Aims. Computer hexapod assisted orthopaedic surgery (CHAOS), is a method to achieve the intra-operative correction of long bone deformities using a hexapod external fixator before definitive internal fixation with minimally invasive stabilisation techniques. The aims of this study were to determine the reliability of this method in a consecutive case series of patients undergoing femoral deformity correction, with a minimum six-month follow-up, to assess the complications and to define the ideal group of patients for whom this treatment is appropriate. Patients and Methods. The medical records and radiographs of all patients who underwent CHAOS for femoral deformity at our institution between 2005 and 2011 were retrospectively reviewed. Records were available for all 55 consecutive procedures undertaken in 49 patients with a mean age of 35.6 years (10.9 to 75.3) at the time of surgery. Results. Patients were assessed at a mean interval of 44 months (6 to 90) following surgery. The indications were broad; the most common were vitamin D resistant rickets (n = 10), growth plate arrest (n = 6) and post-traumatic deformity (n = 20). Multi-planar correction was required in 33 cases. A single level osteotomy was performed in 43 cases. Locking plates were used to stabilise the osteotomy in 33 cases and intramedullary nails in the remainder. Complications included two nonunions, one death, one below-knee deep vein thrombosis, one deep infection and one revision procedure due to initial under-correction. There were no neurovascular injuries or incidence of compartment syndrome. Conclusion. This is the largest reported series of femoral deformity corrections using the CHAOS technique. This series demonstrates that precise intra-operative realignment is possible with a hexapod external fixator prior to definitive stabilisation with contemporary internal fixation. This combination allows reproducible correction of complex femoral deformity from a wide variety of diagnoses and age range with a low complication rate. Cite this article: Bone Joint J 2017;99-B:283–8

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 mechanotransduction which could integrate mechanical cues with genetic regulation. Indeed, expression of cytoskeletal genes has been shown to be affected by immobilisation. In addition to furthering our understanding of a fundamental aspect of cell control and differentiation during development, research in this area is applicable to the engineering of stable skeletal tissues from stem cells, which relies on an understanding of developmental mechanisms including genetic and physical criteria. A deeper understanding of how movement affects skeletogenesis therefore has broader implications for regenerative therapeutics for injury or disease, as well as for optimisation of physical therapy regimes for individuals affected by skeletal abnormalities.

Cite this article: Bone Joint Res 2015;4:105–116