Physical and functional growth and development
Nick Draper, Helen Marshall in Exercise Physiology, 2014
Nearly all bones begin life as cartilage. Both are forms of connective tissue but cartilage is more elastic in nature and therefore less rigid. During the formation of cartilage, chondroblasts (cartilage forming cells) become entrapped in their own network or matrix and develop into chondrocytes (cartilage cells). Most of the skeletal cartilage is replaced by bone as the body develops in a process called ossification. Three types of bone cell are involved in the growth, repair and remodeling of bone tissue. In a similar fashion to cartilage, bone-forming osteoblasts, which combine calcium and phosphorus to produce hydroxyapatite crystals (the mineralised form of bone), become osteocytes when entrapped in their own mineral network. Osteoclasts (from the Greek words for bone and broken), the third form of bone cell, are responsible for the removal and resorption of unwanted bone or the breakdown of bone when the minerals are required elsewhere in the body. While osteocytes are trapped within the matrix of the bone, osteoclasts, which are large multinucleated cells, are free to move along the bone surface as they remove and repair damaged sections of the bone matrix.
Pathophysiology of Fluorosis and Calcium Dose Prediction for Its Reversal in Children: Mathematical Modeling, Analysis, and Simulation of Three Clinical Case Studies
P. Mereena Luke, K. R. Dhanya, Didier Rouxel, Nandakumar Kalarikkal, Sabu Thomas in Advanced Studies in Experimental and Clinical Medicine, 2021
The presence of increased PTH in the blood stream is responsible for the following two major body mechanisms: Significant Loss of Bone Mass: Bone loss is due to increase in the number of osteoblasts and the increase of their activity [9, 10] which causes the stimulation of bone resorption and depletion of bone mass as well as its formation. Osteoclast is a type of bone cell that resorbs bone tissue. Under the normal conditions, where there is an increase in bone resorption, it gets coupled with an effective compensatory increase in an equal magnitude of bone formation and therefore no net bone mass is depleted in the skeletal system. However, during the adjustor mechanism if there is a demand to mobilize calcium from skeletal system to counteract the effects of hypocalcemia, then the bone coupling process gets compromised.Depletion of Bone Formation: It has been reported that despite the effectiveness in a significant increase in bone resorption, bone formation decreased and was significantly inhibited due to PTH [9]. Therefore, the combination of various combined actions such as calcium depletion, bone resorption and decrease in its formation led to a significant loss of bone mass [9].
Cellular and Molecular Basis of Human Biology
Lawrence S. Chan, William C. Tang in Engineering-Medicine, 2019
Many cells in the human body are stationary in nature, that means that they stay in certain body location all their lives. Major stationary cells include the followings: Epithelial cells (of the skin, mucous membranes, hair follicles, cornea, retina, and lining of esophagus, intestines, and bladders).Fibroblasts (cells that produce many extracellular matrices like collagens).Melanocytes (pigment-producing cells of skin, mucous membrane, retina, and iris).Endothelial cells (of the lining of blood or lymphatic vessels).Neurons (of the nerve and brain).Muscle cells (cells that constitute the muscle mass).Bone-building cells (osteoblasts).Bone-breakdown cells (osteoclasts), and many more.
Updating the pathophysiology of arthritic bone destruction: identifying and visualizing pathological osteoclasts in pannus
Published in Immunological Medicine, 2021
Tetsuo Hasegawa
Macrophages follow distinct developmental pathways in response to environmental stimuli in each organ and differentiate into osteoclasts in the bone marrow (BM) cavity. Osteoclasts are myeloid lineage multinucleated cells that have a unique bone-destroying capacity. Macrophage-colony stimulating factor (M-CSF) and receptor activator of NF-κB ligand (RANKL) are essential for their differentiation [1–3], and osteoclasts support steady-state bone remodeling in the BM together with osteoblasts. In contrast, osteoclasts are also involved in pathological joint destruction in patients with rheumatoid arthritis (RA). Synovial inflammation induced by autoimmunity affects the outer surface of articular bone, eventually causing permanent joint destruction. Although the osteoclast precursor (OP)-containing population has been studied extensively in the BM of arthritic mice [4,5], no precise analysis of OPs has been performed in the inflamed synovium, the site of bone erosion in arthritis. Many questions remain regarding pathological osteoclastogenesis in arthritis. Is there a specific subpopulation within OP-containing population that actually differentiates into mature pathological osteoclasts in the synovium? Does the manner of bone resorption by pathological osteoclasts in the joint differ from that of osteoclasts in the BM? Are the osteoclasts formed at the pannus–bone interface derived from BM cells or resident synovial macrophages?
Monoclonal antibodies against RANKL and sclerostin for myeloma-related bone disease: can they change the standard of care?
Published in Expert Review of Hematology, 2019
Martina Kleber, Ioannis Ntanasis-Stathopoulos, Meletios A. Dimopoulos, Evangelos Terpos
Physiological conditions in the bone are defined by a dynamic and balanced process where osteoblasts and osteoclasts remodel bone via bone formation and bone resorption, respectively [11]. Osteoclasts and osteoblasts are mainly involved in bone remodeling and they are supported by osteocytes, cytokines, and hormones. Osteoclasts are multinucleated cells originating from hematopoietic stem cells and mature monocyte-macrophage lineage [27], which are the only cells known to cause bone resorption. Osteoclasts contain multiple proteins such as tartrate-resistant acid phosphatase (TRAP), tartrate-resistant trinucleotide phosphatase, carbonic anhydrase II, calcitonin receptors, and cathepsins (lysosomal) [28]. Osteoblasts are differentiated from mesenchymal stem cells and create the bone matrix by collagen synthesis, osteocalcin production, and mineralization [29]. Osteocytes play a key role in controlling the osteoblastic and osteoclastic activity by secreting cytokines such as sclerostin, DKK1, RANKL, and osteoprotegerin (OPG) to regulate the activity of these cells [27,30].
Cysteinyl leukotriene receptor 1 (cysLT1R) regulates osteoclast differentiation and bone resorption
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2018
Chao Zheng, Xiaoming Shi
Bone is an extensively dynamic structure, which is continuously remodelled to maintain homeostasis [1]. Bone remodelling is mainly regulated by osteoblasts and osteoclasts. Osteoclasts play a pivotal role in bone resorption, while osteoblasts are responsible for bone formation [2]. Excessive bone resorption caused by abnormal activation of osteoclasts results in bone diseases such as rheumatoid arthritis and osteoporosis [3]. Osteoclasts are derived from myeloid lineage cells by cellular differentiation caused by physiological factors, such as macrophage-colony stimulating factor (M-CSF) and receptor activator of nuclear factor κB (NF-κB) ligand (RANKL) [4]. M-CSF is important for maintaining the proliferation and survival of osteoclast precursor cells [5]. RANKL initiates osteoclast differentiation by activating mitogen-activated protein (MAP) kinases and NF-κB by recruiting TNF receptor-associated factor 6 (TRAF6) to its specific receptor RANK [6]. Additionally, phosphorylation of phospholipase Cγ (PLCγ) activates the Ca2+/NFATc1 signalling pathway, which is important in osteoclastogenesis [7]. RANKL also induces the expression of tartrate-resistant acid phosphatase (TRAP), which is a marker gene of osteoclastogenesis [8]. The regulatory mechanisms of osteoclast differentiation are complex. Successful identification of novel signalling pathways governing osteoclast differentiation is helpful for exploring therapeutic targets for osteoporosis.