.30 ± 9.31 years), 15 with generalized AgP, 15 with gingivitis, and 10 who were periodontally healthy. Full-mouth periodontal examinations were performed, and serum and saliva were collected. Levels of calprotectin, CSF-1, MIF, MIG, and MMP-8 were measured using enzyme-linked immunosorbent assays. RESULTS: In serum, mean levels of calprotectin were 2.06-fold higher in patients with AgP than in healthy patients (P = 0.01). Serum levels of MMP-8 were significantly elevated in patients with AgP compared with both healthy patients and those with gingivitis, by 2.60-fold and 2.77-fold, respectively (P = 0.03 and P = 0.009, respectively). In saliva, levels of MMP-8 were 5.66-fold higher in patients with AgP than in healthy patients (P = 0.02). CSF-1, MIF, and MIG levels in both serum and saliva did not differ significantly among the groups. CONCLUSIONS: Serum levels of calprotectin and MMP-8 are elevated in patients with AgP. MMP-8 levels are also increased in saliva from patients with AgP. These results support involvement of innate immune response in the pathogenesis of AgP.

The role of platelets in inflammatory immune responses in generalized aggressive periodontitis.

AIM: To investigate the relationship between inflammatory markers and platelet size in generalized aggressive periodontitis (GAgP). MATERIAL AND METHODS: Periodontal, inflammatory and platelet indices were compared between 59 GAgP patients and 59 healthy subjects. Gingival biopsies from five patients and five healthy subjects were examined by immunohistochemistry and electron microscopy. Changes in patient periodontal and platelet indices were re-evaluated at 3 months after periodontal therapy. RESULTS: Platelet size was decreased significantly in GAgP patients compared to healthy subjects (p ≤ 0.003). Weak negative correlations between platelet size and periodontal parameters were found in GAgP patients (p ≤ 0.025). Platelet aggregates and adhesion to the endothelium or leucocytes were found in venules and connective tissues of gingival biopsies from GAgP patients. Mean platelet volume (MPV) and platelet large cell ratio increased after periodontal therapy in GAgP patients (p ≤ 0.038). The increase in MPV was related to the decrease in bleeding index in GAgP patients after periodontal therapy (p < 0.001; r = 0.357). CONCLUSION: Platelet size was reduced in GAgP patients compared to healthy controls, possibly due to the consumption of large platelets at sites of periodontal inflammation. Platelets may be involved in host responses to periodontal infection in GAgP.

Total and Differential Leukocyte Counts in the Peripheral Blood of Patients with Generalised Aggressive Periodontitis.

PURPOSE: To compare the total and differential leukocyte counts in the peripheral blood of generalised aggressive periodontitis patients with that of periodontally healthy subjects in a central Indian population. MATERIALS AND METHODS: Seventy-five patients with generalised aggressive periodontitis and 63 periodontally healthy subjects were enrolled for the purpose of the study. All participants received a full-mouth periodontal examination in which probing depth and clinical attachment level were recorded. The haematological variables analysed included total leukocyte count, neutrophil count, lymphocyte count, monocyte count, neutrophil percentage, lymphocyte percentage, monocyte percentage and platelet count. RESULTS: The patient group showed a significantly higher total leukocyte count (7.62 ± 1.70 x 109 cells/l, p = 0.008), neutrophil count (5.06 ± 1.47x109 cells/l, p < 0.001) and neutrophil percentage (70.61 ± 8.73, p < 0.001), as well as a significantly lower lymphocyte count (1.82 ± 0.65 x 109 cells/l, p = 0.002) and lymphocyte percentage (26.55 ± 8.05, p < 0.001) compared to the control group. Logistic regression analyses showed significant associations between aggressive periodontitis and elevated total leukocyte (p = 0.012) and neutrophil counts (p = 0.001). CONCLUSION: The findings of the present study suggest that patients with generalised aggressive periodontitis might also demonstrate a systemic inflammatory response, as evidenced by increased leukocyte counts. This systemic inflammatory response observed in patients with generalised aggressive periodontitis may be associated with an increased risk for cardiovascular diseases.

