Imagine a house occupied at the same time by competing construction and demolition crews. Day after day, the construction workers assemble the building’s features with meticulous craftsmanship and care. But at the same time, the hard-hatted workers chip away at the walls and floors, pulverizing pieces into dust and carting away the debris. The house grows or comes apart, depending on which crew has the upper hand. But most times the competing crews work at the same steady and reliable pace, so the house stands solid and useful, but it’s never really finished.
This construction-versus-demolition story can apply to the physiology of your bones. Every year, between 10 and 30 percent of the substance of adult skeletal bones “turns over.” In other words, one group of bone cells (osteoclasts) methodically destroys bone matter while a different group of bone cells (osteoblasts) deposits fresh bone matter to replace what was lost. It really shouldn’t surprise you to discover that your seemingly solid bones are in a constant state of flux. A recurring theme of this book is that the body is built to adapt to ever-changing conditions, and bones are no exception. Bone turnover makes it possible for the body to grow, and it enables bones to repair themselves from daily wear-and-tear. Just as important, bone turnover releases minerals that other organs, especially muscles and nerves, need to function normally.
After an introduction to the skeletal system, this chapter looks at the structure and function of bones as individual, living organs. We will start by noting how anatomists classify bones by shape. Next, we will discuss what bones are made of and introduce the cells that build up bone and tear it down again. Bone cells don’t work without a plan, so it’s equally important to recognize the patterns of bone growth that can occur in the body. As with our discussion of the skin, we finish this chapter by looking at how damaged bones repair themselves.
OVERVIEW OF THE SKELETAL SYSTEM
Together bones, ligaments, and cartilages comprise the skeletal system. Every bone in this system is a living organ composed of a variety of tissues, all of which contribute to the bone’s function. A bone is made mostly of osseous tissue, otherwise known as “bone.” Osseous tissue consists of cells that live on or within a matrix of collagen fibers, ground substance, and calcium salts. The calcium salts give bones their remarkable qualities of hardness, durability, and strength. The living cells in bones include ones that build osseous tissue and ones that break it down. Bones also contain dense connective tissue, adipose tissue and bloodforming tissue, and some bones contain cartilage. In addition, numerous blood vessels and nerves surround and penetrate deep into living bones.
Collectively, bones form the skeleton, the body’s rigid internal framework. A typical adult skeleton consists of 206 bones that anatomists divide into two sets: the axial skeleton and the appendicular skeleton. The axial skeleton includes the bones that form the head, neck, spine, and rib cage. The term “axial” signifies that these bones form a vertical axis or column through the body. In the same way that a trunk forms the structural core of a tree, the axial skeleton forms the body’s structural core.
The appendicular skeleton includes the shoulder bones and hipbones, and the bones of the upper and lower limbs. The shoulder bones attach the upper limbs to the axial skeleton, while the hipbones attach the lower limbs to the axial skeleton. Hence, this division of the skeleton is so named because its bones are appended to (hang from) the axial skeleton. In this respect, the appendicular skeleton is like the branches that successively divide from a tree trunk. Appendicular skeletal bones make it possible for a person to move about and manipulate objects in the surrounding environment.
ACCESSORY PARTS OF THE SKELETAL SYSTEM
Individual bones meet and interact at joints or articulations. Many joints are freely moveable; that is, the bones that form the joint can easily change position with respect to one another. Perhaps the most familiar freely moveable joints are those that form the elbows and knees. Other joints are only slightly moveable, such as those between the vertebrae, the bones that make up the spine. Still other joints, such as those that connect the skull bones, are completely immovable. Bones at joints would either pull apart from each other or damage one another when rubbing together if it weren’t for the presence of the skeleton’s ligaments and cartilages.
Ligaments
A ligament (LIG-a-ment; band) is a strip of dense, regular connective tissue that holds bones together at a joint. Some ligaments may cross between bones deep within a joint, while other ligaments extend around a joint, forming a capsule-like enclosure. Relatively long ligaments hold bones together at freely moveable joints. In contrast, microscopically short ligaments are present between bones at immovable joints. These tiny ligaments act like glue, bonding the bones together so tightly that virtually no movement is possible at the joint.
Skeletal Cartilages
A skeletal cartilage is an avascular connective tissue consisting of chondrocytes living in a matrix of collagen fibers and ground substance. A thin, dense connective tissue membrane called the perichondrium covers the cartilage. The skeletal system has hyaline cartilage at most of its joints, fibrocartilage at some joints, both hyaline and fibrocartilage at a few joints, and elastic cartilage at several locations. Skeletal cartilage attaches and protects bones at joints, and serves as a substitute for bones in certain parts of the skeleton where flexibility is needed as much as mechanical strength. Functions of cartilage include:
- Attaching bones: Like ligaments, some cartilages connect bones at joints by acting like braces. For example, the costal cartilages, made of hyaline cartilage, connect the anterior ends of the ribs to the sternum (breastbone). Fibrocartilage pads called intervertebral discs act like flexible glue to hold the vertebrae together yet allows them to bend and twist. The pubic symphysis is a fibrocartilage pad that holds together the anterior portion of the pelvis.
