12.5 Bone Growth and Homeostasis
LEARNING OUTCOMES
Upon completion of this section, you should be able to
Summarize the process of ossification and list the types of cells involved.
Describe the process of bone remodeling.
Explain the steps in the repair of bone.
The importance of the skeleton to the human form is evident by its early appearance during development. The skeleton starts forming at about 6 weeks, when the embryo is only about 12 mm (0.5 in.) long. Most bones grow in length and width through Page 247adolescence, but some continue enlarging until about age 25. In a sense, bones can grow throughout a lifetime, because they are able to respond to stress by changing size, shape, and strength. This process is called remodeling. If a bone fractures, it can heal by bone repair.
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Identifying Skeletal Remains
Regardless of how, when, and where human bones are found unexpectedly, many questions must be answered. How old was this person at the time of death? Are these the bones of a male or female? What was the ethnicity? Are there any signs this person was murdered?
Clues about the identity and history of the deceased person are available throughout the skeleton (Fig. 12A). Age is approximated by dentition, or the structure of the teeth in the upper jaw (maxilla) and lower jaw (mandible). For example, infants between 0 and 4 months of age will have no teeth present; children approximately 6 to 10 years of age will have missing deciduous, or “baby,” teeth; young adults acquire their last molars, or “wisdom teeth,” around age 20. The age of older adults can be approximated by the number and location of missing or broken teeth. Studying areas of bone ossification also gives clues to the age of the deceased at the time of death. In older adults, signs of joint breakdown provide additional information about age. Hyaline cartilage becomes worn, yellowed, and brittle with age, and the hyaline cartilages covering bone ends wear down over time. The amount of yellowed, brittle, or missing cartilage helps scientists guess the person’s age.
Figure 12A Forensic investigators uncover a skeleton. A knowledge of bone structure and how bones age will help identify these remains.
©Michael Donne/Science Source
If skeletal remains include the individual’s pelvic bones, these provide the best method for determining an adult’s gender. The pelvis is shallower and wider in the female than in the male. The long bones, particularly the humerus and femur, give information about gender as well. Long bones are thicker and denser in males, and points of muscle attachment are bigger and more prominent. The skull of a male has a square chin and more prominent ridges above the eye sockets, or orbits.
Determining ethnic origin of skeletal remains can be difficult, because so many people have a mixed racial heritage. Forensic anatomists rely on observed racial characteristics of the skull. In general, individuals of African or African American descent have a greater distance between the eyes, eye sockets that are roughly rectangular, and a jaw that is large and prominent. Skulls of Native Americans typically have round eye sockets, prominent cheek (zygomatic) bones, and a rounded palate. Caucasian skulls usually have a U-shaped palate, and a suture line between the frontal bones is often visible. Additionally, the external ear canals in Caucasians are long and straight, so that the auditory ossicles can be seen.
Once the identity of the individual has been determined, the skeletal remains can be returned to the family for proper burial.
Questions to Consider
Why do you think long bones are most often found by forensic investigators?
How does an examination of bone ossification provide an indication of age?
Bones are living tissues, as shown by their ability to grow, remodel, and undergo repair. Several different types of cells are involved in bone growth, remodeling, and repair:
Osteoblasts are bone-forming cells. They secrete the organic matrix of bone and promote the deposition of calcium salts into the matrix.
Osteocytes are mature bone cells derived from osteoblasts. They maintain the structure of bone.
Osteoclasts are bone-absorbing cells. They break down bone and assist in returning calcium and phosphate to the blood.
Throughout life, osteoclasts are removing the matrix of bone and osteoblasts are building it up. When osteoblasts are surrounded by calcified matrix, they become the osteocytes within lacunae.
Bone Development and Growth
The term ossification refers to the formation of bone. The bones of the skeleton form during embryonic development in two distinctive ways: intramembranous ossification and endochondral ossification.