Systemic Biomarkers in 2-Phase Antibiotic Periodontal Treatment: A Randomized Clinical Trial.

Accumulating evidence suggests that periodontal infections may have an impact on systemic health. In patients with untreated periodontitis, very high values for several inflammatory markers in serum are expressed simultaneously. We investigated to what extent these peak values change after nonsurgical and surgical periodontal treatment, with adjunctive antibiotics administered during the first or the second treatment phase. In a single-center, randomized, placebo-controlled, and double-masked clinical trial, 80 patients with chronic or aggressive periodontitis were randomized into 2 treatment groups: group A, receiving systemic amoxicillin and metronidazole during the first, nonsurgical phase of periodontal therapy (phase 1), and group B, receiving the antibiotics during the second, surgical phase (phase 2). Serum samples were obtained at baseline (BL), 3 mo after phase 1 (M3), and 6 and 12 mo after phase 2 (M6, M12). Samples were evaluated for 15 cytokines and 9 acute-phase proteins using the Bio-Plex bead array multianalyte detection system. For each analyte, peak values were defined as greater than mean +2 SD of measurements found in 40 periodontally healthy persons. Sixty-six patients showed a peak value of at least 1 analyte at BL. At M12, the number of these patients was only 36 (P = 0.0002). This decrease was stronger in group A (BL: 35, M12: 19, P = 0.0009) than in group B (BL: 31, M12: 17, P = 0.14). Twenty patients displayed peak values of at least 4 biomarkers at BL. The nonsurgical therapy delivered in the first phase reduced most of these peaks (group A, BL: 9, M3: 4, P = 0.17; group B, BL: 11, M3: 2, P = 0.01), irrespective of adjunctive antibiotics. The reductions obtained at M3 were maintained until M12 in both groups. Initial, nonsurgical periodontal therapy reduced the incidence of peak levels of inflammatory markers. Antibiotics and further surgical therapy did not enhance the effect (Clinicaltrials.gov NCT02197260).

Changes in cellular and molecular components of peripheral blood in patients with generalized aggressive periodontitis.

AIM: The association between periodontitis and systemic health is evident; however, until recently, there has been a lack of scientific evidence to define the relationship between aggressive periodontitis and systemic conditions. The aim of the present study was to evaluate the changes in the white blood cell count and levels of serum proteins in patients with generalized aggressive periodontitis (GAP) and to compare it with periodontally-healthy controls. METHODS: Patients with GAP (n = 60) and periodontally-healthy controls (n = 60) were recruited. Clinical parameters, including probing depth and clinical attachment level, were examined. Blood cell variables, including leukocyte, neutrophil, and lymphocyte counts, and serum protein parameters, including total protein, albumin (ALB), globulin (GLB), ALB/GLB (A/G) ratio, and C-reactive protein levels, were analyzed. RESULTS: The results showed a statistically-significant increase in neutrophil numbers and serum GLB and C-reactive protein levels in patients with GAP compared to the controls (P < 0.001), whereas the ALB level and A/G ratio were significantly lower compared to the control group. CONCLUSION: The results showed possible changes in the cellular and molecular components of peripheral blood in patients with GAP compared to periodontally-healthy controls. These changes might represent the contribution of periodontal infections to systemic inflammation in relatively young individuals.

[Analysis of serum IgG titers to Aggregatibacter actinomycetemcomitans serotype c in aggressive periodontitis patients].

