Orthopaedic surgery is in an exciting transitional period as modern surgical interventions, implants and scientific developments are providing new therapeutic options. As advances in basic science and technology improve our understanding of the pathology and repair of musculoskeletal tissue, traditional operations may be replaced by newer, less invasive procedures which are more appropriately targeted at the underlying pathophysiology. However, evidence-based practice will remain a basic requirement of care. Orthopaedic surgeons can and should remain at the forefront of the development of novel therapeutic interventions and their application. Progression of the potential of bench research into an improved array of orthopaedic treatments in an effective yet safe manner will require the development of a subgroup of specialists with extended training in research to play an important role in bridging the gap between laboratory science and clinical practice. International regulations regarding the introduction of new biological treatments will place an additional burden on the mechanisms of this translational process, and orthopaedic surgeons who are trained in science, surgery and the regulatory environment will be essential. Training and supporting individuals with these skills requires special consideration and discussion by the orthopaedic community. In this paper we review some traditional approaches to the integration of orthopaedic science and surgery, the therapeutic potential of current regenerative biomedical science for cartilage repair and ways in which we may develop surgeons with the skills required to translate scientific discovery into effective and properly assessed orthopaedic treatments.
Aseptic loosening is the single most important long-term complication of total joint arthroplasty. Wear debris induced inflammation stimulates osteoclastic resorption of bone. Cellular mechanisms involved in osteoblast viability in PWD induced inflammation is poorly understood. Wear induced inflammation increases osteoblast necrosis and susceptibility to death by apoptosis. PMMA cement has a detrimental effect on osteoblast resistance to apoptosis, and that this is via an receptor mediated pathway. Osteoblast cell cultures (Human and MG63) were grown with and without PMMA cement and assessed for apoptosis and necrosis. TNF-α or Fas antibody simulated inflammation. Viability and apoptosis with PI exclusion, flow cytometry and western blotting assessed response. Cement induced osteoblast necrosis up to 1 hour. This effect was negated after 24 hours. Culture of osteob1asts on cement had no direct effect on spontaneous apoptosis but susceptibility to inflammation was increased. Polymerised cement has no direct effect on osteoblast cell death. Effects are mediated by inhibiting expression of anti-apoptotic protein (Bcl-2), and increasing susceptibility to inflammatory. Osteoblast resistance to death may represent a novel and important factor in aseptic loosening. The role of gene therapy is explored.
Patients with hemiplegic cerebral palsy walk with a well recognised characteristic gait pattern. They also commonly have a significant leg length discrepancy which is less well appreciated. The typical equinus gait in these patients is assumed to be an integral part of the disease process of spasticity and a tendency to develop joint contractures. However an alternative explanation for the presence of an equinus deformity may be that it is a response to the development of a significant leg length discrepancy in these patients. The development of such an equinus deformity would have the effect of functionally lengthening the short hemiplegic leg. We set up a study to examine the correlation between leg length discrepancy and equinus deformity. We reviewed the gait analyses and clinical examinations of 183 patients with hemiplegic cerebral palsy. While 22% had no significant leg length discrepancy, 65% had a measured discrepancy of greater than 1cm. There was a linear correlation between age and limb length discrepancy. We also found that there was a linear relationship between leg length discrepancy and ankle equinus at the point of ground contact. We propose that the equinus deformity seen in the hemiplegic cerebral palsy patient is multifactorial and is related not only to the disease state but also to the presence of leg length discrepancy. The equinus deformity functionally lengthens the short hemiplegic leg. Indeed it may represent an attempt by these patients to functionally equalise their leg lengths. This factor must be taken into account when considering correction of an equinus deformity in patients with hemiplegic cerebral palsy in order to avoid either recurrence of the deformity or the production of functionally unequal leg lengths. We have also highlighted the presence of significant shortening of the hemiplegic leg in these patients.
Aseptic loosening has become the single most important long-term complication of total joint replacements. The pathophysiology of this loosening is multifactorial in origin ranging from mechanical wear, poor surgical technique, thermal damage and the inflammatory response to particulate wear debris. Cytokines are released in response to macrophage activation by particulate wear debris (PWD), the resultant inflammatory cascade stimulates osteoclastic resorption of bone. The failure of remodelling and repair mechanisms may be as a result of Osteonecrosis from cement (PMMA).
Little work has been done on gait initiation in children and there is no published data on gait initiation with cerebral palsy. The aim of this study was to examine the ground reaction forces and centre of pressure in normal children during gait initiation, to compare these to similar values in hemiplegic children and to try to identify differences between the two which may be diagnostic for hemiplegia. Patients and methods: Five normal and five hemiplegic children were studied. Kinematic and dynamic data were collected using a CodaTM motion analysis system and KestlerTM force plate. All subjects stood with one foot on and one foot off the force plate and walked off upon hearing an audible cue. Tests were repeated measuring right and left, normal and hemiplegic legs as both stance and swing legs. Ground reaction forces in the X,Y and Z axes, centre of pressure and kinematic data were collected and studied.
Medio-laterally the stance GRF tending to adduct falls initially and subsequently rises with a bimodal peak. The forces in the swing leg reciprocate these forces. 2) Hemiplegic children. The overall pattern seen when the normal leg is the stance leg are similar to those in normal children with certain specific variations in force development and magnitude. When the hemiplegic leg is the stance leg the overall patterns are again similar but considerably less smooth with characteristic changes indicative of neuro-muscular disturbance. The initial “adjusting” forces tend to be larger indicating the greater force required for control. Discussion: The pattern and relative magnitude of forces measured for normal children are identical to those previously reported for adults. This validates our study design and indicates that central programming for gait initiation develops early in life. It is therefore an early developmental skill and may be used as a diagnostic test in childhood. Significant variations are seen in cerebral palsy. Knowledge of these specific changes may allow earlier and more accurate diagnosis of cerebral palsy in children under investigation for movement disorders. Normal GRF patterns during gait initiations may provide early reassurance for parents of children suspected of having cerebral palsy.
