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The application of Bio-Oss and Bio-Gide as implant materials in the complex treatment of aggressive periodontitis.

In the presented study the results of the complex conservative and surgical periodontological treatment using Bio-Oss implant material and the regenerative Bio-Gide collagen membrane by Geistlich company were subjected to clinical and radiological evaluation. The measure depth of the periodontal pockets PPD was subjected to evaluation, the level of the epithelial attachment CAL and the defect of bone of the alveolar process were observed on radiograms. In all patients the state of oral cavity hygiene was examined using the index of API bacterial plaque and the percent of SBI index of bleeding gingiva. The analysis of the examined parameters concerned the period before surgeries and 8 to 12 months after the surgeries of the guided tissue regeneration. On the basis of the conducted research and the statistic analysis, the reduction of the periodontal pockets depth and the reconstruction of the attachment.

Adult↗

Aggressive periodontal destruction and herpes zoster in a suspected AIDS patient.

An unusual case of spontaneous and rapidly destructive lesions involving the periodontal structures is described in a 54 year old, bi-sexual patients suspected of having AIDS. Concomitant with the periodontal breakdown, the patient developed a severe case of Herpes Zoster involving the area of the face innervated by the 5th cranial nerve. The dermal lesions involved the face, nose, eyes and scalp. Similar lesions were noted on the gingival and palatal mucosa on the same side of the jaw as the skin lesions. The differences between this type of periodontal destruction and more conventional forms of periodontitis are discussed.

Acquired Immunodeficiency Syndrome↗

Proinflammatory cytokines production and PMN-elastase release from activated PMN cells in the periodontal disease.

The aim of this study was to evaluate the local changes in the crevicular gingival fluid (CGF) determined by the inflammatory and immune response in periodontitis and gingivitis. The selected patients presented gingivitis (n = 9) and periodontitis: aggressive periodontitis (n = 21) and adult periodontitis (n = 8). The crevicular fluid was provided from the gingival and periodontal pocket. The measurement of PMN-elastase in the CGF, using the ELISA method, showed a significant (p < 0.01) increase of the enzyme concentration in the aggressive periodontitis group (62.1 +/- 3.91 ng/ml) comparing to the gingivitis group (33.04 +/- 4.14 ng/ml) but also the increase (p < 0.05) of this enzyme in the adult periodontitis (43.6 +/- 2.16 ng/ml) comparing to the gingivitis, which indicated the evolutive aspects of the inflammatory reaction in these diseases. The increased production of PMN-E is the result of the activation of polymorphonuclear cells (PMN) as a reaction of the microbial attack. Degranulation and release of proteolytic enzymes including elastase, which present cytotoxic capacities, follow the activation of neutrophil granulocytes (PMN). The activated granulocytes release proinflammatory cytokines IL-1, TNF-alpha which augment the inflammatory immune response. The aggressive periodontitis group showed an increased CGF level of IL-1 (780.4 +/- 104 pg/ml) comparing to the gingivitis group (275.5 +/- 78 pg/ml) (p < 0.01). TNF-alpha also presented an increased level (p < 0.01) in the aggressive periodontitis group (16.3 +/- 2.3 pg/ml) comparing to the gingivitis group (4.1 +/- 1.2 pg/ml) as a consequence of the periodontium destruction and of the tissular necrosis in the former group. In conclusion, our study shows a significant increase of the PMN-elastase and proinflammatory cytokines level in CGF of patients with gingivitis and periodontitis. The intensity of the inflammatory response in these diseases is strongly correlated to the activation of the neutrophil granulocytes which release these biological active molecules that could be used as evolution markers of the disease.

Adolescent↗

Microbiology and management of periodontal infections.