OBJECTIVE: To analyze the serum IgG titers to Aggregatibacter actinomycetemcomitans(Aa) and associated factors in patients with aggressive periodontitis (AgP). METHODS: Venous blood samples were collected from 62 AgP patients and 45 periodontal healthy controls, unstimulated whole saliva and pooled subgingival plaque samples of AgP patients were also collected for the detection of Aa (PCR method). Serum IgG titers to Aa serotype c were measured by enzyme-linked immunosorbnent assay (ELISA). RESULTS: The detection rates of serum IgG to Aa serotype c in the AgP patients and the healthy controls were both 100%. The AgP patients exhibited significantly higher IgG titers to Aa serotype c than the healthy controls (11.1±1.9 vs. 9.1±1.8, P<0.01). There was no significant difference in serum IgG levels to Aa serotype c and in the prevalence of high-responding patients to Aa serotype c between the incisor-first molar type AgP patients and generalized AgP patients. Serum IgG titers to Aa serotype c in the Aa-positive AgP patients (the patients who were Aa-positive in subgingival plaque or saliva) were significantly higher than those of the Aa-negative patients (11.9±1.3 vs. 10.7±2.1, P<0.05). CONCLUSION: Serotype c was the main serotype of Aa in Chinese patients with AgP. Serum IgG responses in generalized AgP patients were comparable to those in incisor-first molar type AgP patients.

Effects of periodontal therapy on white blood cell count and levels of transforming growth factor beta in serum of subjects with severe periodontitis.

This study aimed to investigate the effects of nonsurgical periodontal therapy on white blood cell (WBC) count and levels of transforming growth factor beta (TGF—β) in serum from subjects with severe periodontitis. Serum from 28 subjects with periodontitis (mean age: 34.36±6.24; 32% men) and 27 healthy controls (mean age: 33.18±6.42; 33% men) were collected prior to therapy. Blood samples were obtained from 23 subjects who completed therapy (9—12 months). A well—controlled periodontal treatment protocol was established in three stages: mechanical periodontal therapy (scaling and root planning), reinstrumentation of dental sites, and supportive periodontal therapy. Periodontal and systemic parameters such as the total number of WBCs and TGF—β levels, accessed by enzyme—linked immunosorbent assay (ELISA), were included. After therapy, all clinical periodontal parameters decreased (p<0.0001). There were no statistical differences in WBC count between experimental and control groups before or after therapy. However, after therapy, the mean value of lymphocytes in patients with localized aggressive periodontitis (LAgP) was statistically higher than that of patients with generalized chronic periodontitis (GCP) (p<0.0357). Additionally, TGF—β levels in LAgP and GCP patients were higher compared to controls before therapy (p<0.05 and p<0.01, respectively). In LAgP patients, periodontal therapy was associated with increased number of lymphocytes.

Association between plasma leptin level and systemic inflammatory markers in patients with aggressive periodontitis.

BACKGROUND: Increasing evidence supports an association between periodontitis and systemic diseases. Leptin is involved both in the energy metabolism and inflammatory processes and is suggested to be a link between periodontal infection and systemic health. The present study aimed to evaluate the peripheral leptin concentration in patients with aggressive periodontitis (AgP) and to explore the relationship between leptin and systemic inflammation. METHODS: Ninety patients with AgP visiting the Clinic of the Periodontology Department, Peking University School and Hospital of Stomatology between July 2001 and May 2006, and 44 healthy controls (staff and student volunteers in the same institute) were recruited. Plasma levels of leptin and inflammatory cytokines including interleukin (IL)-1ß, IL-6, tumor necrosis factor-α (TNF-α) and C-reactive protein (CRP) were measured by enzyme-linked immunosorbent assay. Correlation and multiple linear regression analysis were performed to analyze the association between plasma leptin level and other variables. RESULTS: Plasma leptin level of AgP group was significantly higher than that of the control group (19.7 ± 4.4 ng/ml vs. 7.5 ± 1.3 ng/ml, P < 0.01). After controlling for age, gender, and body mass index, positive correlation was observed between plasma leptin concentration and log-transformed levels of pro-inflammatory cytokines (IL-1ß, IL-6, TNF-α and CRP), and the partial correlation coefficients ranged from 0.199 to 0.376 (P < 0.05). Log-transformed IL-1ß and IL-6 levels entered the final regression model (standardized ß were 0.422 and 0.461 respectively, P < 0.01). CONCLUSIONS: Elevated plasma leptin concentration may be associated with increased systemic levels of inflammatory markers in AgP patients.

Serum and salivary matrix metalloproteinases, neutrophil elastase, myeloperoxidase in patients with chronic or aggressive periodontitis.

