Developmental dysplasia of the hip (DDH) is the most common post-natal skeletal abnormality. It is widely acknowledged that conditions which cause or result in reduced movement in utero are contributing factors to the incidence of DDH. However, the hypothesis that prenatal movement plays a role in normal development of the hip joint has not been tested using embryonic model systems. This research investigates the effects of immobilization in chick embryos on hip joint morphogenesis. Embryonic chicks were treated in ovo using a neuromuscular blocking agent from embryonic days 5 to 9. Limbs were stained for cartilage using alcian blue, and were scanned in 3-D. Standardized virtual sections of the femur were taken and a number of virtual sections from age-matched limbs were overlaid in order to compare between control and immobilized limbs. The results show that not all immobilised limbs were equally affected, with some immobilised embryos having almost normal joint shapes, and other immobilised embryos displaying decreased protuberance of the femoral head and decreased indentation at the femoral neck. Our results demonstrate that the mechanobiological response to immobilisation can vary between individuals, but also that preventing movement during embryonic development can lead to abnormal morphogenesis of the developing proximal femur in some individuals, providing evidence that reduced movement during development can lead to features of DDH.

The steric and electrostatic complementarity of natural proteins and other macromolecules are a result of evolutionary processes. The role of such complementarity is well established in protein-protein interactions, accounting for the known protein complexes. To our knowledge, non-biological systems have not been a part of such evolutionary processes. Therefore, it is desirable to design and develop nonbiological surfaces, such as implant devices (e.g. bone growth for non-cemented fixation), that exhibit such complementarity effects with the natural proteins.

Cell attachment and spreading in vitro is generally mediated by adhesive proteins such as fibronectin and vitronectin [1]. The primary interaction between cells and adhesive proteins occurs through integrin and an RGD amino acid sequence. The adsorption of adhesive proteins plays an important role in cell adhesion and bone formation to an implant surface [1]. The ability of the implant surface to adsorb these proteins determines its aptitude to support cell adhesion and spreading and its biocompatibility. For example, the enhancement of osteoblast precursor attachment on hydroxyapatite (HA) as compared to titanium and stainless steel was related to increased fibronectin and vitronectin absorption [2].

The role of surface characteristics, such as topography, has been studied in recent years without the emergence of a comprehensive and consistent model [1]. For example, while no statistically significant influence of surface roughness on osteoblast proliferation and cell viability was detected in the study of metallic titanium surfaces [3], the TiO2 film enhances osteoblast adhesion, proliferation and differentiation upon an increase in roughness [4].

We designed and produced ceramic [5] and metallic coatings via an ion beam assisted deposition process with spatial dispersion (roughness) comparable to the size of proteins (3–20nm). Our ceramic and cobaltchrome (CoCr) coatings exhibit high hardness and contact angles with serum of 0° and 40° to 50°, respectively. Furthermore, our theoretical calculations and quantum-mechanical modeling clearly indicate that the spatial electric potential variation across our designed ceramic surfaces is comparable to the electrostatic potential variation of proteins such as fibronectin, promoting increased absorption on these surfaces. Therefore, an increase in the concentration of adhesive proteins on the designed surfaces results in the enhancement of the focal adhesion of cells. Our experimental results of the adhesion and proliferation of osteoblast-like stromal cells from mouse bone marrow indicate that our nanostructured coatings are three to five times better than growing on HA and orthopaedic grades of titanium and CoCr. Our results are consistent with the steric and electrostatic complementarity of nanostructured surfaces and adhesive proteins. This paper presents the adhesion and proliferation of osteoblast-like cells on micro-and nanostructured surfaces and provides new models describing the mechanism responsible for the enhancement of cell adhesion on nanostructured ceramic and metallic surfaces compared with orthopaedic materials.