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.

Five cases are reported of periodontitis affecting the deciduous teeth in young children. The purpose of the report is to define prepubertal periodontitis as a clinical entity, establish diagnostic criteria, demonstrate clinical, radiographic, and historical features, document progression, and explore methods of treatment. The disease occurs in localized and generalized forms. In the localized form, either few teeth or many may be affected. The onset appears to be around the age of 4 years or before. The gingival tissue manifests only minor inflammation, if any, and microbial plaque is minimal. Alveolar bone destruction proceeds more rapidly than in adults or teenagers with periodontitis, but much slower than in individuals with generalized prepubertal periodontitis. In some cases, otitis media and upper respiratory infections are also present, although these are not life‐threatening. The progress of the disease can be halted, so far as is known, by curettage coupled with antibiotic therapy and improved toothbrushing. The hallmarks of generalized prepubertal periodontitis include a fiery red acute inflammation pervading the marginal and attached gingiva around all the teeth, gingival proliferation, cleft formation, and recession. Onset is at the time of tooth eruption. Alveolar bone destruction, sometimes accompanied by destruction of the tooth roots, proceeds at an alarming rate. The affected children have otitis media and recurrent, sometimes life‐threatening infections. Their periodontitis seems to be refractory to antibiotic therapy. In one case, the disease was controlled by extraction of the hopeless teeth combined with meticulous plaque control. Abnormalities in peripheral blood leukocyte chemotaxis have been found in all children with prepubertal periodontitis studied so far. In our children with the generalized form of the disease, both neutrophils and monocytes were profoundly abnormal and the basic defect appeared to be in cell adherence, while in children with localized disease, either neutrophils or monocytes but not both cell types were affected, and the defects were not profound. Prepubertal periodontitis seems to be more common in females than in males. In some families susceptibility appears to have a maternal pattern of inheritance, while in others no pattern of transmission is apparent. Prepubertal periodontitis may be followed by severe periodontitis of the permanent teeth or by a normal permanent dentition.

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% exhibited 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.

Predominant bacterial flora resident in subgingival plaque was characterized and evaluated in relation to the etiology of periodontal disease. Small groups of clinically and radiographically identified periodontal patients and control subjects were studied. A comprehensive inventory of cultivable flora was made. The most common group of organisms were the Gram‐positive rods, the majority of which were Actinomyces. A larger proportion of anaerobic Gram‐negative rods were isolated than indicated in the results of previous studies. Considerable variability in floral content was found in different sites in the same patient. However, no statistically significant differences were observed in the flora between clinically normal and pathological sites of the same patients. A significantly greater number of facultative Actinomyces was present in the flora of periodontal patients as compared to control subjects. Sera from the same nine subjects were assayed by indirect immunofluorescence for circulating antibodies to 12 strains of plaque bacteria. No differences in antibody titers were observed between sera from periodontal patients and control subjects.

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.