Abstract

Spinal cord injury (SCI) causes osteoporosis (OP), and the neuropeptide substance P (SP) may play important roles in the pathogenesis of OP after SCI. Our study confirmed SCI-induced sublesional bone loss in young rats at an early stage is associated with a significant increase of SP-immunoreactive nerve fiber innervation density. Spinal cord injury (SCI) causes osteoporosis (OP), and neuropeptides may play important roles in the pathogenesis of OP after SCI. However, few data exist concerning the relationship between neural factors and OP following SCI. One hundred and eight SCI and hindlimb cast immobilization (HCI) rats were studied for skeletal innervation of substance P (SP) and neurofilament 200 (NF200) with immunocytochemistry. Bone and serum SP levels were also assessed using enzyme immunoassay. Developing bone loss was successfully induced by SCI at 3 wks and by HCI at 6 wks. We observed a significant increase of SP-immunoreactive (IR) nerve fibers and decrease of NF200-IR nerve fibers in the tibiae of SCI rats compared with HCI and control (CON) rats at all time points. SP in the proximal tibiae in SCI rats was significantly higher than that in HCI and CON rats at all time points, but no difference was found in the serum. SCI-induced sublesional bone loss in young rats at an early stage is associated with a significant increase of nerve fiber innervation density of SP-IR and decrease of NF200-IR. We speculated that neural factors may play an important role in pathogenesis of OP after SCI.

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