Low prevalence of subgingival viruses in periodontitis patients

Background: Viruses such as Human Cytomegalovirus (HCMV) and Epstein–Barr virus (EBV) have been proposed to be periodontal pathogens. The aim of this study was to analyse the presence of herpesvirus DNA in subgingival plaque samples of patients with different forms of periodontitis and in healthy periodontia.
Materials and Methods: A total of 140 ethnically mixed (prevalently Caucasian) subjects took part in the study. Sixteen were affected by localized aggressive periodontitis (LAgP), 64 by generalized aggressive periodontitis (GAgP), 20 by chronic periodontitis (CP) and 40 were periodontally healthy. Polymerase chain reaction (PCR) analyses were performed to detect HCMV and EBV. Sera were tested for anti-HCMV and EBV IgG antibodies. PCRs for herpes simplex (HSV) and varicella zoster virus (VZV) were performed in subgingival samples from a subset of 20 AgP subjects.
Results: HCMV DNA was not detected in any plaque samples. EBV DNA was detected in four LAgP (25%), two GAgP (3%) subjects and four healthy individuals (10%). HSV DNA and VZV DNA were not detected in the subset of studied individuals.
Conclusions: This study challenges the previously reported high prevalence of herpesvirus DNA in subgingival samples from periodontitis patients and so questions whether they act as pathogens in such patients.     

Mammalian viruses in human periodontitis

A prior investigation has demonstrated a higher prevalence of human cytomegalovirus (HCMV) and Epstein-Barr virus (EBV) in subgingival specimens from periodontitis patients than from gingivitis patients. This study aimed to determine the frequency of HCMV, EBV-1, EBV-2, herpes simplex virus (HSV) and human immunodeficiency virus (HIV) in subgingival samples from 27 adults who each contributed both a periodontitis and a gingivitis site. Viral detection was performed using a nested-polymerase chain reaction method. Twenty-four subjects (89%) yielded at least one of the five test viruses from deep periodontal pockets, wheras only 15 (56%) showed viruses from shallow periodontal sites ( P =0.015; chi-square test). Viral co-infection occurred more frequently in deep than in shallow periodontal sites ( P =0.015). HCMV was detected with higher frequency in deep than in shallow periodontal sites ( P =0.023). The possible periodontopathogenic mechanisms of mammalian viruses in human periodontitis are discussed. The role and importance of HCMV and other mammalian viruses in the initiation and progression of destructive periodontal disease merits further investigation.     

Adjunctive subantimicrobial dose doxycycline: effect on clinical parameters and gingival crevicular fluid transforming growth factor-beta levels in severe, generalized chronic periodontitis

BACKGROUND: At present there is limited data concerning the efficacy of non-surgical periodontal therapy supplemented with subantimicrobial dose doxycycline (SDD) in the treatment of severe, generalized periodontitis. The purpose of the present study was to evaluate the effect of adjunctive SDD therapy on clinical periodontal parameters and gingival crevicular fluid (GCF) transforming growth factor-beta1 (TGF-beta1) levels in patients with severe, generalized chronic periodontitis over a 6-month period. METHODS: Thirty-five patients with severe, generalized periodontitis and 11 periodontally healthy subjects were included in the present study. Patients received full-mouth supragingival debridment at baseline and randomized to take either SDD b.i.d. or placebo b.i.d. for 3 months. Patients received root planing and oral hygiene instruction once a week for four consecutive weeks. Clinical measurements including probing depth (PD), clinical attachment level, papilla bleeding index and plaque index and GCF sampling were performed at baseline, 3 and 6 months. The GCF TGF-beta1 levels were analysed by enzyme-linked immunosorbent assay. RESULTS: Thirteen patients in both study groups completed the 6-month trial. Following scaling and root planing (SRP) plus SDD and SRP plus placebo therapy significant improvements in clinical periodontal parameters of both groups were observed (p<0.025). In the SDD group a significantly higher percentage (%73.4) of deep pockets resolved (PD reduction > or =3 mm from baseline) when compared with placebo group (%49.7) at 6 months (p<0.05). At baseline there were no significant differences in GCF TGF-beta1 levels between three groups. Both total amount and concentration of GCF TGF-beta1 in SDD and placebo groups increased when compared with baseline at 3 months. However, only GCF TGF-beta1 levels of SDD group was significantly higher than baseline (p<0.025) and placebo group (p<0.017) at 3 months. At 6 months GCF TGF-beta1 levels of both groups were similar to baseline levels (p<0.025). CONCLUSIONS: These data indicate that combination of SDD with non-surgical therapy improves clinical parameters of periodontal disease and increases GCF TGF-beta1 levels together with a decrease in prevalence of residual pockets in patients with severe, generalized chronic periodontitis. Increased GCF TGF-beta1 levels following SDD therapy might suggest a novell pleiotrophic mechanism for tetracyclines to inhibit connective tissue breakdown.     

