Abstract
Introduction We have previously reported that inflammatory mediators secreted by osteoclasts increased the expression of calcitonin gene-related peptide (CGRP), a marker of inflammatory pain in dorsal root ganglia (DRG) neurons innervating lumbar vertebrae of osteoporotic rats. We sought to determine whether osteoporotic pain is simply inflammatory pain. We focused on the possibility that pain is exacerbated by mechanical stress on the vertebral body, particularly in elderly people. The purpose of this study was to examine the dynamics of sensory nerve transmission of pain and the effect of mechanical stress on osteoporotic pain using a caudal vertebrae compression model in osteoporotic rats. Materials and Methods As an osteoporosis model, we used female rats ovariectomized (OVX) at 5 weeks ( n = 24). Fluoro-Gold (FG) was applied to the periosteal surface of a caudal vertebra to detect DRG neuronal cells innervating the caudal vertebra. After FG-labeling, we divided into two groups: OVX + CMP group (n = 12) with K-wires inserted above and below a caudal vertebral body compressed using rubber bands and OVX group (n = 12) without compression. After 1, 2, 4, and 8 weeks of FG-labeling, bilateral S1 to S3 DRGs were resected ( n = 3 for each). In FG-labeled neurons, expression of CGRP and activating transcription factor 3 (ATF3), a marker of neuropathic pain, were compared between two groups using immunohistochemistry. Results The proportions of FG-labeled CGRP immunoreactive neurons in the OVX + CMP group were significantly elevated at 4 and 8 weeks compared with the OVX group ( p < 0.05). The proportion of FG-labeled ATF3 immunoreactive neurons significantly increased compared with the FG-positive OVX group at 8 weeks ( p < 0.05). Conclusion The rat caudal vertebra compression model with osteoporosis expressed significantly more ATF3 in DRG cells at 8 weeks. This suggests that micronerve injury occurred in sensory neurons innervating caudal vertebra of these osteoporotic rats. Therefore, mechanical stress may possibly exacerbate osteoporotic pain. I confirm having declared any potential conflict of interest for all authors listed on this abstract Yes Disclosure of Interest None declared
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