SYMPTOMATIC LUMBAR SPONDYLOLYSIS - NEUROIMMUNOLOGIC STUDIES

Objectives. This study characterized the defect using neuroimmunologic and inflammatory cell analysis. Summary of Background Data. Spondylol ysis/spondylolisthesis is thought to be caused by a congenital weaknes s and mechanical stress causing a fracture associated with defective h ealing. Most of the spondylolysis patients are asymptomatic and the me chanisms of pain in symptomatic patients are unknown. Methods. Tissue from the spondylolysis defect was collected from seven patients underg oing posterolateral fusion operations. Results. Histologic examination disclosed delayed union/pseudoarthrosis with fibroblasts and macropha ges in a pseudosynovial lining membrane and occasional perivascular in filtrates containing mainly CD2 lymphocytes and CD11b monocytes/macrop hages. In vascularized connective tissue stroma PGP 9.5, synaptophysin and neurofilament staining disclosed perivascular nerves, which did n ot extend to the synovial lining layer and which mainly represented po stganglionic sympathetic nerve fibers but also calcitonin gene-related peptide end substance P containing sensory fibers. Conclusions. 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 compar ed with those reported in the nonunion of long bones and the sparsity of stromal innervation, indicate that the characteristic defective hea ling is in part clue to lack of neurogenic influences.