Osteoclasts bone-resorbing cells

Sabokbar A, Fujikawa Y, Neale S, Murrary D, Athanasou N. Human arthroplasty derived macrophages differentiate into osteoclastic bone resorbing cells. Arm Rheum Dis 1997 56 414-20. 

The results indicate that metal surfaces made of stainless steel, aluminum or titanium are corroded by human osteoclasts (bone resorbing cells) in vitro. The released ions are taken up by the osteoclasts and immune cells, which are affected in various ways, including induction of metal sensitivity reactions and enhanced activation of osteoclasts. 

Kameda T, Mano H, Yamada Y, Takai H, Amizuka N, Kobori M, Izumi N, Kawashima H, Ozawa H, Ikeda K, Kameda A, Hakeda Y, Kumegawa M. 1998. Calcium-sensing receptor in mature osteoclasts, which are bone resorbing cells. Biochem Biophys Res Commun245 419—22. 

Osteopetrosis is another rare disease in humans that has been analyzed by IR imaging. Patients with this disease have bones that are like rock, impeding their mobility and increasing their pain. In many patients, the cause of the disease is the inability of the bone resorbing cells, osteoclasts, to remodel the bone. For this reason there is a persistence of calcified cartilage. The IR data demonstrated increased mineral content and decreased crystal size, consistent with the properties seen in the bones of animal models of this disease.13... 

Bone can self-adapt and self-repair, which is conducted hy a renewal process of hone called remodeling.This process is maintained through an interplay between different bone cells the bone-forming cells (osteoblasts) and the bone-resorbing cells (osteoclasts). Osteoclasts resorb old bone and leave behind cavities that are later filled with new bone matrix by osteoblasts. The newly deposited matrix, initially collagen... 

Osteopenia (i.e., loss of bone) and osteoporosis (i.e., porous, fragile bone) are noted owing to osteoclasts (i.e., bone-resorbing cells) that are more active than osteoblasts (i.e., bone depositing cells), resulting in decreased bone density and increased bone fragility... 

Besides these basic building blocks, bone cells populated on those structures are fundamental for keeping the bone material alive—osteoblasts and the mature osteo-cytes producing extracellular matrix (ECM) including the mineralized collagen fibrils and osteoclasts, the bone-resorbing cells [8]. Finally, bone-marrow stromal cells have the important role of differentiation into preosteoblasts—and in case of injury—play pivotal benefits in bone regeneration [9]. 

Side effects may include toxic effects of implant derived metal ions [5, 6], inflammation and pain [7], and implant loosening [1, 3]. The cause for side effects is relat to metal wear and corrosive products. However, little is known about bio-corrosion of metal implants and the resulting inflammatory processes. This study focuses firstly on osteoclasts, the only, but very potent bone resorbing cells and their role in bio-corrosion and implant loosening, and secondly on immune cells that are responsible for metal ions related inflammation and pain. 

Bone metabolism comprises the processes of bone formation and bone resorption, the key actions by which skeletal mass, structure and quality are accrued and maintained throughout life. In the mature skeleton, anabolic and catabolic actions are mostly balanced due to the tight regulation of the activity of bone forming ( osteoblast) and bone resorbing ( osteoclast) cells through circulating osteotropic hormones and locally active cytokines. 

The steroid hormone 1,25-dihydroxy vitamin D3 (calcitriol) slowly increases both intestinal calcium absorption and bone resorption, and is also stimulated through low calcium levels. In contrast, calcitonin rapidly inhibits osteoclast activity and thus decreases serum calcium levels. Calcitonin is secreted by the clear cells of the thyroid and inhibits osteoclast activity by increasing the intracellular cyclic AMP content via binding to a specific cell surface receptor, thus causing a contraction of the resorbing cell membrane. The biological relevance of calcitonin in human calcium homeostasis is not well established. 

Gao and Yamaguchi, 1999b Mouse bone marrow cells cultured for 7 d with bone resorbing factors (PTH, PGE2, EPS) +/- genistein osteoclast formation assessed by TRAP enzyme Genistein (10 Yi0 M) inhibited osteoclast formation. Mechanism may involve cAMP signalling. 

Berger, C.E., Horrocks, B.R., and Datta, H.K. 1999. Direct non-genomic effect of steroid hormones on superoxide generation in the bone resorbing osteoclasts. Mol. Cell. Endocrinol. 149, 53-59. 

Steinbeck, M.J., Appel, W.H., Jr., Verhoeven, A.J., and Kamovsky, M.J. 1994. NADPH-oxidase expression and in situ production of superoxide by osteoclasts actively resorbing bone. J. Cell Biol. 126, 765-772. 

Other cells, osteoclasts, are responsible for resorb-ing (taking up) bone. These cells actually digest already-formed bone. 

Bone is a vital, dynamic connective tissue which has evolved to reflect a balance between its two major functions, provision of mechanical integrity for locomotion and protection and involvement in the metabolic pathways associated with mineral homeostatis. In addition, bone is the primary site of hemopoiesis and recent findings support its important role as a component of the immune system [1]. Bones continuously mend and rebuild themselves by opposing actions of two types of cells, the osteoblasts that form bone and the osteoclasts that resorb (destroy) bone. When the activity of the bone destroying osteoclast cell outpaces that of bone forming osteoblasts, the bottom line is bone loss and the result is osteoporosis. 

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