The term periodontal disease refers to all diseases that involve the supportive structures of the periodontium. Peridontal diseases commonly begin as a gingivitis and progress to periodontitis. Necrotizing ulcerative gingivitis (NUG) is the most fulminate form of gingivitis. The two main forms of periodontitis are chronic periodontitis (also known as adult periodontitis) and aggressive periodontitis (also known as early onset periodontitis, destructive periodontitis, and juvenile periodontitis). Gingivitis treatment involves removing dental plaques and maintaining good oral hygiene. Periodontitis therapy should include root debriding, draining the infected root, and surgically resecting inflamed periodontal tissues. Systemic antimicrobials often are indicated in NUG, chronic periodontitis, and aggressive periodontitis. When possible, antimicrobial selection should be based upon culture and susceptibility testing of the subgingival flora.

Adult↗

Prevalence of periodontal pathogens in Brazilians with aggressive or chronic periodontitis.

OBJECTIVES: Previous studies suggest differences between geographically and racially distinct populations in the prevalence of periodontopathic bacteria as well as greater periodontal destruction associated with infection by highly leucotoxic Actinobacillus actinomycetemcomitans. The present study examined these hypotheses in Brazilians with aggressive or chronic periodontitis. MATERIALS AND METHODS: Clinical, radiographical, and microbiological assessments were performed on 25 aggressive periodontitis and 178 chronic periodontitis patients including 71 males and 132 females, 15-69 years of age. RESULTS: The prevalence of Porphyromonas gingivalis was similar to that of other South American populations. The prevalence of A. actinomycetemcomitans and its highly leucotoxic subgroup was higher in Brazilians. Highly leucotoxic A. actinomycetemcomitans was more prevalent in aggressive periodontitis (chi2=27.83) and positively associated with deep pockets (>6 mm, chi2=18.26) and young age (<29 years, chi2=18.68). Greater mean attachment loss was found in subjects with highly leucotoxic A. actinomycetemcomitans than in subjects with minimally leucotoxic (p=0.0029) or subjects not infected (p=0.0001). CONCLUSION: These data support the hypothesis of differences between populations in the prevalence of periodontopathic bacteria and of greater attachment loss in sites infected with highly leucotoxic A. actinomycetemcomitans. Detection of highly leucotoxic A. actinomycetemcomitans in children and adolescents may be a useful marker for aggressive periodontitis.

Acute Disease↗

[Markers of periodontal destruction in saliva of periodontitis patients].

UNLABELLED: Periodontal diseases result from interactions between periodontal microflora and the multifaceted response of the host. Markers of this interrelationship can be found in gingival crevicular fluid and saliva samples indicating early periodontal disease activity. Studies of host defense mediators in saliva of patients with periodontal diseases are very scarce. AIM: The goal of this study was therefore to investigate interrelationships between mediators of local immunity in host saliva and clinical parameters of periodontal destruction in persons with chronic and aggressive periodontitis. METHODS AND SUBJECTS: Host defense indicators were measured using enzyme-immunochemistry tests in unstimulated saliva samples of persons with periodontitis. The degree of periodontal destruction was determined by measuring attachment loss. Subjects were divided into two groups: persons with mild signs of chronic periodontitis and persons with severe signs of aggressive periodontitis. Hypotheses about the structure of those samples and their interrelationship were tested using non-parametric methods. RESULTS: Results indicated that C-reactive protein, C3 component of the complement, alfa 2-macroglobulin and interleukin-6 levels differ significantly between patients with chronic and aggressive periodontitis. Interleukin-6, influencing cells with osteoblastic phenotype, is present at a high level in patients with aggressive periodontitis. Calcium was much lower than in healthy persons. Trypsin levels were lower in patients with periodontitis than in healthy persons. We found a significant interrelationship between host response mediators as measured in saliva and periodontal destruction measured by clinical attachment loss. CONCLUSION: The levels of host defense mediators in saliva are different for chronic and aggressive periodontitis. This findings might help in estimating the course and progression of periodontal destruction, thus providing clinical benefits in treatment planning.

Adult↗

Clonal diversity and stability of subgingival Eikenella corrodens.

