Hukkanen M, Konttinen Y T, Santavirta S, Nordsletten L, Madsen J E, Almaas R, Oestreicher A B, Rootwelt T, Polak J M
Department of Histochemistry, Royal Postgraduate Medical School, London, United Kingdom.
Clin Orthop Relat Res. 1995 Feb(311):247-57.
Neural influences have been associated with fracture healing through clinical observations and experimental procedures. This work was intended to study the reliability of sciatic nerve section as a model of denervation of tibial fracture. Rats were subjected to a standardized fracture with or without simultaneous nerve resection. The fractures were fixed by intramedullary nails, and the legs were immobilized to prevent differential loading. On Day 25 posttrauma, nerve fibers were found in the periosteum, fracture callus, and bone-marrow space. Most fibers expressed growth-associated protein 43 (GAP-43/B-50), suggesting actively ongoing neural regeneration. Additional characterization of the type of innervation revealed an extensive distribution of sensory fibers containing calcitonin gene-related peptide, a neuropeptide with potent vasodilatory actions. Sciatic nerve section reduced all free and some perivascular calcitonin gene-related peptide-containing fibers, although regenerating nerve fibers still were evident in the bone marrow. Radiographs showed an increased callus formation in rats with sciatic nerve section, suggesting involvement of neural factors in the healing process. The results show that sciatic nerve section is not a reliable model for a total denervation of tibial fracture. Hard tissue injury induces proliferation of nerves, probably by production of chemotactic factors to attract neural targeting and regeneration of injured nerves.
通过临床观察和实验程序,已发现神经影响与骨折愈合有关。这项工作旨在研究坐骨神经切断术作为胫骨骨折去神经支配模型的可靠性。对大鼠进行标准化骨折手术,部分大鼠同时进行神经切除。骨折用髓内钉固定,腿部固定以防止不同负荷。创伤后第25天,在骨膜、骨折痂和骨髓腔中发现神经纤维。大多数纤维表达生长相关蛋白43(GAP - 43/B - 50),表明神经正在积极再生。对神经支配类型的进一步表征显示,含有降钙素基因相关肽的感觉纤维广泛分布,降钙素基因相关肽是一种具有强大血管舒张作用的神经肽。坐骨神经切断术减少了所有游离的以及一些血管周围含降钙素基因相关肽的纤维,尽管骨髓中仍可见再生神经纤维。X线片显示坐骨神经切断术的大鼠骨痂形成增加,提示神经因素参与了愈合过程。结果表明,坐骨神经切断术并非胫骨骨折完全去神经支配的可靠模型。硬组织损伤可诱导神经增殖,可能是通过产生趋化因子来吸引神经靶向和损伤神经的再生。