Periodontal disease progression

Citation
Ms. Reddy et al., Periodontal disease progression, J PERIODONT, 71(10), 2000, pp. 1583-1590
Citations number
35
Categorie Soggetti
Dentistry/Oral Surgery & Medicine","da verificare
Journal title
JOURNAL OF PERIODONTOLOGY
ISSN journal
00223492 → ACNP
Volume
71
Issue
10
Year of publication
2000
Pages
1583 - 1590
Database
ISI
SICI code
0022-3492(200010)71:10<1583:PDP>2.0.ZU;2-T
Abstract
Background: The objective of this investigation is to use noninvasive, stat e-of-the-art, diagnostic techniques to measure periodontal disease progress ion and model periodontal disease activity over time. In this investigation , digital subtraction radiography and an electronic controlled force period ontal probe capable of attachment level measurement were used to measure bo ne loss and attachment loss, respectively. The use of these nearly continuo us measures of attachment and bone loss allowed detection of small amounts of disease activity and provided data to be used in modeling of the disease process over time. Methods: Forty-four patients were studied for 18 months. Examinations used clinical attachment level measures at 1-month intervals and quantitative ra diology at 6-month intervals. The sites were analyzed by regression for sta tistically significant changes. These data were used to determine sites of periodontal disease activity for testing various models of periodontal dise ase progression. Results: Overall 22.8% of sites lost attachment, 5.4% gained, and 71.7% dem onstrated no statistically significant change. The mean time to lose 1 mm o f attachment was 8.4 +/- 0.6 months. In the first model tested a step-wise discriminant analysis was used to determine whether or not baseline measure ments of plaque (PI), gingival inflammation (GI), attachment loss, and prob ing depth (PD) could be used to derive a satisfactory model for disease pro gression. Although the overall model was statistically significant with PI, PD, and GI contributing to the model (Wilks' lambda = 0.859, F = 5.71, P < 0.0012), its predictive power was relatively weak. A considerably stronger significant model resulted when the rate of attachment loss over the first 6 months, baseline PI, and baseline GI were included (Wilks' lambda = 0.71 2, F = 14.17, P < 0.00001). A significant model also resulted when bone los s during the first 6 months and baseline probing depth were included (Wilks ' lambda = 0.438, F = 61.48, P < 0.00001). When the last model was applied to each site, the sensitivity in predicting disease progression was 80.0% a nd the specificity in ruling out progressive disease was 93.9%. Conclusions: This study indicates that clinically significant progression o f attachment loss in posterior tooth sites occurs as a frequent event in ad ult periodontitis. The modeling data also suggest that short-term (6 month) measures of periodontal disease progression greatly improve the ability to model attachment loss over a longer period in untreated periodontitis pati ents.