Efficacy of a sonic toothbrush on inflammation and probing depth in adult periodontitis.

This single-blind, 8-week study compared the efficacy of a sonic toothbrush and a manual brush in 40 patients with adult periodontitis. Qualitative clinical indices and quantitative laboratory methods were used to monitor the periodontal status of 3 pockets 5 to 7 mm deep in each subject. Patients were randomly assigned either a sonic or manual toothbrush. The two groups were comparable with respect to age, gender, and anatomical location of the test sites. Data were collected from all sites at baseline and at 2, 4, and 8 weeks. Over the 8-week period, both groups showed significant improvements in the clinical indices used. Descriptive statistics indicated the sonic brush group had greater improvement than the manual group in the clinical parameters (gingival index, bleeding index, probing depth, and clinical attachment level). Gingival crevicular fluid (GCF) flow was significantly lower in the sonic brush group (P = 0.018). Considerable variation was present in the levels detected for both inflammatory cytokines tested, however, concentration of interleukin-1 beta was significantly lower in the GCF of sonic group patients (P = 0.05), while concentration of interleukin-6 was significantly reduced in both groups (P < or = 0.05) (t tests). Under these conditions, there is some evidence to suggest that the sonic toothbrush is more beneficial in resolving inflammation in patients with moderate periodontal disease.

Assessment of serum antibody patterns and analysis of subgingival microflora of members of a family with a high prevalence of early-onset periodontitis.

In a study of members of a large family with a high prevalence of early-onset periodontitis, we sampled the subgingival microflora and characterized 40 isolates from each sample. We surveyed serum samples by enzyme-linked immunosorbent assay for antibodies reacting with any of a panel of 21 periodontal bacteria. The mother and 7 of her 13 children had early-onset periodontitis. Bacteroides gingivalis was not detected in the subgingival flora of any affected or unaffected family member, and Actinobacillus actinomycetemcomitans was isolated from only one affected child. Capnocytophaga ochracea was isolated from five of seven affected children and from none of their normal siblings. We found no significant differences among the floras from family members who had rapidly progressive, juvenile, and prepubertal forms of periodontitis. Elevated levels of serum antibody reacting with one or more of the bacteria tested were found in all family members with disease, but in only one periodontally normal family member. Both children with prepubertal periodontitis had antibodies reacting with C. sputigena, a species not found in their subgingival floras, but with none of the other bacteria tested. All remaining affected family members had antibodies to one or more serotypes of A. actinomycetemcomitans, and four had antibodies reacting with additional bacteria, including C. sputigena, Eikenella corrodens, Fusobacterium nucleatum, and Haemophilus aphrophilus. Sera from patients contained antibodies specific for putative periodontal pathogens not found in their pocket flora, and conversely, putative periodontal pathogens for which no serum antibodies were found frequently comprised a large proportion (10% or more) of the pocket flora. In no case were both the bacterium and its antibody found. These observations are suggestive of sequential infection in the early-onset forms of periodontitis and of induction of protective immunity against reinfection by the same microorganism.

Clinical studies of one family manifesting rapidly progressive, juvenile and prepubertal periodontitis.

We report clinical, radiographic and historical data on a large family with an unusually high prevalence of periodontitis. The proband, a 20-year-old black male, had the classic features of juvenile periodontitis (JP). His father was periodontally normal, while his mother had lost all her teeth at age 27 because of rapidly progressive periodontitis (RP). In addition to the 13 living children the couple had had 2 miscarriages. Of the children, one had RP, five had JP and two had prepubertal periodontitis (PP). Both maternal grandparents of the proband had become edentulous at an early age, presumably because of early-onset periodontitis. Four of 10 siblings of the proband's mother had early-onset periodontitis. In contrast, the paternal grandparents did not have early-onset periodontitis nor was periodontitis unusually prevalent in the siblings of the proband's father. The pedigree for this family is consistent with, but does not prove, an X-linked dominant pattern of genetic transmission. The natural history of early-onset periodontitis and the relationship among PP, JP and RP are not understood. The fact that the mother of the proband had RP and she had offspring with RP, JP and PP indicates a close relationship among these diseases and argues in favor of a common underlying mechanism. JP was not preceded by PP in the proband nor his affected 21-year-old brother, but one sister had PP, and at age 15 manifested JP. In her case, the alveolar bone around the deciduous molars had been destroyed, but it regenerated as the permanent premolars erupted.(ABSTRACT TRUNCATED AT 250 WORDS)