Immunoglobulin G subclass antibody profiles in Porphyromonas gingivalis-associated aggressive and chronic periodontitis patients

BACKGROUND/AIMS: The immunoglobulin G (IgG) antibody response is considered to be protective and beneficial for the control of periodontal lesions. This study analysed IgG subclass antibody levels of Porphyromonas gingivalis in patients with both aggressive periodontitis (AgP) and chronic periodontitis (CP). METHODS: Subgingival plaque and peripheral blood samples were collected from patients with localized AgP (n = 13), generalized AgP (n = 28) and generalized CP (n = 27) and from 14 periodontally healthy controls. P. gingivalis was identified in subgingival pockets using a polymerase chain reaction. Simultaneously, serum IgG subclass antibody against P. gingivalis whole cells/P. gingivalis fimbriae were measured using enzyme-linked immunosorbent assay. RESULTS: P. gingivalis was frequently detected in periodontitis patients. Anti-P. gingivalis whole cell IgG1 was elevated in all P. gingivalis-positive patients in the three periodontitis groups. Although increased anti-P. gingivalis IgG1 was also observed in the bacterium-positive healthy controls, the level was lower than that found in the three periodontitis groups. Levels of IgG1, IgG2, IgG3 and IgG4 to P. gingivalis did not differ among bacterium-positive patients in the three periodontitis groups; a significant increase of IgG2 level was not observed in localized AgP. Anti-fimbriae IgG subclass levels of IgG1, IgG2 and IgG4 did not differ among bacterium-positive subjects in all groups, while the anti-fimbriae IgG3 level in generalized CP was significantly higher than that in localized and generalized AgP. CONCLUSIONS: P. gingivalis infection elicited an IgG subclass antibody response in both periodontitis patients and healthy subjects, while higher anti-P. gingivalis IgG1 levels were found in the three periodontitis groups compared with the healthy control group.     

Differential platelet-activating factor synthesis by monocytes and polymorphonuclear leukocytes from subjects with localized aggressive periodontitis

BACKGROUND AND OBJECTIVE: Platelet-activating factor is elevated in localized aggressive periodontitis. We previously demonstrated that the elevated level of platelet-activating factor in localized aggressive periodontitis is at least partially attributable to low levels of platelet-activating factor acetylhydrolase, the enzyme that catabolizes platelet-activating factor. The objective of this study was to determine if platelet-activating factor synthesis was also elevated in localized aggressive periodontitis. To test this, platelet-activating factor synthesis was quantified in the monocytes and polymorphonuclear neutrophils of periodontally healthy patients and of subjects with localized aggressive periodontitis. MATERIAL AND METHOds: Cells were labeled with [(3)H]acetate and treated with vehicle or stimulated with calcium ionophore A23187. Platelet-activating factor was extracted and quantified by scintillation counting. RESULTS: For both subject groups, resting monocytes and polymorphonuclear neutrophils produced platelet-activating factor, and calcium ionophore A23187 stimulated platelet-activating factor production in both cell types. However, calcium ionophore A23187-activated monocytes from subjects with localized aggressive periodontitis produced less platelet-activating factor than did activated periodontally healthy monocytes (p < 0.0001), suggesting an aberrant calcium ionophore A23187 response in monocytes from subjects with localized aggressive periodontitis. Indeed, when the data were expressed as fold induction of platelet-activating factor synthesis in response to calcium ionophore A23187, monocytes from subjects with localized aggressive periodontitis exhibited only a fourfold increase in platelet-activating factor synthesis, whereas calcium ionophore A23187-stimulated monocytes from periodontally healthy, chronic periodontitis and generalized aggressive periodontitis subjects produced approximately 12 times more platelet-activating factor than did resting monocytes. In contrast, both resting and activated localized aggressive periodontitis polymorphonuclear neutrophils synthesized more platelet-activating factor than did periodontally healthy polymorphonuclear neutrophils. CONCLUSION: These data suggest that high levels of platelet-activating factor in subjects with localized aggressive periodontitis result from both increased synthesis and reduced catabolism. While localized aggressive periodontitis polymorphonuclear neutrophils contribute to increased platelet-activating factor mass through synthesis, the contribution of monocytes is probably the result of reduced catabolism by platelet-activating factor acetylhydrolase.     

