Involvement of the Wnt-ß-catenin signalling antagonists, sclerostin and dickkopf-related protein 1, in chronic periodontitis.

AIM: The regulation of Wnt-ß-catenin signalling, which is crucial for osteoblast differentiation and for bone resorption, is driven by critical inhibitors such as sclerostin (SOST) and dickkopf-related protein 1 (DKK1). As such, the aim of this study was to evaluate the involvement of SOST and DKK1 in human chronic periodontitis. MATERIAL AND METHODS: Gingival biopsies and serum were sampled from systemically healthy non-periodontitis (n = 15) and chronic periodontitis subjects (n = 15). The mRNA and protein levels of SOST, DKK1 and TNF-α in periodontal tissues were measured by qPCR and by enzyme-linked immunosorbent assay (ELISA) respectively. Serum levels of SOST, DKK1 and TNF-α were assessed by ELISA. RESULTS: The mRNA and protein levels of SOST, DKK1 and TNF-α were significantly increased in the gingival tissues of the chronic periodontitis when compared to the non-periodontitis group (p < 0.05). In addition, circulating levels of SOST and TNF-α, but not DKK1, were higher in the periodontitis group than in the non-periodontitis group (p < 0.05). CONCLUSION: SOST and DKK1 were upregulated in the periodontal tissues of chronic periodontitis subjects, suggesting a possible role of these molecules on periodontal tissues.

Preliminary Findings on the Role of Sclerostin in the Osseointegration Process Around Titanium Implants.

PURPOSE: Studies have recognized the importance of Wnt/ß-catenin signals in osteoblastogenesis. Sclerostin is a glycoprotein product of the SOST gene that inhibits Wnt/ß-catenin signaling and reduces osteoblastogenesis. To date, there is little evidence regarding the role of the Wnt/ß-catenin pathway and its inhibitors in the osseointegration process. Therefore, the aim of this study was to evaluate the expression of sclerostin in bone healing around titanium implants inserted in rats. MATERIALS AND METHODS: Fifteen Wistar rats received an implant with primary stability in a tibia, while the contralateral tibia received an implant without primary stability, representing experimental models of implant success and failure, respectively. Animals were then euthanized 7, 14, or 21 days later (five each day). Immunohistochemistry was used to evaluate the specimens for sclerostin-positive cells. RESULTS: The proportion of cells positive for sclerostin was significantly higher around implants without primary stability than those with primary stability at 7 and 14 days after implant placement (P < .05). There were no differences between groups for the proportion of cells positive for sclerostin at 21 days after implant insertion (P > .05). CONCLUSION: Sclerostin expression is upregulated around implants inserted without primary stability, in comparison with that around implants inserted with primary stability, in the tibia of rats. This preliminary evidence reinforces the importance of primary implant stability from the biologic viewpoint.