- Protecting bones: Skeletal cartilages prevent bones at movable joints from damaging each other by reducing friction and absorbing impacts. For example, thin articular cartilages cover the ends of bones at freely moveable joints. These hyaline cartilages are smooth and slippery, which allows the ends of moving bones to slide back and forth over one another. Some joints have fibrocartilage pads that further reduce joint friction by keeping bones properly aligned as they move. Finally, skeletal cartilages keep adjacent bones from pulverizing one another by acting like rubber shock absorbers inside the joint. In particular, the springy fibrocartilage that makes up the intervertebral discs helps absorb and dissipate the physical pounding the spine receives when a person walks or runs.
- Acting like bones: Some cartilages act like bones at places where mechanical flexibility is important, and they help to protect underlying organs. For example, the costal cartilages at the ends of ribs enable the rib cage to expand and contract to produce breathing. These cartilages also shield organs in the lower thoracic and upper abdominal cavities. The nasal cartilages that form the nose are flexible, interlocking hyaline cartilages. The external ears consist mainly of elastic cartilages that surround the entrance to the external ear canals; short ligaments anchor these cartilages to the skull.
FUNCTIONS OF THE SKELETAL SYSTEM
Like the internal framing of a house, the skeleton determines a person’s size and shape. Moreover, the arrangement of the facial bones largely determines a person’s characteristic facial features. Apart from how it influences one’s appearance, the skeletal system plays critical structural and physiological roles in the body. Structurally, the skeleton offers physical support and protection, and it allows for body movement. Physiologically, the skeleton is the site of blood formation in adults, and it serves as a storage site for minerals and fats.
- Support: Healthy bones can withstand tremendous pushing, pulling, and bending forces. Their strength makes bones well suited for supporting the body’s soft tissues, which account for about 80 percent of an average adult’s weight. Even the smallest skeletal bones, such as those that form the ankles and wrists are strong enough to support the body’s full weight without breaking. In most cases, organs and soft tissues hang from the bones much like clothing suspended on hangers. But at some places, the body’s soft tissues rest on a bony platform. The brain, for example, rests in a cradle of bones that form the base and sides of the skull.
- Protection: The bones of the axial skeleton surround the body’s most delicate organs. For example, the bones that form the skull enclose the brain, making it possible for a boxer to survive a punch to the head. The rib cage surrounds and shelters the heart and lungs. The sturdy vertebrae along the spine not only support the trunk, but also enclose the spinal cord, the nervous system’s communications pathway between the brain and most of the body.
- Facilitating movement: Bones that meet at movable joints act like levers, simple machines that can transmit mechanical force. Contracting muscles pull on bones, which then move in relationship to joints and facilitate body movement. For example, to curl your lower arm toward your chest, muscles and their tendons pull on bones of the arm and forearm that meet at the elbow joint. And when you chew food, sets of powerful facial muscles pull against the lower jawbone, which moves at hinge-like joints at the back of the jaw.
- Blood formation: Blood, the body’s softest tissue, forms inside bones, the body’s hardest organs. Blood cells form and differentiate in a process called hemopoiesis (HĒ-mō-poy-Ēsis; hemo, blood; poiesis, making). In adults, blood cells form in red marrow, a specialized connective tissue that is concentrated inside certain bones. Red marrow produces all of the body’s oxygen-carrying red blood cells, its clot-forming platelets, and practically all of its disease-fighting white blood cells.
- Lipid storage: Cavities deep within many bones are filled with yellow marrow. This connective tissue is yellow because it consists almost entirely of lipid-filled adipocytes (fatstoring cells). Yellow marrow comprises part of the body’s chemical energy reserves.
- Mineral storage: Bones are the body’s “mineral bank.” Just as banks store and distribute money, bones store and release minerals depending on the body’s needs. The “currency” that is deposited in bones and can later be withdrawn consists of calcium and phosphorus ions. You probably have read that dietary calcium is required to build strong bones; it’s true – the skeleton contains 99 percent of all the body’s calcium. But organs such as muscles and nerves need steady levels of calcium in the blood and tissue fluids in order to work properly. Bones release calcium ions when blood calcium levels drop, and they tend to take in calcium ions when the blood calcium levels rise.
Figure 9-1.Bone shapes
CLASSIFICATION OF BONES
Bones come in many shapes and sizes. But a closer look at their surface and interior reveals that all bones are derived from a basic blueprint. No two bones in the body are quite alike. But many bones share common physical traits, a fact that enabled anatomists to develop a simple bone classification method based on shape. The four shape-related categories of bones include long bones, short bones, flat bones, and irregular bones (Figure 9-1).