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.     

Subgingival human cytomegalovirus correlates with increased clinical periodontal parameters and bacterial coinfection in periodontitis

BACKGROUND: Viruses from the Herpesviridae family may be implicated in the pathogenesis of periodontal disease. The aim of this investigation was to compare the subgingival frequency of human cytomegalovirus (HCMV) in subjects affected by periodontitis to periodontally healthy subjects and to assess the correlation of HCMV with periodontal clinical parameters and periodontopathic bacteria. METHODS: Thirty subjects with periodontitis (20 with chronic periodontitis and 10 with aggressive periodontitis) were included in the study. A group of 22 periodontally healthy individuals served as controls. Clinical periodontal parameters of probing depth (PD) and clinical attachment level (CAL) were recorded using a computerized periodontal probe. Subgingival plaque samples were processed for viral identification by nested polymerase chain reaction and bacterial identification by culture. Clinical periodontal parameters, frequency of detection of HCMV, and microbial composition were compared between the groups using the two-tailed Student t, chi(2), and Mann-Whitney tests. Logistic and linear regression analyses were performed to measure the association between virus-bacterial coinfection and clinical parameters (P < or =0.05). RESULTS: HCMV detection was more prevalent (P < or =0.05) in periodontally diseased subjects compared to healthy ones. Furthermore, in all groups, PD and CAL were increased in HCMV-positive sites. In the periodontitis groups, higher frequencies and levels of specific periodontopathic bacteria were detected in HCMV-positive sites. CONCLUSIONS: HCMV detection in periodontal pockets was associated with higher levels of periodontopathic bacteria and increased PD and CAL at sampled sites. HCMV/bacteria coinfection may be an important factor in periodontal destruction.     

Calcitonin gene-related peptide in gingival crevicular fluid in periodontal health and disease

The aims of the present study were to investigate whether calcitonin gene-related peptide (CGRP) was present in gingival crevicular fluid in both periodontal health and disease and to study the relationship with periodontal inflammation. Gingival crevicular fluid (GCF) was collected from a healthy, a gingivitis and a periodontitis site in 18 subjects with periodontitis and from a healthy site in 19 subjects without periodontitis. The volume of GCF was measured and each sample subsequently analysed for CGRP by radioimmunoassay. In subjects with periodontitis, CGRP immunoreactivity (CGRP-IR) was not detected in any periodontitis sites, nor in 67% of gingivitis and 28% of periodontally-healthy sites. The total amount of CGRP-IR was significantly elevated in periodontally healthy (p=0.0015) and gingivitis (p=0.027) compared with periodontitis sites. CGRP-IR was present in 89% of the healthy sites sampled in control subjects at comparable levels to those in healthy sites in periodontitis subjects. It is concluded that in periodontal inflammation, particularly in deep pockets, constituents of GCF process and degrade CGRP.     

Plasminogen activator system in smokers and non-smokers with and without periodontal disease

