Bone (redirected from chevron bone)

bone, hard tissue that forms the skeleton of the body in vertebrate animals. In the very young, the skeleton is composed largely of cartilage and is therefore pliable, reducing the incidence of bone fracture and breakage in childhood. The inorganic, or mineral, content of bone is mainly calcium, phosphate and carbonate minerals. The organic content is a gelatinous material called collagen. As the body grows older, decreases in bone mass may lead to an increased vulnerability to fractures. Bone fractures heal naturally, although they are often aided through restriction of movement in the affected area. Bones assume a variety of sizes and shapes; however, all bone tissue has a three-layered composition. A spongy layer forms the interior. Long bones (such as those in the arms and legs) are hollow, the inner spaces being filled with marrow (see bone marrow), important in the formation of blood cells. Surrounding the spongy, inner layer is a hard, compact layer that functions as the basic supportive tissue of the body. The outer layer is a tough membrane called the periosteum, which sheaths most bones. Although bone appears solid, it contains numerous microscopic canals permitting the passage of blood vessels and nerve fibers. Two types of bone are present in most bones: compact, which constitutes the shaft, and cancellous, an extremely strong variety which makes up the enlarged ends of the bone. See also osteoporosis.

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bone

Internal structure of a human long bone, with a magnified cross section of the interior. The …

(credit: © Merriam-Webster Inc.)

Rigid connective tissue of vertebrates, consisting of cells embedded in a hard matrix. Bones serve as the body's supporting framework, provide muscle-attachment points for movement, protect the internal organs, house the blood-cell formation system (red bone marrow), and hold about 99% of the calcium vital to many body processes. Bone consists of a matrix of crystals of calcium, chiefly the phosphate and carbonate, embedded among collagen fibres, providing strength and elasticity, and bone cells (less than 5% of its volume). An external layer of compact bone surrounds a central area of spongy bone, except at the marrow cavity. Bone does not grow by cell division; instead, different types of bone cells generate bone matrix, break it down, and maintain it. Bone is remodeled by this process, which strengthens it in areas under greatest stress, permits healing of fractures, and helps regulate calcium levels in body fluid (see calcium deficiency). The process also causes underutilized bone, as in an immobilized limb, to atrophy. Bone disorders include rheumatoid arthritis, osteoarthritis, rickets, osteoporosis, and tumours. Bone can fracture suddenly or over time, as in stress fractures.

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Bone

The hard connective tissue that, together with cartilage, forms the skeleton of humans and other vertebrates. It is made of calcium phosphate crystals arranged on a protein scaffold. Bone performs a variety of functions: it has a structural and mechanical role; it protects vital organs; it provides a site for the production of blood cells; it serves as a reserve of calcium. See Connective tissue

There are two types of bone in the skeleton: the flat bones (for example, the bones of the skull and ribs) and the long bones (for example, the femur and the bones of the hand and feet). Both types are characterized by an outer layer of dense, compact bone, known as cortical bone, and an inner spongy bone material made up of thin trabeculae, known as cancellous bone. Cortical bone consists of layers of bone (lamellae) in an orderly concentric cylindrical arrangement around tiny Haversian canals. These interconnecting canals carry the blood vessels, lymph vessels, and nerves through the bone and communicate with the periosteum and the marrow cavity. The periosteum is a thin membrane covering the outer surface of bone and consisting of layers of cells that participate in the remodeling and repair of bone. The cancellous bone is in contact with the bone marrow, in which much of the production of blood cells takes place. The interface between the cancellous bone and the marrow is called the endosteum, and it is largely at this site that bone is removed in response to a need for increased calcium elsewhere in the body.

Bone is formed by the laying down of an osteoid matrix by osteoblasts, the bone-forming cells, and the mineralization of the osteoid by the development and deposition of crystals of calcium phosphate (in the form of hydroxyapatite) within it. It is the mineral, organized in a regular pattern on a collagen scaffold, that gives bone its stiffness. Osteoid contains largely fibers of type I collagen and lesser amounts of numerous noncollagenous proteins. Although the role of these proteins in bone is not well understood, it is thought that their particular combination in bone gives this tissue the unique ability to mineralize. It is clear that these proteins interact with each other and that collagen and several of the noncollagenous proteins can bind to specialized receptors on the surface of bone cells. This binding is important for the adhesion of the cells to the bone matrix, and also delivers behavioral signals to the cells. See Collagen

The primary cell types in bone are those that result in its formation and maintenance (osteoblasts and osteocytes) and those that are responsible for its removal (osteoclasts). Osteoblasts form from the differentiation of multipotential stromal cells that reside in the periosteum and the bone marrow. Under the appropriate stimuli, these primitive stromal cells mature to bone-forming cells at targeted sites in the skeleton. Under different stimuli, they are also capable of developing into adipocytes (fat cells), muscle cells, and chondrocytes (cartilage cells). Osteocytes, which are osteoblasts that become incorporated within the bone tissue itself, are the most numerous cell type in bone. They reside in spaces (lacunae) within the mineralized bone, forming numerous extensions through tiny channels (cannaliculi) in the bone that connect with other osteocytes and with the cells on the endosteal surface. Osteocytes are therefore ideally placed to sense stresses and loads placed on the bone and to convey this information to the osteoblasts on the bone surface, thus enabling bone to adapt to altered mechanical loading by the formation of new bone. Osteocytes are also thought to be the cells that detect and direct the repair of microscopic damage that frequently occurs in the bone matrix due to wear and tear. Failure to repair the cracks and microfractures that occur in bone, or when this microdamage accumulates at a rate exceeding its repair, can cause the structural failure of the bone, such as in stress fractures. A large number of molecules that regulate the formation and function of osteoblastic cells have been identified. Circulating hormones, such as insulin, growth hormone, and insulinlike growth factors, combine with growth factors within the bone itself, such as transforming growth factor beta (TGFβ) and bone morphogenetic proteins (BMPs), to influence the differentiation of osteoblasts.