Long Bones are rod shaped and are always longer than they are wide. All long bones are part of the appendicular skeleton, and comprise most of the bones that form the upper and lower limbs. The longest long bone is the femur in the thigh, and the shortest is the bean-like distal phalanx at the end of the little toe. Long bones function as levers that facilitate body movements.
Short Bones are wedge-shaped bones and form the wrists and ankles. These little bones can slide over one another, giving the hands and feet a wide range of motion. The cuneiform bones of the ankle typify the structure of a short bone. Special short bones develop solely in tendons, the connective tissue bands that attach muscles to bones. These are sesamoid bones (SES-a-moyd), so named because they look like sesame seeds. The patella, or kneecap, is the largest sesamoid bone, but rice-sized sesamoid bones may form inside tendons of the hands and feet. It is thought that sesamoid bones stabilize tendons by preventing them from slipping from side to side, as they cross a joint.
Flat Bones have a broad, smooth surface, and are always thinner than they are long or wide. Despite their classification, many flat bones are curved. The bowl-like parietal bone, for example, forms part of the curved dome of the skull. Most flat bones are part of the axial skeleton and shield underlying organs and soft tissues. Some people have extra flat bones between their sutures, the zigzagging joints that hold together the major flat bones of the skull. These tiny bony islands are called sutural bones (Wormian bones).
Irregular Bones. Like the “none-of-theabove” selection from a multiple-choice question, irregular bones have unique and bizarre shapes. These bones may exhibit a variety of projections, indentations, notches, and holes. Ultimately, the odd shapes of irregular bones relate to their functions. For example, a typical vertebra has a hole through its vertical axis that allows for passage of the spinal cord. In addition, the vertebra’s antlerlike projections are sturdy attachment points for powerful back muscles that control posture and trunk movements.
While considerable variation in design exists among short bones, flat bones, and irregular bones, the long bones show the least variation in design. For this reason, we will use a long bone as a model for describing the gross anatomical features of a bone (Figure 9-2).
Figure 9-2. Parts of a long bone
ANATOMY OF A LONG BONE
While long bones come in a wide range of lengths, they all have three external features in common:
- Diaphysis (dī-AF-i-sis; growing between): the relatively long shaft that forms the middle section of the long bone
- Epiphysis (e-PIF-i-sis; upon growth): the enlarged region at the end of the diaphysis. An epiphysis is specified as either proximal or distal, depending on its relative distance from the body’s torso. In most long bones, both epiphyses are covered with articular cartilages (described earlier).
- Metaphysis (me-TAF-i-sis; between growth): the cone-shaped, transition region between the diaphysis and the epiphysis. The proximal or distal metaphysis of both regions in an adult may contain one or two epiphyseal lines, which are remnants of growth zones that existed when the bone was developing.
In addition, all long bones have a periosteum, compact bone, spongy bone, endosteum, medullary cavity, and a rich supply of blood vessels and nerves, and marrow. We will take a closer look at each of these features, beginning on the outer surface of the bone and working inward.
The Periosteum
When bones are cleaned, dried, and sterilized for display in a lab, all that remains is hard osseous tissue. However, living bones appear white because a tough membrane called the periosteum (per-ē-OS-tē-um; peri, around; oste, bone) covers them. This membrane consists of two layers that are structurally and functionally different from one another. The periosteum has an outer fibrous layer that consists of dense regular connective tissue. The inner osteogenic layer contains several types of bone cells. The periosteum is important to the bone in three ways:
- Protection: Densely packed collagen fibers make the fibrous periosteum an effective barrier that separates osseous tissue from surrounding tissues. If bacteria infect a nearby tissue, the periosteum can help prevent their spread into the osseous tissue. However, the periosteum cannot prevent bacteria from entering the bone through blood vessels. The fibrous periosteum also acts like a stretch-resistant jacket that helps prevent bones from bending excessively.
- Attachment site: The fibrous layer of the periosteum is the attachment site for tendons, ligaments, and blood vessels. In fact, the collagen fibers of the fibrous periosteum are continuous with those of tendons and ligaments. Short collagenous fibers, called perforating fibers (Sharpey’s fibers) attach the periosteum firmly to the underlying hard osseous tissue. When tendons or ligaments pull on the bone, the perforating fibers prevent the periosteum from tearing away. Blood vessels and nerves also attach to the fibrous periosteum, and they are distributed throughout this layer.
- Bone growth: The osteogenic layer of the periosteum contains several types of bone cells, including osteoblasts and osteoclasts. Osteoblasts add hard osseous material to the bone’s surface, while osteoclasts remove this material.
