China
Africa
Explore chapters and articles related to this topic
Comparative Anatomy and Development of the Mammalian Disc
Published in Peter Ghosh, The Biology of the Intervertebral Disc, 2019
The dog is a special case since there is a difference between normal breeds and those showing chondrodystrophy, or between strains within a breed.17,80 In all breeds, the nucleus pulposus has a similar form in early life. In normal breeds,17 a gelatinous nucleus pulposus occurs in about 75% of discs at 4 years of age, but in less than 19% beyond 7 years. Chondrodystrophic breeds, however, usually lose their gelatinous nucleus pulposus in the 1st year.
Orthomolecular Parenteral Nutrition Therapy
Published in Aruna Bakhru, Nutrition and Integrative Medicine, 2018
Arturo O'Byrne-Navia, Arturo O'Byrne-De Valdenebro
Mn participates in chondroitin and proteoglycan synthesis. As these are two of the main components in cartilage, Mn can represent an indirect cofactor in the treatment of joint diseases and osteoporosis. In the wide sense, Mn is involved in the biosynthesis of mucopolysaccharides (main components of any extracellular matrix). A deficiency in Mn can then play a role in cartilaginous and collagen disorders. Skeletal abnormalities include chondrodystrophy, or retarded bone growth with bowing. Perosis or “slipped tendon” is a widely recognized condition in chickens and ducks deficient in Mn (Davies 1972, Underwood 1977).
Animal Models and Imaging of Intervertebral Disc Degeneration
Published in Raquel M. Gonçalves, Mário Adolfo Barbosa, Gene and Cell Delivery for Intervertebral Disc Degeneration, 2018
Marion Fusellier, Johann Clouet, Olivier Gauthier, Catherine Le Visage, Jerome Guicheux
Chondrodystrophy is an endochondral ossification defect with disturbance in chondrogenesis that leads to impairment of ossification and growth of long bones. It results in a short-limbed disproportionate dwarfism and, in some cases, in vertebral abnormalities. This anomaly has been fully described in dogs and is even selected in some popular breeds such as Dachshund, Basset Hound, Bulldogs, Beagle, Lhassa Apso, Pekingese, Cavalier King Charles Spaniel, Basset Hounds, and Welsh Corgis (Brisson 2010; Cherrone et al. 2004; Griffin et al. 2009; Priester 1976). As seen in Figure 2.4, these dogs tend to exhibit early onset of IVD degeneration at all levels, with a high incidence of disc herniation at the thoracolumbar junction. DDD in chondrodystrophic breeds is of multigene etiology and is termed chondroid metamorphosis. It is characterized by premature loss of proteoglycans, with an increased metalloproteinase 2 activity and a decrease in glycosaminoglycan (GAG) content. Notochordal cell replacement by chondrocyte-like cells in chondrodystrophic breeds is similar to what is observed in human DDD (Bergknut et al. 2011, 2012; Hunter, Matyas, and Duncan 2003; Johnson, Da Costa, and Allen 2010). Conversely, in nonchondystrophic breeds, notochordal cells are still present in the IVD in adulthood. On MRI, marked similarities have been observed between the different stages of DDD progression in dogs and humans (Bergknut et al. 2011).
Expression of PTHrP and RANKL in acquired middle ear cholesteatoma epithelium
Published in Acta Oto-Laryngologica, 2020
Shumin Xie, Zhen Pan, Tuanfang Yin, Jihao Ren, Wei Liu
The RANKL signaling pathway has been demonstrated to play an essential role in the bone metabolic disturbance. RANKL-knockout mice exhibited severe osteosclerosis, tooth eruption difficulty, obviously reduced skeletal growth, and growth plate chondrodystrophy [15]. Meanwhile, the RANK-knockout mice was also demonstrated to lack osteoclasts, exhibit osteosclerosis, and have a marked deficiency in bone resorption and remodeling [16]. Moreover, the OPG-deficient mice developed early onset osteoporosis characterized by severe trabecular and cortical bone porosity, pronounced thinning of the parietal bones of the skull, and a high incidence of fractures [17]. As for middle ear cholesteatoma, Jeong et al. [12] discovered significantly higher expression of RANKL, lower expression of OPG, and higher RANKL/OPG ratio in cholesteatoma tissues compared with normal postauricular skin, revealing that RANKL participated in the bone resorption process of middle ear cholesteatoma and that the RANKL/OPG ratio might be a reliable indicator of bone resorption in middle ear cholesteatoma. Similarly, in our study, RANKL expression in cholesteatoma epithelium was significantly stronger than that in normal postauricular skin. Furthermore, we have discovered that RANKL protein expression positively correlated with bone resorption degree, indicating that the RANKL signaling pathway may play an essential role in the bone resorption of middle ear cholesteatoma.