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Developmental anomalies and other pathological lesions of the sternum in a medieval osteological sample

机译:中世纪骨科样本中胸骨发育异常和其他病理病变

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We cannot often read about the developmental anomalies of the sternum in paleopathological literature (Brothwell 1965; Tóth and Buda 2001); medical publications on anomalies resulting in chest deformity based on recent population are also rare (Keszler and Szabó 1996). Fractures and inflammation of the sternum are fairly infrequent, and the symptoms of porotic hyperostosis caused by increased red blood cell production are seldom detected in osteological samples. Some developmental anomalies (e. g. sternum fenestratum, alterations of the xiphoid process) do not influence the function or physiological form of the chest, while others may change the shape and diameter of the chest causing difficulties in breathing and in heart function. Some genetic diseases, through the malfunction of the production of the connecting tissues’ basic substantia and fibres, necessarily entail changes in the shape of the sternum. In individuals suffering from Marfan syndrome, sternum excavatum, while in individuals suffering from Hurler- and Morqio-syndrome (and other mucopolysaccharidosis cases), pectus gallinaceum can be observed. Other sternum anomalies resulting from non-genetic factors also seem to run in the family, though how they are inherited is not yet known. An anomaly called synchondrosis sternii develops during postnatal life, and means that the originally cartilaginous sternebrea do not become ossified, there remain synchondrosis between the parts even through the whole lifetime. This, however, does not cause abnormal chest movement. In some cases, the fracture of the sternum may lead to serious respiratory disfunction, and the healing of these injuries without any surgical intervention is not guaranteed. The development of pseudo-articulations may also cause abnormal chest movement. Osteomyelitis spreading to other organs may prove to be dangerous, even fatal.
机译:在古病理学文献中,我们常常不能读到胸骨的发育异常(Brothwell 1965;Tóth和Buda 2001)。关于基于最近人群导致胸部畸形的异常医学出版物也很少(Keszler andSzabó1996)。胸骨骨折和发炎很少见,在骨科样本中很少发现由红细胞产量增加引起的多孔性骨质增生的症状。一些发育异常(例如,胸骨前庭,剑突的改变)不影响胸部的功能或生理形态,而另一些则可能改变胸部的形状和直径,从而导致呼吸和心脏功能困难。一些遗传疾病,由于连接组织的基本物质和纤维产生失灵,必然导致胸骨形状发生变化。在患有马凡氏综合症,胸骨开孔的个体中,而在患有霍勒氏综合征和莫尔奇奥氏综合征(以及其他黏多糖贮积症)的患者中,可以观察到鸡胸肉。由非遗传因素引起的其他胸骨异常似乎也发生在该家族中,尽管如何遗传它们尚不清楚。在产后生活中会出现一种称为胸骨软骨病的异常现象,这意味着最初的软骨性胸骨不会变得骨化,即使在整个一生中,各部位之间仍存在软骨病。但是,这不会引起异常的胸部运动。在某些情况下,胸骨骨折可能导致严重的呼吸功能障碍,并且没有手术干预就无法保证这些损伤的愈合。假关节的发展也可能导致异常的胸部运动。骨髓炎扩散到其他器官可能被证明是危险的,甚至是致命的。

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