Symptomatic lumbar spondylolysis. Neuroimmunologic studies

This study characterized the defect using neuroimmunologic and inflammatory cell analysis.

Spondylolysis/spondylolisthesis is thought to be caused by a congenital weakness and mechanical stress causing a fracture associated with defective healing. Most of the spondylolysis patients are asymptomatic and the mechanisms of pain in symptomatic patients are unknown.

Tissue from the spondylolysis defect was collected from seven patients undergoing posterolateral fusion operations.

Histologic examination disclosed delayed union/pseudoarthrosis with fibroblasts and macrophages in a pseudosynovial lining membrane and occasional perivascular infiltrates containing mainly CD2 lymphocytes and CD11b monocytes/macrophages. In a vascularized connective tissue stroma PGP 9.5, synaptophysin and neurofilament staining disclosed perivascular nerves, which did not extend to the synovial lining layer and which mainly represented postganglionic sympathetic nerve fibers but also calcitonin gene-related peptide and substance P containing sensory fibers.

Pain in spondylolysis/spondylolisthesis might derive from the spondylolytic defect itself, probably from stretching of the local neural elements rather than from their sensitization/stimulation by local inflammatory mediators. The resemblance of neuroimmunohistochemical changes compared with those reported in the nonunion of long bones and the sparsity of stromal innervation, indicate that the characteristic defective healing is in part due to lack of neurogenic influences.