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Bones and fractures
Published in Henry J. Woodford, Essential Geriatrics, 2022
The key components of bone are proteins (especially collagen), cells and calcium salts. Osteoblasts are the cells that form new bone and osteoclasts are the cells that resorb it. They work in balance and, in healthy bone, this produces a constant remodelling process. Their action is coordinated by a number of growth factors, cytokines and hormones. There are two distinct types of bone, termed ‘cortical' and ‘cancellous' (or ‘trabecular'). Long bones are mainly composed of cortical bone and bones of other shapes are mainly composed of cancellous bone (e.g. the pelvis and vertebrae). The metabolism of bone is influenced by a number of external factors. Bone acts as a reservoir of calcium. Vitamin D and parathyroid hormone (PTH) influence its turnover in order to regulate serum calcium levels. The relationship between vitamin D and PTH is shown in Figure 16.1. They are discussed further, along with calcitonin, below.
Biochemistry of Exercise Training: Effects on Bone
Published in Peter M. Tiidus, Rebecca E. K. MacPherson, Paul J. LeBlanc, Andrea R. Josse, The Routledge Handbook on Biochemistry of Exercise, 2020
Panagiota Klentrou, Rozalia Kouvelioti
In understanding the pathophysiology of osteoporosis, bone turnover is an essential concept because it is this process which governs how bone is replaced, lost, or gained at certain sites and ultimately determines bone's three-dimensional structure (35). Bone turnover is considered a continuous process of constant removal and replacement of volumes of bone tissue, conducted by osteoclasts and osteoblasts, in both cortical and trabecular bone (35). Under normal conditions, the processes of bone formation and resorption are coupled to one another, and the maintenance of skeletal balance is achieved through the action of various hormones and local mediators (140). Osteoclasts burrow into bone, forming cavities where osteoblasts can deposit new bone resulting in the formation of new osteons. This process also results in the liberation of calcium and phosphate into the bloodstream. Bone homeostasis is achieved when the amount of bone resorbed is replaced by a similar amount of newly synthesized bone. A sustained increase in the ratio of osteoclast to osteoblast activity may eventually result in osteoporosis. Therefore, the activity of osteoclasts and osteoblasts is not only important in establishing the calcium and phosphate levels necessary for particular bodily functions but also in maintaining the structural integrity of bone.
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.
Morroniside ameliorates glucocorticoid-induced osteoporosis and promotes osteoblastogenesis by interacting with sodium-glucose cotransporter 2
Published in Pharmaceutical Biology, 2023
Hou-Zhi Yang, Runbei Dong, Yutao Jia, Yuqiao Li, Gan Luo, Tianhao Li, Yao Long, Shuang Liang, Shanshan Li, Xin Jin, Tianwei Sun
Osteoblasts are critical cells in bone formation to promote bone synthesis and mineralization, playing a significant role in bone formation (Jilka et al. 2014). In osteoporotic patients, decreased proliferation and differentiation of osteoblasts are the most common pathological processes (Lee et al. 2017). Therefore, promoting the proliferation and differentiation of osteoblasts is critical in preventing and treating OP. Although significant progress in exploring the anti-OP effects of MOR has been made, the molecular targets and the mechanisms underlying MOR functions remain largely unknown. Here, we established a glucocorticoid-induced OP zebrafish model to evaluate the anti-OP function of MOR. We demonstrated that MOR could improve glucocorticoid-induced OP and promote osteoblast proliferation and differentiation. Mechanistically, its action may be associated with SGLT2 interaction. This study provides new insight into the pharmacological mechanism of MOR and reveals a potential therapeutic target for glucocorticoid-induced OP.
Acteoside Derived from Cistanche Improves Glucocorticoid-Induced Osteoporosis by Activating PI3K/AKT/mTOR Pathway
Published in Journal of Investigative Surgery, 2023
Shumei Li, Yajie Cui, Min Li, Wenting Zhang, Xiaoxue Sun, Zhaoxu Xin, Jing Li
Osteoblast differentiation is essential for bone formation. Previous studies have demonstrated that ALP activity is a marker of osteoblast maturation and mineralization and may indirectly reflect the function of osteoblasts. Runx2 and osterix are key transcription factors for osteoblast differentiation, where Runx2 is an upstream regulatory element of osterix that activates the transcription of a series of downstream osteogenic genes and is the master switch for osteogenic factor regulation.COL1A1 is the most abundant matrix protein in bone tissue, accounting for approximately 90% of the organic matrix of bone, and a marker of bone differentiation and maturation [32]. In our study, we found that Dex typically inhibited ALP activity and attenuated mRNA levels of Runx2, osterix, and COL1A1 in both in vivo rat model serum and in vitro osteoblast cell lines, suggesting that osteoblast differentiation was significantly inhibited in GIOP. In contrast, ACT significantly reversed this inhibition and restored osteogenic differentiation.
Romosozumab for the treatment of postmenopausal women at high risk of fracture
Published in Expert Opinion on Biological Therapy, 2023
Piet Geusens, Natasha Appelman-Dijkstra, Willem Lems, Joop van den Bergh
In the context of bone metabolism in humans, the canonical Wnt signaling pathway is a major regulator [39–41]. When Wnt ligands bind to LRP5 or LRP6 and Frizzled co-receptors at the cell surface, this stabilizes the accumulation of intracellular β-catenin. After translocation to the nucleus, β-catenin binds to transcription factors, so that the transcription of bone formation stimulating target genes is started. Bone remodeling is controlled by osteocytes, differentiated osteoblasts, which are embedded in the mineralized matrix and secrete sclerostin, a negative regulator of bone formation produced mainly in the skeleton, but also in chondrocytes, multiple myeloma cells and fibroblast-like synoviocytes [42–47]. When osteocytes produce sclerostin, the osteocyte dendritic network allows it to be transported to the bone surface. There it binds to LRPs, which antagonizes downstream signaling of β-catenin. As a result, the proliferation, differentiation, and survival of osteoblasts is inhibited. In addition, sclerostin also has an autocrine function by upregulating RANKL synthesis in osteocytes which then stimulates osteoclastogenesis. The regulation of sclerostin production is complex and regulated by several mechanisms, including hormones and mechanical load [48–53] (Figure 1).