Salivary, serum matrix metalloproteinase-8 (MMP-8), tissue inhibitor of matrix metalloproteinases-1 (TIMP-1), neutrophil elastase (NE), and myeloperoxidase (MPO) levels were investigated in generalized chronic periodontitis (GCP), generalized aggressive periodontitis (GAgP), and healthy groups. Whole-mouth clinical periodontal measurements were recorded. Salivary, serum concentrations of MMP-8, MPO, TIMP-1, and NE were determined by immunofluorometric assay or ELISA in 18 patients with GCP, 23 patients with GAgP, 18 individuals with healthy periodontium. Patients in the GAgP group were younger than the other groups (p<0.05). The study groups were similar in gender, smoking status. Plaque index was higher in GCP than GAgP group (p<0.05). Biochemical data were similar in periodontitis groups. Salivary, serum MPO, and salivary NE concentrations were higher; TIMP-1 concentrations were lower in the periodontitis groups than the controls (p<0.05). The present data support a close relationship between salivary, serum protease content and clinical periodontal parameters in patients with generalized periodontitis.

Lipid peroxidation levels and total oxidant/antioxidant status in serum and saliva from patients with chronic and aggressive periodontitis. Oxidative stress index: a new biomarker for periodontal disease?

BACKGROUND: In this study, levels of malondialdehyde (MDA), which is a significant product of lipid peroxidation (LPO), total oxidant status (TOS), total antioxidant capacity (TAOC), and the oxidative stress index (OSI), a novel value as a marker of periodontal disease activity, are investigated in serum and saliva from patients with chronic (CP) and generalized aggressive (GAgP) periodontitis. METHODS: A total of 98 patients (33 with CP, 35 patients with GAgP, and 30 periodontally healthy controls) enrolled in the study. After clinical measurements and sample collection, the MDA level, TOS, and TAOC were measured by high-performance liquid chromatography and a novel automatic colorimetric method. The OSI was calculated as [(TOS/TAOC) × 100]. RESULTS: Although the salivary MDA levels and serum and salivary TOS and OSI values were significantly higher in the periodontitis groups than in the control group (P <0.05), the serum and salivary TAOC levels were significantly lower, and no significant difference in serum MDA levels was found (P >0.05). Furthermore, oxidative stress parameters were higher in the GAgP group than in the CP group (except the serum and salivary MDA levels and serum TAOC). Significant positive and negative correlations were observed between periodontal parameters and the MDA levels and TOS, TAOC, and OSI values (except serum MDA) (P <0.05). CONCLUSIONS: The present findings suggest that an increased TOS and decreased TAOC, rather than LPO, play important roles in the pathology of periodontitis and are closely associated with clinical periodontal status. Furthermore, the OSI may be a useful and practical parameter for evaluating periodontal disease activity.

Saliva and serum levels of B-cell activating factors and tumor necrosis factor-α in patients with periodontitis.

BACKGROUND: B-lymphocytes play a central and critical role in the adaptive immune response against invading pathogens. This study evaluates saliva and serum levels of APRIL (a proliferation-inducing ligand), B-cell activating factor (BAFF), tumor necrosis factor-α (TNF-α), interleukin (IL)-6, and IL-10 in patients with chronic periodontitis (CP) or aggressive periodontitis (AgP) and periodontally healthy individuals. METHODS: Twenty-five patients with AgP, 20 patients with CP, and 20 periodontally healthy individuals were included. Smoking status was recorded, and all individuals were divided into non-smokers and smokers. Saliva and serum samples were collected before clinical periodontal measurements. APRIL, BAFF, TNF-α, IL-6, and IL-10 levels in serum and saliva samples were determined by enzyme-linked immunosorbent assay. Statistical analysis was performed using multivariate analysis of variance and bivariate correlation. RESULTS: Serum and saliva levels of TNF-α, APRIL, BAFF, IL-6, and IL-10 were similar in CP and AgP groups. Serum levels of TNF-α, APRIL, and BAFF and saliva levels of BAFF were significantly higher in periodontitis groups than healthy controls (P <0.05). Non-smokers with CP or AgP had lower levels of saliva TNF-α and APRIL and serum APRIL and IL-6 than smokers with CP or AgP (P <0.05). Saliva APRIL and serum TNF-α and IL-6 levels were significantly higher in healthy smokers than healthy non-smokers (P <0.05). Clinical periodontal parameters correlated positively with TNF-family cytokines and negatively with IL-10 (P <0.05). CONCLUSIONS: Within the limits of this study, it may be suggested that elevated salivary and serum TNF-α, APRIL, and BAFF in patients with periodontitis may contribute to the dominance of B cells in periodontitis lesions. Moreover, higher levels in healthy smokers than non-smoking counterparts may play a role in detrimental effects of smoking on periodontal tissues.

