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Pathogenesis of calcium crystal deposition in the ligamentum flavum correlates with lumbar spinal canal stenosis.

OBJECTIVE: To investigate the histological and immunohistochemical properties of degenerative changes and calcium crystal deposition in the lumbar ligamentum favum. METHODS: We examined the ligamentum flavum harvested from 119 surgical cases with symptomatic lumbar spinal stenosis. Sections of the ligament were examined by scanning electron microscopy (SEM), energy dispersive X-ray micro-analysis, and were immunostained for S-100 protein, vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF) and CD34. The results were compared with those of ligament tissue harvested from 10 cases of lumbar disc herniation. RESULT: The elastic fibres of the ligamentum favum showed regular, or sometimes irregular, and fragmented fibre bundles. Large areas of fibrosis with reduced elastic component and increased collagenous tissue were frequently seen in the degenerated ligaments. Calcium crystal deposits were observed in these fibrous ligaments, associated with many hypertrophic chondrocytes, and with small blood vessel formation. These chondrocytes stained positively for S-100 protein, VEGF and bFGF Calcium pyrophosphate dihydrate crystals were identified in the calcium deposit area. CONCLUSION: We believe that rupture of elastic fibre bundles is the first change to occur in degeneration of the ligamentum favum. Calcium crystal deposition was seen within these fibrous and chondrometaplastic areas. Hypertrophic chondrocytes regulate crystal formation and tissue reconstruction by secreting cytokines.

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PubMed1982

[Familial narrow spinal canal (lumbar canal stenosis with narrow cervical canal): case reports of three brothers].

We reported three brothers with lumbar canal stenosis out of six brothers. The three brothers had undergone laminectomy of the lumbar spine. Two of the three who were operated had to undergo emergency operation because of acute onset of paraplegia and micturition disturbance. At surgery we found thick and hypertrophic lamina at stenotic portion of the lumbar spine in case 1 and case 2 and pseudospondylolysthesis in case 3. These three brothers were also found to have narrow cervical canal. Two of them underwent decompressive procedure for cervical spine after lumbar surgery and the rest had already undergone anterior fusion of cervical spine at another hospital. A sister of the six brothers was also demonstrated to have narrow cervical canal. These cases suggested that there is hereditary influence on the pathogenesis of the developmental lumbar canal stenosis. We could find only two reports on familial lumbar canal stenosis in English literature. Our familial cases are considered interesting in the following points. 1) Two of three cases necessitated emergency operation and no mass lesion such as herniated disc, tumor or vascular anomaly was found at surgery. 2) All three cases had narrow cervical canal in association with lumbar canal stenosis.

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