Intramembranous Ossification
Flat bones, such as the bones of the skull, are examples of intramembranous bones. In intramembranous ossification, bones develop between sheets of fibrous connective tissue. Here, cells derived from connective tissue cells become osteoblasts located in ossification centers. The osteoblasts secrete the organic matrix Page 248of bone. This matrix consists of mucopolysaccharides and collagen fibrils. The osteoblasts promote ossification of the matrix by adding calcium salts.
Ossification results in the formation of soft sheets, or trabeculae, of spongy bone. Spongy bone remains inside a flat bone. A periosteum forms outside the spongy bone. Osteoblasts derived from the periosteum carry out further ossification. Trabeculae form and fuse to become compact bone. The compact bone forms a bone collar that surrounds the spongy bone on the inside.
Endochondral Ossification
Most bones of the human skeleton are formed by endochondral ossification, which means the bone forms within the cartilage (Fig. 12.12). During endochondral ossification, bone replaces the cartilaginous (hyaline) models of the bones. Gradually, the cartilage is replaced by the calcified bone matrix that makes these bones capable of bearing weight. Inside, bone formation spreads from the center to the ends. The steps of endochondral ossification include:
The cartilage model (Fig 12.12a). In the embryo, chondrocytes lay down hyaline cartilage, which is shaped like the future bones. Therefore, they are called cartilage models of the future bones. As the cartilage models calcify, the chondrocytes die off.
The bone collar (Fig 12.12b). Osteoblasts are derived from the newly formed periosteum. Osteoblasts secrete the organic bone matrix, and the matrix undergoes calcification. The result is a bone collar, which covers the diaphysis. The bone collar is composed of compact bone. In time, the bone collar thickens.Page 251
The primary ossification center (Fig 12.12c). Blood vessels bring osteoblasts to the interior, and they begin to lay down spongy bone. This region is called a primary ossification center, because it is the first center for bone formation.
The medullary cavity and secondary ossification sites (Fig. 12.12d). The spongy bone of the diaphysis is absorbed by osteoclasts, and the cavity created becomes the medullary cavity. Shortly after birth, secondary ossification centers form in the epiphyses. Spongy bone persists in the epiphyses, and it persists in the red bone marrow for quite some time. Cartilage is present at two locations: the epiphyseal (growth) plate and articular cartilage, which covers the ends of long bones.
The epiphyseal (growth) plate (Fig 12.12e). A band of cartilage called the epiphyseal plate (also called a growth plate) remains between the primary ossification center and each secondary center (see Fig. 12.1). The limbs keep increasing in length as long as the epiphyseal plates are still present.
Figure 12.12 Bone growth by endochondral ossification. In endochondral ossification, the bone begins as hyaline cartilage. Bone cells called osteoblasts colonize the cartilage, then ossify to turn cartilage into bone.
Bone Growth
Figure 12.13 shows that the epiphyseal plate contains four layers. The layer nearest the epiphysis is the resting zone, where cartilage remains. The next layer is the proliferating zone, in which chondrocytes are producing new cartilage cells. In the third layer, the degenerating zone, the cartilage cells are dying off; and in the fourth layer, the ossification zone, bone is forming. Bone formation here causes the length of the bone to increase. The inside layer of articular cartilage also undergoes ossification in the manner described.
Figure 12.13 Increasing bone length. a. Length of a bone increases when cartilage is replaced by bone at the growth plate. Arrows indicate the direction of ossification. b. Chondrocytes produce new cartilage in the proliferating zone, and cartilage becomes bone in the ossification zone closest to the diaphysis.
The diameter of a bone enlarges as a bone lengthens. Osteoblasts derived from the periosteum are active in new bone deposition as osteoclasts enlarge the medullary cavity from inside.
Final Size of the Bones
When the epiphyseal plates close, bone lengthening can no longer occur. The epiphyseal plates in the arms and legs of women typically close at about age 16 to 18, and they do not close in men until about age 20. Portions of other types of bones may continue to grow until age 25.