Periodontal treatment decreases plasma oxidized LDL level and oxidative stress

Periodontitis induces excessive production of reactive oxygen species in periodontal lesions. This may impair circulating pro-oxidant/anti-oxidant balance and induce the oxidation of low-density lipoprotein (LDL) in blood. The purpose of this study was to monitor circulating oxidized LDL and oxidative stress in subjects with chronic periodontitis following non-surgical periodontal treatment. Plasma levels of oxidized LDL and oxidative stress in 22 otherwise healthy non-smokers with chronic periodontitis (mean age 44.0?years) were measured at baseline and at 1 and 2?months after non-surgical periodontal treatment. At baseline, chronic periodontitis patients had higher plasma levels of oxidized LDL and oxidative stress than healthy subjects (p?<?0.001). Periodontal treatment was associated with a significant reduction in plasma levels of oxidized LDL (oxLDL)(p?<?0.001) and oxidative stress (p?<?0.001). At 2?months after periodontal treatment, the degree of change in the oxLDL was positively correlated with that in the oxidative stress (r?=?0.593, p?=?0.004). These observations indicate that periodontitis patients showed higher levels of circulating oxLDL and oxidative stress than healthy subjects. In addition, improved oral hygiene and non-surgical periodontal treatment were effective in decreasing oxLDL, which was positively associated with a reduction in circulating oxidative stress.     

Immunoglobulin G subclass antibody profiles in Porphyromonas gingivalis‐associated aggressive and chronic periodontitis patients

Background/aims: The immunoglobulin G (IgG) antibody response is considered to be protective and beneficial for the control of periodontal lesions. This study analysed IgG subclass antibody levels of Porphyromonas gingivalis in patients with both aggressive periodontitis (AgP) and chronic periodontitis (CP). Methods: Subgingival plaque and peripheral blood samples were collected from patients with localized AgP (n = 13), generalized AgP (n = 28) and generalized CP (n = 27) and from 14 periodontally healthy controls. P. gingivalis was identified in subgingival pockets using a polymerase chain reaction. Simultaneously, serum IgG subclass antibody against P. gingivalis whole cells/P. gingivalis fimbriae were measured using enzyme‐linked immunosorbent assay. Results: P. gingivalis was frequently detected in periodontitis patients. Anti‐P. gingivalis whole cell IgG1 was elevated in all P. gingivalis‐positive patients in the three periodontitis groups. Although increased anti‐P. gingivalis IgG1 was also observed in the bacterium‐positive healthy controls, the level was lower than that found in the three periodontitis groups. Levels of IgG1, IgG2, IgG3 and IgG4 to P. gingivalis did not differ among bacterium‐positive patients in the three periodontitis groups; a significant increase of IgG2 level was not observed in localized AgP. Anti‐fimbriae IgG subclass levels of IgG1, IgG2 and IgG4 did not differ among bacterium‐positive subjects in all groups, while the anti‐fimbriae IgG3 level in generalized CP was significantly higher than that in localized and generalized AgP. Conclusions: P. gingivalis infection elicited an IgG subclass antibody response in both periodontitis patients and healthy subjects, while higher anti‐P. gingivalis IgG1 levels were found in the three periodontitis groups compared with the healthy control group.     

Gingival crevicular fluid levels of RANKL and OPG in periodontal diseases: implications of their relative ratio

AIM: Receptor activator of NF-kappaB ligand (RANKL) and osteoprotegerin (OPG) are a system of molecules that regulate bone resorption. This study aims to compare the levels of RANKL, OPG and their relative ratio in gingival crevicular fluid (GCF) of healthy and periodontal disease subjects. MATERIAL AND METHODS: GCF was obtained from healthy (n=21), gingivitis (n=22), chronic periodontitis (n=28), generalized aggressive periodontitis (n=25) and chronic periodontitis subjects under immunosuppressant therapy (n=11). RANKL and OPG concentrations in GCF were measured by enzyme-linked immunosorbent assays. RESULTS: RANKL levels were low in health and gingivitis groups, but increased in all three forms of periodontitis. OPG levels were higher in health than all three periodontitis, or gingivitis groups. There were no differences in RANKL and OPG levels between chronic and generalized aggressive periodontitis groups, whereas these were lower in the immunosuppressed chronic periodontitis group. The RANKL/OPG ratio was significantly elevated in all three periodontitis forms, compared with health or gingivitis, and positively correlated to probing pocket depth and clinical attachment level. CONCLUSION: GCF RANKL and OPG levels were oppositely regulated in periodontitis, but not gingivitis, resulting in an enhanced RANKL/OPG ratio. This ratio was similar in all three periodontitis groups and may therefore predict disease occurrence.     

