Friday 7 October 2016

What are bones and the skeleton?


Structure and Functions

Bones are active throughout life: the 206 bones of the skeleton establish the size and proportions of the body and interact with all other organ systems. Disorders of the skeleton can have profound effects on the other organ systems and serious health consequences for the organism.



Bone, or osseous tissue, contains specialized cells and a solid, stony matrix. The unique hardened quality of the matrix results from layers of calcium salt crystals such as calcium phosphate, which is responsible for about two-thirds of a bone’s weight, and calcium carbonate. The living cells found in bone account for less than 2 percent of the total bone mass.


Despite the great strength of the calcium salts, their inflexible nature means that they can fracture when exposed to sufficiently great bending or twisting forces, or to sharp impacts. Because the calcium crystals exist as minute plates positioned on a framework of collagen protein fibers, the resulting composite structure does lend a certain degree of flexibility to the bone matrix.


Based on the internal organization of its matrix, bone is classified as either compact (dense) bone or cancellous (spongy) bone. Compact bone is internally more solid, while cancellous bone is made from bony filaments (trabeculae) whose branching interconnections form a three-dimensional network. The cavities of the cancellous bone network are filled usually by bone marrow, the primary location for blood cell formation in adults.


Both types of bone contain bone cells (osteocytes) living in small chambers called lacunae, found periodically between the plates of the matrix. Microscopic channels (canaliculi) connect neighboring lacunae and permit the exchange of nutrients and wastes between osteocytes and accessible blood vessels. Osteocytes provide the collagen fibers and the conditions for proper maintenance of the mineral crystals of the matrix.


A typical skeletal bone has a central marrow cavity that is bordered by cancellous bone. This is enclosed by compact bone, and the outer surface is covered by periosteum. Periosteum consists of a fibrous outer layer and a cellular inner layer. The periosteum plays an important part in the growth and repair of bone, and it is the attachment site for muscles. Collagen protein fibers from the periosteum interconnect with the collagen fibers of the bone.


The marrow cavity inside the bone is lined by endosteum. Endosteum is an incomplete layer covering the trabeculae of cancellous bone and contains a variety of different types of cells. The endosteum also plays important roles during bone growth and repair.


The bone matrix is not an unchanging, permanent structure. During a person's life, the bone matrix is being constantly dissolved while new matrix is synthesized and deposited. Approximately 18 percent of the protein and mineral constituents of bone are replaced each year. Such bone remodeling can result in altered bone shape or internal rearrangement of the trabeculae. It may also result in a change in the total amount of minerals stored in the skeleton. These processes of bone demineralization (osteolysis) and new bone production (osteogenesis) are precisely regulated in the healthy individual.


The type of bone cell responsible for dissolving the mineralized matrix is called an osteoclast. The cells that produce the materials that later become the bony matrix are called osteoblasts. The activities of these cells are influenced by several hormones as well as by the physical stress forces to which a bone may be exposed, such as when a particular muscle becomes stronger as the result of weight training and pulls more strongly on the bones to which it is attached. Increased stress forces on a bone result in that bone becoming thicker and stronger, thereby allowing the bone to withstand the stresses better and reducing the risks of bone fracture. When bones are not subjected to ordinary stresses, such as in persons confined to bed or in astronauts living in microgravity conditions during space flight, there is a corresponding loss of bone mass, with the unstressed bones becoming thinner and more brittle. After several weeks in an unstressed state, a bone can lose nearly a third of its mass. Following the resumption of normal loading stresses, the bone can regain its mass just as quickly.


The skeleton has five major functions: support for the body; protection of the soft tissues and organs; leverage to change the direction and size of the muscular forces; blood cell production, which occurs within the red marrow residing in the marrow cavities of many bones; and storage of both minerals (to maintain the body’s important reserves of calcium and phosphate) and fats (in yellow marrow to serve as an important energy reserve for the body).