BACKGROUND: The present study assessed levels of plasminogen activator (PA) system proteins in gingival crevicular fluid (GCF) and serum of chronic gingivitis, chronic periodontitis patients and periodontally healthy subjects and evaluated how smoking influenced these levels. METHODS: Twenty chronic gingivitis; 20 chronic periodontitis patients and 20 periodontally healthy volunteers were consecutively recruited according to the inclusion criteria so that exactly half of the subjects in each category were smokers. GCF samples from four sites together with serum samples were obtained from each subject. GCF levels of tissue type PA (t-PA), urokinase type PA (u-PA), PA inhibitor-1 (PAI-1) and PA inhibitor-2 (PAI-2) and serum concentrations of cotinine, u-PA and PAI-1 were analysed by enzyme-linked immunosorbent assay. RESULTS: The only statistically significant difference between smokers and non-smokers was a lower GCF PAI-2 concentrations in healthy smokers compared with healthy non-smokers (p<0.01). Gingivitis and periodontitis patients had higher GCF concentrations of PAI-2 than healthy subjects (p<0.002 and p<0.02 respectively). The ratio of u-PA:PAI-1 and t-PA:PAI-1 were significantly higher in GCF of smokers with periodontitis compared with "healthy" smokers, whereas the ratio of t-PA:PAI-2 was significantly lower in smokers with periodontal disease (p<0.05). CONCLUSIONS: GCF levels of the PA system proteins are increased in chronic gingivitis and periodontitis compared with healthy gingiva. Smoking had only subtle effects on the GCF PA system proteins with the exception of PAI-2, and the balance of activators and inhibitors. These findings suggest one mechanism whereby smoking may exert detrimental effects on the periodontal tissues.     

Periodontitis lesions are the main source of salivary cytomegalovirus

Background:  Herpesviruses play causal or cooperative roles in childhood infections, tumorigenesis, ulcerogenesis, and periodontitis. Saliva is a common vehicle of herpesvirus horizontal transmission, but the source of salivary herpesviruses remains obscure. To evaluate the significance of periodontal disease in shedding of oral herpesviruses, this study determined the genome-copy counts of human cytomegalovirus (HCMV) and Epstein–Barr virus (EBV) in whole saliva of subjects with periodontitis, gingivitis, or no natural teeth.
Methods:  Whole saliva was collected from 14 periodontitis patients, 15 gingivitis patients and 13 complete denture wearers. The study subjects were systemically healthy and had not received periodontal treatment in the past 3 months. Real-time TaqMan polymerase chain reaction was used to determine the salivary load of HCMV and EBV.
Results:  Salivary HCMV was detected in seven (50%) periodontitis patients, but not in any gingivitis or edentulous subjects ( P  < 0.001). Salivary EBV was detected in 11 (79%) periodontitis patients, in five (33%) gingivitis patients, and in seven (54%) edentulous subjects ( P  = 0.076). Salivary samples showed copy counts of HCMV in the range of 3.3 × 10³–4.2 × 10⁴/ml and of EBV in the range of 3.6 × 10²–1.6 × 10⁹/ml.
Conclusions:  HCMV and EBV are commonly present in the saliva of periodontitis patients. Periodontitis lesions of systemically healthy subjects seem to constitute the main origin of salivary HCMV, but do not comprise the sole source of salivary EBV.     

Lipid peroxidation levels, total oxidant status and superoxide dismutase in serum, saliva and gingival crevicular fluid in chronic periodontitis patients before and after periodontal therapy

Background:  Recent data have demonstrated increased lipid peroxidation (LPO) levels and oxidative stress in periodontitis. Malondialdehyde (MDA) and superoxide dismutase (SOD) are both increased during oxidative stress. Furthermore, this study examined SOD concentration, total oxidative status (TOS) and MDA levels in periodontal patients and investigated the longitudinal effect of periodontal therapy on the index levels of chronic periodontitis (CP) patients.
Methods:  Serum, saliva and gingival crevicular fluid (GCF) samples were obtained from 48 CP patients and 35 healthy control subjects prior to, as well as after 16 weeks following non-surgical post-periodontal therapy. MDA, TOS and SOD and clinical parameters were determined pre- and post-therapy.
Results:  The levels of TOS and SOD values were significantly higher in the CP group than in the control group (p < 0.05), but only MDA in GCF. Post-periodontal therapy, serum, saliva and GCF TOS and SOD levels significantly decreased compared to basal levels (p < 0.05), but only MDA in GCF.
Conclusions:  LPO was higher in the periodontal region, with TOS and SOD increasing both locally and peripherally. Non-surgical therapy can restore and control the subject antioxidant capacity by locally and systemically modifying the levels of MDA, TOS and SOD.     