Compact Bone
Compact bone (dense bone) is osseous tissue that is solid and heavy, much like concrete (Figure 9-3). It forms the hard exterior, or cortex, of the bone; for this reason, compact bone is also called cortical bone (KOR-tik-al; cortex, bark). Due in part to its high density, compact bone is very strong and able to withstand enormous physical pressure and stress. As you might imagine, strength is an essential property of weight-bearing bones, such as those in your lower limbs. When running or jumping, the forces exerted on these weight-bearing bones in the average adult male may approach 550 kg (~ 1200 lbs.)! However, even bones that seldom support much weight can experience intense compression and bending forces as your muscles contract and relax. For example, simply unscrewing a tight jar lid can apply tremendous pressure to the two long bones within your forearm.
Figure 9-3. Compact and spongy bone
Spongy Bone
Spongy, or cancellous bone (KAN-se-lus; lattice), is osseous tissue that makes up all or part of the interior of bones. In long bones, it makes up most of the epiphyses and lines a tube-like medullary cavity within the diaphysis (shaft). Spongy bone consists of short interlocking struts of osseous tissue called trabeculae that separate numerous tiny cavities. A thin membrane, the endosteum, covers all trabeculae, but unlike the periosteum, the endosteum lacks a fibrous layer. In adult bones, either red or yellow bone marrow may fill the cavities between the trabeculae. Spongy bone reduces a bone’s total weight without overly reducing its strength; in fact, spongy bone actually helps to distribute the stress and strain that bones undergo as muscles pull on them.
Blood vessels, lymphatics, and nerves
Bones, like other organs, contain a rich supply of blood vessels (arteries and veins), lymphatic vessels, and nerves that play important roles in bone homeostasis. Arteries deliver nutrients to the bone, while veins remove substances that the bone releases into the tissue fluid. In most long bones, one nutrient artery enters the diaphysis through an opening called a nutrient foramen (for-Ā-men; opening). The nutrient artery enters the medullary cavity before it branches into smaller arteries that transport blood toward the epiphyses; however, these vessels do not extend past the epiphyseal line. Smaller arteries branch off of the medullary arteries and pass into the inner layers of compact bone in the diaphysis. These small arteries branch into still smaller arteries that transport blood toward the epiphyses. The periosteum has numerous arteries that penetrate and nourish the outer layers of compact bone in the diaphysis. On the other hand, the epiphyses have a blood vessel supply that is separate from that nourishing the metaphyses and diaphysis. Running essentially parallel to the arteries are veins that transport blood out of the bone.
Lymphatic vessels accompany blood vessels along the periosteum and pick up excess tissue fluid that seeps out of the bones. Thus far, however, lymphatic vessels have not been shown to penetrate into bones. Tiny nerves run alongside the bone’s periosteal blood vessels and lymphatic vessels. In addition, tiny nerve branches extend into the medullary cavity and the tiny passageways inside compact bone. When a bone tissue is damaged, nerves alert the person to the damage by sending pain signals to the brain.
Bone Marrow
Bone marrow is a soft, gelatinous material that fills the medullary cavity of long bones and the spaces between trabeculae in spongy bone. There are two types of bone marrow: red marrow and yellow marrow.
- Red marrow consists of blood vessels and hemopoietic tissue (HĒ-mō-poy-e-tik), the latter being responsible for making blood cells. Hemopoietic tissue contains highly branched fibroblasts that produce very delicate collagen filaments. These filaments intertwine in the extracellular fluid to form a network of collagen fibers. The network of fibers supports specialized cells called hemopoietic stem cells that divide repeatedly to form blood cells. During fetal development, red marrow occupies the marrow cavities of all bones, but by age 25, most of the skeleton’s red marrow has changed to yellow marrow. In the adult, red marrow exists mainly in the axial skeleton and in the proximal end of the upper arm bones and the thighbones.
- Yellow marrow consists mostly of adipose tissue that arises from red marrow. Beginning at about age 5, some of the hemopoietic cells in red marrow are replaced by adipocytes. The adipocytes fill with lipid droplets, causing the cells to appear yellow. In the adult, most of the skeleton’s yellow marrow is found in the medullary cavities of long bones. The conversion of red marrow to yellow marrow begins first in the distal bones of the upper and lower limbs. Lipids stored in yellow marrow provide energy for the bone and for other body tissues.
ANATOMY OF SHORT BONES, FLAT BONES, AND IRREGULAR BONES
While these bones come in an assortment of shapes and sizes, they all differ from long bones by not having a diaphysis, epiphyses, or medullary cavity. However, like long bones, they all have an outer layer of compact bone covered with periosteum. Since there is no medullary cavity, the interior of these bones is filled with spongy bone. Endosteum covers the trabeculae, and marrow fills the spaces between the trabeculae. In most flat bones and certain irregular bones (vertebrae), red marrow persists throughout adulthood.