Total oxidant status and bone resorption biomarkers in serum and gingival crevicular fluid of patients with periodontitis.

BACKGROUND: In this study, the relationships between total oxidant status (TOS) and receptor activator of nuclear factor-κB ligand (RANKL) and osteoprotegerin (OPG) levels and RANKL/OPG ratios in serum and gingival crevicular fluid (GCF) are investigated in patients with chronic (CP) and generalized aggressive (GAgP) periodontitis. METHODS: Thirty patients with CP, 30 patients with GAgP, and 28 periodontally healthy controls were included in the study. After clinical measurements and samplings, serum and GCF TOS, RANKL, and OPG levels were determined by a novel automatic colorimetric method and enzyme-linked immunosorbent assays. RESULTS: Serum and GCF TOS, RANKL, and RANKL/OPG values were higher in the periodontitis groups compared with controls, and they were also higher in the GAgP group than the CP group (except serum and GCF RANKL). Furthermore, serum and GCF OPG concentrations were lower in the periodontitis groups than in controls. Strong positive and negative correlations were observed between the periodontal parameters TOS and bone resorption biomarkers. CONCLUSIONS: The present results reveal that TOS, RANKL, and RANKL/OPG values are systemically and locally increased in periodontitis and that this increase is more evident in AgP than CP. These findings further suggest that oxidative stress is closely associated with the severity of periodontitis and bone resorption biomarkers.

Association of aggressive periodontitis with reduced erythrocyte counts and reduced hemoglobin levels.

BACKGROUND AND OBJECTIVE: Studies have shown that erythrocyte counts and hemoglobin levels are reduced in patients with chronic periodontitis, suggesting that this condition may be associated with anemia of chronic disease. Although increased leukocyte counts have been reported in aggressive periodontitis, very little is known about the effects of aggressive periodontitis on erythrocyte counts. The present study was undertaken to determine whether generalized aggressive periodontitis is associated with reduced erythrocyte counts and reduced hemoglobin levels. MATERIAL AND METHODS: The present study was conducted as a case-control study in which 64 patients with generalized aggressive periodontitis were categorized as cases and 58 periodontally healthy individuals were categorized as controls. Erythrocyte parameters (such as erythrocyte count, hemoglobin concentration, and hematocrit and erythrocyte indices) and clinical parameters (such as gingival index, plaque index, probing depth, clinical attachment level and percentage of severe sites) were recorded. RESULTS: Significant differences were observed between cases and controls in mean erythrocyte count (4.45 ± 0.6 × 10(6) erythrocytes/µL and 4.78 ± 0.56 × 10(6) erythrocytes/µL respectively, p = 0.002) and hemoglobin level (12.43 ± 1.83 g/dL and 13.53 ± 1.64 g/dL, respectively, p = 0.001). Other erythrocyte parameters, such as hematocrit, mean corpuscular volume and mean corpuscular hemoglobin, were also significantly lower among cases compared with controls. Logistic regression analyses showed that generalized aggressive periodontitis was significantly associated with lower erythrocyte counts ( p = 0.032) and a lower hemoglobin concentration ( p = 0.017). CONCLUSION: The findings of the present study suggest that patients with generalized aggressive periodontitis tend to have lower erythrocyte counts and lower hemoglobin levels compared with periodontally healthy controls. This suggests that generalized aggressive periodontitis, like chronic periodontitis, may be associated with a risk for anemia of chronic disease.