Do animals have growth plates
Examination of Dogs: Chondrodysplasia
Chondrodysplasia is a genetic disorder of cartilage and bone development. It can occur in both dogs and humans. In general, three types of bone dysplasia, which differ in their severity, are identified - osteodysplasia, chondrodysplasia and dysostosis. In osteodysplasia and chondrodysplasia, the bone and cartilage tissue is affected, while in dysostosis, individual bones or entire groups of bones are affected. Osteodysplasia in particular can be characterized not only by a change in the density of bone minerals but also by chondrodysplasia, which leads to abnormal endochondral bone formation (ossification). This abnormal bone formation within the cartilage causes disturbances in linear bone growth and disproportionate short stature in the affected animal.
During the endochondral ossification / ossification of the long bones, progressive changes occur on the surface and in the interior of the cartilage. This creates individual cartilaginous growth plates that later form whole bone parts. These growth plates are located on the ends of the long bones and are responsible for the length of the bone. They consist of ECM (extracellular matrix / cartilage matrix) and linear columns / nodules that differentiate into chondrocytes. The chondrocytes are arranged in zones. In the proliferation zone, the mature cells in the terminal phase are replaced by trabecular bone.
Chondrodysplasia is currently identified in two breeds of dogs - the Norwegian elkhound and the Karelian bear dog. It is likely that the Karelian bear dog did not develop this disease until after crossing it with the Norwegian elk dog. In contrast to healthy dogs, the affected dogs have much shorter legs. In addition, such skeletal malformations as significantly shorter, sideways-curved fingers on the front paws, curved front legs, shortened vertebrae and significantly delayed ossification of the carpal bones can occur. The histology performed on the affected dogs revealed unusually wide ECM bands, disordered columnar structure, and chondrocytes of atypical size and morphology.
Genes that code for ECM protein are behind the development of chondrodysplasia, namely Cartilage Oligomeric Matrix Protein (COMP), several different collagens and proteoglycans aggrecan and perlacan. Specifically, the mutation c.2083C> T occurs in exon16 of the ITGA10 gene, which codes for the integrin alpha subunit (α10β1). This subunit is responsible for proper chondrocyte proliferation and accumulation of fibrillar collagens near the ECM. The task of this α10β1 subunit is essential for the proper course of endochondral ossification.
Chondrodysplasia is a recessive inherited disease. The disease develops in dogs who have inherited the mutated gene from both parents. These dogs are labeled as P / P (positive / positive). Carriers of the mutated gene, labeled N / P (negative / positive), inherited the mutated gene from only one parent and have no clinical signs, but they pass the disease on to their offspring. If two heterozygos (N / P) are mated, 25% of the offspring will theoretically be healthy, 50% of the offspring will be carriers and 25% of the offspring will inherit the mutated gene from both parents and are therefore affected by chondrodysplasia. By mating a healthy dog (N / N) and a carrier of this mutation (N / P) the litter will theoretically be 50% carrier and 50% healthy puppies. If a carrier (N / P) and an affected dog (P / P) are mated, theoretically 50% affected dogs and 50% carriers would be born.
Kyöstilä, K., Lappalainen, A. K., & Lohi, H. (2013). Canine chondrodysplasia caused by a truncating mutation in collagen-binding integrin alpha subunit 10.PloS one, 8(9), e75621.
Kyöstilä, K. (2015). Identification of Novel Mutations and Molecular Pathways for Canine Neurodegeneration and Chondrodysplasia.Dissertationes Scholae Doctoralis Ad Sanitatem Investigandam Universitatis Helsinkiensis.
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