The Experts below are selected from a list of 468 Experts worldwide ranked by ideXlab platform
Jun Wang - One of the best experts on this subject based on the ideXlab platform.
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dmp1 ablation in the rabbit results in mineralization defects and abnormalities in Haversian Canal osteon microarchitecture
Journal of Bone and Mineral Research, 2019Co-Authors: Tingjun Liu, Jun Wang, Xudong Xie, Ke Wang, Tingting Sui, Di Liu, Liangxue Lai, Hu ZhaoAbstract:DMP1 (dentin matrix protein 1) is an extracellular matrix protein highly expressed in bones. Studies of Dmp1 knockout (KO) mice led to the discovery of a rare autosomal recessive form of hypophosphatemic rickets (ARHR) caused by DMP1 mutations. However, there are limitations for using this mouse model to study ARHR, including a lack of Haversian Canals and osteons (that occurs only in large mammalian bones), high levels of fibroblast growth factor 23 (FGF23), and PTH, in comparison with a moderate elevation of FGF23 and unchanged PTH in human ARHR patients. To better understand this rare disease, we deleted the DMP1 gene in rabbit using CRISPR/Cas9. This rabbit model recapitulated many features of human ARHR, such as the rachitic rosary (expansion of the anterior rib ends at the costochondral junctions), moderately increased FGF23, and normal PTH levels, as well as severe defects in bone mineralization. Unexpectedly, all DMP1 KO rabbits died by postnatal week 8. They developed a severe bone microarchitecture defect: a major increase in the central Canal areas of osteons, concurrent with massive accumulation of osteoid throughout all bone matrix (a defect in mineralization), suggesting a new paradigm, where rickets is caused by a combination of a defect in bone microarchitecture and a failure in mineralization. Furthermore, a study of DMP1 KO bones found accelerated chondrogenesis, whereas ARHR has commonly been thought to be involved in reduced chondrogenesis. Our findings with newly developed DMP1 KO rabbits suggest a revised understanding of the mechanism underlying ARHR. © 2019 American Society for Bone and Mineral Research.
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DMP1 Ablation in the Rabbit Results in Mineralization Defects and Abnormalities in Haversian Canal/Osteon Microarchitecture
Journal of Bone and Mineral Research, 2019Co-Authors: Jun Wang, Ke Wang, Hu Zhao, Zhanjun Li, Jian Q. FengAbstract:DMP1 (dentin matrix protein 1) is an extracellular matrix protein highly expressed in bones. Studies of Dmp1 knockout (KO) mice led to the discovery of a rare autosomal recessive form of hypophosphatemic rickets (ARHR) caused by DMP1 mutations. However, there are limitations for using this mouse model to study ARHR, including a lack of Haversian Canals and osteons (that occurs only in large mammalian bones), high levels of fibroblast growth factor 23 (FGF23), and PTH, in comparison with a moderate elevation of FGF23 and unchanged PTH in human ARHR patients. To better understand this rare disease, we deleted the DMP1 gene in rabbit using CRISPR/Cas9. This rabbit model recapitulated many features of human ARHR, such as the rachitic rosary (expansion of the anterior rib ends at the costochondral junctions), moderately increased FGF23, and normal PTH levels, as well as severe defects in bone mineralization. Unexpectedly, all DMP1 KO rabbits died by postnatal week 8. They developed a severe bone microarchitecture defect: a major increase in the central Canal areas of osteons, concurrent with massive accumulation of osteoid throughout all bone matrix (a defect in mineralization), suggesting a new paradigm, where rickets is caused by a combination of a defect in bone microarchitecture and a failure in mineralization. Furthermore, a study of DMP1 KO bones found accelerated chondrogenesis, whereas ARHR has commonly been thought to be involved in reduced chondrogenesis. Our findings with newly developed DMP1 KO rabbits suggest a revised understanding of the mechanism underlying ARHR. © 2019 American Society for Bone and Mineral Research.
Hu Zhao - One of the best experts on this subject based on the ideXlab platform.