Severe periodontitis is associated with systemic inflammation and a dysmetabolic status: a case-control study

BACKGROUND AND AIM: A cluster of metabolic factors defines a syndrome that predisposes to diabetes and cardiovascular disease. Chronic infections such as periodontitis might alter these individual metabolic factors and the systemic inflammatory burden. The aim of this study was to investigate the association between severe periodontitis and increase in inflammatory and metabolic risk factors for cardiovascular disease. MATERIALS AND METHODS: We examined 302 patients with severe periodontitis and 183 healthy controls, and we collected a blood sample from each subject in order to investigate differences in inflammatory (leukocyte numbers and differential counts) and metabolic markers (lipids and glucose). RESULTS: After correcting for differences in age, gender, smoking and ethnicity, periodontitis subjects exhibited a low-grade systemic inflammation (increased white cell counts, 1.10+/-1.02 x 10(9)/l, 95%CI 1.05-1.15, p=0.0001), dyslipidemia [lower high-density lipoprotein cholesterol, 1.14+/-1.03 mmol/l, 95%CI 1.08-1.20, p<0.0001 and higher low-density lipoprotein cholesterol, 1.12+/-1.03, 95%CI 1.05-1.19, p<0.0001) and increased non-fasting serum glucose levels (1.04+/-1.01 mmol/l, 95%CI 1.02-1.06, p=0.01) when compared with controls. The associations were confirmed in a subpopulation of Caucasian non-smokers. A trend for a dose dependent effect of the number of periodontal pockets on the tested inflammatory and metabolic markers was observed. Conclusions: These data suggest a possible link between severe generalized periodontitis, systemic inflammation and a dysmetabolic state in otherwise healthy individuals.     

Intracytoplasmic enzymes in gingival crevicular fluid of patients with aggressive periodontitis

Castro CE, Koss MA, López ME. Intracytoplasmic enzymes in gingival crevicular fluid of patients with aggressive periodontitis. J Periodont Res 2011; 46: 522–527. © 2011 John Wiley & Sons A/S Background and Objective: Biochemical parameters of crevicular fluid could provide evidence of periodontal tissue disease. The aim of this study was to analyze enzymes in crevicular fluid in aggressive localized and generalized periodontitis. Material and Methods: One hundred and twenty‐four subjects were classified as having localized (n = 36) or generalized aggressive periodontitis (n = 38) and subclassified into moderate and severe groups. Controls were 50 periodontitis‐free subjects. Activities of the enzymes lactate dehydrogenase, neutrophil elastase, alkaline phosphatase and aspartate aminotransferase were determined. Data were analyzed using one‐way ANOVA and Tukey’s test. Results: Among the subjects with localized aggressive periodontitis, values of lactate dehydrogenase and alkaline phosphatase increased notably in moderate and severe periodontitis compared with control subjects. Values for aspartate aminotransferase increased with the severity of the disease, and neutrophil elastase was increased in the moderate and severe states. In generalized aggressive periodontitis, lactate dehydrogenase showed higher values than in control subjects in both periodontal subgroups. Alkaline phosphatase and neutrophil elastase showed higher significant differences between moderate and severe periodontitis compared with the control group. Aspartate aminotransferase showed differences between the severe and moderate periodontitis groups compared with the control group. Of all the enzymes analyzed, only lactate dehydrogenase showed higher values in localized than in generalized aggressive periodontitis. Conclusion: Lactate dehydrogenase may distinguish localized and generalized aggressive periodontitis. Alkaline phosphatase increases from moderate to severe states in both types of periodontitis. Aspartate aminotransferase and neutrophil elastase only increase with strong evidence of periodontal destruction.     

