Literature DB >> 8911474

Studies in cranial suture biology: IV. Temporal sequence of posterior frontal cranial suture fusion in the mouse.

J P Bradley1, J P Levine, D A Roth, J G McCarthy, M T Longaker.   

Abstract

The biology underlying normal and premature cranial suture fusion remains unknown. To develop a model for normal cranial suture fusion, the temporal sequence of the posterior frontal cranial suture fusion in the mouse was determined. To do this, all the cranial sutures of three distinct strains of mice (CD-1, CF-1, and C57bl-6) were studied histologically for fusion at sequential time points. Two studies were set up using group A mice (n = 72, all sutures studied) and group B mice (n = 78, only the posterior frontal suture studied, but more precisely along its anatomic length). In the group A cranial suture study, mice were sacrificed starting at newborn age and then every 5 days until age 50 days. In addition, two mature mice (250 days old) from each strain were sacrificed. In all three mouse strains, histologic examinations showed that the anterior frontal, sagittal, coronal, lambdoid, and occipitointerparietal sutures remained patent at up to 50 days of age and were patent in the 250-day mature mice. However, examination of the midpoint of the posterior frontal suture showed patency at 30 days, partial fusion at 35 days, and complete fusion by 40 days. These data prompted the posterior frontal suture fusion study. In the group B posterior frontal suture fusion study, mice were sacrificed at age 23 days and then every 2 days until 47 days of age. The anterior, midpoint, and posterior aspects of the posterior frontal suture were examined: The anterior aspect fused between 25 and 29 days; the midpoint fused between 31 and 37 days; and the posterior aspect fused between 39 and 45 days. These data indicate that fusion of the posterior frontal cranial suture in the mouse proceeds in a defined temporal sequence from an anterior to posterior direction in three distinct strains of mice, while in the same mice all other cranial sutures remain patent. By describing and understanding the fusion of the normal posterior frontal suture, a biologic basis of normal suture development and fusion can be established and used as a comparison for murine cranial sutures altered surgically, biochemically (with growth factors), or genetically (with craniosynostotic phenotypes).

Entities:  

Mesh:

Year:  1996        PMID: 8911474     DOI: 10.1097/00006534-199611000-00018

Source DB:  PubMed          Journal:  Plast Reconstr Surg        ISSN: 0032-1052            Impact factor:   4.730


  17 in total

1.  In vivo modulation of FGF biological activity alters cranial suture fate.

Authors:  J A Greenwald; B J Mehrara; J A Spector; S M Warren; P J Fagenholz; L E Smith; P J Bouletreau; F E Crisera; H Ueno; M T Longaker
Journal:  Am J Pathol       Date:  2001-02       Impact factor: 4.307

2.  Tissue interactions between craniosynostotic dura mater and bone.

Authors:  Gregory M Cooper; Emily L Durham; James J Cray; Michael I Siegel; Joseph E Losee; Mark P Mooney
Journal:  J Craniofac Surg       Date:  2012-05       Impact factor: 1.046

3.  Bone up: craniomandibular development and hard-tissue biomineralization in neonate mice.

Authors:  Khari D Thompson; Holly E Weiss-Bilka; Elizabeth B McGough; Matthew J Ravosa
Journal:  Zoology (Jena)       Date:  2017-01-29       Impact factor: 2.240

4.  Neurodevelopmental and esthetic results in children after surgical correction of metopic suture synostosis: a single institutional experience.

Authors:  Mathias Kunz; Markus Lehner; Alfred Heger; Lena Armbruster; Heike Weigand; Gerson Mast; Aurelia Peraud
Journal:  Childs Nerv Syst       Date:  2013-12-13       Impact factor: 1.475

5.  Disruption of the mouse Jhy gene causes abnormal ciliary microtubule patterning and juvenile hydrocephalus.

Authors:  Oliver K Appelbe; Bryan Bollman; Ali Attarwala; Lindy A Triebes; Hilmarie Muniz-Talavera; Daniel J Curry; Jennifer V Schmidt
Journal:  Dev Biol       Date:  2013-07-29       Impact factor: 3.582

Review 6.  Growth of the normal skull vault and its alteration in craniosynostosis: insights from human genetics and experimental studies.

Authors:  Gillian M Morriss-Kay; Andrew O M Wilkie
Journal:  J Anat       Date:  2005-11       Impact factor: 2.610

Review 7.  Role of thyroid hormones in craniofacial development.

Authors:  Victoria D Leitch; J H Duncan Bassett; Graham R Williams
Journal:  Nat Rev Endocrinol       Date:  2020-01-23       Impact factor: 43.330

8.  Runx2 is required for early stages of endochondral bone formation but delays final stages of bone repair in Axin2-deficient mice.

Authors:  Meghan E McGee-Lawrence; Lomeli R Carpio; Elizabeth W Bradley; Amel Dudakovic; Jane B Lian; Andre J van Wijnen; Sanjeev Kakar; Wei Hsu; Jennifer J Westendorf
Journal:  Bone       Date:  2014-06-25       Impact factor: 4.398

Review 9.  Understanding craniosynostosis as a growth disorder.

Authors:  Kevin Flaherty; Nandini Singh; Joan T Richtsmeier
Journal:  Wiley Interdiscip Rev Dev Biol       Date:  2016-03-22       Impact factor: 5.814

10.  Runx2 protein represses Axin2 expression in osteoblasts and is required for craniosynostosis in Axin2-deficient mice.

Authors:  Meghan E McGee-Lawrence; Xiaodong Li; Krista L Bledsoe; Hai Wu; John R Hawse; Malayannan Subramaniam; David F Razidlo; Bridget A Stensgard; Gary S Stein; Andre J van Wijnen; Jane B Lian; Wei Hsu; Jennifer J Westendorf
Journal:  J Biol Chem       Date:  2013-01-07       Impact factor: 5.157

View more

北京卡尤迪生物科技股份有限公司 © 2022-2023.