Eikenella corrodens is a commensal subgingival bacterium commonly found in both periodontally nondiseased and diseased subjects. The present study examined the clonal diversity and stability of subgingival E. corrodens over time. Ninety-five subjects were enrolled at the baseline examination, including 44 periodontally nondiseased subjects and 51 subjects with aggressive periodontitis. Twenty-two nondiseased subjects and 11 subjects with aggressive periodontitis were subsequently reexamined after an average interval of 14 months. Two subgingival plaque samples were obtained from each subject to determine the total cultivable bacteria. In addition, multiple E. corrodens isolates from each sample were recovered for clonal analysis by arbitrarily primed PCR. The mean numbers of distinct E. corrodens clones harbored by nondiseased subjects and subjects with aggressive periodontitis were 1.3 and 3.0, respectively. Thirty-nine percent of the nondiseased subjects and 63% of the subjects with aggressive periodontitis harbored multiple clones of E. corrodens. The numbers of distinct E. corrodens clones increased significantly (Mann-Whitney ranking test, P < 0.05) in sites from patients with aggressive periodontitis, in sites with pocket depths of 4 mm or greater, in sites with a clinical attachment loss of 2 mm or greater, and in sites coinfected with Porphyromonas gingivalis. Comparison of E. corrodens clones recovered at the baseline and those recovered at the follow-up examination showed that E. corrodens colonization was not stable. Thirty-eight of the 66 follow-up samples (58%) showed a complete change (including de novo colonization of the sites or complete elimination of the organism from the sites) of the subgingival E. corrodens clonal types between the baseline and the follow-up examinations. Our results suggest a complexity of subgingival microbiota not seen previously.

Adolescent↗

Detection of highly and minimally leukotoxic Actinobacillus actinomycetemcomitans strains in patients with periodontal disease.

This study examined the prevalence of highly and minimally leukotoxic Actinobacillus actinomycetemcomitans in patients with periodontal disease. Pooled subgingival plaque samples from 136 patients with some form of periodontal disease were examined. Subjects were between 14 and 76 years of age. Clinical examinations included periodontal pocket depth (PD), plaque index (PI) and bleeding index (BI). The obtained plaque samples were examined for the presence of highly or minimally leukotoxic A. actinomycetemcomitans strains by the polymerase chain reaction (PCR). Chi-square and logistic regression were performed to evaluate the results. Forty-seven subjects were diagnosed with gingivitis, 70 with chronic periodontitis and 19 with aggressive periodontitis. According to chi-square there was no significant correlation detected between PD (chi2 = 0.73), PI (chi2 = 0.35), BI (chi2 = 0.09) and the presence of the highly leukotoxic A. actinomycetemcomitans. The highly leukotoxic A. actinomycetemcomitans strains were correlated with subjects that were 28 years of age and younger (chi2 = 7.41). There was a significant correlation between highly leukotoxic A. actinomycetemcomitans and aggressive periodontitis (chi2 = 22.06). This study of a Brazilian cohort confirms the strong association between highly leukotoxic A. actinomycetemcomitans strains and the presence of aggressive periodontitis.

Adolescent↗

Immunoglobulin G profiles in different forms of periodontitis.

BACKGROUND: Races and Gm(23) allotypes can modify the serum levels of IgG subclasses. The average serum levels of IgG subclasses of African-Americans have been reported to be higher than those of Caucasians in both healthy young adults and patients with aggressive periodontitis; Gm(23)-positive subjects generally had higher IgG2 levels than Gm(23)-negative subjects. OBJECTIVE: We examined serum immunoglobulin G (IgG) concentrations in Taiwanese patients with different forms of periodontitis. METHODS: The serum levels of four IgG subclasses were determined by enzyme-linked immunosorbent assay and Gm(23) allotypes were verified by radial immunodiffusion tests in 50 patients with chronic periodontitis, 30 patients with aggressive periodontitis, and 74 healthy controls. RESULTS: There were no differences in the concentrations of four IgG subclasses in patients with chronic periodontitis compared with age-matched controls. However, in subjects younger than 35 years, levels of IgG2 were significantly elevated in patients with aggressive periodontitis compared with controls. We also found significant differences in IgG2 levels within the control group when stratified by age (< or = 35 years and > 35 years). Gm(23) allotypes were not correlated with the serum levels of IgG2 in either patient group. CONCLUSION: Microbial challenge might not provoke significant changes in systemic IgG response in patients with chronic periodontitis. However, in patients with aggressive periodontitis, IgG2 levels were increased when compared with age-matched controls. Gm(23) allotypes had no influence on IgG2 levels in well-established generalized chronic periodontitis or aggressive periodontitis.

