1217 Periodontal Breakdown Correlates with Lower Periostin Levels in Inflammatory Model

Saturday, March 24, 2012: 8 a.m. - 9:30 a.m.
Presentation Type: Oral Session
J. RODRIGUEZ, M. PADIAL-MOLINA, S.L. VOLK, A.D. TAUT, W.V. GIANNOBILE, and H.F. RIOS, Periodontics and Oral Medicine, University of Michigan, Ann Arbor, MI
Periostin, a matricellular molecule highly expressed by periodontal ligament fibroblasts, is implicated in the maintenance of periodontal integrity. Objective: To explore the influence of chronic inflammation on the expression of the matricellular adapter protein Periostin over time. Methods: Periodontal breakdown was induced in male Sprague-Dawley rats using a ligature periodontal inflammatory disease model (n=10). Periodontal tissue specimens were harvested at baseline, 2 weeks, and 4 weeks and prepared for histologic, immunofluorescence (Periostin), and micro-CT (linear and volumetric) examination. Statistical analyses were conducted using ANOVA, Fisher’s, and Spearman’s tests. Results: The areas with lower levels of Periostin corresponded to the areas with more detrimental tissue changes in the coronal-apical direction. Interestingly, although no significant differences in terms of alveolar bone loss (ABL) were observed between the 2 weeks and 4 weeks time points, the Periostin levels continued to decrease over time in this inflammation-challenged model. The immunofluorescence normalized Periostin expression was reduced over time (1±0.0; 0.83±0.22; 0.54±0.34; p<0.001) in response to the inflammatory process, i.e. decreased to about half its initial level after 4 weeks. ABL increased (0.41±0.05; 1.38±0.24; 1.32±0.47[µm]; p<0.001); the higher the ABL (ρ=-0.824), the lower the Periostin expression (p<0.001, Spearman). Volumetric analyses showed significant tissue mineral content and density reductions as the inflammatory process evolved. Conclusion: Physiologically relevant differences in Periostin levels are yet to be determined in humans. However, these observations in rodents do suggest a potential role of Periostin in the pathogenesis of inflammation-induced periodontal breakdown.
This abstract is based on research that was funded entirely or partially by an outside source: NIH/NIDCR K23DE019872 (HFR) and DE13397 (WVG)

Keywords: Animal, Inflammation, Periodontal disease, Periodontium-gingiva and Periostin
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