Maxillary alveolar cleft repair in dogs using recombinant human bone morphogenetic protein-2 and a polymer carrier.

Maxillary alveolar cleft repair in dogs using recombinant human bone morphogenetic protein-2 and a polymer carrier.
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使用重组人骨形态发生蛋白 2 和聚合物载体修复犬上颌牙槽裂。

DOI:
10.1097/00006534-199608000-00006
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发表时间:
1996
影响因子:
3.6
通讯作者:
J. Wozney
J. Wozney
中科院分区:
医学1区
文献类型:
--
作者:
M. Mayer;J. Hollinger;E. Ron;J. Wozney

文献摘要

被引文献

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研究了重组人骨形态发生蛋白-2在24只成年、骨骼发育成熟的猎犬上颌牙槽裂中的作用。制备双侧裂缝,骨宽度为1cm,两侧内衬健康上皮,两侧各有功能牙齿,预计不会自发愈合。对24只犬进行双侧唇裂准备,48个受者部位平均分为四种处理和两个时间段(2个月和4个月),每次处理产生6个重复。该研究的总体目标是使用以下三种治疗方法中的一种来再生骨裂:(2)200微克重组人骨形态发生蛋白-2与共聚物聚(乳酸-羟基乙酸酯)和自体血液结合,(2)聚(乳酸-羟基乙酸酯)和自体血液结合,或(3)从髂后嵴移植自体骨。第四组为未经治疗的牙槽裂缺损。在指定的时间,对狗实施安乐死,并对有连续骨的受体床进行回收、处理和放射学和组织学评估。自体移植缺损2个月时骨量高于其他治疗;然而,到4个月时,除聚乳酸-羟基乙酸酯组骨量最少外,各组间无差异。对重组人骨形态发生蛋白-2的反应可能是次优的,这可能是因为剂量太低,或者是因为聚(乳酸-羟基乙酸酯)自体血液输送系统没有在受体床上暂时维持和空间定位重组人骨形态发生蛋白-2。此外,狗的上颌骨出现不愈合的、临界大小的缺损,似乎需要更积极地切除骨头,以阻止自发的骨再生。
Recombinant human bone morphogenetic protein-2 was evaluated in maxillary alveolar clefts in 24 adult, skeletally mature Foxhound dogs. Bilateral clefts were prepared, 1 cm in bony width, lined with healthy epithelium with functional teeth on each side, and were expected not to heal spontaneously with new bone. Preparation of bilateral clefts in 24 dogs permitted 48 recipient sites divided evenly among four treatment and two time periods (2 and 4 months), yielding six replicates per treatment per time. The overall goal for the study was to regenerate bone in the cleft using one of three treatments: (2) 200 microgram recombinant human bone morphogenetic protein-2 combined with the copolymer poly(lactide-co-glycolide) and autogenous blood, (2) poly(lactide-co-glycolide) and autogenous blood, or (3) an autograft from the posterior iliac crest. A fourth group consisted of untreated alveolar cleft defects. At designated times, dogs were euthanized, and the recipient beds with contiguous bone were recovered, processed, and assessed radiographically and histologically. Autograft-treated defects had more bone than other treatments at 2 months; however, by 4 months, there were no differences among treatments, except for the poly(lactide-co-glycolide) group, which had the least amount of bone. Response to the recombinant human bone morphogenetic protein-2 may have been suboptimal either because the dose was too low or because the poly(lactide-co-glycolide)-autogenous blood delivery system did not temporally maintain and spatially position recombinant human bone morphogenetic protein-2 at the recipient bed. In addition, the development of a nonhealing, critical-sized defect in the maxilla of the dog appears to require a more aggressive resection of bone to preclude spontaneous osseous regeneration.