Altered neutrophil function in localized juvenile periodontitis: intrinsic cellular defect or effect of immune mediators?
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Patients suffering from periodontitis or periodontosis were selected for the study. Further subdivision of these groups was based on the presence or absence of herpes and/or adenoviruses in their oral lymphocytes and epithelial cells. The phagocytic and bactericidal activities of oral leukocytes isolated from the same individuals were compared with virus carriage. In the periodontitis group, 60.5%, and in the periodontosis group 61.5% of patients carried viruses, while this was established only in 21.1% of control cases. On the other hand, emigration and sulcular gathering of the less viable polymorphonuclear leukocytes was elevated but their phagocytotic activity was decreased among periodontitis patients. Bactericidal capacity was significantly lowered among those subjects who carried viruses in their cells, as compared with virus-free persons, especially in the periodontitis group. The functions of the polymorphonuclear leukocytes accumulated in the sulcus gingivalis may be modified by mediators released from the virus-carrying cells. These mediators could achieve a greater concentration locally, and the damaged leukocytes would not be able to eliminate the microbes continuously so that the accumulation of bacterial products, among them endotoxins, could lead to periodontal inflammation.
OBJECTIVES: In order to elucidate the genetic background to EOP it is useful to investigate associations with genetic polymorphisms of immune response genes, whose products play a r le in the inflammatory process. The aim of this study was to examine IL1A and IL1B genetic polymorphisms in unrelated European white Caucasian patients with generalised early-onset periodontitis (GEOP). MATERIAL AND METHODS: Polymerase chain reaction (PCR) amplification of the ILIA (-889) gene and IL1B (+3953) gene (56 patients, 56 controls) was carried out and PCR products subjected to restriction fragment length polymorphism (RFLP) analysis. RESULTS: There were no significant differences between patients and controls for any of the genotype or allele frequencies investigated (p = 1.0). Smoking status was also included as a covariate but this did not alter the results. Furthermore, expression of the composite genotype described by Kornman and coworkers was also investigated in these subjects. No significant differences were found between patients and controls whether smoking was included as a covariate or not. CONCLUSION: The lack of any association between the IL1 polymorphisms and GEOP, in the population presented here, brings into doubt the usefulness of these candidate genes as markers of susceptibility to this form of periodontitis.
OBJECTIVE: To describe the prevalence of the cultivable subgingival microbiota in periodontal diseases and to draw attention to the polymicrobial nature of periodontic infections. METHODS: The study population consisted of 95 patients, 51 females and 44 males, aged 14-62 years. Twenty-nine patients exhibited adult periodontitis (AP), six localized juvenile periodontitis (LJP), and 60 rapidly progressive periodontitis (RPP). Two to four pooled bacterial samples were obtained from each patient. Samples were collected with sterile paper points from the deepest periodontal pockets. The samples were cultured under anaerobic and microaerophilic conditions using selective and non-selective media. Isolates were characterized to species level by conventional biochemical tests and by a commercial rapid test system. RESULTS: Prevotella intermedia and Capnocytophaga spp. were the most frequently detected microorganisms in all diagnostic groups. Porphyromonas gingivalis and Peptostreptococcus micros were found more frequently in AP and RPP patients, while Actinobacillus actinomycetemcomitans and Eikenella corrodens were associated with AP, LJP and RPP patients. The other bacterial species, including Actinomyces spp., Streptococcus spp. and Eubacterium spp., were detected at different levels in the three disease groups. CONCLUSIONS: The data show the complexity of the subgingival microbiota associated with different periodontal disease groups, indicating that the detection frequency and levels of recovery of some periodontal pathogens are different in teeth affected by different forms of periodontal disease.
The purpose of the present study was to investigate the clinical differences between individuals highly susceptible and individuals insusceptible to periodontal breakdown. The susceptible group consisted of 7 patients with a diagnosis of juvenile periodontitis. The insusceptible group consisted of 7 individuals selected on the basis of age (52 years or older), presence of at least 18 teeth, no evidence of extractions due to periodontal breakdown, no loss of attachment, shallow pockets, gross amounts of plaque and no history of interdental cleaning. Results showed that the susceptible group had more bleeding, less plaque and deeper pockets than the insusceptible group. Since the 2 groups seem to behave differently with regard to bleeding upon probing and amount of plaque, bleeding/plaque ratios were calculated. Testing showed a highly significant difference between the 2 groups. The same results were obtained if only sites with shallow pockets were included in the analysis. On the basis of these results, it is hypothesized that a high value of the ratio between bleeding and plaque may act as a prognostic indicator for periodontal breakdown.
