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Connexin43 (Cx43) is the main gap junction protein expressed in bone forming cells, where it modulates peak bone mass acquisition and cortical modeling. Genetic ablation of the Cx43 gene ( Gja1 ) results in cortical expansion with accentuated periosteal bone formation associated with decreased expression of the Wnt inhibitor sclerostin. To determine whether sclerostin ( Sost)  down-regulation might contribute to periosteal expansion in  Gja1  deficient bones, we took a gene interaction approach and crossed mice harboring germline null alleles for  Gja1  or  Sost  to generate single  Gja1   +/–  and  Sost   +/–  and double  Gja1   +/–   ;Sost   +/–  heterozygous mice. In vivo μCT analysis of cortical bone at age 1 and 3 months confirmed increased thickness in  Sost   –/–  mice, but revealed no cortical abnormalities in single  Gja1  +/– or  Sost   +/–  mice. Double heterozygous  Gja1   +/–   Sost   +/–  also showed no differences in mineral density, cortical thickness, width or geometry relative to wild type control mice. Likewise, 3-point bending measurement of bone strength revealed no significant differences between double  Gja1   +/–   ;Sost   +/–  or single heterozygous and wild type mice. Although these data do not exclude a contribution of reduced sclerostin in the cortical expansion seen in  Gja1  deficient bones, they are not consistent with a strong genetic interaction between  Sost  and  Gja1  dictating cortical modeling.

Heterozygous deletion of both sclerostin (Sost) and connexin43 (Gja1) genes in mice is not sufficient to impair cortical bone modeling