The human skeleton contains 206 bones. These are distributed between two subdivisions of the skeleton: the axial skeleton and the appendicular skeleton. The axial skeleton contains 80 bones distributed among the skull (29 bones), the chest (25 bones), and the spinal (vertebral) column (26 bones). The remaining 126 bones are found in the appendicular skeleton’s components: 4 bones in the shoulder (pectoral) girdles, 60 bones in the arms (including the 54 bones located in both of the hands and wrists), 2 bones in the hip (pelvic) girdle, and 60 bones in the legs (including the 52 bones found in the ankles and feet).


Skeletal bones are classified according to their shape. Long bones occur in the upper arm, the forearm, the thigh, the lower leg, the palm, the fingers, the sole of the foot, and the toes. Short bones are cuboid in shape and are found in the wrist and the ankle. Flat bones form the top of the skull, the shoulder blade, the breastbone, and the ribs. Sesamoid bones are typically small, round, and flat. They are found near some joints, such as the kneecap on the front of the knee joint. Irregular bones have shapes that are difficult to describe because of their complexity. Examples of irregular bones are found in the spinal column and the skull.


Learning to name the bones solely by their appearance is made somewhat easier by the fact that each one has a definitive form and distinctive surface features. The places where blood vessels and nerves enter into a bone, or lie along its surface, are commonly discernible as indentations, grooves, or holes. The locations where muscles are connected to bones by tendons, or where a bone is tethered to another bone by ligaments, are often clearly visible as elevations, projections, or ridges of bony matrix, or as roughened areas on the surface of the bone. Finally, the areas of the bone that are involved in forming joints (articulations) with other bones have characteristic shapes that impart particular properties to the joint. Various specialized terms are used to name these features.


Articulations are found wherever one bone meets another. The amount of motion permitted between the bones forming an articulation ranges from none (for example, between the skull bones) to considerable (as at the shoulder joint). The anatomy of the joint determines its functional capability, and the parts of the bones that form the joint have distinctive structural features.




Disorders and Diseases

Among the disorders of the skeleton, a number of them occur during the growth and development of the bones. The problems usually result in abnormal (most often decreased) stature or abnormal shape of the bones. The aberrations may alter the entire skeleton or be restricted to a portion of it. The basis of the pathology is to be found in a disruption of the normal, orderly sequence of events that take place during the growth and remodeling of the bones.


Osteopetrosis belongs to this class of disturbance. It is an inherited condition in which abnormal remodeling results in increased bone density. This seems to result from a reduced level of activity by the cells responsible for dissolving the bone matrix—the osteoclasts. In healthy, normal individuals, there is a precisely regulated relationship between osteoclast and osteoblast activity. Depending on the current needs of the body, or merely those of a single bone, the rate of bone matrix formation by osteoblasts may be greater than, equal to, or less than the rate of bone resorption by osteoclasts.


Osteoclasts are derived from cells that are made in the bone marrow. For this reason, bone marrow transplantation
has been tried as a treatment for osteopetrosis; however, this approach is risky and not always successful. There has also been improvement in the condition of some osteopetrosis patients following treatment with a hormone related to vitamin D. This particular hormone can increase bone resorption and thereby may prevent the increase in bone density that characterizes this condition.


Another member of this category of disturbance is congenital hypothyroidism.
The basic problem in this condition is underactivity of the thyroid gland during the development of the fetus, resulting in a decrease in the production of thyroid hormones in the fetus. This condition can be caused by an insufficient supply of the element iodine in the pregnant mother, or it may result from inherited errors in the production of the thyroid hormones.


Among the organ systems seriously affected by this condition is the skeleton. The bones do not develop correctly; consequently, the bones are shorter and thicker than normal, with corresponding changes in the appearance of the child. Early diagnosis of the condition and timely treatment with drug forms of the thyroid hormones can halt the disease. Otherwise, the adult skeleton has stubby arms and legs, a somewhat flattened face, and disproportionately large chest and head.


