What causes pars interarticularis injuries?

Updated: Jan 22, 2019
  • Author: Gerard A Malanga, MD; Chief Editor: Craig C Young, MD  more...
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Spondylolysis is considered by most to represent a fatigue fracture that results from repeated mechanical stress with microtrauma and eventual overload to the pars interarticularis rather than as a result of a single traumatic event. [27] However, a traumatic event may result in the completion of a developing fracture. [27] Studies have shown a remarkably low or absent rate of occurrence in newborns and very young children, as well as in those patients who have never been ambulatory.

Rosenberg et al studied 143 patients who had never walked, with an average age of 27 years, and found no cases of spondylolysis. [28] This finding appears to support the theory that loading of the pars interarticularis during upright, weight-bearing activities plays a role in the pathogenesis of these lesions.

Another study investigating the mechanical loading of the spine tested cadaveric lumbar vertebrae that were cyclically loaded at the inferior articular processes to simulate shear force. [27] The authors found 55 of 74 vertebrae to sustain pars fractures. They concluded that the pars interarticularis was particularly vulnerable to this type of repetitive loading. Further analysis of the vertebrae of those subjects without a fracture revealed a larger cross-sectional area of cortical bone in the pars compared with the control group. [27] This led Wiltse et al to hypothesize that a genetic predisposition may be related to the cortical bone density of the pars. This study also suggested that the strength of the neural arch may increase up to the 4th or 5th decade of life. [27]

In an experimental model, Dietrich and Kurowski found that the greatest mechanical loads occur at L5 and S1 with flexion and extension movements. [29] Furthermore, the greatest mechanical stress was found to occur at the region of the pars interarticularis. The investigators also noted that the loads and stresses across this region are related to the physical dimensions of the vertebrae, which may offer a partial explanation regarding the varying incidence among different races and the sexes. Repeated flexion and extension maneuvers, and to a lesser degree rotation, typically have been thought to be the movements that are responsible for generating the forces across the pars interarticularis that result in spondylolysis. [29, 30]

In a retrospective analysis of 213 young athletes, Gregory et al found left-sided lower lumbar pain was more common than the right side, and a marked increase in scintigraphic uptake was noted on the left side of the neural arch more often than the right side. [31] Unilateral spondylolysis was identified by reverse gantry computed tomography (CT) scanning on the left pars 36 times and on the right pars 16 times. These findings support the hypothesis that asymmetric repetitive movements associated with certain sports may be responsible for the development of unilateral spondylolysis. [31]

Green et al concluded from their cadaveric study on pars interarticularis stress, which investigated mechanical loading, that activities involving alternating flexion and extension movements cause large stress reversals in the pars interarticularis, thereby creating the highest risk for developing a pars defect. [32] The authors found compressive or axial loading to have little effect in generating these stresses likely responsible for spondylolysis. [32] Other anatomic studies have suggested that shear stresses on the isthmic pars are the greatest with lumbar spine extension. [33]

The specific cause of LBP associated with spondylolysis and spondylolytic spondylolisthesis has not been definitively established. Theories include nerve root compression by floating laminae, intervertebral disc pain, lumbar facet joint pain resulting from spinal instability, or a combination of these pathologies. [34] . A fibrocartilage mass of scar tissue forms at the site of lumbar spondylolysis and eventually develops into a structure frequently indistinguishable from a normal ligament by adulthood.

Eisenstein et al identified nerve fibers in the fibrocartilage masses histologically, [35] and Nordstrom et al detected the existence of the slow-conducting type C pain fibers and substance P in spondylolytic tissue obtained from patients who underwent resection. [36] Mechanoreceptors were later identified in these masses as well.

Hasegawa et al concluded that these fibrocartilage masses appear to be one source of pain, as LBP was induced by injecting hypertonic saline and was blocked by injecting lidocaine into these masses in all patients in their study before resection of the lesion. [37] The authors hypothesized that the fibrocartilage mass plays a protective role by sensing instability through the mechanoreceptor and then conveying this information through nociceptive fibers as pain, while at the same time, stabilizing this area of instability by acting as a ligamentlike structure across the defect. [37]

Given the high number of asymptomatic spondylolytic lesions, an important issue that is lacking in the literature and warrants further investigation is determining the factors that are responsible for producing pain in one patient but not another.

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