Adult↗

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.

Actinobacillus Infections↗

Levels of leukotriene B4 in gingival crevicular fluid and gingival tissue in specific periodontal diseases.

BACKGROUND: Leukotriene B4 (LTB4), a product of the lipoxygenase pathway of arachidonic acid metabolism, exhibits numerous activities that can account for most of the features of host responses seen in periodontal diseases. The aim of the present study was to examine the role of LTB4 in the pathogenesis of specific periodontal diseases. METHODS: LTB4 levels were investigated in gingival crevicular fluid (GCF) and gingival tissue (GT) samples of 10 patients with chronic periodontitis (CP), 12 patients with generalized aggressive periodontitis (GAgP), 6 patients with localized aggressive periodontitis (LAgP), 6 patients with gingivitis (G), and 6 periodontally healthy subjects (H). Periodontal status was evaluated by measuring probing depth, gingival index, papillary bleeding index, and plaque index. LTB4 was extracted from the samples by solid-phase method using C18 cartridge and was purified by high performance liquid chromatographic method and then analyzed by radioimmunoassay. RESULTS: All patient groups had significantly higher levels of GCF and GT LTB4 compared to the control group (P<0.005). The CP patients had the highest LTB4 levels compared to those in other patient groups (P<0.005). GAgP, LAgP, and G groups had similar amounts of GCF and GT LTB4 (P>0.005). When the data were expressed as concentration, the CP group was found to have higher concentration of LTB4, compared to that of control group (P<0.005). GAgP, LAgP, and G groups had similar LTB4 concentration compared to that of control group (P>0.005). No significant difference was found between GAgP, LAgP, and G groups (P>0.005). The CP group had higher LTB4 concentration compared to both GAgP and LAgP groups (P<0.005). Although the CP group had a higher GCF LTB4 concentration compared to G group, this difference did not reach significance (P>0.005). No significant correlation was found between GCF and GT LTB4 levels and clinical parameters. CONCLUSIONS: The results of the present study indicate that LTB4 is likely to be an important mediator in regulating inflammatory responses in the human periodontal tissues. This lipid mediator may play an important role in the pathophysiology of periodontal disease.

Adult↗

Anti-cardiolipin antibodies in sera from patients with periodontitis.

Antiphospholipid antibodies are commonly found in patients with systemic lupus erythematosus or the antiphospholipid syndrome, and a subset of such antibodies is associated with prothrombotic events such as stroke and with adverse pregnancy outcomes and fetal loss. We examined sera from 411 patients who were clinically characterized as to their periodontal disease status for serum levels of beta2-glycoprotein I-dependent anti-cardiolipin autoantibodies (anti-CL). The prevalence of patients with chronic periodontitis (CP) and generalized aggressive periodontitis (GAgP) positive for anti-CL (16.2% and 19.3%, respectively) was greater than that in healthy controls (NP) and localized aggressive periodontitis (LAgP) patients (6.8% and 3.2%). Patients with these autoantibodies demonstrated increased pocket depth and attachment loss compared with patients lacking the antibodies. Analysis of the data indicates that patients with generalized periodontitis have elevated levels of autoantibodies reactive with phospholipids. These antibodies could be involved in elevated risk for stroke, atherosclerosis, or pre-term birth in periodontitis patients.