C-reactive protein levels in patients with aggressive periodontitis

BACKGROUND: Sera from patients with periodontal infections contain elevated levels of C-reactive protein (CRP) compared to periodontally healthy individuals. Most studies to date have included patients with chronic periodontitis, and few investigators have studied CRP levels in subjects with aggressive periodontitis (AgP). The purpose of this study was to determine the relative levels of serum CRP in AgP patients and periodontally healthy subjects and to examine patients' characteristics that might account for intergroup differences. METHODS: Serum samples were collected from 93 patients with generalized AgP (GAgP), from 97 patients with localized AgP (LAgP), and from 91 healthy controls (non-periodontitis [NP]). Periodontal examination consisted of plaque index, gingival index, probing depth, bleeding index, and attachment loss measurements. Current smoking was assessed by determination of serum cotinine levels by enzyme-linked immunosorbent assay (ELISA), and serum CRP levels were determined using a high-sensitivity ELISA assay. RESULTS: The three groups were significantly different from one another (P <0.0001). The 95% confidence interval for serum CRP concentrations were as follows: NP, 0.65919 (0.4901 to 0.8869); LAgP, 1.10138 (0.8265 to 1.468); and GAgP, 2.05318 (1.5313 to 2.7538) mg/l. CRP levels in both LAgP and GAgP subjects were significantly greater than those in NP subjects, and levels in GAgP were significantly greater than those in LAgP. Following adjustment of the data for periodontal and demographic variables and current smoking, both mean probing depth and periodontal diagnosis remained correlated with CRP levels. CONCLUSIONS: Patients with AgP have statistically significant elevations in serum CRP levels compared to subjects without periodontitis. Elevated CRP in these subjects might represent a contribution of periodontal infections to systemic inflammation in relatively young individuals.     

Evidence for a specific crevicular lymphocyte profile in aggressive periodontitis

BACKGROUND AND OBJECTIVE: It is undisputed that the periodontal pocket is a particular region of the host defense that is dominated by polymorphonuclear leukocytes. However, little is known about the lymphocytes in the crevice. It was the aim of this study to analyse the proportions of T cells (CD3+), T-helper cells (CD4+), T-suppressor cells (CD8+), and B cells (CD20+) in the crevice of patients with localized aggressive periodontitis (LAP), generalized aggressive periodontitis (GAP), and generalized chronic periodontitis (CP). The results were compared with those obtained from periodontally healthy controls. MATERIAL AND METHODS: Crevicular cells were collected according to a previously described method. The lymphocyte subpopulations were analysed by using an indirect immunofluorescence method. RESULTS: Significant differences were established between the test groups and the controls regarding the mean number of CD8+ lymphocytes (LAP > CP and controls; p < 0.05) and CD20+ lymphocytes (LAP/GAP > CP, p < 0.05 and LAP/GAP > controls; p < 0.001). Significant variations in the CD4+/CD8+ ratio were observed (LAP < controls and GAP < controls; p < 0.01), as well as a correlation between the number of T cells and the degree of inflammation. CONCLUSION: In the present study, patients with LAP and patients with GAP were found to have increased numbers of crevicular T-suppressor/cytotoxic and B cells. This supports the hypothesis of a changed immune pathology in patients with aggressive periodontitis.     

Influence of periodontal therapy on the regulation of soluble cell adhesion molecule expression in aggressive periodontitis patients

BACKGROUND: Inflammatory periodontal disease is associated with an increased risk of cardiovascular disease. Circulating cell adhesion molecules (CAM) (intercellular adhesion molecule-1 [ICAM-1], vascular cell adhesion molecule-1 [VCAM-1], and E-selectin) have been suggested as potential candidate markers of endothelial dysfunction, which contribute to the pathogenesis of cardiovascular diseases. The regulation of CAM in subjects with severe periodontitis and the influence of periodontal intervention on systemic CAM levels are not clear. The aim of this study was to determine whether intensive periodontal therapy reduces serum levels of CAM in patients with generalized aggressive periodontitis. METHODS: Blood samples were collected at six treatment time points from 21 patients with previously untreated generalized aggressive periodontitis (mean age: 34.6 +/- 4.3 years). Patients received subgingival scaling and root planing and antibiotic therapy and were monitored over a 6-month recall period. Serum levels of soluble ICAM-1 (sICAM-1), VCAM-1 (sVCAM-1), and E-selectin (sE-selectin) were measured by enzyme-linked immunosorbent assay. RESULTS: sE-selectin plasma levels decreased significantly (P <0.01) during periodontal therapy. Mean plasma levels were 65.95 ng/ml before treatment and 44.71 ng/ml 6 months after antibiotic therapy. sICAM-1 and sVCAM-2 serum levels were unaffected by therapeutic intervention. CONCLUSIONS: Periodontal therapy reduces plasma sE-selectin levels. Whether this leads to a reduction in risk of future cardiovascular events in patients with aggressive periodontal disease warrants further studies.     

