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Spinal Cord Injury and Osteoporosis
´ëÇÑ°ñ´Ù°øÁõÇÐȸÁö 2014³â 12±Ç 1È£ p.1 ~ p.6
¹ÚÁØ¿µ(Park Jun-Yeong) - Ãæ³²´ëÇб³ ÀÇÇÐÀü¹®´ëÇпø Á¤Çü¿Ü°úÇб³½Ç
À̽ÂÇö(Lee Seung-Hyun) - Ãæ³²´ëÇб³ ÀÇÇÐÀü¹®´ëÇпø Á¤Çü¿Ü°úÇб³½Ç
¾çÁØ¿µ(Yang Jun-Young) - Ãæ³²´ëÇб³ ÀÇÇÐÀü¹®´ëÇпø Á¤Çü¿Ü°úÇб³½Ç
Abstract
Osteoporosis is one of the major complications in patients with SCI (spinal cord injury). The neurologic lesion and subsequent immobilization induce early and acute bone loss. During the first months post-injury, demineralization occurs exclusively in the sublesional areas and predominantly in weight-bearing sites. The high bone loss associated with modification in bone matrix composition is very likely at the origin of the pathologic fractures occurring spontaneously or in response to minor trauma. The pathogenesis of osteoporosis after SCI was generally considered disuse. But, the lack of mechanical factors alone cannot explain the considerable bone loss. Currently, the pathogenesis of SCI-induced bone loss is considered the result of high rate of bone turnover characterized by bone formation?resorption uncoupling. But, the duration and patterns of bone loss after SCI remain still unknown. In addition the question of whether alterations in qualitative bone properties are confined to the paralyzed limbs or affect the whole skeleton remains open.
Å°¿öµå
Bone metabolism, Osteoporosis, Spinal cord injury
KMID :
1007020140120010001
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