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Review Article Biology of Bone Tissue: Structure, Function, and Factors That Influence Bone Cells

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Review Article Biology of Bone Tissue: Structure, Function, and Factors That Influence Bone Cells Hindawi Publishing Corporation BioMed Research International Volume 2015, Article ID 421746, 17 pages http://dx.doi.org/10.1155/2015/421746 Review Article Biology of Bone Tissue: Structure, Function, and Factors That Influence Bone Cells Rinaldo Florencio-Silva,1 Gisela Rodrigues da Silva Sasso,1 Estela Sasso-Cerri,2 Manuel Jesus Simões,1 and Paulo Sérgio Cerri2 1 Department of Morphology and Genetics, Laboratory of Histology and Structural Biology, Federal University of Sao˜ Paulo, 04023-900 Sao˜ Paulo, SP, Brazil 2Department of Morphology, Laboratory of Histology and Embryology, Dental School, Universidade Estadual Paulista (UNESP), 14801-903 Araraquara, SP, Brazil Correspondence should be addressed to Paulo Sergio´ Cerri; [email protected] Received 3 December 2014; Revised 30 April 2015; Accepted 4 May 2015 Academic Editor: Wanda Lattanzi Copyright © 2015 Rinaldo Florencio-Silva et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Bone tissue is continuously remodeled through the concerted actions of bone cells, which include bone resorption by osteoclasts and bone formation by osteoblasts, whereas osteocytes act as mechanosensors and orchestrators of the bone remodeling process. This process is under the control of local (e.g., growth factors and cytokines) and systemic (e.g., calcitonin and estrogens) factors that all together contribute for bone homeostasis. An imbalance between bone resorption and formation can result in bone diseases including osteoporosis. Recently, it has been recognized that, during bone remodeling, there are an intricate communication among bone cells. For instance, the coupling from bone resorption to bone formation is achieved by interaction between osteoclasts and osteoblasts. Moreover, osteocytes produce factors that influence osteoblast and osteoclast activities, whereas osteocyte apoptosis is followed by osteoclastic bone resorption. The increasing knowledge about the structure and functions of bone cells contributed to a better understanding of bone biology. It has been suggested that there is a complex communication between bone cells and other organs, indicating the dynamic nature of bone tissue. In this review, we discuss the current data about the structure and functions of bone cells and the factors that influence bone remodeling. 1. Introduction three phases: (1) initiation of bone resorption by osteoclasts, (2) the transition (or reversal period) from resorption to new Bone is a mineralized connective tissue that exhibits four bone formation, and (3) the bone formation by osteoblasts types of cells: osteoblasts, bone lining cells, osteocytes, and [10, 11]. This process occurs due to coordinated actions osteoclasts [1, 2]. Bone exerts important functions in the of osteoclasts, osteoblasts, osteocytes, and bone lining cells body, such as locomotion, support and protection of soft which together form the temporary anatomical structure tissues, calcium and phosphate storage, and harboring of called basic multicellular unit (BMU) [12–14]. bone marrow [3, 4]. Despite its inert appearance, bone is a Normal bone remodeling is necessary for fracture healing highly dynamic organ that is continuously resorbed by osteo- andskeletonadaptationtomechanicaluse,aswellasfor clasts and neoformed by osteoblasts. There is evidence that calcium homeostasis [15]. On the other hand, an imbalance osteocytes act as mechanosensors and orchestrators of this of bone resorption and formation results in several bone bone remodeling process [5–8]. The function of bone lining diseases. For example, excessive resorption by osteoclasts cells is not well clear, but these cells seem to play an important without the corresponding amount of nerformed bone by role in coupling bone resorption to bone formation [9]. osteoblasts contributes to bone loss and osteoporosis [16], Bone remodeling is a highly complex process by which whereas the contrary may result in osteopetrosis [17]. Thus, oldboneisreplacedbynewbone,inacyclecomprisedof the equilibrium between bone formation and resorption is 2 BioMed Research International Oc B B BV Ot B BV Ob Ob B (a) (b) Ob B B B Ob B B B (c) (d) Figure 1: (a)–(d) Light micrographs of portions of alveolar bone of rats. (a) HE-stained section showing a portion of a bony trabecula (B). Polarized osteoblasts (Ob) and giant multinucleated osteoclasts (Oc) are observed in the bone surface; osteocyte (Ot) surrounding bone matrix is also observed. (b) Section subjected to immunohistochemistry for osteocalcin detection and counterstained with hematoxylin. Note osteocalcin-positive