Hormones, chemical messengers that are produced by one part of the body and act on a different part of the body, are secreted by the endocrine glands and distributed about the body by the bloodstream. Hormones control the activity of the epiphyseal plate, as is discussed next.
Hormones Affect Bone Growth
Several hormones play an important role in bone growth.
Vitamin D is formed in the skin when it is exposed to sunlight, but it can also be consumed in the diet. Milk, in particular, is often fortified with vitamin D. In the kidneys, vitamin D is converted to a hormone that acts on the intestinal tract. The chief function of vitamin D is intestinal absorption of calcium. In the absence of vitamin D, children can develop rickets, a condition marked by bone deformities, including bowed long bones.
Growth hormone (GH) directly stimulates growth of the epiphyseal plate, as well as bone growth in general. However, growth hormone is somewhat ineffective if the metabolic activity of cells is not promoted. Thyroid hormone, in particular, promotes the metabolic activity of cells (see Section 16.6). Too little growth hormone in childhood results in dwarfism. Too much growth hormone during childhood (prior to epiphyseal fusion) can produce excessive growth and even gigantism (see Fig. 16.9). Acromegaly results from excess GH in adults following epiphyseal fusion. Page 252This condition produces excessive growth of bones in the hands and face (see Fig. 16.10).
Adolescents usually experience a dramatic increase in height, called the growth spurt, due to an increased level of sex hormones. These hormones apparently stimulate osteoblast activity. Rapid growth causes epiphyseal plates to become “paved over” by the faster-growing bone tissue within 1 or 2 years of the onset of puberty.
Bone Remodeling and Calcium Homeostasis
Bone is constantly being broken down by osteoclasts and re-formed by osteoblasts in the adult. As much as 18% of bone is recycled each year. This process of bone renewal, often called bone remodeling, normally keeps bones strong. In Paget disease, new bone is generated at a faster-than-normal rate. This rapid remodeling produces bone that’s softer and weaker than normal bone and can cause bone pain, deformities, and fractures.
Bone recycling allows the body to regulate the amount of calcium in the blood. To illustrate that the blood calcium level is critical, recall that calcium is required for blood to clot (see Section 6.4). Also, if the blood calcium concentration is too high, neurons and muscle cells no longer function. If calcium falls too low, nerve and muscle cells become so excited that convulsions occur. Calcium ions are also necessary for the regulation of cellular metabolism by acting in cellular messenger systems. Thus, the skeleton acts as a reservoir for storage of this important mineral—if the blood calcium rises above normal, at least some of the excess is deposited in the bones. If the blood calcium dips too low, calcium is removed from the bones to bring it back up to the normal level.
Two hormones in particular are involved in regulating the blood calcium level. Parathyroid hormone (PTH) stimulates osteoclasts to dissolve the calcium matrix of bone. In addition, parathyroid hormone promotes calcium reabsorption in the small intestine and kidney, increasing blood calcium levels. Vitamin D is needed for the absorption of Ca2+ from the digestive tract, which is why vitamin D deficiency can result in weak bones. It is easy to get enough of this vitamin, because your skin produces it when exposed to sunlight, and the milk you buy at the grocery store is fortified with vitamin D.
Calcitonin is a hormone that acts opposite to PTH. The female sex hormone estrogen can actually increase the number of osteoblasts; the reduction of estrogen in older women is often given as reason for the development of weak bones, called osteoporosis. Osteoporosis is discussed in the Health feature “You Can Avoid Osteoporosis.” In the young adult, the activity of osteoclasts is matched by the activity of osteoblasts, and bone mass remains stable until about age 45 in women. After that age, bone mass starts to decrease.
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You Can Avoid Osteoporosis
Osteoporosis is a condition in which the bones are weakened due to a decrease in the bone mass that makes up the skeleton. The skeletal mass continues to increase until ages 20 to 30. After that, there is an equal rate of formation and breakdown of bone mass until ages 40 to 50. Then, reabsorption begins to exceed formation, and the total bone mass slowly decreases (Fig. 12C).
