Mineralization

Donnelly, Eve; Boskey, Adele L.

doi:10.1016/b978-0-12-381978-9.10021-6

Cited by 5 publications

(4 citation statements)

References 143 publications

(146 reference statements)

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“…Therefore, addressing the impact of cell-free iron is essential for the orange-spotted grouper's against P. plecoglossicida. Biologic mineralization refers to the physicochemical process by which organic ions are converted into inorganic crystals and deposited within cells [40]. Iron mineralization involves the conversion of organic ferrous ions into ferric ions stored as ferritin [41].…”

Section: Discussionmentioning

confidence: 99%

Ferroptosis and iron mineralization involved in the death and survival of orange‐spotted groupers challenged with Pseudomonas plecoglossicida

Sun,

Weng,

Dong

et al. 2024

Animal Research and One Health

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Pseudomonas plecoglossicida (P. plecoglossicida) is a pathogen in aquaculture that causes considerable economic loss. According to artificial infection experiments, the fish were classified into control group, moribund group, and survival group. Compared to the control group, both the moribund group and the survival group of fish had fewer red blood cells (RBCs) and lower oxygen saturation (SaO2). Furthermore, the fish in the survival group has more RBCs and SaO2 compared to the moribund group. The concentrations of total iron, ferrous iron, ferric iron, and mineralized iron in the fish spleen of the moribund and survival groups were lower compared to those of the control group. Additionally, the concentrations of these iron components in the fish spleen of the survival group were higher than those of the moribund group. The results demonstrated that iron mineralization is involved in the survival of fish challenged with P. plecoglossicida. Compared to the control and survival groups, the fish spleen had several distinguishing features in the moribund group, including less reduced glutathione (GSH), higher mitochondrial complex V activity, more lipid peroxidation, and reactive oxygen species, as well as reduced glutathione peroxidase 4 (gpx4) expression. Moreover, there were intact cell membranes, a normal nucleus size, no chromatin concentration, and disappearance of cristae in the mitochondria of the spleens of the moribund group. The characteristics of spleen cells in the moribund group were consistent with ferroptosis, suggesting that ferroptosis was involved in the death of fish challenged with P. plecoglossicida.

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Section: Discussionmentioning

confidence: 99%

Ferroptosis and iron mineralization involved in the death and survival of orange‐spotted groupers challenged with Pseudomonas plecoglossicida

Sun,

Weng,

Dong

et al. 2024

Animal Research and One Health

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“…Adequate mineralization of cartilage is required for normal deposition of bone on cartilage during ossification (Mackie, Tatarczuch, & Mirams, ); if the cartilage matrix is not sufficiently mineralized, the defective framework limits the potential scaffolding that osteoblasts need in order to express osteoid. The lack of adequate mineral accumulations that occur during vitamin D deficiency also limits mineralization of organic matrix expressed by osteoblasts, compromising both endochondral and appositional skeletal growth (Donnelly & Boskey, ; Pettifor, ). Osteoblast formation, activity and survival are also impaired during severe vitamin D deficiency (Montecino et al, ).…”

Section: Vitamin D In Endochondral Growthmentioning

confidence: 99%

“…Vitamin D deficiency in particular, has been directly associated with growth stunting in clinical studies (e.g., Jaffe, ; Koo & Waylat, ). Vitamin D is a steroid hormone that exerts direct effects on chondrocyte and osteoblast activity as well as cartilage and skeletal mineralization (Boyan, Doroudi, & Schwartz, ; Donnelly & Boskey, ). An active deficiency is therefore capable of significantly moderating endochondral bone growth and causing long bone bending deformities due to weight‐bearing pressure on bones weakened by defective mineralization (Hess, ; Kreiter et al, ; Rajah et al, ; Thacher, Fischer, & Pettifor, ).…”

Section: Introductionmentioning

confidence: 99%

Endochondral growth disruption during vitamin D deficiency rickets in a mid‐19th century series from Bethnal Green, London, UK

Ives

Humphrey

2018

American J Phys Anthropol

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Pronounced growth faltering existed in children with active rickets and affected the upper and lower limb, indicating systemic growth failures during the deficiency. Poor maternal health, early weaning and inadequate infant feeding, and lack of sunlight exposure likely contributed to the development of rickets. Complex interactions between pathological conditions, nutritional deficiencies and vitamin D deficiency may have exacerbated growth impacts.

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“…Vitamin D is a steroid hormone that can affect the body's handling of calcium and phosphate, which are necessary for the mineralization of osteoid and cartilage tissue (Boyan et al, 2011; Donnelly & Boskey, 2011; Jowsey, 1977). Although genetic factors can impact the formation and utilization of vitamin D, vitamin D deficiency is predominately caused by insufficient sunlight exposure for synthesis in the skin or insufficient dietary uptake (Brickley et al, 2020).…”

Section: Introductionmentioning

confidence: 99%

The impact of vitamin D deficiency on cortical bone area and porosity at the femoral midsection in children from post‐medieval London

Swan

Humphrey

Ives

2022

American Journal of Biological Anthropology

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Objectives: Cortical bone structure undergoes dynamic changes during appositional growth and is highly sensitive to mechanical, hormonal, and nutritional influences.Vitamin D deficiency rickets can significantly disrupt the normal mineralization of newly formed bone leading to compromised bone structure. Here, we document ontogenetic trends in femoral cortical bone area and porosity during early growth and examine how vitamin D deficiency during childhood may impact these parameters in a sample of children from post-medieval London, UK.Materials and Methods: Micro-CT scans of the femur were collected from a documented sample of 138 children aged from birth to 8.5 years who were grouped by the presence and stage of rickets. Cross-sections were extracted at the midsection and area and porosity measurements recorded. A local regression (LOESS) was used to fit curves to the dataset of children without rickets, which were used as comparative baselines for children with active and healed rickets.Results: Cortical bone porosity was elevated in all children with active rickets most likely reflecting delayed mineralization of osteoid and increased resorption due to secondary hyperparathyroidism. Total subperiosteal area and cortical bone area were higher in children with healed rickets than children without rickets reflecting the mineralization of osteoid following recovery from the deficiency. Discussion:The results demonstrate marked differences in cortical bone structure in children with rickets, which vary according to age and disease stage. This study illustrates the complex interaction between metabolic bone diseases and bone formation and the importance of considering ontogenetic changes in bone structure in the study of disease during childhood.

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Mineralization

Cited by 5 publications

References 143 publications

Ferroptosis and iron mineralization involved in the death and survival of orange‐spotted groupers challenged with Pseudomonas plecoglossicida

Ferroptosis and iron mineralization involved in the death and survival of orange‐spotted groupers challenged with Pseudomonas plecoglossicida

Endochondral growth disruption during vitamin D deficiency rickets in a mid‐19th century series from Bethnal Green, London, UK

The impact of vitamin D deficiency on cortical bone area and porosity at the femoral midsection in children from post‐medieval London

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