Flat bones consist of equally thick layers of compact bone and spongy bone. In the parietal bone of the skull, for example, two layers of compact bone sandwich an equally thick layer of spongy bone called diploë (DIP-lō-ē; double). Short bones and irregular bones are made mostly of spongy bone surrounded by a thin shell of compact bone. In terms of their composition, short bones and irregular bones look much like the epiphyses of long bones.
OSSEOUS TISSUE
As fascinating as an individual bone may look, its gross anatomy barely hints at the constant chemical tug-of-war that takes place in its osseous tissue. A bone can grow, and it can rearrange its tissue to help it withstand mechanical stress. These qualities are due to the actions of different kinds of bone cells, and the extracellular environment in which they act. Moreover, the microscopic structure of both compact bone and spongy bone reveals that bone cells act in a coordinated manner. In this section, we will describe the stuff that makes up bones and how bone cells assemble osseous tissue into characteristic patterns.
Bone Matrix
The strength of osseous tissue is an attribute of its extracellular material, called bone matrix. Like the matrix of other connective tissues, bone matrix has two parts: (1) a homogeneous ground substance, and (2) a fibrous portion. The ground substance, which makes up about 65% of the bone matrix, consists of inorganic and organic materials. The most abundant inorganic material in the ground substance of bone matrix is hydroxyapatite, a mineral salt containing calcium phosphate, Ca3(PO4)2. The major organic components of the ground substance are proteoglycans, which contain chondroitin sulfate and hyaluronic acid. Collagen fibers make up the fibrous portion of bone matrix. The entire organic component of bone matrix, including the collagen fibers and proteoglycans, is called osteoid (OS-tē-oyd; ost, bone; oid, resembles).
A bone receives two benefits of having its bone matrix as a mixture of mineral salts and collagen fibers:
(1) Since mineral crystals bind tightly to collagen fibers, they cannot easily shift or slide past one another under stress.
(2) Collagen is less dense than mineral salts, so a mixture of collagen and minerals is lighter than an equal amount of minerals alone. Altogether, the arrangement of mineral salts and collagen fibers in bone matrix helps bones to resist compression, tension (pullingforces), and torsion (twisting forces).
The balance of mineral salts and collagen in the matrix is crucial to maintaining a bone’s physical integrity. If the concentration of either component in the matrix falls below normal, the bone may become either too brittle or too soft. On the one hand, a bone deficient in bone salts would be too flexible; it would twist or warp when stressed, just as a rubber dog bone would. On the other hand, a bone that is deficient in collagen would still be very hard, but it might shatter like glass when bent.
Classification of Bone Matrix
Based on the arrangement of the ground substance and collagen fibers in its bone matrix, osseous tissue is classified as either woven bone or lamellar bone.
- Woven bone is so named because it contains delicate, interlacing strands that look like threads in woven cloth. The tiny strands that make up woven bone contain irregularly arranged collagen fibers surrounded by tiny crystals of hydroxyapatite. Woven bone is found in the embryonic skeleton or in broken bones that are healing, and it represents the earliest stage of bone development.
- Lamellar bone (la-MEL-lar; lamella, plate) has parallel collagen fibers surrounded by ground substance that is assembled in layers called lamellae. Lamellar bone is “mature” bone tissue, and it comprises almost all of the osseous tissue in the adult skeleton. Depending on how the lamellae are arranged, lamellar bone is classified as either compact bone or spongy bone. These two types of osseous tissue have strikingly different patterns of lamellae, and these patterns determine how nutrients travel through the osseous tissue. Most compact bone is nourished from the “inside out,” while spongy bone is nourished from the “outside in.”
Compact Bone and Osteons
The lamellae of compact bone form groups of tiny cylinders called osteons, or Haversian systems. Researchers estimate that the adult skeleton contains around 20 million osteons. The average osteon has about 30 concentric lamellae, giving it the appearance of a sliced onion when viewed in cross section. The innermost lamella surrounds a narrow tunnel called the central canal, or Haversian canal, through which blood vessels and nerves run. Smaller branches extend from these vessels and nerves and pass into small perforating canals (Volkmann’s canals) that lead to the bone’s surface or into the medullary cavity. Nutrients from blood vessels in the central canal diffuse outward through tiny canals, called canaliculi (kan-a-LIK-ū-lī; little canals) to reach tiny cavities called lacunae, which house bone cells called osteocytes. Cellular wastes diffuse in the opposite direction; osteocytes in the outer lamella of an osteon are seldom more than 1/2 mm from the central canal.
The lamellae of compact bone form other patterns besides the concentric circles that identify osteons. Circumferential lamellae make up a few layers of a bone’s outer surface, and they are formed by osteoblasts in the osteogenic layer of the periosteum. After they are surrounded by calcified bone matrix, the osteocytes in circumferential lamellae are nourished through canaliculi that communicate with blood vessels in the periosteum. In addition, wedge-shaped features called interstitial lamellae exist within compact bone. These structures are the remains of older osteons that were destroyed as the result of bone resorption (discussed shortly).
