Sean Gallagher

Musculoskeletal Disorders


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lining cells, osteocytes, and osteoclasts (Figure 3.17). They also contain nervous tissue, epithelial cells, and various types of hematopoietic cells. During bone growth and remodeling, there is a delicate balance between osteoblast and osteoclast function. This balance is orchestrated by osteocyte signaling, which dictates the outcome of loading on bone.

       Osteoblasts—the producers of bone matrix

Photos depict bone cells.

       Bone lining cells—effector cells on standby

       Osteocytes—the mechanotransducers and maintainers of bone

      Osteocytes are mature bone cells that live within the substance of bone and comprise 90–95% of all bone cells (Bonewald, 2007). Osteocytes are embedded in spaces (lacunae) in the interior of bone and are connected to adjacent cells by long cytoplasmic processes radiating from the cell body that lie within channels (canaliculi) throughout the mineralized matrix of bone (Figure 3.17) (Hirose et al., 2007; Lian & Stein, 2008). The processes of adjacent osteocytes make contact via gap junctions as well as with the osteoblasts and bone lining cells, maintaining the vitality of osteocytes by passing nutrients and metabolites between blood vessels and distant osteocytes (Jiang, Siller‐Jackson, & Burra, 2007).

      Osteocytes are believed to be the bone‐sensing cells involved in mechanotransduction and thus the key regulators of bone remodeling. The gap junctions mentioned earlier aid in this function. Also, the osteocyte cell membrane is surrounded by interstitial fluid and extracellular matrix in which microtubules are embedded in order to transmit extracellular matrix mechanical changes to the osteocyte’s actin filaments (Bakker et al., 2009). Osteocytes also communicate with surrounding cells via the release of biochemical factors and signaling molecules, such as bone morphogenetic proteins (BMPs), prostaglandin E2 (PGE2), and nitric oxide (NO) (Klein‐Nulend, Bacabac, & Bakker, 2012).

      Osteocytes are also actively involved in maintaining the bony matrix. They express osteoblast stimulating factor‐1 after mechanical or muscular loading (Klein‐Nulend & Bonewald, 2008). Osteocytes send inhibitory signals to osteoclasts to prevent bone loss during normal loading (Nakashima et al., 2011). Local damage (microcracks) of the osteoid matrix can compromise the osteocyte environment, disrupting the fluid flow, consequently reducing nutrients and oxygen supply to the embedded cells and creating oxidative stress (Al‐Dujaili et al., 2011).

       Osteoclasts—reallocate and remodel bone

      Osteoclasts differentiate after the fusion of bone marrow‐derived mononuclear precursor cells of the monocyte–macrophage lineage in a process termed osteoclastogenesis. Osteoclasts are large multinucleated cells with a ruffled bottom in contact with the bone matrix (Figure 3.17d). They work in concert with osteoblasts in the constant turnover and remodeling of bone. They do this via their ability to secrete hydrochloric acid and other degradative enzymes, which, once activated, dissolve the bone matrix, creating a resorption pit underneath the cell. Osteoclasts are regulated by parathyroid hormone, calcitonin (from the thyroid gland), and pro‐inflammatory cytokines (Boyce & Xing, 2007; Brabnikova Maresova, Pavelka, & Stepan, 2013; Nakashima & Takayanagi, 2011). As mentioned earlier, osteoclast activation is also mediated by the binding of osteoblast or osteocyte produced RANKL (a protein that plays an essential role in the recruitment, differentiation, activation, and survival of osteoclasts) (Burgess et al., 1999). Estrogen has a dual effect: Its presence increases bone formation and reduces bone resorption by enhancing osteoblast proliferation and function (Ernst, Heath, & Rodan, 1989; Majeska, Ryaby, & Einhorn, 1994); it also reduces bone turnover by reducing osteoclast activity (Hofbauer et al., 1999).

      Extracellular matrix

      Organization