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Results for “Aggressive Periodontitis”

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PubMed2005

Crestal bone changes around titanium implants. Part I: A retrospective radiographic evaluation in humans comparing two non-submerged implant designs with different machined collar lengths.

BACKGROUND: Experimental studies demonstrated that peri-implant crestal hard and soft tissues are significantly influenced in their apico-coronal position by the rough/smooth implant border as well as the microgap/ interface between implant and abutment/restoration. The aim of this study was to evaluate radiographically the crestal bone level changes around two types of implants, one with a 2.8 mm smooth machined coronal length and the other with 1.8 mm collar. METHODS: In 68 patients, a total of 201 non-submerged titanium implants (101 with a 1.8 mm, 100 with a 2.8 mm long smooth coronal collar) were placed with their rough/smooth implant border at the bone crest level. From the day of surgery up until 3 years after implant placement crestal bone levels were analyzed digitally using standardized radiographs. RESULTS: Bone remodeling was most pronounced during the unloaded, initial healing phase and did not significantly differ between the two types of implants over the entire observation period (P >0.20). Crestal bone loss for implants placed in patients with poor oral hygiene was significantly higher than in patients with adequate or good plaque control (P <0.005). Furthermore, a tendency for additional crestal bone loss was detected in the group of patients who had been diagnosed with aggressive periodontitis prior to implant placement (P = 0.058). In both types of implants, sand-blasted, large grit, acid-etched (SLA) surfaced implants tended to have slightly less crestal bone loss compared to titanium plasma-sprayed (TPS) surfaced implants, but the difference was not significant (P >0.30). CONCLUSION: The implant design with the shorter smooth coronal collar had no additional bone loss and may help to reduce the risk of an exposed metal implant margin in areas of esthetic concern.

Adult↗
PubMed2005

Enhanced root planing and systemic metronidazole administration improve clinical and microbiological outcomes in a two-step treatment procedure.

BACKGROUND: Recently we described a non-surgical two-step treatment concept, in which we distinguished between a first scaling and root planing step (SRP) and an additional second enhanced root planing step (ERP). Until now it is difficult to determine how often a root surface should be instrumented during ERP. METHODS: The aim of the present study was to investigate the outcomes after different root planing intensities during ERP in 37 patients with aggressive periodontitis after SRP. During ERP a full-mouth root planing was performed. The patients were randomly assigned to one of two root planing regimens (group 1, N = 12 and group 2, N = 11), based on number of curet strokes per root surface (instrumentation frequency, IF) and probing depth. Group 1: PD 1 to 3.5 mm, 4 IF (for group 2, 8 IF); PD 4 to 6 mm, 8 IF (group 2, 14 IF); PD 6.5 to 9 mm, 12 IF (group 2, 20 IF); and PD >9 mm, 16 IF (group 2, 24 IF). Group 3 patients (controls; N = 14) received only the initial SRP. All three groups received the same adjunctive systemic antibiotic treatment. RESULTS: In all groups, the results showed statistically significant differences in PD and clinical attachment level (CAL) after 6 and 24 months compared to baseline data. Compared with the controls, a significant reduction in PD was observed in groups 1 and 2. The reduction in mean PD was distinctly greater in group 2 (higher IF). Furthermore, Porphyromonas gingivalis (Pg) and Actinobacillus actinomycetemcomitans (Aa) were completely suppressed in group 2 after 24 months. CONCLUSIONS: The present results show that the extent of root planing has a distinct influence on treatment outcomes. Patients treated with the highest instrumentation frequency showed the best long-term results.

Adult↗
PubMed2003

Migrating third molar: a report of a case.

Pathologic migration is an abnormal change in the position of a tooth within the dental arch. There are many etiologic factors associated with this phenomenon, but the exact cause is often difficult to diagnose. The following is a report of a 42-year-old man exhibiting a unique form of bilateral migration of his mandibular third molars. He was asymptomatic and unaware of this occurrence. The morbidity to remove these teeth was deemed too great to justify extraction. Biopsy of the overlying tissue associated with a left-impacted third molar revealed no significant pathologic process other than inflammation and some hyperplasia within the dental follicle. Histologic-radiographic correlation was inconclusive in determining whether epithelium from pericoronal soft tissue involving the right third molar was from a hyperplastic dental follicle or a small dentigerous cyst. It is speculated that the ultimate cause of the migration of the third molars was severe, aggressive periodontal disease of the adjacent molars.

Adult↗
PubMed2002

Analysis of genetic polymorphisms at the interleukin-10 loci in aggressive and chronic periodontitis.