Comparison of CCL28, interleukin‐8, interleukin‐1β and tumor necrosis factor‐alpha in subjects with gingivitis,chronic periodontitis and generalized aggressive periodontitis

Background and Objective: Cytokines produced by various cells are strong local mediators of inflammation. Mucosa‐associated epithelial chemokine (CCL28), interleukin‐8 (IL‐8), interleukin‐1beta (IL‐1β) and tumor necrosis factor‐alpha (TNF‐α) are major cytokines that play important roles in the periodontal inflammatory process. In this study we aimed to compare the levels of CCL28, IL‐8, IL‐1β and TNF‐α in the gingival crevicular fluid of both periodontally healthy subjects and in subjects diagnosed with gingivitis, chronic periodontitis and generalized aggressive periodontitis. Material and Methods: A total of 84 subjects participated in the study: 21 subjects had gingivitis, 21 subjects had chronic periodontitis, 21 subjects had generalized aggressive periodontitis and 21 were periodontally healthy. The levels of CCL28, IL‐8, IL‐1β and TNF‐α were analyzed using enzyme‐linked immune sorbent assay (ELISA). Results: The total levels of CCL28 and IL‐8 in the gingival crevicular fluid of the generalized aggressive periodontitis group (324.74 ± 42.62 pg/30 s, 487.62 ± 49.21 pg/30 s) were significantly higher than those of the chronic periodontitis group (268.81 ± 28.64 pg/30 s, 423.65 ± 35.24 pg/30 s), the gingivitis group (146.35 ± 17.46 pg/30 s, 310.24 ± 48.20 pg/30 s) and the periodontally healthy group (92.46 ± 22.04 pg/30 s, 148.41 ± 24.64 pg/30 s). Similarly, the total levels of IL‐1β and TNF‐α in the generalized aggressive periodontitis group (110.23 ± 9.20 pg/30 s, 1284.46 ± 86.32 pg/30 s) were significantly higher than those in the chronic periodontitis group (423.65 ± 35.24 pg/30 s, 82.64 ± 9.12 pg/30 s), the gingivitis group (52.10 ± 7.15 pg/30 s, 824.24 ± 44.68 pg/30 s) and the periodontally healthy group (36.44 ± 8.86 pg/30 s, 628.26 ± 34.61 pg/30 s). Conclusion: CCL28, IL‐8, IL‐1β and TNF‐α may play key roles in the host response to inflammation in periodontal diseases. As the severity of periodontal diseases increases, destruction of periodontal tissues also increases. Inflammation is one among many factors that trigger periodontal tissue destruction. Identification of the mediators that influence the development and progression of inflammation in periodontal diseases may be very important in understanding the prognoses of periodontal diseases.     

Anti-cardiolipin and increased serum adhesion molecule levels in patients with aggressive periodontitis