Osteoclasts are typically large, multinucleated cells, rich in the intracellular machinery required for bone resorption. This is accomplished when the cells form a tight sealing zone by attachment of the cell membrane against the bone matrix, creating a bone-resorbing compartment. Into this space, the cell secretes acid to dissolve the bone mineral, and enzymes to digest the collagen and other proteins in the bone matrix. The removal of bone by osteoclasts is necessary to enable the repair of microscopic damage and changes in bone shape during growth and tooth eruption. Osteoclast-mediated bone resorption is also the mechanism for releasing calcium stored in bone for the maintenance of calcium levels in the blood. Most agents that promote bone resorption act on osteoblastic cells, which in turn convey signals to osteoclast precursors to differentiate into mature osteoclasts. These agents include the active form of vitamin D, parathyroid hormone, interleukin-1, interleukin-6, and interleukin-11, and prostaglandins such as prostaglandin E₂. Differentiation to fully functional osteoclasts also requires close contact between osteoclast precursors and osteoblastic cells. This is due to a molecule called osteoclast differentiation factor (ODF) which is located on the surface of osteoblasts, binds to receptors on the surface of osteoclast precursor cells, and induces their progression to osteoclasts.

Flat bones and long bones are formed by different embryological means. Formation of flat bones occurs by intramembranous ossification, in which primitive mesenchymal cells differentiate directly into osteoblasts and produce bony trabeculae within a periosteal membrane. The initial nature of this bone is relatively disorganized and is termed woven bone. Later, this woven bone is remodeled and replaced by the much stronger mature lamella bone, consisting of layers of calcified matrix arranged in orderly fashion. Long bones are formed by intracartilaginous development in which the future bone begins as cartilage. The cartilage template is gradually replaced by bone in an orderly sequence of events starting at the center of the growing bone. Cartilage remains at the ends of long bones during growth, forming a structure at each end termed the growth plate. Cartilage cells (chondrocytes) that arise in the growth plates proliferate and add to the length of the bone. This occurs during a complex series of events, with expansion both away from and toward the center of the bone. When the bone achieves its final length in maturity, expansion from the growth plate ceases. Cartilage persists at the ends of the long bones in a specific form called articular cartilage, which provides the smooth bearing surfaces for the joints.

Bone is a dynamic tissue and is constantly being remodeled by the actions of osteoclasts and osteoblasts. After bone removal, the osteoclasts either move on to new resorption sites or die; this is followed by a reversal phase where osteoblasts are attracted to the resorption site. It is thought that growth factors that are sequestered in an inactive form in the bone matrix are released and activated by the osteoclast activity and that these in turn promote fresh osteoid production by the recruited osteoblasts. The new osteoid eventually calcifies, and in this way the bone is formed and replaced in layers (lamellae), which are the result of these repeated cycles. In growing bone, the activities of bone cells is skewed toward a net increase in bone. However, in healthy mature bone there is an equilibrium between bone resorption and bone formation. When the equilibrium between these two cell types breaks down, skeletal pathology results.

The most common bone disease is osteoporosis, in which there is a net loss of bone due to osteoclastic bone resorption that is not completely matched by new bone formation. The best-understood cause of osteoporosis is that which occurs in women due to the loss of circulating estrogen after menopause. Another cause of osteoporotic bone loss is seen in disuse osteoporosis. Just as bone can respond to increased loading with the production of additional bone, bone is also dependent on regular loading for its maintenance. Significant bone loss can occur during prolonged bed rest or, for example, in paraplegia and quadriplegia. Likewise, an unloading of the skeleton (due to a lack of gravitational pull) in space flight results in severe bone loss in astronauts unless the effects of gravity are simulated by special exercises and devices. See Osteoporosis

Many metabolic and genetic diseases can affect the amount and quality of bone. Metabolic diseases such as diabetes, kidney disease, oversecretion of parathyroid hormone by the parathyroid glands, anorexia nervosa, and vitamin D-dependent rickets may cause osteopenias (the reduction in bone volume and bone structural quality). Immunosuppressive therapy in organ transplant patients can lead to reduced bone mass, as can tumors of bone and other sites. Tumors can produce substances that cause the activation of osteoclastic bone resorption. In the genetically based disease osteogenesis imperfecta, mutations in the gene for type I collagen result in the production of reduced amounts of collagen or altered collagen molecules by osteoblasts. Other common diseases of the skeleton are diseases of the joints, such as rheumatoid arthritis and osteoarthritis. See Thyroid gland