Prevalence of periodontal pathogens in subgingival lesions, atherosclerotic plaques and healthy blood vessels: a preliminary study

Background and Objective:  Previous studies have reported different periodontal bacteria in atherosclerotic lesions, but their involvement in plaque formation remains unclear. The aim of the present study was to investigate the presence of 20 periodontal bacteria in atherosclerotic samples and healthy blood vessels (used as controls) and to clarify their relationship in regard to clinical and bacteriological periodontal status.
Material and Methods:  The day before vascular surgery the patients had a thorough periodontal examination and bacteriological samples were taken from periodontally diseased sites. Atheromatous plaques, internal mammary arteries and saphenous veins were harvested during surgery. A DNA–DNA hybridization procedure was used to screen periodontal and vascular samples for the 20 selected bacterial species.
Results:  Periodontal samples from the severe periodontitis group were found to have a higher prevalence and biomass of bacterial species than the moderate periodontitis group. In vessel samples, the prevalence of the same 20 bacterial species analyzed together was similar in the two groups, except for saphenous veins.
Conclusion:  The presence of periodontal pathogens in atherosclerotic plaques and in apparently healthy vessels appeared to reflect a higher level of bacteremia rather than infection of endothelial cells.     

Periodontal disease in mothers indicates risk in their children

Introduction.  It is well established that severe periodontitis clusters in families, but there are no data about the relationship between mothers with chronic periodontitis and their children's periodontal status.
Objective.  To evaluate a risk for periodontal diseases in children of periodontally diseased and healthy mothers.
Methods.  Four study groups were included: (I) 20 female patients with untreated generalized severe chronic periodontitis, (II) their children (34), (III) 13 periodontally healthy mothers and (IV) their children (13). Material was collected from years 2004–2006. The clinical examination included registration of visible plaque index, modified gingival index and, bleeding sites on probing. Periodontal microbiological samples were obtained from all study subjects and the isolates were identified according to morphology and biochemical profiles; similar interfamilial pathogens were compared by PCR-technique.
Results.  The children of diseased mothers more frequently had periodontal diseases, especially gingivitis. In addition, clinical parameters of gingival inflammation were more expressed and oral hygiene was worse in this group of children. VPI and VPI% of the diseased and healthy mothers differed significantly. The most common oral pathogens were P. intermedia/nigrescens and A. actinomycetemcomitans . The children of healthy mothers harboured pathogens less frequently than the children of diseased mothers. The sharing of P. intermedia/nigrescens was more frequent (5 families) than A. actinomycetemcomitans (2 families).
Conclusion.  Maternal indicators, such as periodontitis, hygiene habits, and periodontal microflora are risk factors for childhood periodontal diseases, and might be predictive of future childhood and adolescent periodontitis.     

Comparison of nested polymerase chain reaction (PCR), real-time PCR and viral culture for the detection of cytomegalovirus in subgingival samples

Introduction:  The purpose of this study was to compare nested polymerase chain reaction (PCR), real-time PCR, and shell vial for the detection of human cytomegalovirus (HCMV) in subgingival samples in periodontitis patients.
Methods:  A group of 44 patients and 24 individuals without periodontitis were included in the study. A full periodontal examination was conducted in each subject. Gingival crevicular fluid (GCF) was collected by pocket lavage and used for viral culture (shell vial). Additional subgingival samples were obtained with paper points and used for molecular analysis. Nested PCR and real-time PCR were used to detect and quantify HCMV. Student's t -test and chi-squared test were used to compare groups. The sensitivity and specificity for the tests were calculated on 2 × 2 tables considering the nested PCR as the gold standard.
Results:  The detection of HCMV was greater using nested PCR than with either real-time PCR or shell vial ( P  < 0.0001). However, the frequency detection of both molecular techniques was higher than in viral culture ( P  < 0.0001). Only one case of chronic periodontitis was positive by viral culture. Agreement between nested PCR and real-time PCR was observed 47.7% and 4.1% of the time in the periodontitis and control groups, respectively. The sensitivity of real-time PCR was 60%, compared with 2.8% for the shell vial technique.
Conclusions:  In conclusion, this study confirmed that active HCMV infection occurs in human periodontitis; however, its frequency seems to be low. In contrast, latent periodontal HCMV infection seems to be a more frequent event.     