Osteons are one reason why bones, especially long bones, are strong. Imagine that you could pull out the lamellae of an osteon like the tubes of a telescope. The osteon would look like a series of tubes-within-tubes. The outer lamellae reinforce the inner ones, an arrangement that helps an osteon to withstand tremendous compression. A spiraling pattern of collagen fibers within each lamella also resists tension. Also, the orientation of the collagen fibers alternates from one lamella to the next helping an osteon resist torsion. When a force twists an osteon clockwise, all the collagen fibers that spiral clockwise tighten and oppose the force. This is similar to the way a wet towel becomes progressively harder to twist as you add more twists to it. Half of an osteon’s lamellae have collagen fibers spiraling in one direction, while the remaining lamellae have fibers spiraling in the opposite direction. This allows an osteon to be resistant to torsion applied from any direction.
Spongy Bone and Trabeculae
Whereas lamellae form osteons in compact bone, they form trabeculae in spongy bone. The lamellae in a trabecula look like irregular or flattened ovals when viewed in cross section, and they seldom stack more than a few layers deep from center to edge. Unlike that of an osteon, the innermost lamella of a trabecula does not surround a central canal with a nourishing blood vessel. Instead, osteocytes within trabeculae receive nutrients through canaliculi that open through the endosteum to the bone marrow. This means that the osteocytes inside trabeculae are nourished from “outside in,” compared to the osteocytes in the osteons of compact bone, which are nourished from “inside out.” The outer lamella of a trabecula is covered by the endosteum, which consists of different kinds of bone cells, including osteoblasts and osteoclasts. We will discuss these cells, along with osteocytes, in the context of how osseous tissue is built up and broken down. Table 9-1 summarizes the characteristics in spongy and compact bone tissue.
BONE DEPOSITION BY OSTEOBLASTS
Bone deposition refers to the formation of osseous tissue, and this process requires (1) the formation of osteoid secreting bone cells, (2) the secretion of osteoid, and (3) the precipitation of calcium salts in the osteoid to form a hard matrix. These steps are described below:
Table 9-1. Comarison of trabeculae and osteons
Figure 9-4. Bone cells
- Development of osteoblasts. Osteoblasts are cells that secrete osteoid, the organic component of the bone matrix (Figure 9-4). Osteoblasts develop from osteogenic cells, unspecialized stem cells in the osteogenic layer of the periosteum and in the endosteum. Osteogenic cells are the only cells that divide in osseous tissue. Prior to secreting osteoid, the osteoblasts develop long cytoplasmic projections that extend in all directions to connect with adjacent osteoblasts. The tips of these projections contain gap junctions through which materials pass from one osteoblast into another.
- Secretion of osteoid. Spider-shaped osteoblasts begin bone deposition by secreting (depositing) osteoid, the bone’s organic matrix, into the extracellular space. The osteoid spreads around the cell’s “body” (containing the nucleus) and around the cell’s cytoplasmic extensions. At the same time, osteoblasts secrete enzymes that cause the bone matrix to harden. One such enzyme is alkaline phosphatase, which increases the concentration of phosphate ions (PO43-) in the osteoid.
- Calcification of the osteoid. The abundance of PO43- ions in the osteoid causes mineral salts, particularly calcium phosphate, to crystallize and precipitate like snow in the osteoid; this process is called calcification. As osteoid calcifies, the osteoblast’s body becomes trapped within a lacuna, and its cytoplasmic extensions become enclosed within canaliculi. After being “buried alive” in bone matrix, the osteoblasts are called osteocytes. Osteocytes are the most abundant cells in osseous tissue, and represent the “building superintendents” of bones, patiently maintaining and recycling the bone matrix. They do this by secreting enzymes that can dissolve mineral salts from the matrix or ones that cause mineral salts to precipitate in it. Osteocytes receive nutrients through the canaliculi and through gap junctions with adjacent osteocytes.
BONE RESORPTION BY OSTEOCLASTS
Just as it is necessary to withdraw money from a bank account periodically, under certain conditions, it is necessary to “withdraw” minerals from the calcified matrix of bones. The destruction of bone matrix and subsequent diffusion of its minerals into the blood is called bone resorption. The term “resorption” implies that the bone’s minerals are being absorbed into the blood a second time. This is true since they entered the body in food and were first absorbed into the blood through the intestines. Osteocytes can cause a small amount of bone resorption, but most resorption involves cells called osteoclasts.
- Development of osteoclasts: Osteoclasts are the most important matrix-destroying cells. These multinucleated cells are found mostly in the endosteum, but small numbers live in the periosteum’s osteogenic layer (Figure 9-4). In the marrow, specialized blood cells, called monocytes, fuse to form a single osteoclast. Like a tiny scrubbing brush, the part of an osteoclast’s plasma membrane that is in contact with the bone surface has hundreds of tiny finger-like processes, collectively known as a ruffled membrane. The ruffled membrane greatly increases the amount of osteoclast surface in contact with the bone surface, thereby increasing its ability to destroy bone matrix.
