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Molecular Pathways Regulating the Geometric Induction of Bone Formation
Published in Ugo Ripamonti, The Geometric Induction of Bone Formation, 2020
The newly formed collagenous matrix forms a network onto which the osteoblasts become embedded to secrete newly formed bone matrix. The early patterning events involve osteoclastic activity and Ca++ release on the surface of concavities of the macroporous bioreactors. Without these events, there is a delay in the differentiation of BMPs and perturbation of the proper organisational structure of the newly formed bone. Molecular profiling has unequivocally shown that bone formation takes place via the BMPs’ pathway. This was shown by the effect of the inhibitor Noggin that abrogated the signalling of the TGF-β superfamily of genes. Moreover, how hTGF-β3 is capable of inducing substantial bone when added to the 7% HA/CC macroporous devices requires further investigation. Studies now need to focus on the global changes that take place at both the gene and protein levels. Only by understanding how the microenvironment and molecular pathways function, can mechanistic aspects underlying the intrinsic induction of bone formation be manipulated for optimal results in pre-clinical and clinical contexts.
Introduction and Review of Biological Background
Published in Luke R. Bucci, Nutrition Applied to Injury Rehabilitation and Sports Medicine, 2020
The cells that produce, maintain, and repair bone are known as osteoblasts. Like chondrocytes, osteoblasts have encased themselves in extracellular matrix (bone), but unlike chondrocytes, osteoblasts enjoy a rich blood supply and direct links to adjacent osteocytes in canaliculi. The ability of osteoblasts to respond to trauma enables bone to regenerate and heal completely. Furthermore, bone is constantly being remodeled, which means that osteoblasts are periodically required to produce osseous matrix. Osteoblasts synthesize bone tissue by first depositing osteoid or organic bone matrix. Osteoid is composed of collagen, PGs, and noncollagenous proteins that resemble cartilage. Mineralization of osteoid proceeds with the assistance of specialized proteins and after removal of most PGs. Osteoblasts are hormone-responsive, which greatly affects how these cells convert nutrients into bone. Rapid mobilization of calcium and other minerals (magnesium, phosphate, zinc, copper) from lacunae surfaces is termed osteocytic osteolysis and is vital for maintenance of serum calcium levels.
Nutrition
Published in Jagdish M. Gupta, John Beveridge, MCQs in Paediatrics, 2020
Jagdish M. Gupta, John Beveridge
In rickets and prematurity the skull is soft because of inadequate calcification. In osteogenesis imperfecta there is deficiency of bone matrix. In lacunar skull there are defects in the vault in the form of depressions or 'holes' extending to the outer surface of the skull, mainly in the frontal or parietal regions. There is no softening of the skull in thalassaemia minor.
Cell and molecular toxicity of lanthanum nanoparticles: are there possible risks to humans?
Published in Nanotoxicology, 2021
Amir Mohammad Malvandi, Sara Shahba, Abbas Mohammadipour, Seyed Hamidreza Rastegar-Moghaddam, Mahmoud Abudayyak
Free La3+ ions have shown a strong tendency to competitively replace and block biological functions of the essential cellular elements, such as Ca2+ in ion-binding proteins according to similar properties, ionic radii, coordination chemistry, and electric charge. The toxicity of La3+ on metabolism can originate from its degree of deviation in charge from Ca2+, and that cations, such as La3+ tend to replace Ca2+. The bone matrix consists of 90% of hydroxyapatite (Ca10[PO4]6[OH]2). Therefore, the toxic effects of La NPs on bone hemostasis are expected through changes in Ca2+ absorption level (Dai et al. 2008). It is approved that the Ca2+ level decreases in the La2O3 NPs-treated rat bones and thus higher amounts of other bone elements are detected at the external part of the bone tissue (Dressler et al. 2020). However, it remains to understand the La2O3 NPs behavior whether the La3+ ions have replaced Ca2+ ions. An assessment of bacterial toxicity suggests that specific antibacterial activity of the La2O3 NP against Staphylococcus aureus might be attributed to the La ions replacing the Ca2+ ions (Balusamy et al. 2012). However, the probable functions of free La3+ ions are valuable to determine in the context of bone and other tissues.
Bioavailability of Calcium from Chia (Salvia hispanica L.) in Ovariectomized Rats Fed a High Fat Diet
Published in Journal of the American College of Nutrition, 2021
Marcella Duarte Villas Mishima, Bárbara Pereira da Silva, Renata Celi Lopes Toledo, Neuza Maria Brunoro Costa, Hércia Stampini Duarte Martino
With aging and post-menopause, the efficiency of calcium absorption is decreased. Low estrogen levels are known to induce bone remodeling and skeletal frailty, determinants of osteoporosis pathogenesis (1–3). Skeletal abnormalities such as bone loss occur when there is an imbalance in bone matrix synthesis and bone resorption, controlled by osteoblasts and osteoclasts, respectively. This imbalance is also caused by hormonal changes and inflammation (4). In this sense, bone resorption is affected by low estrogen in the postmenopausal period and inflammation induced by obesity. Consumption of a high fat diet increases inflammation (5), adipocyte hypertrophy stimulates the secretion of proinflammatory cytokines. In turn, these cytokines stimulate the differentiation of osteoclasts and bone resorption (6, 7). Recommendation of calcium intake is based on bone health since calcium is one of the main strategies to ensure bone construction and maintenance (8), thus its adequate intake is important (9).
Bone health and hyperglycemia in pediatric populations
Published in Critical Reviews in Clinical Laboratory Sciences, 2020
Wojciech J. Bilinski, Przemyslaw T. Paradowski, Grazyna Sypniewska
The mechanisms leading to deterioration of bone quality in diabetic conditions are illustrated in Figure 1. The most important factors involved in the pathophysiology of bone quality worsening in diabetics are AGEs that accumulate in the bone matrix and decreased circulating insulin and insulin-like growth factor 1 (IGF-1) levels [84]. In diabetes, a state of low bone turnover leads to enhanced post-translational glycation of collagen in the bone matrix, which decreases cross-link strength and increases bone fragility; simultaneously, the bone mineralization process is more complete. This could explain the higher fracture risk in subjects with T2DM despite increased or normal BMD. In vitro experiments demonstrated that accumulation of AGEs interfere with the function of osteoclasts and osteoblasts, inhibiting their maturation [77].