Download Craniofacial sutures: development, diseases and treatment: by David P. Rice PDF

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By David P. Rice

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The exception is the intermaxillary suture which starts to fuse between the age of 30 and 35 years [66]. In the mouse, all calvarial sutures, except for the posterior section of the interfrontal suture, remain patent. The posterior section of the interfrontal suture fuses between 25 and 45 days postnatal, and it does this in an anterior to posterior manner [67]. The Sprague-Dawley rat exhibits a similar pattern with posterior section of the interfrontal suture fusing between 12 and 30 days postnatal.

Mice lacking the non-receptor tyrosine kinase, c-Src, can form multifunctional osteoclastic cells but these are nonfunctional. Osteoclast function including dissolution of mineral and collagen is regulated by the enzymes TRAP, carbonic anhydrase II, Hϩ-ATPase and cathepsin K. p52 (NF␬B2), p65 (RelA), C-Rel (Rel) and RelB. Mice lacking both p50 and p52 subunits exhibit a severe osteopetrotic phenotype, but here osteoclast differentiation is affected at a slightly later stage compared to the mice described above.

As a consequence bone mineral density is reduced. This phenotype can be rescued by transcriptional overactivation ␤-catenin [23]. , pp. 107–143 and Intramembranous Bone and Suture Formation and Function 27 Hajihosseini, pp. 160–177]. FGF2 increases cell to cell adhesion and N-cadherin expression in calvarial cell cultures and the effect on cell adhesion is blocked by application of neutralizing antibodies to N-cadherin. The S252W mutation in FGFR2 confers a gain-of-function which results in Apert syndrome craniosynostosis.

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