Study design: We propose that chronic spondylolytic defects at L5 are influenced by insufficient differential mediolateral distances between inferior articular facets of L4 and the superior facets of S1, which results in these structures impinging on adjacent sides of the par interarticularis during hyperlordosis. Individuals with adequate increase in interfacet distances from L4 through S1 are less likely to develop or maintain defects.
Objectives: We test the above hypothesis by comparing the transverse interfacet dimensions throughout the lumbar columns of normal and spondylolytic individuals.
Summary of background data: Spondylolysis is a common condition, yet its etiology is poorly understood. It is generally considered to be the result of a vaguely defined fatigue fracture through the pars interarticularis. The cause(s) of spondylolysis, however, have not been clearly identified.
Methods: Lumbar vertebrae from the Hamann-Todd osteological collection at the Cleveland Museum of Natural History were examined. Thirty individuals with bilateral spondylolysis at L5 were compared with 30 age- and sex-matched controls. Differences in transverse distances between articular facets and in transverse breadths of vertebral bodies were compared using two-tailed t tests.
Results: Results show that normal individuals have a significantly greater increase in interfacet dimensions progressing down the spine from L4 to S1 than do those with spondylolysis. These differences are not the result of normal individuals having increasingly large vertebrae, as results are significant even when standardized for vertebral body breadth. Vertebral body size itself does not differ systematically between groups.
Conclusions: Spondylolysis is the direct result of contact pressures on both sides of the pars interarticularis resulting from inadequate separation between the inferior articular processes of L4 and the superior articular facets of S1. Individuals lacking sufficient increase in transverse interfacet dimensions in their lumbar columns are at greater risk of developing and maintaining spondylolytic defects.