Osteogenesis in calvarial defects: Contribution of the dura, the pericranium, and the surrounding bone in adult versus infant animals
Osteogenesis in calvarial defects: Contribution of the dura, the pericranium, and the surrounding bone in adult versus infant animals
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DOI：
10.1097/01.prs.0000070728.56716.51
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发表时间：
2003-08-01
影响因子：
3.6
通讯作者：
Madoub, HS
中科院分区：
文献类型：
--
作者：
Gosain, AK;Santoro, TD;Madoub, HS
引导性骨再生是一种很有前途的颅骨缺损修复方法。本研究的目的是更好地定义影响颅骨成骨的因素。作者研究了一个单一的动物模型，研究了成熟和未成熟动物颅骨再生过程中硬脑膜、颅骨膜和邻近颅骨的作用。对未成熟（n = 16）和成熟（n = 16）家兔进行双侧100 mm（2）顶骨颅骨切除术。根据膨胀聚四氟乙烯膜对硬脑膜和/或颅骨膜的不同阻滞，将顶骨缺损随机分为四组。12周后人道处死动物，并进行组织学分析以定量原始骨缺损、新骨形成和新骨密度的面积。骨形成分别在周围和中心的缺陷进行量化。还对屏障的硬脑膜和颅周侧的部位外骨形成进行了定量。在12周的研究期间，所有组的骨再生都是不完全的，这表明在任何组中都没有观察到完全的骨愈合。在成熟和未成熟动物中，硬脑膜的成骨性高于颅骨膜，因为在双层膨胀聚四氟乙烯屏障组中，硬脑膜侧形成的骨外骨显著更多。在硬脑膜和双层膨体聚四氟乙烯屏障组中，未成熟动物的硬脑膜骨生成显著高于成熟动物。硬脑膜似乎是中央新骨的来源，因为硬脑膜和双膨胀聚四氟乙烯组中的硬脑膜阻滞导致成熟和未成熟动物的中央骨密度显著降低。奇怪的是，在成熟动物中分离颅骨膜导致总新骨面积显著减少，而颅骨膜接触似乎增强外周新骨形成，对照组具有最大的总新骨面积。本研究建立了一个模型，定量研究颅骨缺损的骨再生过程，并突出了硬脑膜和颅骨膜对婴儿和成年动物颅骨骨再生的贡献的差异。基于这些发现，作者提出，在后续研究中，改变膨胀聚四氟乙烯膜的渗透性以允许骨诱导蛋白迁移到缺损中，同时阻止邻近软组织脱垂，这可能有助于使引导骨再生成为修复颅骨缺损的现实替代方案。
Guided bone regeneration is a promising means for reconstructing bone defects in the cranium. The present study was performed to better define those factors that affect osteogenesis in the cranium. The authors studied a single animal model, investigating the contribution of the dura, the pericranium, and the adjacent calvarial bone in the process of calvarial regeneration in both mature and immature animals. Bilateral, 100-mm(2), parietal calvariectomies were performed in immature (n = 16) and mature (n = 16) rabbits. Parietal defects were randomized to one of four groups depending on the differential blockade of the dura and/or the pericranium by expanded polytetrafluoroethylene membranes. Animals were humanely killed after 12 weeks, and histometric analysis was performed to quantitate the area of the original bone defect, new bone formation, and new bone density. Bone formation was quantified separately both at the periphery and in the center of the defects. Extrasite bone formation was also quantified both on the dural and on the pericranial sides of the barriers. Bone regeneration was incomplete in all groups over the 12-week study period, indicating that complete bone healing was not observed in any group. The dura was more osteogenic than the pericranium in mature and immature animals, as there was significantly more extrasite bone formed on the dural side in the double expanded polytetrafluoroethylene barrier groups. In both the dural and the double expanded polytetrafluoroethylene barrier groups, dural bone production was significantly greater in immature compared with mature animals. The dura appeared to be the source of central new bone, because dural blockade in the dural and double expanded polytetrafluoroethylene groups resulted in a significant decrease in central bone density in both mature and immature animals. Paradoxically, isolation of the pericranium in mature animals resulted in a significant reduction in total new bone area, whereas pericranial contact appeared to enhance peripheral new bone formation, with the control group having the greatest total new bone area. The present study establishes a model to quantitatively study the process of bone regeneration in calvarial defects and highlights differences in the contribution of the dura and pericranium to calvarial bone regeneration between infant and adult animals. On the basis of these findings, the authors propose that subsequent studies in which permeability of the expanded polytetrafluoroethylene membranes is altered to permit migration of osteoinductive proteins into the defect while blocking prolapse of adjacent soft tissues may help to make guided bone regeneration a realistic alternative for the repair of cranial defects.