- Secretion of acids and enzymes: Osteoclasts begin bone resorption by secreting acids and enzymes onto a bone surface. The acids dissolve mineral salts within the ground substance of the matrix, while the enzymes break down the collagen fibers distributed throughout the ground substance. The ruffled membrane also engulfs pieces of digested bone matrix by phagocytosis.
- Formation of resorption pit: As an osteoclast does its work, it leaves behind a little dimple in the bone surface called a resorption pit, or Howship’s lacuna. Much of the calcium freed during bone resorption enters the blood; therefore, when osteoclasts become more active, the amount of calcium ions in the blood rises.
DEVELOPMENT AND GROWTH OF BONES
Our discussions to this point have focused on the osseous tissue in an adult human body. Now consider an X-ray that reveals what your body probably looked like when you were a fetus only 12 weeks old. There are no bones to be found! What you can see instead are cloudy patches of membranes and little bone-shaped pieces of cartilage that together look like a human skeleton. Two processes take place that transform this tiny skeleton-to-be into a network of sturdy bones. First, the soft fetal “models” of bones seen in the X-ray must ossify. Second, the ossified bones must keep growing in a coordinated fashion until adulthood.
To trace out the processes of bone development and growth, we will start by describing ossification (os-i-fi-KĀ-shun), or osteogenesis (os-tē-ō-JEN-e sis; osteo, bone; genesis, creating), the process in which hard bones arise from soft tissues during fetal life. Then we will examine two ways in which bones grow and look at the activities of osteoblasts and osteoclasts that make bone growth happen. Bones can neither ossify nor grow, however, without precise hormonal controls and the right balance of nutrients, so we will discuss these topics to finish this section.
Ossification starts early during fetal life when connective tissues arrange themselves into bone models. These models consist of soft tissues but look something like future bones. The models for bones have two different origins: some bones arise from mesenchymal membranes, but most arise from hyaline cartilage. Keep in mind that regardless of their origin, bones ossify in two main steps: (1) osteoblasts secrete osteoid into the bone model; and (2) the osteoid calcifies. But since bones arise from two kinds of bone models, physiologists distinguish between two kinds of ossification: intramembranous ossification and endochondral ossification.
Intramembranous Ossification
A few bones in the skeleton develop through intramembranous ossification (en-tra-MEM bra-nus). As the name implies, this form of ossification occurs “within a membrane;” in this case, the membrane consists of dense irregular connective tissue. Intramembranous ossification begins around the eighth week of fetal development and forms the flat bones of the skull, parts of the lower jaw, and the diaphyses of the collarbones. In the skull, the process begins after fibroblasts weave a dense fibrous membrane, consisting mostly of collagen fibers, between the scalp and brain. Intramembranous ossification unfolds in four steps.
- Formation of ossification center: Some osteogenic cells in the membrane differentiate to become osteoblasts. The site where this occurs is called an ossification center. The osteoblasts secrete osteoid, which calcifies to form threadlike trabeculae around the collagen fibers of the membrane.
- Development of woven bone: The first trabeculae in the ossification center consist of only one layer of bone matrix. As more of these “nonlamellar” trabeculae emerge, they interconnect to form a delicate net-like tissue called woven bone (described earlier). At the same time, blood vessels within the fibrous membrane become trapped in between the trabeculae.
- Development of lamellar bone and periosteum: The osteoblasts on the surface of woven bone secrete osteoid, which calcifies to form another layer of bone matrix. Now, the woven bone is becoming lamellar bone. Meanwhile, a periosteum develops as fibroblasts and collagen fibers cluster together along the perimeter of the fibrous membrane model. Osteoblasts in the periosteum deposit layers of bone matrix that form a shell of compact bone around the membrane.
- Formation of marrow: As the trabeculae grow thicker, the spaces between them (and around the intertwining blood vessels) get smaller and the tissue is called spongy bone. In flat bones of the skull, this spongy bone is also called diploë. Eventually, blood vessels between the trabeculae give rise to red marrow (hemopoietic tissue) and begin making blood cells.
At birth, not all of the flat bones in the skull are completely ossified. Where certain flat bones will eventually connect to one another, sections of the fibrous membrane remain and are called fontanels (fon-ta-NELZ; little fountains), or “soft spots.” Fontanels allow the skull to deform slightly as it passes through the birth canal, and they allow the skull to expand as the brain grows. Fontanels completely ossify within 1-2 years after birth.
Endochondral Ossification
Most bones in the skeleton develop through a process called endochondral ossification (en dō-KON-dral). As the name implies, this process occurs “inside cartilage” tissue. We will discuss the steps of endochondral ossification using a “generic” long bone as an example (Figure 9-5).
