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)

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)

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.