Purpose: Non-ambulatory persons with cerebral palsy are prone to low bone mineral density. In ambulatory persons with cerebral palsy, bone mineral density deficits are expected to be small or absent, but a consensus conclusion is lacking. In this systematic review bone mineral density in ambulatory persons with cerebral palsy (Gross Motor Function Classification Scales I–III) was studied.
Materials and methods: Medline, Embase, and Web of Science were searched. According to international guidelines, low bone mineral density was defined as Z-score?≤??2.0. In addition, we focused on Z-score?≤??1.0 because this may indicate a tendency towards low bone mineral density.
Results: We included 16 studies, comprising 465 patients aged 1–65?years. Moderate and conflicting evidence for low bone mineral density (Z-score?≤??2.0) was found for several body parts (total proximal femur, total body, distal femur, lumbar spine) in children with Gross Motor Function Classification Scales II and III. We found no evidence for low bone mineral density in children with Gross Motor Function Classification Scale I or adults, although there was a tendency towards low bone mineral density (Z-score?≤??1.0) for several body parts.
Conclusions: Although more high-quality research is needed, results indicate that deficits in bone mineral density are not restricted to non-ambulatory people with cerebral palsy.
Implications for Rehabilitation
Although more high-quality research is needed, including adults and fracture risk assessment, the current study indicates that deficits in bone mineral density are not restricted to non-ambulatory people with CP.
Health care professionals should be aware that optimal nutrition, supplements on indication, and an active lifestyle, preferably with weight-bearing activities, are important in ambulatory people with CP, also from a bone quality point-of-view.
If indicated, medication and fall prevention training should be prescribed.
FGFR–TACC, found in different tumor types, is characterized by the fusion of a member of fibroblast grown factor receptor (FGFR) tyrosine kinase (TK) family to a member of the transforming acidic coiled-coil (TACC) proteins. Because chromosome numerical alterations, hallmarks of FGFR–TACC fusions are present in many hematological disorders and there are no data on the prevalence, we studied a series of patients with acute myeloid leukemia and myelodysplastic syndrome who presented numerical alterations using cytogenetic traditional analysis. None of the analyzed samples showed FGFR3–TACC3 gene fusion, so screening for this mutation at diagnosis is not recommended. 相似文献
??Objective To investigate the effect of tooth movement at different time after the repair of alveolar bone defects. Methods Defective alveolar bone model was established on one side in forty white rabbits??which were filled with bone meal and attached with Bio-Gide membrane as experiment sides. The other side was performed routine tooth extraction as control. Track the mandibular second molar in both sides respectively in 1 week??1 month??2 months and 3 months after operation. One month later??the distance between the mandibular second molar and third molar was measured with electronic vernier caliper in the experiment side and control side. The mandibular tissue was made paraffin section and hematoxylin eosin staining. Three views of the periodontal ligament in a third place of the mesial roots of the second molar was randomly chosen to count the total number of osteoclasts. Paired-t test analysis was made to evaluate the displacement of the mandibular second molar in experiment and control side??and to evaluate the number of osteoclasts in two side. Results In Group 1w and Group 1 m??the displacement of the mandibular second molar in experiment group was smaller than that in the control side??P??0.05??. There was no statistical significance in Group 2 m and Group 3 m. The number of osteoclasts in the experiment side was less than the control group in Group 1 w and Group1 m??P??0.05??. No statistical significance in Group 2 m and Group 3 m was found. Conclusion Orthodontic treatment can be performed two months after the repair of alveolar bone defects. 相似文献
The objective of this study was to investigate the absorption behavior of chikusetsusaponin IVa (CHS‐IVa) in the rat intestine using single‐pass intestinal perfusion (SPIP) and to classify CHS‐IVa into the biopharmaceutics classification system (BCS). The equilibrium solubility of CHS‐IVa was determined by the shaker method. The absorption mechanism of CHS‐IVa in the intestine was studied by comparing the Peff of different concentrations of CHS‐IVa. The intestinal site dependence of CHS‐IVa absorption was studied by comparing the Peff of the same concentration of CHS‐IVa in different intestinal segments. The relationship between CHS‐IVa and intestinal efflux protein was studied by perfusion with an efflux protein inhibitor. The permeability of CHS‐IVa was investigated by comparing the Peff of CHS‐IVa and the reported value. The solubility of CHS‐IVa over the pH range 1.0–7.5 was 14.4 ± 0.29 to 16.9 ± 0.34 mg/ml. The Peff of CHS‐IVa in the duodenum was 1.76 × 10?3 to 2.00 × 10?3 cm/min. The Peff of CHS‐IVa in the jejunum was 1.26 × 10?3 to 1.39 × 10?3 cm/min. The Peff of CHS‐IVa in the ileum was 1.25 × 10?3 to 1.31 × 10?3 cm/min. The Peff of CHS‐IVa in the colon was 1.02 × 10?3 to 1.08 × 10?3 cm/min. There was no statistical difference of the Peff in the four segments at different CHS‐IVa concentrations. The Peff of CHS‐IVa (0.07, 0.7 and 7.0 mg/ml) were all notably smaller than the reported Peff (3.00 × 10?3 cm/min) in the jejunum. The Peff of CHS‐IVa was not influenced by verapamil (P‐gp inhibitor), indomethacin (MRP inhibitor) and pantoprazole (BCRP inhibitor). CHS‐IVa was classified as high solubility, low permeability and BCS III. The main absorptive tracts were the upper intestinal tracts and the rank order of intestinal permeability was duodenum > jejunum ≈ ileum > colon. The transport mechanism of CHS‐IVa in all intestinal segments might be primarily passive transport. CHS‐IVa was not a substrate of P‐gp, MRP and BCRP. 相似文献
Fibrous dysplasia is a non‐neoplastic developmental process that affects the craniofacial bones, characterized by painless enlargement as a result of bone substitution by abnormal fibrous tissue. Postzygotic somatic activating mutations in the GNAS1 gene cause fibrous dysplasia and have been extensively investigated, as well as being helpful in the differential diagnosis of the disease. Fibrous dysplasia may involve one (monostotic) or multiple bones (polyostotic), sporadically or in association with McCune‐Albright syndrome, Jeffe‐Lichenstein syndrome, or Mazabreud syndrome. This review summarizes the current knowledge on fibrous dysplasia, emphasizing the value of integrating the understanding of its molecular pathogenesis with the clinical, radiological, and histopathological features. In addition, we address important aspects related to the differential diagnosis and patient management. 相似文献