2024-03-29T01:12:23Z
https://niigata-u.repo.nii.ac.jp/oai
oai:niigata-u.repo.nii.ac.jp:00005380
2022-12-15T03:38:16Z
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453:455
下歯槽神経切断部に局所投与したBDNF抗体の神経腫形成に対する影響
Effect of a local application of an antibody to BDNF on neuroma formation after transection of the inferior alveolar nerve in the rat
Effect of a local application of an antibody to BDNF on neuroma formation after transection of the inferior alveolar nerve in the rat
Valverde, Guevara Yessenia Maria
50178
nerve injury
neuroma
IAN
BDNF
trkB
新潟大学
博士(歯学)
Peripheral nerve injury sometimes induces neuroma formation at the injury site. The inferior alveolar nerve (IAN) is often damaged by dental treatment, resulting in painful symptoms. Antagonizing neurotrophins has been reported to reduce neuroma formation and neuropathic pain without damaging the transecting neurons following peripheral nerve injury, indicating the possibility that the inhibition of BDNF at the injury site can repress neuroma formation. The present study examined the effects of a local application of an antibody to BDNF at the injury site immediately after complete IAN transection, using immunohistochemistry and in situ hybridization histochemistry for trkB and BDNF. Histological analysis revealed a regular increase in the number of cellular elements and collagen fibers in the nerve cutting sites at both postoperative (PO) Weeks 1 and 2. At PO Week 2, a local administration of an antibody to BDNF clearly inhibited any proliferation of connective tissue at the injury site. Immunohistochemistry for PGP9.5 confirmed nerve fiber integrity in the anti BDNF-treated group. However, the control vehicle group showed no continuity of positive PGP 9.5 nerve fibers with neuroma formation at the proximal site. A fluorogold labeling technique revealed a significant difference (p<0.05) with a higher number of labeled trigeminal ganglion neurons in the anti BDNF- treated group than in the vehicle control groups. In situ hybridization histochemistry found intense signals for both BDNF and trkB mRNAs at the injury site of the vehicle control group. However, the signal for mRNAs for trkB and BDNF was localized in the area of the perineurium on the intact nerve fibers, indicating that fibroblasts encountered within the connective tissue were the cells expressing these signals. These findings suggest that a local inhibition of BDNF at a low dose clearly inhibited the proliferation of connective tissue at the injury site and neuroma formation.
学位の種類: 博士(歯学). 報告番号: 甲第3818号. 学位記番号: 新大院博(歯)甲第284号. 学位授与年月日: 平成25年9月20日
新大院博(歯)甲第284号
thesis
新潟大学
2013-09-20
2013-09-20
application/pdf
application/pdf
1
19
13101A3818
https://niigata-u.repo.nii.ac.jp/record/5380/files/h25ndk284.pdf
https://niigata-u.repo.nii.ac.jp/record/5380/files/h25ndk284_a.pdf
eng