Reduction and Fixation of Sacroiliac joint Dislocation by the Combined Use of S1 Pedicle Screws and an Iliac Rod
Kai-Uwe Lewandrowski, Donald L. Wise, Debra J. Trantolo, Michael J. Yaszemski, Augustus A. White in Advances in Spinal Fusion, 2003
Osteoblasts are bone-building cells and are responsible for bone formation, maintenance, and degradation through their influence on osteoclast function. They are mesenchymal stem cells (MSC) derivatives and proceed through a number of osteoblastic iterations throughout their lifecycle. This cycle begins after the MSC is exposed to the appropriate environmental cues, both chemical and mechanical, and starts to express various preosteoblast characteristics. This includes expression of nuclear transcription factors such as core binding factor alpha 1 (CBFA1), protein production to include alkaline phosphatase and collagen type I (col I), and responsiveness to growth factors and cytokines such as prostaglandin (PGE2), epidermal growth factor (EGF), and transforming growth factor (31 (TGF-(31) [1-3]. Determination of the osteoblast phenotype by morphology alone is near impossible; therefore, functional classification based on extracellular matrix (ECM) is preferred. As the osteoblast matures, protein production alters and the ECM develops into mature bone matrix with the addition of osteopontin, osteonectin, and osteocalcin, all of which are important for mineralization of the osteoid either in the development or in the ossifying callus of the spinal fusion site. Osteoclasts
Evaluation of PCL/Chitosan/Nanohydroxyapatite/Tetracycline Composite Scaffolds for Bone Tissue Engineering
Naznin Sultana, Sanchita Bandyopadhyay-Ghosh, Chin Fhong Soon in Tissue Engineering Strategies for Organ Regeneration, 2020
In this chapter, PCL/chitosan-based scaffolds were fabricated for bone tissue engineering applications. Normal human osteoblast cell studies will provide insight into the performance of the scaffolds as an implant for bone regeneration. The osteoblast is a fully differentiated cell that is responsible for the synthesis and mineralization of bone during bone formation and remodeling. It can produce many cell products such as the enzymes alkaline phosphate and collagenase, growth factors, hormones and many others (Velasco et al. 2015). VEGF growth factors were used as their “enhanced vascularization” provides abundant osteoprogenitor cells to the defect site along with a direct stimulating effect on the osteoblast migration and differentiation, leading to higher bone deposition” (Bose et al. 2012).
Postnatal Bone Growth: Some Methods of Assessment
D. Dixon Andrew, A.N. Hoyte David, Ronning Olli in Fundamentals of Craniofacial Growth, 2017
Although growth of bones is greatest in the young, nevertheless bone tissue is in a state of continuous change throughout life as a result of an interplay of formation and destruction. In regions where bone is being apposed, osteoblasts are found arranged in a continuous single layer, like cuboidal epithelium, on the surface of the bone. Osteoclasts are found in areas where bone is being destroyed or resorbed. The osteoclasts are multinucleated giant cells of varying size and shape and are found in shallow hollows (Howship’s lacunae) on the surface of the bone trabeculae. The process of bone formation and destruction, and the role of the osteoclasts and osteoblasts are at best incompletely understood (Marks and Popoff, 1988). Bhaskar (1953) compared the prenatal and postnatal growth, and development of the mandible in normal rats and in those characterized by retardation of bone resorption.
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.
MiR-152 influences osteoporosis through regulation of osteoblast differentiation by targeting RICTOR
Published in Pharmaceutical Biology, 2019
Li Feng, Bo Xia, Bao-Fang Tian, Gong-Biao Lu
Osteoporosis is a relatively prevalent degenerative disease that mainly leads to loss of bone mass and microstructural deterioration of bone tissues and eventually increases the susceptibility of patients to bone fractures (Rachner et al. 2011). As estimated, it is more prevalent in middle-aged and elderly people, and especially, postmenopausal women had approximately over 60% incidence, posing a large threat to the health of the elderly population (Li et al. 2013; Spilmont et al. 2014). Osteoporosis has been generally believed as the consequence of osteoclast-regulated bone resorption exceeding osteoblast-regulated bone formation in the process of bone remodelling (Harvey et al. 2014). In a factual manner, the restoration and maintenance of the balance between bone formation and bone resorption constitutes an effective perspective in the clinical treatment of osteoporosis (Marie and Kassem 2011). Meanwhile, osteoblast is the major cell type of bone formation, playing important roles in metabolic balance, growth and damage repair of bone tissues (Li et al. 2015). Thus, exploring new targets for controlling osteogenesis of osteoblasts would provide new strategies and methods for the treatment of osteoporosis.
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.