Adult↗

Gingival crevicular fluid transforming growth factor-beta1 in several forms of periodontal disease.

BACKGROUND: Transforming growth factor-beta(1) (TGF-beta(1)) has significant effects on periodontal host response regulation. Limited knowledge on the role of TGF-beta(1) in various periodontal disease types and particularly in advanced periodontitis forms warranted the present study. The aim of the present study was to evaluate the gingival crevicular fluid (GCF) TGF-beta(1) levels in patients with different forms of periodontal disease. METHODS: GCF TGF-beta(1) levels were investigated in 32 chronic periodontitis (CP), 30 generalized aggressive periodontitis (G-AgP), 15 gingivitis patients and 16 periodontally healthy subjects. Periodontal status was evaluated by measuring probing depth, clinical attachment loss, plaque and bleeding on probing. TGF-beta(1) levels were analyzed by enzyme-linked immunosorbent assay. The results were expressed in terms of total amount (pg) and concentration (pg/microl). RESULTS: G-AgP and CP groups had significantly elevated GCF TGF-beta(1) total amount compared to healthy group (p<0.008). Moreover, GCF TGF-beta(1) total amount of G-AgP group was significantly higher than that of gingivitis group (p<0.008). G-AgP and CP groups had similar GCF TGF-beta(1) total amount (p>0.008). Significant correlation was found between GCF TGF-beta(1) total amount and all clinical periodontal parameters (p<0.05). CONCLUSIONS: The results of the present study suggest contribution of TGF-beta(1) to the pathogenesis of advanced chronic and aggressive periodontitis. TGF-beta(1) may thus be one of the components modulating exaggerated host response together with other major mediators of inflammation.

Adult↗

Sister chromatid exchange (SCE) analysis in periodontitis.

BACKGROUND: Emerging data indicate that genetic factors may be associated with the etiopathogenesis of aggressive periodontitis. Sister chromatid exchange (SCE) is a sensitive method that might reflect an instability of DNA or a deficiency of DNA repair. The aim of the present study was to investigate SCE frequency of patients with different forms of periodontal disease and to determine whether this cytogenetic marker in patients with aggressive periodontitis can be differential compared to patients with chronic periodontitis and control subjects. METHODS: SCE was analysed in peripheral blood lymphocyte chromosomes of 13 patients with generalised aggressive periodontitis (G-AP), 10 patients with chronic periodontitis (CP) and 10 control subjects. The periodontal parameters of probing depth, clinical attachment level, the presence of bleeding on probing and plaque were recorded. Peripheral blood lymphocytes obtained from both patient groups and control subjects were cultured in the presence of 5-Bromo-2-deoxyuridine in complete darkness for 72 h. For scoring SCE frequency, 20 metaphases were studied from each donor. RESULTS: The frequency of SCE was found to be 6.7 +/- 0.9 per cell in patients with G-AP, 6.5 +/- 1.5 per cell in CP patients and 6.9 +/- 1.1 in control subjects. No statistically significant differences were found between groups (p > 0.05). CONCLUSIONS: The data indicate that there the cyotogenetic damage in the aggressive type of periodontal disease is not greater than in chronic periodontitis and control subjects. Although no aberrant cytogenetic damage was observed in different forms of periodontitis compared to control, this does not discount the importance of other genetic factors in the pathogenesis of periodontal disease.

Acute Disease↗

Resistance of fluorescent-labelled Actinobacillus actinomycetemcomitans strains to phagocytosis and killing by human neutrophils.