Real-time polymerase chain reaction quantification of human cytomegalovirus and Epstein-Barr virus in periodontal pockets and the adjacent gingiva of periodontitis lesions

BACKGROUND: Genomic sequences of human cytomegalovirus (HCMV) and Epstein-Barr virus (EBV), two herpesviruses, can frequently be detected in periodontal pockets of progressive periodontitis lesions, but the prevalence and load of the two viruses in gingival tissue are unknown. This study determined levels of HCMV and EBV DNA in the periodontal pocket and in the adjacent gingiva of periodontitis lesions using a real-time polymerase chain reaction (PCR) assay. MATERIAL AND METHODS: A total of 20 systemically healthy periodontitis patients participated in the study. Nine patients below 35 years of age were tentatively diagnosed as having aggressive (early onset) periodontitis, and 11 patients 36-56 years of age as having chronic (adult) periodontitis. Clinical parameters were evaluated using established methods. Using periodontal curettes, specimens were harvested from 6-10 mm periodontal pockets and from the adjacent inflamed periodontal pocket wall. A 5'-nuclease (TaqMan) real-time PCR assay was used to identify and quantify genomic copies of periodontal HCMV and EBV. RESULTS: HCMV DNA was detected in 78% of subgingival and 33% of gingival tissue samples from aggressive periodontitis lesions, but only in 46% of subgingival and 9% of gingival tissue samples from chronic periodontitis lesions. In aggressive periodontitis, HCMV subgingival and gingival tissue counts were positively correlated with periodontal pocket depth and probing attachment loss at sample sites (p6 mm, but none of 14 patients having mean pocket depth at sample teeth相似文献   

Viruses in periodontal disease - a review

The purpose of this review was to evaluate the evidence supporting the hypothesis that viral infection plays a role in the development of periodontitis. An involvement in periodontal diseases has been suspected specifically for human immunodeficiency virus (HIV) and herpes viruses. An association has been demonstrated between HIV infection and some distinct forms of periodontal infection, i.e. necrotizing lesions. Furthermore, reports of increased prevalence and severity of chronic periodontitis in HIV-positive subjects suggests that HIV infection predispose to chronic periodontitis. Several studies, most of them from the same research group, have demonstrated an association of herpesviruses with periodontal disease. Viral DNA have been detected in gingival tissue, gingival cervicular fluid (GCF) and subgingival plaque from periodontaly diseased sites. In addition markers of herpesviral activation have been demonstrated in the GCF from periodontal lesions. Active human cytomegalovirus (HCMV) replication in periodontal sites may suggest that HCMV re-activation triggers periodontal disease activity. Concerns regarding sampling, methods and interpretation cast doubts on the role of viruses as causes of periodontal disease.     

Analysis of neutrophil-derived antimicrobial peptides in gingival crevicular fluid suggests importance of cathelicidin LL-37 in the innate immune response against periodontogenic bacteria

Introduction:  During periodontitis, an innate immune response to bacterial challenge is primarily mediated by neutrophils. We compared neutrophilic content and the level of neutrophil-derived antimicrobial peptides in gingival crevicular fluid (GCF) in two clinical forms of severe periodontitis.
Methods:  GCF was collected from 14 patients with aggressive periodontitis, 17 patients with chronic periodontitis, and nine healthy subjects. Samples were analyzed for periodontopathogen load using real-time polymerase chain reactions. The amounts of myeloperoxidase and α-defensins (HNP1–3) were determined by enzyme-linked immunosorbent assay, and the level of cathelicidin (hCAP18/LL-37) was assayed by Western blot.
Results:  Myeloperoxidase concentration was not correlated with levels of LL-37 and HNP1–3 in samples from patients, compared to controls. The amount of HNP1–3 was twofold and fourfold higher in patients with aggressive and chronic periodontitis, respectively. Those with chronic disease had significantly elevated amounts of mature LL-37. The increased concentration of both peptides in chronic periodontitis correlated with the load of Porphyromonas gingivalis , Tannerella forsythia , and Treponema denticola.
Conclusion:  The lack of a correlation between LL-37, HNP1–3, and myeloperoxidase content suggests that neutrophils are not the sole source of these bactericidal peptides in the GCF of patients with periodontitis; and that other cells contribute to their local production. The bacterial proteases of P. gingivalis , T. forsythia , and T. denticola might degrade hCAP18/LL-37, because the 11-kDa cathelicidin-derived fragment was present in GCF collected from pockets infected with these bacteria. Collectively, it appears that a local deficiency in LL-37 can be considered as a supporting factor in the pathogenesis of severe cases of periodontitis.     