osteoblasts (arrows) on the surface of a bony trabecula (B). BV: blood vessel. (c) Undecalcified section subjected to the Gomori method for the detection of alkaline phosphatase, evidencing a portion of bone matrix (B) positive to the alkaline phosphatase (in brown/black). Ob: osteoblasts. (d) Undecalcified section subjected to the von Kossa method for calcium detection (brown/dark color). von Kossa-positive bone matrix (B) is observed; some positive granules (arrow) can also be observed on the surface of the bone trabeculae. Scale bar: 15 m. necessary and depends on the action of several local and as various secretory vesicles [22, 23]. As polarized cells, the systemic factors including hormones, cytokines, chemokines, osteoblasts secrete the osteoid toward the bone matrix [24] and biomechanical stimulation [18–20]. (Figures 1(a), 1(b),and2(a)). Recent studies have shown that bone influences the Osteoblasts are derived from mesenchymal stem cells activity of other organs and the bone is also influenced by (MSC). The commitment of MSC towards the osteopro- otherorgansandsystemsofthebody[21], providing new genitor lineage requires the expression of specific genes, insights and evidencing the complexity and dynamic nature following timely programmed steps, including the synthesis of bone tissue. of bone morphogenetic proteins (BMPs) and members of In this review we will address the current data about bone the Wingless (Wnt) pathways [25]. The expressions of Runt- cellsbiology,bonematrix,andthefactorsthatinfluencethe related transcription factors 2, Distal-less homeobox 5 (Dlx5), bone remodeling process. Moreover, we will briefly discuss and osterix (Osx) are crucial for osteoblast differentiation theroleofestrogenonbonetissueunderphysiologicaland [22, 26]. Additionally, Runx2 is a master gene of osteoblast pathological conditions. differentiation, as demonstrated by the fact that Runx2-null mice are devoid of osteoblasts [26, 27]. Runx2 has demon- 2. Bone Cells strated to upregulate osteoblast-related genes such as ColIA1, ALP, BSP, BGLAP,andOCN [28]. 2.1. Osteoblasts. Osteoblastsarecuboidalcellsthatarelocated Once a pool of osteoblast progenitors expressing Runx2 along the bone surface comprising 4–6% of the total resident and ColIA1 has been established during osteoblast differenti- bone cells and are largely known for their bone forming ation, there is a proliferation phase. In this phase, osteoblast function [22].Thesecellsshowmorphologicalcharacteristics progenitors show alkaline phosphatase (ALP) activity, and of protein synthesizing cells, including abundant rough endo- are considered preosteoblasts [22]. The transition of pre- plasmic reticulum and prominent Golgi apparatus, as well osteoblasts to mature osteoblasts is characterized by an BioMed Research International 3 and the fibrillar phases [40, 41]. The vesicular phase occurs when portions with a variable diameter ranging from 30 to 200 nm, called matrix vesicles, are released from the apical Ob membrane domain of the osteoblasts into the newly formed Ob bone matrix in which they bind to proteoglycans and other B organic components. Because of its negative charge, the Otd Ob B sulphated proteoglycans immobilize calcium ions that are stored within the matrix vesicles [41, 42]. When osteoblasts Otd secrete enzymes that degrade the proteoglycans, the calcium B ions are released from the proteoglycans and cross the (a) calcium channels presented in the matrix vesicles membrane. These channels are formed by proteins called annexins [40]. On the other hand, phosphate-containing compounds are BLC N degraded by the ALP secreted by osteoblasts, releasing phos- Otd phate ions inside the matrix vesicles. Then, the phosphate N Otd and calcium ions inside the vesicles nucleate, forming the B hydroxyapatite crystals [43]. The fibrillar phase occurs when the supersaturation of calcium and phosphate ions inside the (b) matrix vesicles leads to the rupture of these structures and the hydroxyapatite crystals spread to the surrounding matrix Figure 2: Electron micrographs of portions of alveolar bone of rats. [44, 45]. (a) Oteoblasts exhibiting abundant rough endoplasmic reticulum are observed adjacent to the bone (B) surface. A layer of bundles Mature osteoblasts appear as a single layer of cuboidal of collagen fibrils situated between osteoblasts (Ob) and calcified cells containing abundant rough endoplasmic reticulum and bone surface (B) constitutes the osteoid (Otd). Scale bar: 2.7 m. (b) large Golgi complex (Figures 2(a) and 3(a)). Some of these Bone lining cells (BLC) exhibiting scarce cytoplasm are situated on osteoblasts show cytoplasmic processes towards the bone the osteoid surface (Otd). Bone lining cells (BLC) extend some thin matrix and reach the osteocyte processes [46]. At this stage, cytoplasmic
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