A disorder of the pituitary gland can result in skeletal development abnormalities that are opposite to those observed in congenital hypothyroidism: namely, excessive growth in the length of bones. This condition is called giantism (or gigantism) and results from the overproduction of growth hormone by the pituitary gland before normal adult stature has been achieved. The most common cause of this situation is a tumor in the pituitary gland. Cases are known of people attaining heights of more than eight feet tall. Unfortunately, because of complications involving other organ systems as a result of the excessive production of growth hormone, the persons suffering from this disorder usually die before the age of thirty.


Surgical removal of the pituitary tumor is often attempted. If the tumor is successfully removed, then the overproduction of growth hormone will be stopped. In other cases, radiation treatments are used to destroy the tumor. It is also possible to combine both of these treatment techniques. Drug therapy is also possible. Because of the high doses necessary and the accompanying side effects of high drug dosages, however, the reduction of growth hormone levels through drug treatment is usually applied only in conjunction with one or both of the other therapies.


There are also disorders that afflict adult bone. Most of the remodeling disorders involve a loss of bone mass. The group of disorders known as osteoporosis (porous bone) is a rather common example; according to the International Osteoporosis Foundation, by 2013, osteoporosis affected more than 200 million people worldwide. The reduction in bone mass is sufficient to result in increased fragility and ease of breakage. There is also slower healing of bone fractures. In advanced cases, bones have been known to break when the person sneezes or simply rolls over in bed.


Loss of bone mass is a normal feature of aging, becoming quite marked after the age of seventy-five, particularly in the hip and leg bones. Because of the normal decrease in bone mass with aging, there is not a clear distinction to be made between normal, age-related skeletal changes and the clinical condition of osteoporosis. The occurrence of excessive fragility at a relatively early age is an indication that osteoporosis is developing. Normally, between the ages of thirty and forty, the activity of the osteoblast cells (those that form bone matrix) begins to decrease while the osteoclast cells (those that dissolve the matrix) maintain their previous level of activity. This results in the loss of about 8 percent of the total bone mass each decade for women and about 3 percent for men. Because of unequal loss in the different regions of the skeleton, the outcome is a gradual reduction in height, the loss of teeth, and the development of fragile limbs.


Osteoporotic bones are indistinguishable from normal bones with respect to their bone composition. The problem is simply too little of the strength-imparting matrix, with both compact and spongy bone being affected.


There are multiple causes of osteoporosis. Some cases have no known cause (idiopathic osteoporosis), some are inherited, and others are brought about as a result of hormonal (endocrine) disorders, vitamin or mineral deficiency, or effects of the long-term use of certain drugs.


The fact that women are more often affected than men, and that the process is most conspicuous in women beyond the age of the menopause, has implicated the female sex hormones (and, specifically, their decreased production) in the initiation of the osteoporotic process. One form of therapy is the administration of certain female sex hormones (specifically estrogens) to postmenopausal women (who have decreased production of estrogens). This treatment slows their loss of bone mass. While hormone therapy has been the mainstay of osteoporosis treatment for many years, controversy regarding the risks of hormone therapy has caused many women to stop using this treatment altogether. In 2002, two major studies found that the risks associated with hormone therapy outweigh the benefits. Following these studies, doctors began to look closer at the roles that high-impact exercise and the use of calcium and vitamin D play in decreasing bone density loss.


Other treatments of osteoporosis include administering the hormone calcitonin and increasing the dietary intake of the mineral calcium. The hormone calcitonin, produced by the thyroid gland, is sometimes used to treat osteoporosis because it stimulates the production of bone matrix by increasing the activity of the osteoblasts. At the same time, calcitonin inhibits the breakdown of bone by decreasing the activity of osteoclasts. Although this treatment theoretically should produce the desired result of preventing the accelerated loss of bone mass characteristic of osteoporosis, actual clinical results are not always positive.


For those cases of osteoporosis that are the result of endocrine gland disturbances, the appropriate treatment depends on the specific glandular disorder that is present. In some instances, hormone therapy can produce improvement in the patient’s condition.