Detection of human viruses in patients with chronic periodontitis and the relationship between viruses and clinical parameters

BACKGROUND: Recent studies have demonstrated that various human viruses, especially cytomegalovirus (HCMV), Epstein-Barr virus type-1 (EBV-1), and herpes simplex virus (HSV), seem to play a part in the pathogenesis of human periodontitis. Little information is available on the relationship between these viruses and clinical periodontal parameters in patients with chronic periodontitis. This study examined the occurrence of HCMV, EBV-1, and HSV in patients with chronic periodontitis and the relationship between these viruses and clinical parameters. METHODS: A nested polymerase chain reaction (PCR) method determined the presence of HCMV, EBV-1, and HSV. Subgingival plaque samples from 30 patients with chronic periodontitis and 21 randomly selected healthy controls were collected by paper points, and clinical measurements were recorded from both sampling sites and entire dentition. The following indices were measured: plaque index (PI), gingival index (GI), probing depth (PD), and clinical attachment loss (CAL). Results: HCMV was detected in 44.3% of chronic periodontitis patients and 14.3% of healthy persons (P < 0.05); EBV-1 in 16.7% of chronic periodontitis patients and 14.3% of healthy persons (P = 1.00); and HSV in 6.7% of chronic periodontitis patients and in no healthy persons. HCMV and EBV-1 detected and undetected sites in patients with periodontitis showed statistically significant differences in sampling clinical depth (SPD) and sampling clinical attachment loss (SCAL). Differences in the measurements of PI of entire dentition and GI of entire dentition between HSV detected and undetected sites were statistically significant. CONCLUSIONS: Findings of the present study confirm the frequent presence of HCMV in crevicular samples of chronic periodontitis lesions, and suggest a strong relationship between the presence of HCMV and EBV-1 in subgingival areas and the measurements of probing depth and probing attachment loss.     

Detection of gingival crevicular fluid MMP-8 levels with different laboratory and chair-side methods

Objective:  The aim of the study was to compare four methods for gingival crevicular fluid (GCF) matrix metalloproteinase (MMP)-8 detection.
Methods:  Matrix metalloproteinase-8 levels from 20 GCF samples from two periodontally healthy subjects, 18 samples from two patients with gingivitis and 45 samples from six patients with moderate to severe periodontitis, altogether 83 samples, were analysed using (1) a time-resolved immunofluorometric assay (IFMA), (2) an MMP-8 specific chair-side dip-stick test, (3) a dentoAnalyzer device and (4) the Amersham ELISA kit. Western immunoblot using same monoclonal anti-MMP-8 as in IFMA and dentoAnalyzer was used to identify molecular forms of MMP-8 in GCFs.
Results:  Correlation between IFMA and dentoAnalyzer results calculated with Spearman's correlation coefficient was 0.95 ( P  = 0.01). The chair-side dip-stick test results were well in line with these assays. Periodontitis sites with unstable characteristics were differentiated with these methods. The Amersham ELISA results were not in line with the findings by other methods.
Conclusions:  Immunofluorometric assay and dentoAnalyzer can detect MMP-8 from GCF samples and these methods are comparable. Using Western immunoblot, it was confirmed that IFMA and dentoAnalyzer can detect activated 55 kDa MMP-8 species especially in periodontitis-affected GCF. dentoAnalyzer is among the first quantitative MMP-8 chair-side testing devices in periodontal and peri-implant diagnostics and research.     

Gingival crevicular fluid EMAP-II, MIP-1alpha and MIP-1beta levels of patients with periodontal disease

BACKGROUND: Periodontal diseases may differ, which could be attributed to the factors that might modify the host response to microbial pathogens. The aim of this study was to examine gingival crevicular fluid (GCF) levels of EMAP-II, MIP-1alpha and MIP-1beta in patients with different periodontal diseases (EMAP-II, endothelial-monocyte activating polypeptide; MIP-1alpha, macrophage inflammatory protein-1alpha; MIP-1beta, macrophage inflammatory protein-1beta). METHODS: Eighty-two subjects were included in this study. GCF samples were collected from 26 patients with generalized aggressive periodontitis (G-AgP), 26 patients with chronic periodontitis (CP), 15 with gingivitis and 15 periodontally healthy subjects. Clinical periodontal parameters were recorded. GCF EMAP-II, MIP-1alpha and MIP-1beta levels were quantified by enzyme immunoassay. RESULTS: GCF EMAP-II levels of G-AgP group were higher than those of gingivitis and healthy groups (p<0.008). G-AgP group showed a trend for higher GCF EMAP-II levels compared with CP group (p>0.008). G-AgP, CP, gingivitis and healthy groups had comparable GCF MIP-1alpha and MIP-1beta levels. CONCLUSIONS: Our results suggest that elevated GCF EMAP-II could contribute to the pathogenesis of G-AgP. Alternatively, EMAP-II reflects the extent of the inflammatory activity in the periodontal tissues. At this point, MIP-1alpha and MIP-1beta levels in GCF do not seem to play a discriminatory role in periodontitis. Our data document for the first time the essential role of EMAP-II in the pathogenesis of different periodontal diseases.     

