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Khurana - Bone Pathology

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Khurana Bone Pathology

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Jasvir S. Khurana (ed.) Bone Pathology 10.1007/978-1-59745-347-9_1 Humana Press, a part of Springer Science+Business Media, LLC 2009
1. Bone Structure, Development and Bone Biology
Fayez F. Safadi 1, Mary F. Barbe 2, Samir M. Abdelmagid 3, Mario C. Rico 4, Rulla A. Aswad 5, Judith Litvin 6 and Steven N. Popoff 7
(1)
Department of Anatomy and Cell Biology, Temple University School of Medicine, Philadelphia, PA 19140, USA
(2)
Department of Physical Therapy, College of Health Professions; Department of Anatomy and Cell Biology, Temple University School of Medicine, Philadelphia, PA 19140, USA
(3)
Department of Plastic and Reconstructive Surgery, Children Hospital of Philadelphia, University of Pennsylvania, Philadelphia, PA 19104, USA
(4)
Department of Physiology, Temple University School of Medicine, Philadelphia, PA 19140, USA
(5)
Department of Periodontology and Oral Implantology, Kronberg School of Dentistry, Temple University, Philadelphia, PA, 19140, Pennsylvania
(6)
Department of Anatomy and Cell Biology, Temple University School of Medicine, Philadelphia, PA 19140, USA
(7)
Department of Anatomy and Cell Biology, Temple University School of Medicine, Philadelphia, PA 19140, USA
Abstract
The skeleton serves as an internal structural support system for vertebrates. It has mechanisms to grow and change in shape and size to suit varying stressors including the ability to resist the mechanical forces. In addition, bone is a major source of inorganic ions, and actively participates in the bodys calcium/phosphate balance.
Bone tissue is continuously formed and remodeled throughout life. Initially, the bone achieves its increase in size and shape through growth (increase in size) and a complicated process known as skeletal modeling . In late childhood and adulthood there is continuous renewal of the skeleton via a process termed remodeling. Both modeling and remodeling require two separate processes namely bone resorption and bone formation to occur simultaneously to be effective. This requirement is known as coupling.
Keywords
Runx-2 (runt-related transcription factor 2) cbfa-1 (core binding factor alpha1) Pebp2aA (Polyoma enhancer binding protein 2aA) Osterix cleidocranial dysplasia osteopontin Leptin osteoblast specific factor-1, N-syndecan osteoblast/osteocyte factor-45 (OF45) dentin matrix protein 1 fibroblast growth factor 23 sclerostin Sclerosteosis SOST gene osteocyte osteoclastogenesis parathyroid hormone 1, 25 dihydroxyvitamin D3 transforming growth factor alpha epidermal growth factor tartrate resistant acid phosphatase osteoprotegerin integrins integral membrane proteins fibronectin collagen type I bone sialoprotein II osteopontin suppressor of cytokine signaling-1 osteoclast-associated receptor apposition growth plate drosophila sarcolemma myofilaments motorend plate somites skeletogenesis osteoactivin biglycan decorin calcitonin calcitriol bone morphogenetic proteins connective tissue growth factor
Introduction
The skeleton serves as an internal structural support system for vertebrates. It has mechanisms to grow and change in shape and size to suit varying stressors including the ability to resist the mechanical forces. In addition, bone is a major source of inorganic ions, and actively participates in the bodys calcium/phosphate balance.
Bone tissue is continuously formed and remodeled throughout life. Initially, the bone achieves its increase in size and shape through growth (increase in size) and a complicated process known as skeletal modeling . In late childhood and adulthood there is continuous renewal of the skeleton via a process termed remodeling. Both modeling and remodeling require two separate processes namely bone resorption and bone formation to occur simultaneously to be effective. This requirement is known as coupling.
Overview
Bone forms the skeletal framework of all vertebrates. It is a composite tissue consisting of organic matrix, inorganic minerals, cells, and water. Bone is formed by the hardening of this matrix entrapping osteoblasts which then become osteocytes.
The inorganic portion of bone matrix is composed mainly of crystalline calcium phosphate salts, present in the form of hydroxylapatite. This allows bone to serve as a reservoir of calcium and phosphate that can be stored or mobilized in a controlled fashion. Bone also contains carbonate, fluoride, acid phosphate, magnesium, and citrate. Hydroxyapatite crystals also form in tissues that are not normally calcified, including in atherosclerotic plaque, in soft tissues of some patients with abnormally high circulating calcium or phosphate, and in articular cartilage of some patients with degenerative joint diseases. Crystals in these situations are often distinctly larger.
The organic component of bone matrix comprises 40% of the dry weight of bone. Most of the organic component is Type I collagen, which is synthesized intracellularly as tropocollagen and then exported as collagen fibrils. Pathological disorders of the bone matrix exist, such as osteogenesis imperfecta , a disorder caused by a defect in Type I collagen. This defect results in less organized bone with loss of normal osteon structure. With loss of normal osteons, which function to withstand deformation, the bone fails (fractures) with only minimal amounts of force. In addition to collagen, bone matrix is composed of proteoglycans, glycoproteins, phosopholipids and phosphoproteins, as well as various growth factors including osteocalcin, osteonectin, and bone sialoprotein.
Bones are fashioned in the form of a hollow tube or a bilaminar plate of bone, each commonly termed compact bone . Additionally, the architecture is strengthened by internal struts of trabecular bone that follow the lines of stress. Trabecular or cancellous bone is a metabolically active component of bone and has about nine times greater turnover than the outer compact bone. This kind of design is known in engineering terms as composite and allows bone to take advantage of the strength of components. This type of design also allows bone to resist mechanical compression and able to deform significantly before failing (i.e. breaking).
Part 1 Bone Structure
Macroscopic Features of Bone
At the gross level, bone can be broadly categorized into five types: long bones (femur, tibia, ulna and radius), short bones (carpal bones of the hand), flat bones (skull, sternum and scapula), irregular shaped bones (vertebra and ethmoid), and sesamoid bones (bones embedded in tendons). These bones form through different mechanisms during embryonic development. The long bones form by endochondral mechanisms, while the flat bones form by intramembranous mechanisms. These processes are discussed later in this chapter. Both long and flat bones are organized with a hard, but relatively thin, outer region composed of dense, compact bone called the cortex or cortical bone . Inside the cortex is the marrow cavity containing hematopoietic elements, fat and spicules of bone. The bone spicules are also referred to as trabecular, spongy , or cancellous bone (Fig. ).
Fig 1 Adult long bone Sagittal section through long bone showing the - photo 1
Fig. 1
Adult long bone . Sagittal section through long bone showing the internal structure of the bone. Note the outer dense compact bone (also called cortical bone) and the inner cancellous bone filled with spicules (trabeculae), these latter small bundles of bone traverse the inner substances of bone and are usually interconnected with one another.
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