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.

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.

No abstract

Experiments were done to learn whether or not the blastogenic responsiveness of peripheral blood mononuclear cells (PBM) from 34 patients to mitogens and homogenates of a panel of periodontal bacteria differs significantly from that of cells from 16 normal individuals. Groups of control individuals and patients with juvenile (JP), rapidly progressive (RP) and adult periodontitis (AP) were formed. Blastogenic responsiveness was assessed after 72 and 120 h incubation by measuring the uptake of radioactive precursor into DNA. Bacterial preparations and mitogens used as stimulators included Bacteroides melaninogemcus (BMEL), Capnocytophaga (CAPNO), Fusobacterium nucleatum (FUSO), Actinomyces viscosus (AVIS), phytohemagglutinin (PHA), and pokeweed mitogen (PWM). When the data were calculated as Stimulation Index (E/C), responsiveness of cells from patients with AP and JP was enhanced relative to that of cells from normal control subjects, but the enhancement was not statistically significant. In contrast, responsiveness of cells from RP patients to FUSO and AVIS was significantly suppressed. Except in the case of AP cells activated with PHA, mitogenic responsiveness of all patient cells was significantly suppressed. When responsiveness was calculated as E minus C, these differences between patient and control cells disappeared except for suppression of the level of blastogenesis by AP and RP cells exposed to AVIS. After 120 h incubation, unstimulated cultures of AP cells incorporated significantly less, and RP cells significantly more, radioactivity than did unstimulated cultures from normal individuals indicating an abnormal autologous mixed lymphocyte reaction. Cells were harvested and tested from a group of AP patients before, during and following periodontal therapy. PBM responsiveness to horaogenates of CAPNO did not change significantly during therapy, but responsiveness to all of the other bacterial preparations including autologous plaque increased following initial therapy. Values for AVIS, FUSO, and PLAQ were statistically significant. Responsiveness to the bacterial preparations either remained at the enhanced levels or increased to even greater levels following completion of therapy, except in the case of autologous plaque, where the values had begun to return toward pretreatment levels. In addition, responsiveness to PWM and PHA dropped to about one‐half the pretreatment values and responsiveness of unstimtilated cultures increased significantly to levels observed in cultures of ceils from normal donors.