[Studies on microflora and host defensive function of a mother and daughter with early onset periodontitis].
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The point of this study was to examine the presence or absence of cytokine-positive cells by means of immunohistochemical methods in the samples of inflamed gingival tissues obtained from an 11-year-old girl with Papillon-Lefevre syndrome (PLS). Interleukin-8 (IL-8)-positive cells were found to be present. In addition, IL-1alpha-and IL-1beta-positive cells were detected. No dysfunction in the phagocytosis and the bacterial killing of peripheral blood polymorphonuclear neutrophils (PMNs) was observed in this patient. Our findings suggest that these cytokines may be members responsible for modulating the process of rapidly progressive periodontitis for patient with PLS.
HLA-A, B, C and DR antigen frequencies were determined in a group of patients with juvenile periodontitis and rapidly progressive periodontitis. In juvenile periodontitis patients, HLA-A24 and DR4 were found at a significantly higher level than in the control group, and in rapidly progressive periodontitis patients, A9 and DR4 were found at a significantly higher level than the control group. The presence of these antigens gives evidence as to the susceptibility of various forms of early onset periodontitis.
OBJECTIVE: To arrest the advancement of periodontitis. PATIENT: A 17-year-old boy diagnosed with Pierre-Robin sequence at birth exhibited localized juvenile periodontitis. Severe bone loss and mobile teeth were localized in the incisors and molars, which were irregularly positioned, possibly associated with a residual scar from palatoplasty for a soft palate cleft at an early age. CONCLUSION: Combined orthodontic-periodontic-prosthodontic treatment arrested the advancement of the periodontitis and established a stable occlusion.
An in vivo assay was recently developed to monitor the crevicular leucocyte response to chemotactic agents, e.g., casein and N-formyl peptides. This method was used to monitor humans with little or no gingival disease (C group), gingivitis (G group), chronic periodontitis (CP group) and localized juvenile periodontitis (LJP group). Casein (0.2 microliters, 2 mg/ml) was placed into an isolated gingival crevice of each subject with a calibrated wire loop and the time recorded (t = 0). Leucocytes were counted in crevicular washes (10 microliters) 15 minutes later and every 5 minutes thereafter up to t = 50 minutes. This protocol was repeated for the crevice of an adjacent tooth except that the crevicular fluid flow response to the chemotactic challenge was monitored. The C, G and CP subjects showed a similar pattern of response to the chemoattractant with a single "peak" of leucocytes at approximately t = 25 minutes. However, the peak cell count was much greater in the G and CP groups than in the C group. LJPs showed an abnormal pattern with two leucocyte peaks, one at approximately 25 minutes and the other at 45 minutes. Both peaks tended to be higher than the single peak seen in Cs but were significantly lower than that in Gs or CPs, even at similar levels of inflammation. In addition, the peak leucocyte response (to casein) in LJPs did not increase with increasing leucocyte counts in the unchallenged (resting) crevice, whereas a positive relationship was seen in the other groups of subjects. These data suggest that this new assay may provide important diagnostic information on in vivo neutrophil migration in the gingival crevice and on susceptibility to periodontal disease.
Four patients, ages 14-17, who demonstrated characteristics of juvenile periodontitis, underwent antibiotic and surgical therapy to control microbial etiologic factors. No occlusal equilibration or bone grafting techniques were employed. Subsequent to treatment, all four patients demonstrated decreased pocket depths and mobility on teeth associated with vertical osseous defects. Osseous repair was evident on postoperative radiographs. Reentry procedures, on one patient, confirmed that osseous repair had occurred in 2- to 3-wall, 3-wall, hemi-circumferential and furcal defects. If infection and inflammation are controlled, it appears that the potential for osseous repair in juvenile periodontitis patients is greater than has been thought.
The periodontal pathogen Actinobacillus actinomycetemcomitans produces a leukotoxin that is considered a primary virulence factor in localized juvenile periodontitis (LJP). Select strains of the bacterium contain a 530-bp deletion in the promoter region of the leukotoxin gene operon which results in enhanced transcription of the leukotoxin. DNA hybridization and polymerase chain reaction (PCR) were used to examine genetic variants of A. actinomycetemcomitans in 24 LJP-susceptible children from 21 families having a history of the disease and 34 control children from non-LJP families. A significant association was found between the detection of variants that had a deletion in the leukotoxin promoter region, indicative of a high level expression leukotoxin genotype, and conversion from a healthy periodontal status to disease. Subjects harboring A. actinomycetemcomitans of this genotype were more likely to convert to LJP than those subjects who had variants containing the full length leukotoxin promoter region (odds ratio = 22.5; 95% C.I., 2.84 < 206.66) [corrected]. These findings support the concept that highly virulent strains or clonal types of periodontal pathogens play a major role in the initiation of periodontal disease in susceptible hosts.
A total of 131 Actinobacillus actinomycetemcomitans clinical strains from 28 periodontally healthy or diseased subjects were serologically categorized by indirect enzyme-linked immnosorbent assay. Sepecies-specific and serotype b, c-specific monoclonal antibodies against Actinobacillus actinomycetemcomitans were used. Preliminary data revealed that each subject harbored only one serotype of Actinobacillus actinomycetemcomitans. The distribution of serotype a, b and c were respectively 11%, 21% and 68%, both of periodontally healthy subjects harbered serotype b, 7 of 9 juvenile periodontitis subjects harbered serotype c, 12 of the other subjects which included 3 adult periodontitis and 14 gingivitis harbered serotype c.
The ingestion of opsonized zymosan particles by neutrophil blood granulocytes and the chemiluminescence in samples of whole blood, induced by zymosan, Streptococcus mutans as well as phorbol myristate acetate, as a measure of the generation of reactive oxygene species were studied in patients with various forms of marginal periodontitis. Compared to a control group the phagocytic activity was found to be enhanced in progressive adult periodontitis and diminished in juvenile periodontitis whereas no differences to controls were found in chronic nonprogressive or postjuvenile periodontitis. With respect to the height of the chemiluminescence signals increased values were only measured in chronic nonprogressive periodontitis after stimulation by phorbol myristate acetate. The results indicate that impairment of blood granulocyte functions may be a pathogenetic factor for the development and the progression of marginal periodontitis.
The prevalence and severity of periodontal diseases in young people are significant. Recent progress in understanding the etiology and pathogenesis of periodontal diseases in this group of patients has allowed significant improvement in periodontal classifications. Actinobacillus actinomycetemcomitans characteristically is the major pathogen involved; black-pigmented anaerobic rods and other organisms can also be important. Treatment of periodontitis should focus on meticulous plaque control and eradication of periodontal pathogens, possibly by means of systemic or topical antimicrobial therapies.
Recent microbiological studies support the concept that specific gram negative bacteria play a major role in the etiology and pathogenesis of human chronic inflammatory periodontal disease. Actinobacillus actinomycetemcomitans has been isolated frequently from juvenile periodontitis and Porphyromonas gingivalis has been shown to be a prominent species in adult periodontitis in humans. The purpose of this study was to determine levels of the specific antibodies to A.actinomycetemcomitans and P.gingivalis in 17 patients with juvenile and 15 patients with adult periodontitis and 24 healthy subjects. IgG and IgM antibody titers against these antigens were determined by enzyme-linked immunosorbent assay (ELISA). The levels of antibodies against A.actinomycetemcomitans were significantly higher in the juvenile periodontitis compared to the adult periodontitis patients and controls. Anti-P.gingivalis antibodies were elevated in adult periodontitis compared to juvenile periodontitis patients and controls.
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