The influence of the protein Wnt10b as a marker of bone repair of critical size defects fille with autogenous adipose tissue graft: A study in rabbit calvaria

  • Luiz Gustavo Klug
  • Carmen Lucia Mueller Storrer
  • Aline Monise Sebastiani
  • Bruna Lorena Barbaresco
  • Allan Fernando Giovanini
  • Tatiana Miranda Deliberador


 The proteins Wnts are considered a key regulator of the early development of the skeleton. Aim: The aim of this study was to evaluate the presence of the protein Wnt10b as a marker of bone repair in critical size defects surgically created in the calvaria of rabbits treated with fragmented autogenous adipose tissue graft. Methods: A total of 28 rabbits were divided into two groups: the Control group (C) and Adipose Tissue Graft group (ATG). A CSD measuring 15 mm in diameter was created in the calvaria of each animal. In rabbits of the C group, the defect was filled only with blood clot, and in ATG group, the defect was filled with fragmented adipose tissue graft. The two groups were divided into two subgroups (n = 7) for euthanasia 15 and 40 days after surgery. Histological and immunohistochemically analyses were performed to evaluate the neoformed bone and the presence/concentration of Wnt10b protein. The Kruskal-Wallis test was performed to compare the means and standard deviations of the number of Wnt10b + cells/mm2 in both groups in each postoperative period. It was assumed a significance level of 5%. Results: After 40 days, the mean concentration of the protein Wnt10b in ATG group was 26.26 (+-6.97) significant higher (p<0,001) than the mean in C group that was 305 (37.41). Conclusion: The protein Wnt10b would play a crucial role in the signaling of bone formation in bone defects treated with fragmented autogenous adipose tissue graft.


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How to Cite
KLUG, Luiz Gustavo et al. The influence of the protein Wnt10b as a marker of bone repair of critical size defects fille with autogenous adipose tissue graft: A study in rabbit calvaria. Brazilian Journal of Oral Sciences, [S.l.], p. e170082, dec. 2016. ISSN 1677-3225. Available at: <>. Date accessed: 21 july 2019. doi:
Original Research

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