Slow stretching that mimics embryonic growth rate stimulates structural and mechanical development of tendon-like tissue in vitro.

A distinctive feature of embryonic tendon development is the steady increase in collagen fibril diameter and associated improvement of tissue mechanical properties. A potential mechanical stimulus for these changes is slow stretching of the tendon during limb growth. Testing this hypothesis in vivo is complicated by the presence of other developmental processes including muscle development and innervation. Here we used a cell culture tendon-like construct to determine if slow stretch can explain the increases in fibril diameter and mechanical properties that are observed in vivo. Non-stretched constructs had an ultrastructural appearance and mechanical properties similar to those of early embryonic tendon. However, slowly stretching during 4 days in culture increased collagen fibril diameter, fibril packing volume, and mechanical stiffness, and thereby mimicked embryonic development. 3D EM showed cells with improved longitudinal alignment and elongated nuclei, which raises the hypothesis that nuclear deformation could be a novel mechanism during tendon development.

The spatial and temporal pattern of collagens I and II and keratan sulphate in the developing chick metatarsophalangeal joint.

Both intrinsic and extrinsic factors are known to be involved in the morphogenesis of diarthrodial joints. The use of specific antibodies to collagens I and II and keratan-sulphate-containing proteoglycans (KSPG) has enabled the distributions of these macromolecules to be followed during the development of the third metatarsophalangeal joint in the chicken embryo. Our study shows that cartilage differentiation occurs as a continuous rod, which is then subsequently divided into separate elements. Further development also reveals that, unlike the matrix of the cartilaginous elements, there is a differential distribution of collagen (type II) and KSPG in the presumptive joint region. It is proposed that a decrease in KSPG in the presumptive joint region at stages 28/30 may be involved in the mechanism for the flattening of cells in formation of the interzone. Whereas, a decrease in collagen across the joint interzone region may provide an area of weakness, which might allow forces produced by the developing musculature to cause cavitation.