A comparison of antimicrobial activity of four disclosant dyes.

Four disclosant dyes were tested for antimicrobial activity against 27 oral reference strains and five non-oral human pathogens. Erythrosine and fluorescein inhibited most gram-positive and gram-negative organisms associated with dental plaque, and were bactericidal to selected strains. Fast green and brilliant blue demonstrated little antimicrobial activity.

Clinical, microbiological and immunological studies of a family with a high prevalence of early-onset periodontitis.

Extensive clinical, laboratory and microbiological studies were performed on members of a family with an unusually high prevalence of early-onset severe periodontitis. Clinical observations included intraoral photographs and assessment of inflammation, plaque, probing depths and bone loss. Pocket bacteria were sampled, cultivated and identified. Immunological studies included assessment in vitro of neutrophil (PMN) and monocyte (MN) chemotaxis, assessment of PMN phagocytosis and other functions using the iodination assay, measurement of serum opsonic and chemoattractant activities and determination of levels of serum antibodies specific to various putative periodontal pathogens. The proband, a 19-year-old white woman, had rapidly progressive periodontitis (RP). Of her six siblings available for study, all had juvenile periodontitis (JP), and both parents had been edentulous since early adulthood. Early edentulism and recurrent infections, especially otitis media, were prevalent in the forebearers, especially on the maternal side. Two married sisters of the proband had young male children with recurrent infections. Abnormalities in leukocyte chemotaxis were found in the proband, in two of her siblings and in both parents. The pocket flora was predominantly Gram-negative, anaerobic rods with a high prevalence of Bacteroides species, and serum antibodies specific to Bacteroides species were detected in the sera of five of the seven patients studied. Actinobacillus actinomycetemcomitans was not found in any of the pockets studied, nor were antibodies specific to any of the three known serotypes of this bacterium detected in the serum of any of the patients. There was a relatively good correlation between the bacterial species isolated from the periodontal pockets and the antibodies found in the serum. PMN iodination and serum opsonic activity were normal in all of the patients. Thus not all JP patients have detectable Actinobacillus species in their periodontal pockets, nor do all have antibody detectable with the techniques we used specific to these bacteria in their serum. In contrast, JP patients may have Bacteroides species in their periodontal pockets and antibody specific to Bacteroides species in their serum. Although abnormal leukocyte chemotaxis is generally common in RP and JP patients, in this family the correlation between this defect and the presence of these diseases was poor.

Rapidly progressive periodontitis. A distinct clinical condition.

We report radiographic, clinical, historical, and laboratory observations on seven patients selected to illustrate the features and characteristics of rapidly progressive periodontitis, with the aim of establishing this disease as a distinct clinical entity. This form of periodontitis is seen most commonly in young adults in their twenties, but it can occur in postpubertal individuals up to approximately 35 years of age. During the active phase, the gingival tissues are extremely inflamed and there is hemorrhage, proliferation of the marginal gingiva, and exudation. Destruction is very rapid, with loss of much of the alveolar bone occurring within a few weeks or months. This phase may be accompanied by general malaise, weight loss, and depression, although these symptoms are not seen in all patients. The disease may progress, without remission, to tooth loss, or alternatively, it may subside and become quiescent with or without therapy. The quiescent phase is characterized by the presence of clinically normal gingiva that may be tightly adapted to the roots of teeth with very advanced bone loss and deep periodontal pockets. The quiescent phase may be permanent, it may persist for an indefinite period, or the disease activity may return. Most patients with rapidly progressive periodontitis have serum antibodies specific for various species of Bacteroides, Actinobacillus, or both, and manifest defects in either neutrophil or monocyte chemotaxis. Affected patients generally respond favorably to treatment by scaling and open or closed curettage, especially when accompanied by standard doses of antibiotics for conventional time periods. A small minority of patients do not respond to any treatment, including antibiotics, and the disease progresses inexorably to tooth loss even in the presence of aggressive periodontal therapy and maintenance. At the present time it is not possible to distinguish prior to treatment which individuals will respond to therapy and which will not.

Clinical and laboratory studies of a family with a high prevalence of juvenile periodontitis.

