Construction of a functional skeleton is accomplished
through co-ordination of the developmental processes of chondrogenesis,
osteogenesis, and synovial joint formation. Infants whose movement in
utero is reduced or restricted and who subsequently suffer
from joint dysplasia (including joint contractures) and thin hypo-mineralised
bones, demonstrate that embryonic movement is crucial for appropriate
skeletogenesis. This has been confirmed in mouse, chick, and zebrafish
animal models, where reduced or eliminated movement consistently yields
similar malformations and which provide the possibility of experimentation
to uncover the precise disturbances and the mechanisms by which
movement impacts molecular regulation. Molecular genetic studies have
shown the important roles played by cell communication signalling
pathways, namely Wnt, Hedgehog, and transforming growth factor-beta/bone
morphogenetic protein. These pathways regulate cell behaviours such
as proliferation and differentiation to control maturation of the
skeletal elements, and are affected when movement is altered. Cell
contacts to the extra-cellular matrix as well as the cytoskeleton
offer a means of