Figure 12C Preventing osteoporosis. a. Normal bone. b. Bone from a person with osteoporosis.
(a): ©Susumu Nishinaga/Science Source; (b): ©Ed Reschke/Photolibrary/Getty Images
Over time, men are apt to lose 25% and women 35% of their bone mass. But we have to consider that men—unless they have taken asthma medications that decrease bone formation—tend to have denser bones than women anyway. Whereas a man’s testosterone (male sex hormone) level generally declines slowly after the age of 45, estrogen (female sex hormone) levels in women begin to decline significantly at about age 45. Sex hormones play an important role in maintaining bone strength, so this difference means that women are more likely than men to suffer a higher incidence of fractures, involving especially the hip, vertebrae, long bones, and pelvis. Although osteoporosis may at times be the result of various disease processes, it is essentially a disease that occurs as we age.
Osteoporosis
How to Avoid Osteoporosis
Everyone can take measures to avoid having osteoporosis later in life. Adequate dietary calcium throughout life is an important protection against osteoporosis. The National Osteoporosis Foundation (www.nof.org) recommends that adults under the age of 50 take in 1,000 mg of calcium per day. After the age of 50, the daily intake should exceed 1,200 mg per day.
A small daily amount of vitamin D is also necessary for the body to use calcium correctly. Exposure to sunlight is required to allow skin to synthesize a precursor to vitamin D. If you reside on or north of a “line” drawn from Boston to Milwaukee, to Minneapolis, to Boise, chances are you’re not getting enough vitamin D during the winter months. Therefore, you should take advantage of the vitamin D present in fortified foods such as low-fat milk and cereal. If you are under age 50, you should be receiving 400–800 IU of vitamin D per day. After age 50, this amount should increase to 800–1,000 IU of vitamin D daily.
Very inactive people, such as those confined to bed, lose bone mass 25 times faster than people who are moderately active. On the other hand, moderate weight-bearing exercise, such as regular walking or jogging, is another good way to maintain bone strength (Fig. 12C).
Diagnosis and Treatment
Postmenopausal women with any of the following risk factors should have an evaluation of their bone density:
White or Asian race
Thin body type
Family history of osteoporosis
Early menopause (before age 45)
Smoking
A diet low in calcium or excessive alcohol consumption and caffeine intake
Sedentary lifestyle
Bone density is measured by a method called dual-energy X-ray absorptiometry (DEXA). This test measures bone density based on the absorption of photons generated by an X-ray tube. Blood and urine tests are used to detect the biochemical markers of bone loss. Over the past several years, it has become easier for physicians to screen older women and at-risk men for osteoporosis.
If the bones are thin, it is worthwhile to take all possible measures to gain bone density, because even a slight increase can significantly reduce fracture risk. Although estrogen therapy does reduce the incidence of hip fractures, long-term estrogen therapy is rarely recommended for osteoporosis. Estrogen is known to increase the risk of breast cancer, heart disease, stroke, and blood clots. Other medications are available, however. Calcitonin, a thyroid hormone, has been shown to increase bone density and strength while decreasing the rate of bone fractures. Also, the bisphosphonates are a family of nonhormonal drugs used to prevent and treat osteoporosis. To achieve optimal results with calcitonin or one of the bisphosphonates, patients should also receive adequate amounts of dietary calcium and vitamin D.
Questions to Consider
How may long-term digestive system problems promote the chances of developing osteoporosis?
Why are individuals at risk for osteoporosis encouraged to increase their exercise regimes, including load-bearing exercises?
Page 253Bone remodeling also accounts for why bones can respond to stress. If you engage in an activity that calls upon the use of a particular bone, the bone enlarges in diameter at the region most affected by the activity. During this process, osteoblasts in the periosteum form compact bone around the external bone surface and osteoclasts break down bone on the internal bone surface around the medullary cavity. Increasing the size of the medullary cavity prevents the bones from getting too heavy and thick. Today, exercises such as walking, jogging, and weightlifting are recommended. These exercises strengthen bone because they stimulate the work of osteoblasts instead of osteoclasts.