Neutrophils are initially the predominant cells involved in the host defence of bacterial infections, including periodontal disease. Aggressive periodontitis is associated with Actinobacillus actinomycetemcomitans, a Gram-negative capnophilic microorganism. Infections caused by A. actinomycetemcomitans are not resolved by the host immune response despite the accumulation of neutrophils at the site of inflammation. To better understand the role of natural host defence mechanisms in A. actinomycetemcomitans infections, the interaction of phenotypically diverse strains of this pathogen with human neutrophils was assessed directly using techniques such as genetic labelling with the gene for green fluorescent protein, fluorescence-activated cell sorting and fluorescence imaging. The study included clinical isolates of A. actinomycetemcomitans represented by self-aggregating, biofilm-associated and isogenic planktonic variants. Data obtained showed that complement-mediated phagocytosis of A. actinomycetemcomitans was generally inefficient regardless of strain-specific serotype or leukotoxin production. Furthermore, the majority of ingested bacteria remained viable after exposure to neutrophils for 1 h. Interestingly, uptake of antibody-opsonized bacteria resulted in the rapid cell death of neutrophils. This was in contrast to ingestion of complement-opsonized bacteria, which did not affect neutrophil viability. The methods used in this study provided reliable and reproducible results with respect to adherence, phagocytosis and killing of A. actinomycetemcomitans when encountering human neutrophils.

Aggregatibacter actinomycetemcomitans↗

Expression of CD14, CD16 and CD45RA on monocytes from periodontitis patients.

BACKGROUND AND OBJECTIVE: Peripheral blood monocytes are a heterogeneous population, with phenotypes that change on activation or differentiation. Most of the monocytes express lipopolysaccharide (LPS) receptor, CD14 intensely, and do not express Fc gamma receptor III, CD16 (CD14++CD16- monocytes). But monocytes expressing CD16 with reduced CD14 (CD14+CD16+ monocytes) increase in inflammatory diseases as well as sepsis and bacteremia in hemodialysis patients. CD45RA is expressed on activated monocytes, and is regarded as an activation marker of peripheral blood monocytes. The purpose of this study was to determine the phenotypic and functional alteration of monocytes in periodontitis patients. METHODS: Peripheral blood was collected from 33 aggressive periodontitis patients (22 females, 11 males), 55 chronic periodontitis patients (35 females, 20 males) and 30 healthy subjects (16 females, 14 males), and the expression of CD14, CD16 and CD45RA on monocytes was determined using flow cytometry. The production of interleukin-6 (IL-6) by CD16+ and CD16- monocytes stimulated with LPS from Escherichia coli and Actinobacillus actinomycetemcomitans was also examined using flow cytometry. RESULTS: The percentage of CD14+CD16+ monocytes was significantly increased in chronic periodontitis patients. Percentage of monocytes expressing CD45RA was significantly increased in aggressive periodontitis patients compared to healthy subjects. CD16+ and CD16- monocytes produced IL-6 in response to LPS from E. coli and A. actinomycetemcomitans, and the percentage of IL-6 producing cells was higher in CD16+ monocytes than CD16- monocytes, suggesting that CD14+CD16+ monocytes represent a hyper-reactive phenotype. CONCLUSIONS: The present study demonstrated that CD14+CD16+ monocytes and CD45RA+ monocytes were increased in chronic and aggressive periodontitis, respectively. These findings suggest that alteration of monocytes in periodontitis patients could be evaluated by monitoring the surface expression of CD14, CD16 and CD45RA on monocytes.

Adult↗

Periodontal diseases in the child and adolescent.

BACKGROUND: Periodontal diseases are among the most frequent diseases affecting children and adolescents. These include gingivitis, localized or generalized aggressive periodontitis (a.k.a., early onset periodontitis which includes generalized or localized prepubertal periodontitis and juvenile periodontitis) and periodontal diseases associated with systemic disorders. The best approach to managing periodontal diseases is prevention, followed by early detection and treatment. METHODS: This paper reviews the current literature concerning the most common periodontal diseases affecting children: chronic gingivitis (or dental plaque-induced gingival diseases) and early onset periodontitis (or aggressive periodontitis), including prepubertal and juvenile periodontitis. In addition, systemic diseases that affect the periodontium and oral lesions commonly found in young children are addressed. The prevalence, diagnostic characteristics, microbiology, host-related factors, and therapeutic management of each of these disease entities are thoroughly discussed.

Adolescent↗