1 Department of Orthopaedics, University Medical Center Utrecht , Utrecht, The Netherlands .
2 Department of Biomechanical Engineering, Faculty of Mechanical, Maritime, and Materials Engineering, Delft University of Technology , Delft, The Netherlands .
Tissue Eng Part C Methods. 2017 Nov;23(11):673-685. doi: 10.1089/ten.TEC.2017.0151. Epub 2017 Aug 21.
Pathologic conditions associated with bone formation can serve as models to identify bone-promoting mediators. The inflammatory response to bacterial infections generally leads to osteolysis and impaired bone healing, but paradoxically, it can also have pro-osteogenic effects. As a potential model to investigate pro-osteogenic stimuli, this study characterizes the bone formation in an established rabbit tibia model of periprosthetic infection. Our hypothesis was that the infection with Staphylococcus aureus (S. aureus) correlates with bone formation as a response to local inflammation. Fluorochromes showed excessive subperiosteal bone formation in infected tibiae, starting the first week and continuing throughout the study period. Despite the observed cortical lysis on micro-CT after 28 days, infection resulted in a twofold higher bone volume in the proximal tibiae compared to uninfected controls. The ipsilateral fibulae, nor the contralateral fibulae or tibiae were affected by infection. Next, we sought to confine the cause of stimulated bone formation to the isolated S. aureus cell wall. In absence of virulent bacterial infection, the S. aureus cell wall extract induced bone in a more favorable way without cortical lysis. This suggests that the sterile inflammatory reaction to bacterial antigens may be harnessed for bone regenerative purposes. Future investigations in this rabbit tibia model can lead to further identification of effective stimuli for clinical application.
与骨形成相关的病理状况可作为鉴定促骨形成介质的模型。细菌感染的炎症反应通常导致溶骨和骨愈合受损，但矛盾的是，它也可能具有促成骨作用。作为研究促成骨刺激的潜在模型，本研究对已建立的假体周围感染兔胫骨模型中的骨形成进行了特征描述。我们的假设是金黄色葡萄球菌（S. aureus）感染与骨形成相关，作为局部炎症的反应。荧光染料显示感染胫骨有大量骨膜下骨形成，从第一周开始，并持续整个研究期间。尽管在 28 天后 micro-CT 观察到皮质溶解，但与未感染对照相比，感染导致胫骨近端的骨量增加了两倍。同侧腓骨，以及对侧腓骨或胫骨均不受感染影响。接下来，我们试图将刺激骨形成的原因局限于分离的金黄色葡萄球菌细胞壁。在没有毒力细菌感染的情况下，金黄色葡萄球菌细胞壁提取物以一种更有利的方式诱导骨形成，而不会发生皮质溶解。这表明，针对细菌抗原的无菌炎症反应可被用于骨再生目的。在这种兔胫骨模型中的进一步研究可以进一步确定用于临床应用的有效刺激物。