The composition of subgingival plaque, from healthy and periodontally diseased regions, as well as the clinical periodontal condition of 6 patients, 17 to 24-years-old suffering from juvenile periodontitis were examined. 6 older patients with rapidly progressive periodontitis served as a control. Samples of subgingival plaque were taken from first molars and central incisors and were analysed morphologically by dark-field microscopy. In the control group in healthy regions the ratio between non-motile and motile bacteria was 27:1 and about 1:1 in deep pockets. In the juvenile periodontitis group in diseased regions, motile bacteria made up only 1/4 of the bacteria present. The results clearly show that our relatively old patients with juvenile periodontitis had a completely different microflora in their periodontally diseased regions than patients with common periodontitis. As regards our observations by dark-field microscopy, one can assume, however, that with increasing age, there might be a shift of the flora associated with juvenile periodontitis lesions from a rather simple composition to a more complex composition very similar to the flora seen in rapidly progressive adult periodontitis lesions.
The generation rate of free oxygen radicals as measured by maximal light intensity of luminol-enhanced chemiluminescence from peripheral blood granulocytes (PMN) stimulated with differently opsonized Staphylococcus aureus was studied in 13 patients with juvenile periodontitis (JP) and pair-matched, healthy controls. Plasma proteins related to inflammation were also assayed. When stimulated with bacteria opsonized with autologous serum, the PMN from the JP patients showed a more intensive chemiluminescence than did their pair-matched controls (p less than or equal to 0.0005). The difference was consistent but slightly reduced when using heat-treated serum (p less than or equal to 0.006) or heterologous gammaglobulin (p less than or equal to 0.19) for opsonization. When testing freeze preserved sera from 11 of the compared pairs, the sera from JP patients induced a slightly higher chemiluminescence in PMN from a healthy donor (p less than or equal to 0.031). Protein analysis of the patient sera revealed a slightly higher concentration of complement 4 (p less than or equal to 0.032) and IgM (p less than or equal to 0.030) when compared with their respective pair-matched healthy controls. The influence of other blood components contaminating our assay system was checked on healthy PMN cells. Lymphocytes, platelets, relevant amounts of ADP and serum had no effect on the chemiluminescence. In conclusion, the increased chemiluminescence of peripheral blood granulocytes from patients with juvenile periodontitis seems to be related mainly to the cells. The association with free oxygen radicals and their tissue-damaging potency might be a contributing factor in the pathogenesis of periodontal disease.
In 12 patients with juvenile periodontitis (JP), stimulation of peripheral polymorphonuclear neutrophils (PMN) by opsonized bacteria showed increased release of free oxygen radicals and of elastase activity in relation to that of pair-matched healthy controls. The elastase increase was not associated with higher intracellular content of elastase, since the measurement of homogenized PMN cells did not differ between the patient group and the control group; nor did the spontaneous elastase activity of nonstimulated cells differ. Release of elastase by contaminating lymphocytes and platelets could be excluded, since no elastase activity from these cells or interference by these cells could be demonstrated in the assay system used. When formyl-methionyl-leucyl-phenylalanine was used as a stimulant, the chemiluminescence in the patient PMN cells did not differ with statistical significance from their pair-matched controls. The increased release of free oxygen radicals and of elastase seems to be a characteristic of the PMN cells in juvenile periodontitis, indicating hyperactive cells with possible pathogenic effects.
Longitudinal investigations concerning immunological responses and periodontal disease activity support a relationship between serum antibody levels and the micro-organisms associated with dental plaque. To define this host response further, we studied the relationship of antibody avidity to Actinobacillus actinomycetemcomitans (Aa) in 11 adult periodontitis and 6 localized juvenile periodontitis (LJP) patients with Aa infections. Patients were monitored every 3-4 months for immunological and clinical variables including probing pocket depths (PD), bleeding on probing (BOP), plaque index (PLI), and the number of disease active sites (DA). Avidity indices were determined using an ELISA and significant changes from each patients' baseline level were determined. The results showed different response patterns between and within the patient groups. A subset of the subjects experienced significant changes in antibody avidity over time. Between group comparisons yielded no significant differences in the number of positive or negative avidity index changes, although there were more frequent changes in the disease active adult periodontitis group. There were also no significant correlations between clinical parameters and antibody avidity, although there were changes in the clinical parameters between baseline and significant avidity change points, and also between baseline and the determination of active disease. Further studies will be necessary to define fully the role of antibody avidity and its relationship to the pathogenesis of periodontal diseases.