The form of periodontitis with onset at puberty and affecting predominantly the first molars and incisors is called juvenile periodontitis (JP). The disease has been the object of intense study because from its analysis may come insights into understanding other, more common, forms of periodontitis. We recently had the opportunity to study an unusual family in which both parents developed JP in their teens. We did clinical examinations, measured leukocyte chemotaxis, analyzed the pocket microflora, looked for serum antibodies against a large panel of putative periodontal pathogens and correlated the results. The couple had two affected and two unaffected children. One of the unaffected children was not available for study. Neutrophil chemotaxis was abnormal in both parents and in the two affected children, but not in the unaffected child. Actinobacillus actinomycetemcomitans accounted for 17.5% of the pocket flora isolated from one affected child and 2.5% of that from the unaffected child, but was not detected in the remaining family members. Antibodies specific for A. actinomycetemcomitans, Hemophilus aphrophilus and Eikenella corrodens were present in the serum of both affected children and for Capnocytophaga sputigena and C. ochracea in the father, but no antibodies directed against any of the species studied were found in the mother and the unaffected child. The distribution of disease in this family was more compatible with an X-linked dominant than with an autosomal recessive mode of inheritance. The correlations among presence or absence of disease, abnormal neutrophil chemotaxis and presence of serum antibodies reacting with A. actinomycetemcomitans were excellent.(ABSTRACT TRUNCATED AT 250 WORDS)

Prevalence of viridans streptococci exhibiting lactose-inhibitable coaggregation with oral actinomycetes.

Fresh oral isolates from human dental plaque were selected on the basis of their spherical morphology. In a double-blind experiment, their species identity and ability to coaggregate with human oral Actinomyces viscosus and Actinomyces naeslundii were determined. Of the 110 isolates characterized, 30 were identified as either Streptococcus mutans, Streptococcus anginosus-constellatus, or Veillonella parvula; none of these coaggregated with the actinomycetes. The remaining 80 isolates were identified as Streptococcus sanguis, Streptococcus mitis, Streptococcus MG-intermedius, or Streptococcus morbillorum. Of these 49 isolates (61%) coaggregated with actinomycetes, and nearly 90% (43 of 49 isolates) exhibited lactose-inhibitable coaggregations. Compared with previously characterized coaggregation properties determined with stock culture strains of streptococci, 82% of the fresh isolates exhibited identical coaggregations. The other 18% made up a new coaggregation group that possessed a related lactose-inhibitable coaggregation pattern. Thus, most fresh isolates that coaggregated exhibited lactose-inhibitable coaggregations with human oral actinomycetes. It is suggested that these coaggregations are mediated by a network of lectin-carbohydrate interactions similar to those already characterized in previous studies with stock cultures of actinomycetes and streptococci.

Lactose-reversible coaggregation between oral actinomycetes and Streptococcus sanguis.

Freshly isolated strains of oral actinomycetes were obtained from human dental plaque and were tested for the ability to coaggregate with common laboratory stock strains of Streptococcus sanguis. Strains belonging to the genera Actinomyces, Arachnia, Bifidobacterium, and Bacterionema were isolated. Only members of the genus Actinomyces coaggregated with the streptococci, and only Actinomyces viscosus and Actinomyces naeslundii exhibited lactose-reversible interactions. A total of 61 strains, consisting of all of the A. viscosus isolates and 86% of the A. naeslundii isolates, coaggregated; 87% inhibited lactose-reversible coaggregation. On the basis of this property and the altered ability of strains to coaggregate after heat treatment of the cells, we delineated four coaggregation groups. The other 13% of the strains constituted a fifth group, which was characterized by a pattern of closely related interactions that were not reversed by lactose. Compared with previously characterized coaggregation properties determined with stock culture strains of actinomycetes, more than 80% of these fresh isolates exhibited identical coaggregation properties. Thus, most of the coaggregation between freshly isolated oral actinomycetes and streptococci involves lactose-reversible cell-cell interactions, which suggests that such coaggregation is mediated by a network of lectin-carbohydrate interactions between complementary cell surface structures on the two cell types.

Bacteriology of dental abscesses of endodontic origin.

Aspirates have been cultured from 10 dental abscesses of endodontic origin, all of which had penetrated beyond the bony alveolus to produce fluctuant swelling. Sampling was by syringe aspiration. Strict anaerobic techniques, including the use of an anaerobic chamber, were used for serial dilution and plating. Randomly selected colonies (100) from each culture were purified, characterized, and identified. Seventy percent of the bacterial isolates were either strict anaerobes or microaerophilic. One abscess yielded a pure culture of a viridans streptococcus, Streptococcus milleri. Streptococcus intermedius dominated the flora in a second abscess. The common oral streptococcus, Streptococcus sanguis, constituted only 2% of the isolates from one additional infection. Fusobacterium nucleatum, Bacteroides melaninogenicus, other Bacteroides including B. oralis and B. ruminicola, anaerobic diphtheroids, Peptostreptococcus micros, and Staphylococcus epidermis were other predominant isolates.

Subgingival microflora of periodontal patients on tetracycline therapy.

