Mouse models in skeletal physiology and osteoporosis: experiences and data on 14,839 cases from the Hamburg Mouse Archives.

TY - JOUR

T1 - Mouse models in skeletal physiology and osteoporosis: experiences and data on 14,839 cases from the Hamburg Mouse Archives.

AU - Pogoda, Pia

AU - Priemel, Matthias

AU - Schilling, Arndt F

AU - Gebauer, Matthias

AU - Catalá-Lehnen, Philip

AU - Barvencik, Florian

AU - Beil, F Timo

AU - Münch, Christian

AU - Rupprecht, Martin

AU - Müldner, Cordula

AU - Rueger, Johannes M

AU - Schinke, Thorsten

AU - Amling, Michael

PY - 2005/1/1

Y1 - 2005/1/1

N2 - Our understanding of the developmental biology of the skeleton, like that of virtually every other subject in biology, has been transformed by recent advances in human and mouse genetics, but we still know very little, in molecular and genetic terms, about skeletal physiology. Thus, among the many questions that are largely unexplained are the following: why is osteoporosis mainly a women's disease? How is bone mass maintained nearly constant between the end of puberty and the arrest of gonadal functions? Molecular genetics has emerged as a powerful tool to study previously unexplored aspects of the physiology of the skeleton. Among mammals, mice are the most promising animals for this experimental work. The input that transgenic animals can offer to our field depends on our means of phenotypic characterization of the mouse skeleton. In fact, full appreciation of the skeletal characteristics of a given mouse model requires the application of standardized protocols for noninvasive imaging, histology, histomorphometry, biomechanics, and individually adapted in vitro and in vivo analysis. Over the past years we have established a mouse archive that consists of 14,839 cases from more than 120 different mouse models that we have phenotypically characterized in Hamburg. Today, this is one of the biggest databases on the mouse skeleton. This review focuses on one aspect of skeletal physiology, namely skeletal aging, and demonstrates that mouse models can be a valuable tool to gain insights in certain facets of skeletal physiology that have been unexplored previously.

AB - Our understanding of the developmental biology of the skeleton, like that of virtually every other subject in biology, has been transformed by recent advances in human and mouse genetics, but we still know very little, in molecular and genetic terms, about skeletal physiology. Thus, among the many questions that are largely unexplained are the following: why is osteoporosis mainly a women's disease? How is bone mass maintained nearly constant between the end of puberty and the arrest of gonadal functions? Molecular genetics has emerged as a powerful tool to study previously unexplored aspects of the physiology of the skeleton. Among mammals, mice are the most promising animals for this experimental work. The input that transgenic animals can offer to our field depends on our means of phenotypic characterization of the mouse skeleton. In fact, full appreciation of the skeletal characteristics of a given mouse model requires the application of standardized protocols for noninvasive imaging, histology, histomorphometry, biomechanics, and individually adapted in vitro and in vivo analysis. Over the past years we have established a mouse archive that consists of 14,839 cases from more than 120 different mouse models that we have phenotypically characterized in Hamburg. Today, this is one of the biggest databases on the mouse skeleton. This review focuses on one aspect of skeletal physiology, namely skeletal aging, and demonstrates that mouse models can be a valuable tool to gain insights in certain facets of skeletal physiology that have been unexplored previously.

KW - Animals

KW - Bone and Bones

KW - Disease Models, Animal

KW - Female

KW - Male

KW - Mice

KW - Mice, Knockout

KW - Osteoporosis

U2 - 10.1007/BF03026332

DO - 10.1007/BF03026332

M3 - SCORING: Journal article

C2 - 15984423

VL - 23

SP - 97

EP - 102

JO - J BONE MINER METAB

JF - J BONE MINER METAB

SN - 0914-8779

ER -