Regular exercise is a means both of preventing the onset of osteoporosis and of slowing its progression. Because muscular activity is critical for the maintenance of bone mass, extended periods of inactivity or immobilization can actually induce osteoporosis. For women, it is known that the amount and regularity of their exercise during the teenage years is strongly associated with their chances of developing osteoporosis thirty and more years later. The exercise need only be of moderate intensity in order to decrease significantly the risk of developing osteoporosis. Indeed, exercise that is at a level of intensity so high that it interferes with the normal female menstrual cycle (stopping the occurrence of menstruation completely or causing irregular cycle lengths) can actually increase the risk of developing osteoporosis later in life.




Perspective and Prospects

One of bone's primary functions is the protection of softer, more vulnerable tissues and organs. The physical properties of bone—it is as strong as cast iron but only weighs as much as an equally large piece of pine wood—make it ideally suited for this job. This combination of strength and lightness derives from the bony matrix of mineral crystals and the architecture of the bone, which unites compact and spongy bone.


The physical and chemical properties of the mineral crystals also result in the permanency of bone following death. Often the only trace of a dead body is the skeleton. Because of the resistance of bone to the processes of decomposition that befall the other tissues of the body following death, investigators are often able to determine the sex of the person whose skeleton has been found even though all other tissues have long since disappeared. This is possible because of the characteristic differences between male and female adult skeletons. Racial differences in the detailed structure of the skull and pelvis, age-related changes in the skeleton, signs of healed bone fractures, and the prominence of ridges where muscles attach (giving clues about the degree of muscular development) are also valuable sources of information when attempting to identify skeletal remains.


The sexual differences in the human skeleton are most obvious in the adult pelvis. These are genetically determined differences that are structural adaptations for childbearing. For example, the pelvis is smoother and wider in the female than in the male. Other differences include a lighter and smoother female skull, a more sloping male forehead, a larger and heavier male jawbone, and generally heavier male bones that also typically possess more prominent markings.


Among the common age-related changes found in skeletons are a general reduction in the mineral content and less prominent bone markings, both of which become more obvious after about age fifty. Various bones in the skull fuse together at characteristic ages ranging from one to thirty years of age. Other bones throughout the body can also be examined to achieve more accurate estimates of the age of a skeleton at the time of death.


Another consequence of the permanent nature of bone is that it provides a record of the changes in the skeletal anatomy of humans that have occurred during the hundreds of thousands of years of human evolution. Expert examination of skeletal remains can actually reveal an amazing wealth of information concerning the health and even the lifestyle of the deceased.




Bibliography


Ballard, Carol. Bones. Chicago: Heinemann Library, 2002.



Currey, John D. Bones: Structures and Mechanics. Princeton, N.J.: Princeton University Press, 2002.



International Osteoporosis Foundation. "Facts and Statistics." International Osteoporosis Foundation, 2013.



Joyce, Christopher, and Eric Stover. Witnesses from the Grave: The Stories Bones Tell. Boston: Little, Brown, 1991.



KidsHealth. "Bones, Muscles, and Joints." Nemours Foundation, 2013.



Marieb, Elaine N., and Katja Hoehn. Human Anatomy and Physiology. 9th ed. San Francisco: Pearson/Benjamin Cummings, 2010.



NIH Osteoporosis and Related Bone Diseases National Resource Center. "Bone Health for Life." National Institutes of Health, November 2011.



OrthoInfo. "Bone Health Basics." American Academy of Orthopaedic Surgeons, May 2012.



Seeley, Rod R., Trent D. Stephens, and Philip Tate. Anatomy and Physiology. 7th ed. New York: McGraw-Hill, 2006..



Van De Graaff, Kent M., and Stuart Ira Fox. Concepts of Human Anatomy and Physiology. 5th ed. Dubuque: Iowa: Wm. C. Brown, 2000.

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