Samples of subgingival plaque were collected from periodontal patients receiving two different tetracycline treatment regimens following conventional periodontal therapy. Four patients had received an oral dose of 1000 mg/day for 2 weeks and nine had received 1000 mg/day for 1 week followed by 250 mg/day for extended time periods. The latter regimen is similar so that commonly prescribed for the chronic skin disease, acne vulgaris. Taxonomic characterization of plaque isolates indicated that the predominant organisms cultured from both treatment groups were species of Streptococcus and the branching, filamentous Gram-positive rods, Actinomyces and Rothia. A much greater microbial complexity was observed among the flora isolated from patients taking 250 mg/day. The latter group harbored many of the fastidious Gram-negative organisms presently implicated in the etiology of periodontal disease. All bacterial strains isolated were tested for resistance to tetracycline by replica-plating cultures on an agar medium containing two-fold dilutions of the antibiotic. Streptococcus, Veillonella and Neisseria were the bacterial genera found to be consistently resistant to tetracycline, with minimum inhibitory concentrations as high as 128 micrograms/ml. Among the Actinomyces, selection for antibiotic resistance was common only within a single species, A. odontolyticus. However, A viscosus strains isolated at 54% of the subgingival flora from one patient did demonstrate an intermediate resistance level, growing on concentrations up to 8 micrograms/ml. Tetracycline resistance was shown by a variety of Gram-negative rods isolated from the low dosage group. Although a minimum number of patients were studied, extensive microbial analyses of the predominating subgingival bacteria indicated that the goal of tetracycline therapy was achieved during the 2-week therapy period at 1000 mg/day.

Synonymy of strains of Center for Disease Control group DF-1 with species of Capnocytophaga.

Of eight strains of Center for Disease Control group DF-1 examined, seven had 62 to 87% deoxyribonucleic acid homology with the neotype strain of Capnocytophaga ochracea and one had 72% deoxyribonucleic acid homology with the type strain of C. gingivalis. Deoxyribonucleic acid homology of four strains of Bacteroides ochraceus with the neotype strain of C. ochrecea was 76 to 86%.

Effects of short-term administration of metronidazole on the subgingival microflora.

The effect of a 5-day course of systemic metronidazole was investigated in 11 recall maintenance patients over a period of 3 months. Crevicular fluid flow, bleeding on probing, pocket depth, and composition of the subgingival microbiota as observed by dark-field microscopy, were measured. The study design allowed patients to act as their own controls. At baseline 1 (day 0), each patient had a randomly assigned quadrant scaled and root-planed, and received oral hygiene instruction. Microbiological and clinical parameters were measured at baseline 1 (before treatment) and at 3, 6, and 12 weeks in both the root-planed and a designated no-treatment quadrant. At baseline 2 (12 weeks), the contralateral quadrant was scaled and root-planed, and the oral hygiene instruction was reinforced. At this appointment, each patient was given 15 metronidazole tablets (250 mg), 1 to be taken 3 times per day for 5 days. At the end of this period, patients were seen 1-2 h after taking their last tablet, and blood and crevicular fluid samples were taken to determine the concentration of metronidazole by microbiological assay in the serum and crevicular fluid. Microbiological and clinical parameters were measured at baseline 2 (before treatment) and at 13, 15, 18, and 24 weeks in both the root-planed and designated non-root-planed (metronidazole only) quadrants. Results demonstrated that in this group of recall maintenance patients, metronidazole was no more effective than root-planing alone in reducing the relative % of total motile organisms and spirochetes in 5-8 mm pockets. Crevicular fluid flow was, however, significantly reduced for 11 weeks; serum and crevicular fluid levels of metronidazole were similar 1 to 2 h after drug ingestion.

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.

Laboratory studies of a family manifesting premature exfoliation of deciduous teeth.

In a previous publication, we described the clinical and radiographic findings of a family in which the children manifested premature exfoliation of the deciduous teeth. We now report for the same family the results of extensive laboratory studies performed on blood and urine, analysis of periodontal microflora, and a family pedigree. We demonstrated the presence of putative periodontal pathogens in the subgingival microflora, elevated levels of serum antibodies reacting to Bacteroides gingivalis, Capnocytophaga gingivalis, and C. sputigena in 2 of the children, and significantly suppressed monocyte chemotaxis in all 3 children. Phosphoethanolamine was found in the urine of the father and all 3 children, but not in the mother. Likewise, serum alkaline phosphatase was abnormally low for all 3 children, and was at the extreme low end of normal range for the father, but was normal for the mother. On the basis of the alkaline phosphatase and phosphoethanolamine measurements, we assigned a diagnosis of hypophosphatasia to the 3 children. Phosphoethanolamine and alkaline phosphatase were also abnormal in the paternal grandmother and her brother. The son of this brother who was deceased had a daughter manifesting premature loss of the primary teeth. The data are consistent with an autosomal dominant mode of transmission. In the light of our findings, hypoplastic cementum must be considered in the etiology of some forms of early-onset periodontitis.