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Background And Objective: Wnt signaling pathways regulate osteoblast differentiation and bone formation and are associated with inflammatory responses driven by innate and adaptive immunity via the NF-κB pathway. The aim of this study was to compare the levels of sclerostin (SOST), WNT-5a, and TNF-α between chronic periodontitis and periodontally healthy sites and determine their value as diagnostic markers of chronic periodontitis.
Material And Methods: In a cross-sectional assessment 25 chronic periodontitis cases and 25 periodontally healthy controls were selected upon clinical and radiographic periodontal evaluation. Gingival crevicular fluid (GCF) was collected cross-sectionally from diseased and healthy sites in periodontitis patients and from healthy sites in each control subject. In a subgroup analysis, ten patients with generalized moderate and severe chronic periodontitis and ten generalized periodontally healthy individuals were included. The protein levels of SOST, WNT-5a, and TNF-α in GCF were measured by sandwich ELISA. The Shapiro-Wilk test was utilized to assess the normality of the distribution and non-parametric comparisons were performed.
Results: The protein levels of SOST were significantly higher in the generalized moderate and severe chronic periodontitis subgroup when compared to the generalized healthy (P = 0.002), while the WNT-5a and TNF-α GCF total amounts were similar (P > 0.05). Diseased sites in the periodontitis patients exhibited significantly higher total protein levels of WNT-5a than in healthy sites (P = 0.017), whereas no differences were detected for SOST and TNF-α (P > 0.05). The total protein levels of SOST, WNT-5a, and TNF-α in GCF were similar in periodontitis and non-periodontitis patients (P > 0.05).
Conclusions: Sclerostin and WNT-5a gingival protein levels demonstrated a high diagnostic value for generalized moderate and severe chronic periodontitis, while a low accuracy was detected for localized chronic periodontitis.
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http://dx.doi.org/10.1111/jre.12659 | DOI Listing |
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