Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0851184 (thinning)
11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We present two cases of bilateral, symmetrical pedicular clefts associated with dural ectasia in von Recklinghausen's disease (neurofibromatosis). In one case the pedicular cleft was at the T12 level, while in the other it was at L4, and was responsible for spondylolisthesis. Two hypotheses are advanced to explain the cleft: (1) a congenital, dysplastic osseous defect and (2) bilateral stress fractures related to thinning of the pedicle caused by dural ectasia.
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PMID:Neurofibromatosis with dural ectasia and bilateral symmetrical pedicular clefts: report of two cases. 160 5

Internal fixation of the spine combined with limited or no fusion has been advocated in the treatment of thoracolumbar fractures, spondylolisthesis, and severe juvenile spinal deformities. Internal fixation without arthrodesis of canine facet joints has been shown to result in the irreversible gross and histologic findings typical of osteoarthritis. Surgery was performed in eight patients for the treatment of thoracolumbar fractures. In each patient, Harrington distraction instrumentation was placed across at least two vertebral segments above and below the fused area. Instrumentation was removed six to 26 months following the initial surgery. A unilateral partial facetectomy was performed at the facet joint above the lower Harrington hook. Gross examination of the facet joints revealed areas of fibrillation, fissures, and thinning of the normal cartilaginous surface characteristic of osteoarthritis. Histologic examination revealed consistent areas of erosion of the vascular tidemark, osteophyte formation, subchondral remodeling, fibrillation, and loss of the normal cartilage cellularity. These findings were consistent with the histologic appearance of osteoarthritis. Internal fixation of the spine without arthrodesis is not an innocuous procedure and may be a predisposing factor in the development of symptomatic spinal arthritis.
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PMID:The effect of internal fixation without arthrodesis on human facet joint cartilage. 647 98

The intervertebral disc is a highly organized matrix laid down by relatively few cells in a specific manner. The central gelatinous nucleus pulposus is contained within the more collagenous anulus fibrosus laterally and the cartilage end plates inferiorly and superiorly. The anulus consists of concentric rings or lamellae, with fibers in the outer lamellae continuing into the longitudinal ligaments and vertebral bodies. This arrangement allows the discs to facilitate movement and flexibility within what would be an otherwise rigid spine. At birth, the human disc has some vascular supply within both the cartilage end plates and the anulus fibrosus, but these vessels soon recede, leaving the disc with little direct blood supply in the healthy adult. With increasing age, water is lost from the matrix, and the proteoglycan content also changes and diminishes. The disc-particularly the nucleus-becomes less gelatinous and more fibrous, and cracks and fissures eventually form. More blood vessels begin to grow into the disc from the outer areas of the anulus. There is an increase in cell proliferation and formation of cell clusters as well as an increase in cell death. The cartilage end plate undergoes thinning, altered cell density, formation of fissures, and sclerosis of the subchondral bone. These changes are similar to those seen in degenerative disc disease, causing discussion as to whether aging and degeneration are separate processes or the same process occurring over a different timescale. Additional disorders involving the intervertebral disc can demonstrate other changes in morphology. Discs from patients with spinal deformities such as scoliosis have ectopic calcification in the cartilage end plate and sometimes in the disc itself. Cells in these discs and cells from patients with spondylolisthesis have been found to have very long cell processes. Cells in herniated discs appear to have a higher degree of cellular senescence than cells in nonherniated discs and produce a greater abundance of matrix metalloproteinases. The role that abnormalities play in the etiopathogenesis of different disorders is not always clear. Disorders may be caused by a genetic predisposition or a tissue response to an insult or altered mechanical environment. Whatever the initial cause, a change in the morphology of the tissue is likely to alter the physiologic and mechanical functioning of the tissue.
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PMID:Histology and pathology of the human intervertebral disc. 1659 36