KOMANG AGUNG IRIANTO S., 090810122 D (2011) PERUBAHAN SUBSELULER SEL KONDROID NUKLEUS PULPOSUS PADA DEGENERASI DISKUS INTERVERTEBRALIS. Disertasi thesis, UNIVERSITAS AIRLANGGA.

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Abstract

Back ground: Degenerated intervertebral disc (IVD) has always been considered as the major cause of low back pain. These were aberrant cell-mediated response to progressive structural failure, combined with accelerated or advanced signs of aging. Eighty percent of the population ever experiencing such back pain once in the life time. The pathogenesis itself is remained unclear; intriguing to find out the starting point where the disc structures started to decrease the ability to resist the load. While these notochord-origin chondroid IVD cells lessen into1% of population and mostly were forming clusters. Understanding the sub cellular changes would guide the right management of degenerative disc disease. Objective: the aim of this study is to show the sub cellular changes of chondroid cells in the degenerative disc. Method: Fifty one discus specimens sampled from MED (Micro Endoscopic Discectomy) of Herniation Disc patients and two child discus specimens from scoliosis patients were looked into proportional of chondroid cell clustering. Immunohistochemistry evaluated for protein expressions of HSP70, CD68, Caspase-3, Collagen I and Collagen II. Data analyzed statistic with Paired t-test and Wilcoxon Sign Rank Test, and Pearson correlation test (p< 0.05). Results: Chondroid cell clustering was significantly higher than the single cells in degenerative disc. There was strong correlation of HSP70, CD68, Caspase-3, and Collagen II in chondroid cell cluster, but not for Collagen I. There was strong correlation of CD68 and Caspase-3 in cell cluster (p #8804;0,05, r=0,734) Conclusion: The subcellular changes in IVD cell clustering showed adaptation and regeneration process by the expression of HSP70, CD68, and persist Collagen II. The Caspase-3 and Collagen I expressions showed degeneration process. The strong correlation of CD68 and Caspase-3 expressed equilibrium of adapting and apoptotic process.

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