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  • bone
  • Using a mouse mutant that fractures spontaneously and dies at a very young age, we identified that a deletion of the GULO gene, which is involved in the synthesis of vitamin C, is the cause of impaired osteoblast differentiation, reduced bone formation, and development of spontaneous fractures. (jax.org)
  • mice
  • We established that ascorbic acid deficiency caused by deletion of the GULO gene (38,146-bp region) contributes to fractures and premature death because the sfx phenotype can be corrected in vivo by treating sfx mice with ascorbic acid and because osteoblasts derived from sfx mice are only able to form mineralized nodules when treated with ascorbic acid. (jax.org)
  • CONCLUSION: The sfx is a mutation of the GULO gene, which leads to ascorbic acid deficiency, impaired osteoblast cell function, and fractures in affected mice. (jax.org)
  • Recurrent
  • Nasu-Hakola disease (NHD), also referred to as polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL), is a rare inherited leukodystrophy characterized by progressive presenile dementia associated with recurrent bone fractures due to polycystic osseous lesions of the lower and upper extremities. (nih.gov)
  • Patients then start suffering from recurrent bone fractures due to polycystic osseous and osteoporotic lesions in the limb bones (osseous stage). (nih.gov)
  • skeletal
  • Although bisphosphonates effectively prevent vertebral fractures, and their safety has been tested in randomized trials, we must emphasize the need for awareness of the possibility that long-term suppression of bone turnover with bisphosphonates may eventually lead to an accumulation of fatigue-induced damage and adverse skeletal effects such as delayed fracture healing. (kjim.org)
  • osteopenia
  • Localized osteopenia is evident in X-rays of tumours or infections of bone, in osteonecrosis (death of bony tissue), in fracture, and in conditions of diminished mechanical demand. (britannica.com)
  • Deficient calcium intake combined with excessive phosphate intake causes osteopenia, fractures, and loss of teeth in dogs, cats, and other animals by excessive compensatory parathyroid hormone action. (britannica.com)
  • phenotype
  • We established that ascorbic acid deficiency caused by deletion of the GULO gene (38,146-bp region) contributes to fractures and premature death because the sfx phenotype can be corrected in vivo by treating sfx mice with ascorbic acid and because osteoblasts derived from sfx mice are only able to form mineralized nodules when treated with ascorbic acid. (jax.org)
  • occur
  • This rare injury is discussed, addressing the mechanism of the injury, the treatment, and the types of sports that this fracture has been reported to occur. (sportsfootankle.com)
  • cause
  • There are things you can do to get these two biological mechanisms on an equal footing, so as we age we don't suffer from this and the fractures they can cause. (healthcentral.com)