Spondylolysis is defined as a defect in the pars interarticularis without vertebral slipping [1]. Lumbar spondylolysis is a condition specific to humans due to our unique anatomical characteristic of lumbar lordosis, facilitating upright posture [2]. Clinical features include chronic lower back pain exacerbated by hyperlordosis [3], but spondylolysis may also develop without symptoms [4]. This defect occurs most commonly at L5 and is generally bilateral [5].

The precise cause of lumbar spondylolysis is not fully understood. It is thought that repetitive microtrauma and stress fracture is the likely cause [1]. Mechanical studies have shown that during flexion and extension of the normal lumbar spine the loading forces are maximal in the L5 neural arch, with the greatest mechanical stresses found within the pars interarticularis [6]. It is proposed that during hyperlordosis the L4 inferior facets and the S1 superior facets impinge the L5 pars interarticularis resulting in bone lysis and/or an accumulation of stress fracture leading to spondylolysis [2]. Repetitive lumbar hyperextension in athletes has been linked with pars interarticularis fractures [7]. Gymnasts, who were included in the previously mentioned study, have an increased incidence of pars interarticularis fractures [8].

Morphological differences of the neural arch, relating to the configuration of the L4 and L5 inter-facet region, have been described and associated with L5 pars interarticularis fractures. These anatomical differences enhance the forces applied to the pars interarticularis during torsional spinal motion and increase the risk of fracture [9,10].

While there is a suggestion that an increased angle of lumbar lordosis may be associated with an increased incidence of pars interarticularis fracture there is as yet no strong evidence to support this.  The aim of this research is to test the hypothesis that there is an association between lumbar lordosis and the presence of a pars L5 interarticularis fracture.