Sihvo H-K, Airas N, Lindén J, Puolanne E
Department of Veterinary Biosciences, University of Helsinki, P.O. Box 66, FI-00014, Finland; Department of Food and Environmental Sciences, University of Helsinki, P.O. Box 66, FI-00014, Finland.
Department of Veterinary Biosciences, University of Helsinki, P.O. Box 66, FI-00014, Finland.
J Comp Pathol. 2018 May;161:1-10. doi: 10.1016/j.jcpa.2018.04.002. Epub 2018 Jun 1.
In wooden breast myopathy (WBM) of broiler chickens, the pectoralis major muscles show abnormally hard consistency and microscopical myodegeneration of unknown aetiology. To date, previous studies have focused primarily on chronic WBM and ultrastructural descriptions of early WBM are lacking. The aim of this study was to elucidate the pathogenesis of WBM by light microscopical morphometry of vessel density and the ultrastructural description of early WBM changes with transmission electron microscopy. The pectoral vessel density was compared between unaffected chickens (n = 14) and two areas of focal WBM in affected chickens (n = 14). The transverse myofibre area per vessel was highest in the unaffected area of muscle from cases of focal WBM, significantly higher (P = 0.01) than in macroscopically unaffected tissue, indicating that relatively decreased blood supply may trigger the development of WBM. The ultrastructural study included unaffected chickens (n = 3), two areas of focal WBM from affected chickens (n = 3) and areas of diffuse WBM from affected chickens (n = 3). The morphologically least affected myofibres within the WBM lesion areas in light microscopy exhibited ultrastructural changes of increased sarcoplasmic reticulum diameter and mitochondrial hyperplasia. Such changes originate typically from osmotic imbalance, for which the most likely aetiologies in WBM include tissue hypoxia or myodegeneration of the surrounding myofibres. The findings suggest that a relative reduction of blood supply in the major pectoral muscle occurs in the early phase of WBM, which may be linked to the ultrastructural changes of osmotic imbalance.
在肉鸡的木胸肌病（WBM）中，胸大肌表现出异常坚硬的质地以及病因不明的微观肌变性。迄今为止，先前的研究主要集中在慢性WBM上，缺乏对早期WBM的超微结构描述。本研究的目的是通过血管密度的光学显微镜形态计量学以及透射电子显微镜对早期WBM变化的超微结构描述来阐明WBM的发病机制。比较了未受影响的鸡（n = 14）和受影响的鸡中两个局灶性WBM区域（n = 14）的胸肌血管密度。在局灶性WBM病例的肌肉未受影响区域，每根血管的横向肌纤维面积最大，显著高于（P = 0.01）宏观上未受影响的组织，表明相对减少的血液供应可能触发WBM的发展。超微结构研究包括未受影响的鸡（n = 3）、受影响的鸡的两个局灶性WBM区域（n = 3）和受影响的鸡的弥漫性WBM区域（n = 3）。在光学显微镜下，WBM病变区域内形态学上受影响最小的肌纤维表现出肌浆网直径增加和线粒体增生的超微结构变化。这种变化通常源于渗透压失衡，在WBM中最可能的病因包括组织缺氧或周围肌纤维的肌变性。研究结果表明，在WBM的早期阶段，胸大肌的血液供应相对减少，这可能与渗透压失衡的超微结构变化有关。