不同糖蛋白B基因型人巨细胞病毒感染与慢性牙周炎的关系

目的探讨不同糖蛋白B（gB）基因型人巨细胞病毒（HCMV）感染与慢性牙周炎（CP）的关系。方法采用套式聚合酶链反应（nPCR）检测65例CP患者龈下菌斑标本和24名牙周健康者龈沟液标本中HCMV的gB基因，并进行限制性片段长度多态性分析（RFLP）对gB基因进一步分型。分析HCMV及其不同gB基因型感染与牙周炎严重程度的关系。结果以位点计，CP的HCMV感染率59．23％（154／260），明显高于牙周健康者的感染率32．29％（31／96）（P〈0．01）。cP的HCMV感染者中gBⅠ型、gBⅡ型、gBⅠ和Ⅱ混合型分别占11．7％（18／154）、80．5％（124／154）和7．8％（12／154）；牙周健康的HCMV感染者中gBⅠ型占45．2％（14／31），gBⅡ型占38．7％（12／31），gBⅠ和Ⅱ型混合感染占16．1％（5／31）。与牙周健康者相比，CP患者感染HCMV以gBⅡ型明显占多数（P〈0．01）。不同gB基因型HCMV感染在不同临床附着丧失、探诊深度和牙龈指数的位点中的分布差异均无统计学意义（P〉0．05）。结论HCMV感染与cP密切相关，但与牙周炎严重程度无直接关系。gBⅡ型可能是与CP相关的HCMV优势基因型。     

Relationship of Actinobacillus actinomycetemcomitans serotypes to periodontal condition: prevalence and proportions in subgingival plaque

No study available has utilized the new classification scheme (the consensus report of the American Academy of Periodontology 1999) to determine the prevalence of Actinobacillus actinomycetemcomitans in different periodontal conditions. The purpose of this study was to investigate prevalence and proportions of A. actinomycetemcomitans serotypes in subgingival plaque samples from a young Taiwanese population with aggressive periodontitis, chronic periodontitis and no periodontal disease. A total of 221 subgingival plaque samples from 171 diseased subjects (70 had aggressive periodontitis, and 101 had chronic periodontitis) (mean age 25.0 +/- 8.2 yr) and 50 periodontally healthy subjects (mean age 18.4 +/- 9.5 yr) were screened for A. actinomycetemcomitans. Serotypes of A. actinomycetemcomitans were determined by an indirect immunofluorescence assay using serotype-specific polyclonal antisera to A. actinomycetemcomitans strains ATCC 29523 (serotype a), ATCC 43728 (serotype b) and ATCC 33384 (serotype c). Prevalence (% of positive samples) of A. actinomycetemcomitans was 84.3% in aggressive periodontitis, 60.4% in chronic periodontitis, and 64.0% in periodontally healthy subjects. Proportions of A. actinomycetemcomitans (mean percentage per total bacteria) in periodontally healthy subjects were significantly lower than in aggressive periodontitis subjects. The proportion of serotype b in subjects with aggressive periodontitis and subjects with chronic periodontitis were significantly greater than that in periodontally healthy subjects. The proportion of serotype c in periodontally healthy subjects was much higher than that in chronic periodontitis subjects. The results of this study suggest that prevalence and proportions of A. actinomycetemcomitans are significantly greater in patients with aggressive periodontitis than in those with chronic periodontitis. Serotype b is the predominant serotype of A. actinomycetemcomitans in patients with diseased periodontal conditions. Serotype c is a more common serotype detected in periodontally healthy subjects.