BACKGROUND/AIMS: Different cytokine genotypes have been described in periodontal disease. The aim of the present study was to investigate the genetic association of two previously described interleukin-10 (IL-10) polymorphisms in patients with aggressive (AP) and chronic periodontitis (CP) and to investigate possible associations with clinical manifestations. METHODS: Based on clinical parameters and radiographs, 23 patients with CP and 18 patients with AP were included in the study. Additionally, 21 age-matched healthy subjects served as a control group. Genomic DNA was isolated from whole blood samples and the IL-10 promoter sequences from positions - 597 to - 824 were amplified by polymerase chain reaction (PCR). Polymorphisms were detected by restriction-enzyme cleavage. The A and C alleles at the - 597 position were associated with the T and C alleles at the - 824 position, respectively. Fisher's exact test was used for the statistical analysis. RESULTS: No significant differences were observed in the allele frequencies between controls and AP patients (p = 0.70) or CP patients (p = 0.43), although the previously reported association between allele A at position - 597 and allele T at position - 824 was observed in our population. CONCLUSION: We conclude that the investigated polymorphisms are not associated with periodontal disease.

Acute Disease↗
PubMed2004

[The concept of maintenance therapy for periodontal inflammations characterized by an aggressive course].

Long-term studies have reported significance of supportive periodontal therapy in patients with aggressive forms of periodontitis. The success of periodontal care depends on a long commitment of both the patient and the dentist. The continuing, periodic assessment of periodontal structures aims to determine treatment needs. The main aim of supportive periodontal treatment in case of aggressive periodontitis is to prevent the recurrence and progression of periodontal disease. This paper contains information concerning significance and methods of plaque removal by the patient after appropriate periodontal therapy.

Dental Care↗
PubMed2005

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 (p 6 mm, but none of 14 patients having mean pocket depth at sample teeth<or=6 mm revealed more than 100,000 copies of HCMV or EBV in subgingival or gingival samples (p=0.001; chi-squared test). In periodontitis lesions demonstrating herpesviruses in paired subgingival and gingival tissue samples, the tissue samples showed the higher HCMV copy counts in three of four patients and the higher EBV copy counts in six of eight patients. CONCLUSIONS: The elevated occurrence of HCMV and EBV DNA copies in periodontal pockets and in the gingival tissue of aggressive periodontitis lesions relative to chronic periodontitis lesions, and the increase in herpesvirus counts with increasing severity of periodontitis lend substantial support to a periodontopathic role of the two viruses. Real-time PCR determination of herpesvirus DNA in periodontal sites may become a promising marker to monitor the course of destructive periodontal disease. Herpesviruses and bacteria, now mostly studied in isolation, may cooperate synergistically in the development of periodontitis, and should probably be considered as a pathogenetic consortium in future investigations of periodontal infections.

Adult↗
PubMed2003

Genes and gene polymorphisms associated with periodontal disease.

The scientific literature during the last ten years has seen an exponential increase in the number of reports claiming links for genetic polymorphisms with a variety of medical diseases, particularly chronic immune and inflammatory conditions. Recently, periodontal research has contributed to this growth area. This new research has coincided with an increased understanding of the genome which, in turn, has permitted the functional interrelationships of gene products with each other and with environmental agents to be understood. As a result of this knowledge explosion, it is evident that there is a genetic basis for most diseases, including periodontitis. This realization has fostered the idea that if we can understand the genetic basis of diseases, genetic tests to assess disease risk and to develop etiology-based treatments will soon be reality. Consequently, there has been great interest in identifying allelic variants of genes that can be used to assess disease risk for periodontal diseases. Reports of genetic polymorphisms associated with periodontal disease are increasing, but the limitations of such studies are not widely appreciated. While there have been dramatic successes in the identification of mutations responsible for rare genetic conditions, few genetic polymorphisms reported for complex genetic diseases have been demonstrated to be clinically valid, and fewer have been shown to have clinical utility. Although geneticists warn clinicians on the over-enthusiastic use and interpretation of their studies, there continues to be a disparity between the geneticists and the clinicians in the emphasis placed on genes and genetic polymorphism associations. This review critically reviews genetic associations claimed for periodontal disease. It reveals that, despite major advances in the awareness of genetic risk factors for periodontal disease (with the exception of periodontitis associated with certain monogenetic conditions), we are still some way from determining the genetic basis of both aggressive and chronic periodontitis. We have, however, gained considerable insight into the hereditary pattern for aggressive periodontitis. Related to our understanding that it is autosomal-dominant with reduced penetrance comes a major clinically relevant insight into the risk assessment and screening for this disease, in that we appreciate that parents, offspring, and siblings of patients affected with aggressive periodontitis have a 50% risk of this disease also. Nevertheless, we must exercise caution and proper scientific method in the pursuit of clinically valid and useful genetic diagnostic tests for chronic and aggressive periodontitis. We must plan our research using plausible biological arguments and carefully avoid the numerous bias and misinterpretation pitfalls inherent in researching genetic associations with disease.