BACKGROUND: We observed that a significant proportion of patients with periodontitis have elevated serum levels of beta2-glycoprotein-I-dependent anti-cardiolipin (anti-CL). These prothrombotic autoantibodies, commonly found to be elevated in patients with systemic lupus erythematosus and the antiphospholipid syndrome, are associated with adverse pregnancy outcomes, such as fetal involution, prematurity, and low birth weight, and with cardiovascular sequelae, such as atherosclerosis, stroke, and myocardial infarction. Anti-CL is known to promote vascular inflammation and thrombosis. METHODS: We measured serum levels of markers of vascular inflammation, including soluble intercellular adhesion molecule (sICAM)-1, soluble vascular cell adhesion molecule (sVCAM)-1, and sE-selectin, in 190 subjects with generalized aggressive or chronic periodontitis and in 90 periodontally healthy subjects. RESULTS: sVCAM-1 and sE-selectin levels were significantly higher in patients with elevated anti-CL (>15 U/ml). This relationship also was observed in the never-smoker subset of subjects, even after correction for demographic and periodontal variables. Within the diagnostic categories, sICAM-1, sVCAM-1, and sE-selectin were significantly higher in generalized aggressive periodontitis patients who had elevated anti-CL compared to those with normal anti-CL. Statistical correction for demographic and periodontal variables indicated that elevated anti-CL remained significantly associated with increased sVCAM-1 and sE-selectin in generalized aggressive periodontitis patients. CONCLUSIONS: Systemic markers of vascular inflammation in patients with aggressive periodontitis are associated with elevated levels of anti-CL. We hypothesize that a subset of periodontitis patients with elevated antiphospholipid antibodies could represent a subgroup at increased risk for obstetrical and cardiovascular sequelae.     

Elevated serum IgG titer and avidity to Actinobacillus actinomycetemcomitans serotype c in Japanese periodontitis patients

AIM: The purpose of this study was to characterize serum antibody responses to different serotypes of Actinobacillus actinomycetemcomitans strains in various forms of periodontitis and to determine whether any specific type of A. actinomycetemcomitans was associated with any specific form of periodontitis in a Japanese population. METHODS: Sonicated whole cell and autoclaved serotype antigens of A. actinomycetemcomitans were used. Serum IgG titer and avidity to A. actinomycetemcomitans were measured by enzyme-linked immunoabsorbant assay (ELISA) and ammonium thiocyanate-dissociation ELISA, respectively, in 46 aggressive periodontitis patients (8 localized, 38 generalized), 28 chronic periodontitis patients, and 18 periodontally healthy subjects. The presence of A. actinomycetemcomitans in plaque and saliva samples was determined using polymerase chain reaction. RESULTS: Generalized aggressive and chronic periodontitis patients exhibited significantly higher IgG titers than healthy subjects to both sonicated and autoclaved antigens of serotype c strains, while IgG titer to serotype b (Y4) was significantly higher in localized aggressive periodontitis patients compared to healthy subjects. No A. actinomycetemcomitans was detected in localized aggressive periodontitis patients. A. actinomycetemcomitans-positive patients exhibited significantly higher IgG titer and avidity to serotype c than A. actinomycetemcomitans-negative patients. In A. actinomycetemcomitans-positive patients, a significantly positive correlation was observed between antibody titer and avidity to serotype c. A. actinomycetemcomitans-positive patients with generalized aggressive periodontitis showed lower IgG avidities to serotype c than those with chronic periodontitis, though no statistically significant difference was found. CONCLUSION: A. actinomycetemcomitans serotype c may play a significant role in chronic and generalized aggressive periodontitis, while A. actinomycetemcomitans serotype b may be associated with localized aggressive periodontitis in a Japanese population.     

Differential regulation of innate immune response genes in gingival epithelial cells stimulated with Aggregatibacter actinomycetemcomitans

Background and Objective:  The gingival epithelium provides the first line of defense against colonization by periodontal pathogens, both as a physical barrier and by the production of inducible innate immune mediators such as β-defensins and pro-inflammatory cytokines. The gram-negative bacterium Aggregatibacter actinomycetemcomitans is implicated in the pathogenesis of localized aggressive periodontitis, although the bacterium is found widely in the healthy population. We hypothesized that gingival epithelial cell-derived innate immune mediators triggered in response to A. actinomycetemcomitans infection may play an important role in increased susceptibility to infection.
Material and Methods:  Primary cultures of human gingival epithelial cells were cultured in the presence of A. actinomycetemcomitans . Total mRNA was examined for the presence of innate immune markers using RT-PCR.
Results:  We show here that the mRNA levels of human β-defensin 2 and interleukin-8 are elevated by live cultures of a clinical isolate of A. actinomycetemcomitans in cultured gingival epithelial cells from healthy individuals, but not by A. actinomycetemcomitans lipopolysaccharide. Cells from a patient with localized aggressive periodontitis, however, did not respond to this bacterial stimulation. In contrast, the pro-inflammatory cytokine interleukin-19 was induced in cells from both localized aggressive periodontitis and healthy subjects. Examination of Toll-like receptors and associated adapter molecules indicated lower levels of Toll-like receptor 2 mRNA in the localized aggressive periodontitis patient-derived cells compared with cells from healthy subjects.
Conclusion:  These results suggest that a differential expression of innate immune response genes to A. actinomycetemcomitans in the gingival epithelium could be an underlying factor of susceptibility to localized aggressive periodontitis.     