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dmp1 ablation in the rabbit results in mineralization defects and abnormalities in Haversian Canal osteon microarchitecture
Journal of Bone and Mineral Research, 2019Co-Authors: Tingjun Liu, Jun Wang, Xudong Xie, Ke Wang, Tingting Sui, Di Liu, Liangxue Lai, Hu ZhaoAbstract:DMP1 (dentin matrix protein 1) is an extracellular matrix protein highly expressed in bones. Studies of Dmp1 knockout (KO) mice led to the discovery of a rare autosomal recessive form of hypophosphatemic rickets (ARHR) caused by DMP1 mutations. However, there are limitations for using this mouse model to study ARHR, including a lack of Haversian Canals and osteons (that occurs only in large mammalian bones), high levels of fibroblast growth factor 23 (FGF23), and PTH, in comparison with a moderate elevation of FGF23 and unchanged PTH in human ARHR patients. To better understand this rare disease, we deleted the DMP1 gene in rabbit using CRISPR/Cas9. This rabbit model recapitulated many features of human ARHR, such as the rachitic rosary (expansion of the anterior rib ends at the costochondral junctions), moderately increased FGF23, and normal PTH levels, as well as severe defects in bone mineralization. Unexpectedly, all DMP1 KO rabbits died by postnatal week 8. They developed a severe bone microarchitecture defect: a major increase in the central Canal areas of osteons, concurrent with massive accumulation of osteoid throughout all bone matrix (a defect in mineralization), suggesting a new paradigm, where rickets is caused by a combination of a defect in bone microarchitecture and a failure in mineralization. Furthermore, a study of DMP1 KO bones found accelerated chondrogenesis, whereas ARHR has commonly been thought to be involved in reduced chondrogenesis. Our findings with newly developed DMP1 KO rabbits suggest a revised understanding of the mechanism underlying ARHR. © 2019 American Society for Bone and Mineral Research.
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DMP1 Ablation in the Rabbit Results in Mineralization Defects and Abnormalities in Haversian Canal/Osteon Microarchitecture
Journal of Bone and Mineral Research, 2019Co-Authors: Jun Wang, Ke Wang, Hu Zhao, Zhanjun Li, Jian Q. FengAbstract:DMP1 (dentin matrix protein 1) is an extracellular matrix protein highly expressed in bones. Studies of Dmp1 knockout (KO) mice led to the discovery of a rare autosomal recessive form of hypophosphatemic rickets (ARHR) caused by DMP1 mutations. However, there are limitations for using this mouse model to study ARHR, including a lack of Haversian Canals and osteons (that occurs only in large mammalian bones), high levels of fibroblast growth factor 23 (FGF23), and PTH, in comparison with a moderate elevation of FGF23 and unchanged PTH in human ARHR patients. To better understand this rare disease, we deleted the DMP1 gene in rabbit using CRISPR/Cas9. This rabbit model recapitulated many features of human ARHR, such as the rachitic rosary (expansion of the anterior rib ends at the costochondral junctions), moderately increased FGF23, and normal PTH levels, as well as severe defects in bone mineralization. Unexpectedly, all DMP1 KO rabbits died by postnatal week 8. They developed a severe bone microarchitecture defect: a major increase in the central Canal areas of osteons, concurrent with massive accumulation of osteoid throughout all bone matrix (a defect in mineralization), suggesting a new paradigm, where rickets is caused by a combination of a defect in bone microarchitecture and a failure in mineralization. Furthermore, a study of DMP1 KO bones found accelerated chondrogenesis, whereas ARHR has commonly been thought to be involved in reduced chondrogenesis. Our findings with newly developed DMP1 KO rabbits suggest a revised understanding of the mechanism underlying ARHR. © 2019 American Society for Bone and Mineral Research.
Mahoney Patrick - One of the best experts on this subject based on the ideXlab platform.
