False positive rates associated with changes in periodontal probing measurements (changes which are of such magnitude as to be construed as due to disease or healing when the observed changes are actually due to measurement error) were estimated by computerized simulation. In the first phase of the simulation study, various distributions of error variances among sites were evaluated for their ability to produce matches to an empirical distribution of differences between replicate measurements. In the second phase of the study, distributions of variances identified in Phase I were used to estimate the false positive rate, under conditions of no actual change, for detection methods based on critical differences between averaged pairs of measurements. This rate was found to be substantially greater than that predicted using normal distribution probabilities and, for a difference of ≥2.5 mm, approached one false detection per examination of 168 sites. In the third phase of the study, simulation procedures were extended to the tolerance detection methodology and the false positive rate, in the absence of real change, was almost one detection per two examinations. This simulation suggested that perhaps one third of tolerance detected “bursts” of periodontal attachment change may be false positives attributable to measurement error.
A theory of periodontal attachment loss which postulates discrete bursts of activity has recently been proposed. This paper identifies several problems in the interpretation of the experimental data that have been used to support the burst model. Major obstacles to valid inferences are associated with the following: substantial measurement error, insufficient evidence supporting a dichotomy of disease state and the use of diagnostic decision criteria with undesirable properties. The nature of these problems is discussed from the framework of receiver operating characteristic (ROC) analysis. "Bursts" of attachment loss can be explained, in whole or in part, by these factors in the absence of real change. Types of research evidence that would offer more compelling support for the burst model are identified. The questionable validity of evidence supporting the burst model may impact on both the direction of future research efforts and clinical applications.
Distributions of periodontal attachment levels at probing sites within patients have traditionally been used in clinical diagnosis and treatment planning. Progression from mild to moderate to severe disease is generally associated with increasing magnitudes of attachment loss at greater percentages of sites. Recent analyses of distributions of periodontal attachment levels have suggested three general patterns of loss defined by: (1) loss at less than about one third of all sites, (2) more widespread disease with multiple peaks and (3) normally distributed loss with virtually all sites being affected. In attempting to stimulate these three patterns using a model based on the burst theory of periodontal attachment loss, divergent assumptions about burst magnitude, frequency, and possible local immunity were required. These findings were used to support the hypothesis that distinctly different disease processes are associated with the different patterns of attachment level. In the present investigation an alternative model was developed which was theoretically consistent with the view that the three patterns reflect arbitrary stages in a continuous disease "aging" process. Simple assumptions concerning attachment loss probabilities and rates enabled the generation of attachment level distributions that matched all three patterns previously attributed to separate disease processes, depending only upon the duration of the process.
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