Aggressive Periodontitis↗
PubMed2002

Interactions between stress, interleukin-1beta, interleukin-6 and cortisol in periodontally diseased patients.

BACKGROUND/AIMS: The aim of the present study was to measure interleukin-1beta, interleukin-6 and cortisol levels in the peripheral blood of periodontally diseased patients in order to record any interactions with psychosocial stress. MATERIAL AND METHODS: The test group comprised 16 patients with untreated and 14 with treated aggressive generalized periodontitis (AGP), five patients with untreated aggressive localized periodontitis (ALP) and five with chronic generalized periodontitis (CGP). The control group comprised 40 periodontally healthy probands. Blood was taken from the cephalic vein of all patients and controls at the same time (8 a.m.) each day. IL-1beta, IL-6 and cortisol levels were then measured with a sensitive ELISA, the 'Quantikine HS Immunoassay Kit' (Biermann Diagnostica, Bad Nauheim, FRG). The clinical examination covered probing depth, gingival recession, gingival index, plaque index and clinical attachment level. A questionnaire was used to ask the patients and controls about their attitude to life and the stress induced by their jobs and their families. Previous and current levels of tobacco consumption were also recorded. Statistical evaluation was based on the Mann-Whitney U-Wilcoxon test for comparison of blood serum values and clinical parameters between patients and controls, and the Kruskal-Wallis test for intergroup comparison. All data were correlated by means of Spearman's rank correlation coefficient, and significance levels relating to stress and smoking were determined with the chi-square test. RESULTS: With respect to cortisol, the results showed no significant differences either between the patient groups or in comparison with the controls. IL-1beta was detected only in the AGP patients and their controls, but with no significant differences. IL-6 was detected in virtually all patients and controls, but with no significant differences. Only in the untreated AGP patients was IL-6 significantly elevated (P < 0.05) and a slight correlation with attachment loss recorded. In all AGP patients a slight correlation between IL-1beta and IL-6 was recorded. Evaluation of the questionnaire revealed a higher proportion of untreated AGP patients than of controls with a pessimistic attitude to life. In all AGP patients, family-induced stress and smoking were found to correlate with attachment loss. In the untreated AGP patients, smoking correlated with IL-1beta protein content, and in the controls there was a moderate correlation between smoking and IL-6 levels. CONCLUSIONS: The present study found no correlation between the immunological mediators (IL-1beta, IL-6), glucocorticoids (cortisol) and the registered stress values. However, the patients with untreated AGP showed signs of a pessimistic attitude to life, and an elevated IL-6 level was recorded in the peripheral blood. As a restrictive factor it should be borne in mind that the number of patients investigated was too small for adequate conclusions to be drawn.

Adult↗
PubMed2004

Update on human cytomegalovirus in destructive periodontal disease.

AIM: Human cytomegalovirus (HCMV), a herpesvirus, is discussed in this review as it relates to destructive periodontal disease in humans. RESULTS: HCMV genomic sequences, detected by polymerase chain reaction identification, occur with elevated frequency in severe adult periodontitis, localized and generalized aggressive (juvenile) periodontitis, Papillon-Lefèvre syndrome periodontitis, acute necrotizing ulcerative gingivitis, and periodontal abscesses. DISCUSSION: Herpesviruses establish lifelong persistent infections. HCMV infection involves an asymptomatic latent phase interrupted by periods of recrudescence where viral replication and possibly clinical disease become manifest. HCMV reactivation is triggered by a number of immunosuppressive factors, some of which have been shown also to be risk factors/indicators of periodontitis. HCMV periodontal infection may cause release of tissue-destructive cytokines, overgrowth of pathogenic periodontal bacteria, and initiation of cytotoxic or immunopathologic events. CONCLUSIONS: A growing body of data supports the concept that HCMV contributes to severe types of periodontal disease. HCMV infection of the periodontium may alter the immune control of resident microorganisms and be important in a multistage pathogenesis of periodontitis involving viral activation, periodontopathic bacteria, and host immune responses. Understanding the significance of HCMV and other herpesviruses in the development of periodontal disease may have important therapeutic implications. Vaccines against HCMV, which are in various stages of development, need to be evaluated for their ability to decrease the incidence of destructive periodontal disease.

Animals↗
PubMed2005

Tissue destruction in periodontitis: bacteria or cytokines fault?

The pathogenesis of periodontal disease involves the sequential activation of a great variety of components of the host immune response, primarily acting to defend periodontal tissues against bacterial aggression, but also functioning as mediators of tissue destruction. The expression of the disease results from the interaction of host, microbiological agents, and environmental factors. Leukocytes play a critical role in the pathogenesis of the disease, producing different cytokines, chemokines, and other mediators, thus generating a host defense response, as well as inducing tissue inflammation and bone destruction. The aim of this review is to address the role of some inflammatory mediators in response to bacterial aggression in periodontitis.

Cytokines↗