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Secondary osteon variants and remodeling in human bone
'Wiley', 2021Co-Authors: Cooke, Karen M., Mahoney Patrick, Miszkiewicz, Justyna J.Abstract:Histomorphometric analysis of human cortical bone has documented the occurrence of secondary osteon variants. These include drifting osteons which form tails as they move erratically through the cortex and Type II osteons which show partial resorption and redeposition within the cement line of the osteon. Little is known about the biological significance of these variants. Prior studies suggested correlations with age, biomechanics, diet, and mineral homeostasis. No study has yet tested for osteon variant associations with static measures of bone remodeling. In this study, thin sections (n = 112) of the posterior femur representing a late English Medieval adult human osteological collection, subdivided by age, sex, and socio-economic status, were examined to determine whether remodeling indicators reconstructed from osteon parameters (area, diameter, area ratios) and densities differed between categories of presence or absence of Type II and drifting osteon variants. Of the 112 sections, 33 presented with Type II osteons, and 38 had drifting osteons. Sporadic statistically significant results were identified. Haversian Canal:osteon area ratio differed (p = 0.017) with Type II osteon presence, Type II osteons were more prevalent in males than females (p = 0.048), and drifting osteons were associated with smaller osteon (p = 0.049) and Haversian Canal area (p = 0.05). These results may be explained through some biological (sex) and social (status) processes such as a period of physiological recovery (e.g., following lactation, malnutrition). However, the general lack of consistent relationships between osteon variants and remodeling indicators suggests they occur as a result of natural variation
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Microscopic markers of an infradian biorhythm in human juvenile ribs
'Wiley', 2019Co-Authors: Pitfield Rosie, Miszkiewicz, Justyna J., Mahoney PatrickAbstract:Recent studies have indicated that an infradian systemic biorhythm may coordinate aspects of human hard tissue growth and adult body size. Here we investigate if evidence of this biorhythm retained in human teeth as the periodicity of Retzius lines (RP) corresponds with the microstructural growth of a non-weight bearing bone, the rib. Using static histomorphometric methods, the RP of permanent first molars was calculated and combined with measures of bone remodelling for ribs from 50 human juvenile skeletons. Results provide the first evidence that the infradian biorhythm is linked to bone remodelling in children. Retzius periodicity was negatively correlated with relative osteon area and Haversian Canal size in children aged between eight to 12 years. Results imply that a faster biorhythm (fewer days) relates to increased bone deposition during remodelling leading to larger osteons relative to Haversian Canal size in ribs from these children. A faster biorhythm was also correlated with the relative cortical area of their ribs. Relationships between bone remodelling and the biorhythm were much more variable in younger children aged between three to seven years of age. Our results provide the first evidence that an infradian biorhythm is linked to bone remodelling in older children
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Microscopic markers of an infradian biorhythm in human juvenile ribs
'Elsevier BV', 2018Co-Authors: Pitfield Rosie, Miszkiewicz, Justyna J., Mahoney PatrickAbstract:Recent studies have indicated that there may be an infradian systemic biorhythm that coordinates aspects of human hard tissue growth and influences adult body size. Here we investigate if evidence of this biorhythm retained in human teeth as the periodicity of Retzius lines (RP) corresponds with the microstructural growth of a non-weight bearing bone, the rib, in a sample of 50 human juvenile skeletons. Using static histomorphometric methods, the RP of one permanent tooth from each skeleton was calculated and combined with measures of bone remodeling in a rib from the same individual. Results provide the first evidence that the infradian biorhythm is linked to bone remodeling in children. Retzius periodicity was negatively correlated with relative osteon area (r = -0.563, p = 0.008) and positively related to Haversian Canal area (r = 0.635, p = 0.002) and diameter (r = 0.671, p = 0.001) in children between the age of 8 to 12 years. There was also a negative correlation between RP and the relative cortical area of ribs (r = -0.500, p = 0.048). Relationships between bone remodeling and the biorhythm were much more variable in younger children. Results imply that as the biorhythm speeds up there is increased bone deposition during remodeling of the rib, leading to the larger osteonal lamellar bone areas and smaller Haversian Canals in children between 8 and 12 years of age. Our results support the idea that there is an infradian biorhythm that coordinates aspects of human hard tissue growth
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Ancient Human Bone Microstructure in Medieval England: Comparisons between Two Socio-Economic Groups
Wiley, 2016Co-Authors: Miszkiewicz Justyna, Mahoney PatrickAbstract:Understanding the links between bone microstructure and human lifestyle is critical for clinical and anthropological research into skeletal growth and adaptation. The present study is the first to report correspondence between socio-economic status and variation in bone microstructure in ancient humans. Products of femoral cortical remodeling were assessed using histological methods in a large human medieval sample (N = 450) which represented two distinct socio-economic groups. Osteonal parameters were recorded in posterior midshaft femoral sections from adult males (N = 233) and females (N = 217). Using univariate and multivariate statistics, intact, fragmentary, and osteon population densities, Haversian Canal area and diameter, and osteon area were compared between the two groups, accounting for sex, age, and estimated femoral robusticity. The size of osteons and their Haversian Canals, as well as osteon density, varied significantly between the socio-economic groups, although minor inconsistencies were observed in females. Variation in microstructure was consistent with historical textual evidence that describes differences in mechanical loading and nutrition between the two groups. Results demonstrate that aspects of ancient human lifestyle can be inferred from bone microstructure. Anat Rec, 299:42–59, 2016
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Ancient Human Bone Microstructure in Medieval England: Comparisons between Two Socio-Economic Groups
'Wiley', 2015Co-Authors: Miszkiewicz, Justyna J., Mahoney PatrickAbstract:Understanding the links between bone microstructure and human lifestyle is critical for clinical and anthropological research into skeletal growth and adaptation. The present study is the first to report correspondence between socio-economic status and variation in bone microstructure in ancient humans. Products of femoral cortical remodeling were assessed using histological methods in a large human medieval sample (N:450) which represented two distinct socio-economic groups. Osteonal parameters were recorded in posterior midshaft femoral sections from adult males (N:233) and females (N:217). Using univariate and multivariate statistics, intact, fragmentary, and osteon population densities, Haversian Canal area and diameter, and osteon area were compared between the two groups, accounting for sex, age, and estimated femoral robusticity. The size of osteons and their Haversian Canals, as well as osteon density, varied significantly between the socio-economic groups, although minor inconsistencies were observed in females. Variation in microstructure was consistent with historical textual evidence that describes differences in mechanical loading and nutrition between the two groups. Results demonstrate that aspects of ancient human lifestyle can be inferred from bone microstructure
Jian Q. Feng - One of the best experts on this subject based on the ideXlab platform.
