Alroy J, Knowles K, Schelling S H, Kaye E M, Rosenberg A E
Department of Pathology, Tufts University School of Medicine and Veterinary Medicine, Boston, MA 02111, USA.
Virchows Arch. 1995;426(2):141-8. doi: 10.1007/BF00192635.
The development of skeletal lesions in two canine models of GM1-gangliosidosis, English springer spaniels and Portuguese water dogs, has been studied and compared to osseous abnormalities in a child with the infantile form of the disease. In the canine models, skeletal dysplasia was progressive. Lesions were noted at 2 months of age and characterized by retarded endochondral ossification and osteoporosis. Older puppies had focal cartilage necrosis within lumbar vertebral epiphyses. At the cellular level, lesions were characterized by chondrocytic hypertrohy and lysosomal accumulation of storage compounds. Our studies illustrate that the skeletal lesions in both canine models are similar to those in a child with GM1-gangliosidosis. Furthermore, we proposed that the abnormal storage of partially degraded compounds in affected chondrocytes might explain, at least in part, the retarded bone formation noted in patients with GM1-gangliosidosis.
在两种GM1神经节苷脂贮积症犬模型(英国激飞猎犬和葡萄牙水犬)中,对骨骼病变的发展进行了研究,并与一名患有婴儿型该疾病儿童的骨骼异常进行了比较。在犬模型中,骨骼发育异常呈进行性。在2月龄时发现病变,其特征为软骨内成骨延迟和骨质疏松。年龄较大的幼犬腰椎椎体骨骺内有局灶性软骨坏死。在细胞水平上,病变的特征为软骨细胞肥大和储存化合物的溶酶体蓄积。我们的研究表明,两种犬模型中的骨骼病变与GM1神经节苷脂贮积症患儿的病变相似。此外,我们提出,受影响软骨细胞中部分降解化合物的异常储存可能至少部分解释了GM1神经节苷脂贮积症患者中所观察到的骨形成延迟。