Plasma osteoprotegerin levels are decreased in smoker chronic periodontitis patients

Background: The aim of this study was to evaluate plasma levels of soluble receptor activator of nuclear factor‐kappa B ligand (sRANKL) and osteoprotegerin (OPG) in smoker versus non‐smoker chronic periodontitis patients. Methods: Plasma samples were obtained from 13 smoker and 31 non‐smoker systemically healthy chronic periodontitis patients, as well as 13 smoker and 29 non‐smoker systemically and periodontally healthy subjects. Before commencing any periodontal intervention, venous blood samples were obtained and whole‐mouth clinical periodontal measurements were recorded. sRANKL and OPG concentrations in plasma samples were determined by enzyme‐linked immunosorbent assay (ELISA) technique. Data were tested statistically by student’s t test, Wilcoxon matched pairs test, and Spearman’s correlation analysis. Results: All clinical periodontal measurements were significantly higher in chronic periodontitis groups than the healthy controls (p < 0.05). Smoker and non‐smoker chronic periodontitis patients exhibited similar values in all clinical periodontal measurements and plasma sRANKL, OPG concentrations (p > 0.05). Smoker chronic periodontitis patients exhibited significantly lower (p = 0.007) plasma OPG concentrations and higher sRANKL/OPG ratio (p = 0.01) than smoker healthy controls. Conclusions: Within the limits of this study, periodontal inflammation in smoker chronic periodontitis patients seems to lower plasma osteoprotegerin levels and thereby increase the RANKL/OPG ratio, and possibly play a role in the increased susceptibility for alveolar bone destruction in smoker subjects.     

Real-time PCR quantification of cytomegalovirus in aggressive periodontitis lesions using TaqMan technology

BACKGROUND: Herpesviruses are implicated in the pathogenesis of human periodontitis. However, the quantity of herpesviruses in periodontal sites remains unknown. OBJECTIVE: The aim of this study was to compare levels of subgingival human cytomegalovirus (HCMV) in aggressive periodontitis patients and in periodontally healthy subjects. METHODS: A total of 16 consecutive subjects with aggressive periodontitis and 15 healthy control subjects were included in the study. Subgingival specimens were collected by a periodontal curette. TaqMan real-time polymerase chain reaction (PCR) assay was used to quantify HCMV. RESULTS: HCMV was detected in 68.8% of aggressive periodontitis lesions but not in any of the periodontally healthy study sites. HCMV viral load in positive subgingival specimens ranged from 5 x 10(2) to 7.4 x 10(3) copies/ml. CONCLUSIONS: The TaqMan real-time PCR technology seems to provide a rapid and sensitive method for quantifying HCMV in periodontal pockets. The present findings confirm the frequent presence of HCMV in aggressive periodontitis lesions. Determining HCMV levels in different types of periodontitis may help elucidate the periodontopathic role of the virus and advance our understanding of the disease pathogenesis.     

C-reactive protein associated with periodontitis in a Thai population

Aim: C‐reactive protein (CRP) has been implicated as a possible mediator of the association between periodontitis and several systemic diseases. Previous studies suggest an association between increased CRP levels and periodontitis predominantly in Caucasians. This study evaluated the associations of chronic periodontitis and Porphyromonas gingivalis with CRP in systemically healthy Thai adults. Material and Methods: Serum high‐sensitivity CRP was measured in 21 generalized periodontitis, 62 localized periodontitis, and 38 periodontally healthy control subjects. P. gingivalis in subgingival plaque samples was analyzed by polymerase chain reaction. Results: Overall, these subjects had a median CRP level lower than that reported in the western populations. Subjects with generalized periodontitis and localized periodontitis had higher median CRP levels than controls (1.78 and 0.65 mg/l versus 0.25 mg/l, p<0.001). Multivariate linear regression showed that log CRP levels were increased in subjects with generalized periodontitis (p<0.01) and localized periodontitis (p=0.03) compared with the controls, adjusted for age, body mass index and smoking. Presence of P. gingivalis was also independently associated with elevated log CRP levels (p<0.001). Conclusion: Periodontitis and subgingival P. gingivalis are associated with increased CRP levels. These findings suggest that periodontal infection may contribute to systemic inflammatory burden in otherwise healthy individuals.     

