Familial aggregation of early onset or juvenile Periodontitis (JP), a disorder that varies in expression and age of onset, has been recognized for some time. Autosomal recessive and X‐linked inheritance patterns have been suggested, and one large pedigree has demonstrated autosomal dominant inheritance. The variability and age limitations in clinical phenotypic diagnosis present several problems to genetic analysis, because information on members of the youngest and older generations may be lost to the analysis. The purpose of the present study was to elucidate the genetic basis of JP by formal pedigree analysis and comparison of competing genetic models. Twenty‐eight families were included, with general and specific autosomal models, and an X‐linked model being compared. The autosomal recessive model provided the most parsimonious explanation of the data, and its likelihood was not significantly different from the more general model. Likelihoods for the sporadic (nongenetic) and X‐linked models were considerably lower than the autosomal models. While comparison of genetic models suggests recessive inheritance of JP, the serious complications to pedigree analysis posed by limitations warns against acceptance of this conclusion, without more exhaustive evaluation of: (1) a more extensive collection of family data, (2) more complete investigation of the effects of age limitations on comparisons among competing models, and (3) elucidation of the importance of diagnosis and phenotype assignment of adults through past dental records.
Clinical and laboratory data were compared in 72 patients with localized Periodontitis (LP) and 103 patients with generalized Periodontitis (GP). Significantly more LP than GP cases had decreased neutrophil Chemotaxis (CTX), and were seropositive for Actinobacillus actinomycetemcomitans (Aa). Significantly, more GP cases were seropositive for Bacteroides gingivalis (Bg). All clinical indices were similar on affected teeth in LP and GP, but the attachment loss was greater on clinically unaffected teeth in GP when compared with LP. LP cases with CTX defects had a significantly lower mean age, were more often seropositive for Aa antibodies, and were more often female than LP patients with normal CTX. Significantly more GP cases with CTX defects were seropositive for Aa antibody. GP patients with normal CTX had a higher plaque index on both affected and unaffected teeth than did GP patients with a CTX defect. Our data suggest that Chemotaxis and/or specific bacteria may be contributory, but not always necessary, factors in these disorders. The overlap in clinical and laboratory profiles of LP and GP continues to cloud the distinction of these early onset forms of Periodontitis. {J Periodontol 1989;60:557–563)
A mechanism for analyzing a patient pool using the computer is described. This system, used by the division of dental hygiene at Virginia Commonwealth University, is presented as a model for evaluating patients profiles. The in‐depth analysis provided by this method is helpful in determining whether the patient‐related needs of the education program are being met. Descriptions of the various patients parameters are provided, and guidelines are presented to assist those institutions considering such a system
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