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DMP1 Ablation in the Rabbit Results in Mineralization Defects and Abnormalities in Haversian Canal/Osteon Microarchitecture
Journal of Bone and Mineral Research, 2019Co-Authors: Jun Wang, Ke Wang, Hu Zhao, Zhanjun Li, Jian Q. FengAbstract:DMP1 (dentin matrix protein 1) is an extracellular matrix protein highly expressed in bones. Studies of Dmp1 knockout (KO) mice led to the discovery of a rare autosomal recessive form of hypophosphatemic rickets (ARHR) caused by DMP1 mutations. However, there are limitations for using this mouse model to study ARHR, including a lack of Haversian Canals and osteons (that occurs only in large mammalian bones), high levels of fibroblast growth factor 23 (FGF23), and PTH, in comparison with a moderate elevation of FGF23 and unchanged PTH in human ARHR patients. To better understand this rare disease, we deleted the DMP1 gene in rabbit using CRISPR/Cas9. This rabbit model recapitulated many features of human ARHR, such as the rachitic rosary (expansion of the anterior rib ends at the costochondral junctions), moderately increased FGF23, and normal PTH levels, as well as severe defects in bone mineralization. Unexpectedly, all DMP1 KO rabbits died by postnatal week 8. They developed a severe bone microarchitecture defect: a major increase in the central Canal areas of osteons, concurrent with massive accumulation of osteoid throughout all bone matrix (a defect in mineralization), suggesting a new paradigm, where rickets is caused by a combination of a defect in bone microarchitecture and a failure in mineralization. Furthermore, a study of DMP1 KO bones found accelerated chondrogenesis, whereas ARHR has commonly been thought to be involved in reduced chondrogenesis. Our findings with newly developed DMP1 KO rabbits suggest a revised understanding of the mechanism underlying ARHR. © 2019 American Society for Bone and Mineral Research.
Xudong Xie - One of the best experts on this subject based on the ideXlab platform.
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dmp1 ablation in the rabbit results in mineralization defects and abnormalities in Haversian Canal osteon microarchitecture
Journal of Bone and Mineral Research, 2019Co-Authors: Tingjun Liu, Jun Wang, Xudong Xie, Ke Wang, Tingting Sui, Di Liu, Liangxue Lai, Hu ZhaoAbstract:DMP1 (dentin matrix protein 1) is an extracellular matrix protein highly expressed in bones. Studies of Dmp1 knockout (KO) mice led to the discovery of a rare autosomal recessive form of hypophosphatemic rickets (ARHR) caused by DMP1 mutations. However, there are limitations for using this mouse model to study ARHR, including a lack of Haversian Canals and osteons (that occurs only in large mammalian bones), high levels of fibroblast growth factor 23 (FGF23), and PTH, in comparison with a moderate elevation of FGF23 and unchanged PTH in human ARHR patients. To better understand this rare disease, we deleted the DMP1 gene in rabbit using CRISPR/Cas9. This rabbit model recapitulated many features of human ARHR, such as the rachitic rosary (expansion of the anterior rib ends at the costochondral junctions), moderately increased FGF23, and normal PTH levels, as well as severe defects in bone mineralization. Unexpectedly, all DMP1 KO rabbits died by postnatal week 8. They developed a severe bone microarchitecture defect: a major increase in the central Canal areas of osteons, concurrent with massive accumulation of osteoid throughout all bone matrix (a defect in mineralization), suggesting a new paradigm, where rickets is caused by a combination of a defect in bone microarchitecture and a failure in mineralization. Furthermore, a study of DMP1 KO bones found accelerated chondrogenesis, whereas ARHR has commonly been thought to be involved in reduced chondrogenesis. Our findings with newly developed DMP1 KO rabbits suggest a revised understanding of the mechanism underlying ARHR. © 2019 American Society for Bone and Mineral Research.