Immune response to cytolethal distending toxin of Aggregatibacter actinomycetemcomitans in periodontitis patients

Ando ES, De‐Gennaro LA, Faveri M, Feres M, DiRienzo JM, Mayer MPA. Immune response to cytolethal distending toxin of Aggregatibacter actinomycetemcomitans in periodontitis patients. J Periodont Res 2010; 45: 471–480. © 2010 John Wiley & Sons A/S Background and Objective: Cytolethal distending toxin (CDT) is a genotoxin produced by Aggregatibacter actinomycetemcomitans. In spite of its association with pathogenesis, little is known about the humoral immune response against the CDT. This study aimed to test whether subgingival colonization and humoral response to A. actinomycetemcomitans would lead to a response against CDT. Material and Methods: Sera from periodontally healthy, localized and generalized aggressive periodontitis and chronic periodontitis subjects (n = 80) were assessed for immunoglobulin G titers to A. actinomycetemcomitans serotypes a/b/c and to each CDT subunit (CdtA, CdtB and CdtC) by ELISA. A. actinomycetemcomitans subgingival levels and neutralization of CDT activity were also analyzed. Results: Sera from 75.0% localized and 81.8% generalized aggressive periodontitis patients reacted to A. actinomycetemcomitans. A response to serotype b was detected in localized (66.7%) and generalized aggressive periodontitis (54.5%). Reactivity to A. actinomycetemcomitans correlated with subgingival colonization (R = 0.75, p < 0.05). There was no correlation between A. actinomycetemcomitans colonization or response to serotypes and the immunoglobulin G response to CDT subunits. Titers of immunoglobulin G to CdtA and CdtB did not differ among groups; however, sera of all generalized aggressive periodontitis patients reacted to CdtC. Neutralization of CDT was not correlated with levels of antibodies to CDT subunits. Conclusion: Response to CdtA and CdtB did not correlate with the periodontal status of the subject in the context of an A. actinomycetemcomitans infection. However, a response to CdtC was found in sera of generalized but not of localized aggressive periodontitis subjects. Differences in response to CdtC between generalized and localized aggressive periodontitis subjects indicate that CDT could be expressed differently by the infecting strains. Alternatively, the antibody response to CdtC could require the colonization of multiple sites.     

Plasma and crevicular fluid osteopontin levels in periodontal health and disease

BACKGROUND AND OBJECTIVE: The level of osteopontin in gingival crevicular fluid has been found to correlate with clinical measures of periodontal disease. The present study was designed to assess the relationship between clinical parameters and osteopontin levels of the gingival crevicular fluid from inflamed gingivae, periodontitis sites and after treatment of periodontitis sites, and to correlate them to the osteopontin levels of the plasma. MATERIAL AND METHODS: Thirty, gender-matched subjects were divided into three groups--healthy, gingivitis and chronic periodontitis--based on modified gingival index scores and clinical attachment loss. The fourth group consisted of 10 subjects in the periodontitis group, 6-8 wk after initial therapy. Plasma and gingival crevicular fluid samples were collected and quantified for osteopontin using an enzyme immunoassay. RESULTS: The highest mean gingival crevicular fluid and plasma osteopontin concentrations were observed in the periodontitis group (1575.01 and 1273.21 ng/mL, respectively) and the lowest in the healthy group (1194.80 and 476.35 ng/mL, respectively). After treatment of the periodontitis group, the level of osteopontin decreased to 1416.15 in gingival crevicular fluid and to 1051.68 ng/mL in plasma. In all groups the gingival crevicular fluid osteopontin levels showed a statistically significant positive correlation with that of plasma and clinical attachment loss. CONCLUSION: Osteopontin levels were highest in the gingival crevicular fluid from sites with periodontal destruction; however, periodontal treatment resulted in the reduction of osteopontin levels. Gingival crevicular fluid and plasma osteopontin levels showed a positive correlation in all of the groups.