Bone Repair
Repair of a bone is required after it breaks or fractures. Fracture repair takes place over a span of several months in a series of four steps, shown in Figure 12.14:
Hematoma. After a fracture, blood escapes from ruptured blood vessels and forms a hematoma (mass of clotted blood) in the space between the broken bones. The hematoma forms within 6 to 8 hours.
Fibrocartilaginous callus. Tissue repair begins, and a fibrocartilaginous callus fills the space between the ends of the broken bone for about 3 weeks.
Bony callus. Osteoblasts produce trabeculae of spongy bone and convert the fibrocartilage callus to a bony callus that joins the broken bones together. The bony callus lasts about 3 to 4 months.
Remodeling. Osteoblasts build new compact bone at the periphery. Osteoclasts absorb the spongy bone, creating a new medullary cavity.
Figure 12.14 Bone repair following a fracture. The stages in the repair of a fracture.
In some ways, bone repair parallels the development of a bone except that the first step, hematoma, indicates that injury has occurred. Further, a fibrocartilaginous callus precedes the production of compact bone.
The naming of fractures tells you what type of break has occurred. A fracture is complete if the bone is broken clear through, and incomplete if the bone is not separated into two parts. A fracture is simple if it does not pierce the skin, and is compound if it does pierce the skin. Impacted means that the broken ends are wedged into each other. A spiral fracture occurs when the break is ragged due to twisting of a bone.
Blood Cells Are Produced in Bones
The bones of your skeleton contain two types of marrow: yellow and red. Fat is stored in yellow bone marrow, thus making it part of the body’s energy reserves.
Red bone marrow is the site of blood cell production. The red blood cells are the carriers of oxygen in the blood. Oxygen is Page 254necessary for the production of ATP by aerobic cellular respiration. White blood cells also originate in the red bone marrow. The white cells are involved in defending your body against pathogens and cancerous cells; without them, you would soon succumb to disease and die.
CHECK YOUR PROGRESS 12.5
Describe how bone growth occurs during development.
Answer
Through intramembranous ossification, in which bone develops between sheets of fibrous connective tissue, and endochondral ossification, in which bone replaces a cartilage model.
Summarize the stages in the repair of bone.
Answer
A hematoma is formed. Next, tissue repair begins, and a fibrocartilaginous callus is formed between the ends of the broken bone. Then, the fibrocartilaginous callus is converted into a bony callus and remodeled by osteoblasts and osteoclasts.
Explain how the skeletal system is involved in calcium homeostasis.
Answer
When blood calcium is low, parathyroid hormone is secreted, causing osteoclasts to dissolve the bone matrix, releasing calcium into the blood. When blood calcium is high, calcitonin from the thyroid gland activates the bone-forming activity of osteoblasts.
CONNECTING THE CONCEPTS
For more on bone development and the hormones that influence bone growth, refer to the following discussions:
Section 9.6 provides additional information on inputs of vitamin D and calcium in the diet.
Section 16.2 examines the role of growth hormones in the body.
Section 16.3 describes the action of the hormones calcitonin and PTH.
CONCLUSION
For the first painful month or so after having her knee replaced, Jackie wondered if she had made the right decision. Just walking down the hall or up stairs was excruciating at first. Within 2 months, however, she was walking and swimming. Her physical therapist attributed her rapid return to her previous habits of staying in shape. But Jackie knows that without twenty-first-century medicine, she might have a difficult time walking by the time she is 60. Still, she has been reminded by her doctor that all bones, even those of adults, are dynamic structures. Whereas her bone could be replaced by bone remodeling, the plastic and ceramic parts of her knees would eventually wear out. So there was a very good chance she would have to undergo a repeat replacement of her knee in about 20 years. For Jackie, the ability to once again lead an active lifestyle was a worthwhile trade for a few months of discomfort.