Figure 9-5. Endochondral ossification
- Formation of cartilage model: Prior to the sixth week of fetal development, chondroblasts (cartilage cells) gather at the site of the bone -to-be and secrete a cartilage matrix. The matrix forms a hyaline cartilage model, a soft, miniature version of a bone, and the chondroblasts within the matrix become chondrocytes. At the same time, dense fibrous connective tissue condenses around the cartilage model, forming a tough covering, the perichondrium. As the cartilage model grows, nutrients cannot reach the chondrocytes deep inside the model fast enough to sustain them. Malnutrition and a lack of oxygen cause the chondrocytes to swell and release alkaline compounds into the cartilage matrix. As the matrix pH rises in those areas, calcium salts precipitate, causing the cartilage to calcify.
- Formation of primary ossification center: At 6-8 weeks of fetal development, blood vessels penetrate and grow throughout the perichondrium in the diaphysis of the cartilage model. Shortly thereafter, osteogenic cells in the perichondrium differentiate and become osteoblasts. After this happens, the perichondrium is now called the periosteum. The osteoblasts secrete osteoid onto the cartilage surface, which calcifies to form a hard bone collar around the diaphysis. The bone collar (1) prevents the cartilage from growing wider, and (2) effectively stops the diffusion of nutrients to the deepest cartilage. Consequently, the chondrocytes deep within the diaphysis swell, expand their lacunae, and die. This deep portion of the diaphysis is the first place where bone will replace cartilage, so it is called the primary ossification center.
- Formation of spongy bone in the inner diaphysis: Blood vessels, along with osteoblasts and osteoclasts, penetrate the primary ossification center. Osteoclasts begin destroying some of the calcified cartilage, causing large cavities to develop. At the same time, osteoblasts secrete osteoid that calcifies to form woven bone (simple trabeculae without lamellae) around any remaining calcified cartilage.
- Formation of medullary cavity: Osteoblasts in the periosteum create osteons by depositing concentric layers of bone matrix around periosteal blood vessels. The compact bone along the diaphysis continues to thicken as the bone collar spreads toward the epiphyses. Deep in the diaphysis, osteoclasts begin removing some of the woven bone that was deposited by the osteoblasts. Eventually, a large hollow channel, the medullary cavity (MED-ū-lar-ē; medulla, marrow) emerges, but spongy bone remains along the inside wall of this cavity. In addition, hemopoietic cells brought into the bone by blood vessels divide rapidly and fill the medullary cavity with red marrow.
- Formation of secondary ossification centers and epiphyseal plate: Near the time of birth, chondrocytes deep in the epiphyses swell and die; this event marks the beginning of secondary ossification centers. Blood vessels and osteoblasts enter the cavities left by the departed chondrocytes. The osteoblasts produce spongy bone, which spreads outward to the edges of the epiphyses. Eventually, only two structures in the maturing bone consist of cartilage from the original model: (1) an epiphyseal plate (ep-i-FIZ-ē-al), or growth plate, a thin layer of cartilage in one or both metaphyses, and (2) articular cartilage covering the end of one or both epiphyses.
PATTERNS OF BONE GROWTH
Although ossification starts early in fetal life, most bones in the body keep growing long after they initially ossify from either a fibrous membrane or cartilage model. Interestingly, long bones have two independent growth processes: one that makes the bone longer, and one that makes the bone wider.
Longitudinal Growth
Most long bones face the daunting challenge of having to grow longer (experience longitudinal growth) even as they bear weight or endure other types of physical stress. Amazingly enough, the way a long bone grows longer can be compared to making a skyscraper grow taller by simultaneously stuffing in additional floors part way from the top and bottom of the building. In a long bone, these “action sites” of growth are the epiphyseal plates. An epiphyseal plate in a long bone has four zones, each of which contributes to longitudinal growth.
- Growth zone: the cartilage expands: The layer of the epiphyseal plate that faces the epiphysis is where cartilage grows most quickly, and it is where a long bone lengthens. Until early adulthood, the chondrocytes closest to the nourishing blood vessels in the epiphysis undergo mitosis and cytokinesis. Like one acrobat climbing atop the shoulders of another, the daughter cells push apart to form long stacks or rows of chondrocytes that stretch from the epiphysis toward the diaphysis. The recently divided chondrocytes secrete fresh cartilage matrix into the growth zone, which pushes the epiphysis away from the diaphysis. This action is sort of like squeezing a toothpaste tube with a loose cap. The rising mass of toothpaste (cartilage matrix) pushes the cap (the epiphysis) up and away from the neck of the tube (the diaphysis).
- Transformation zone: the cartilage calcifies: As the cartilage matrix grows, the epiphysis and its nourishing blood vessels move away from the rows of chondrocytes. Consequently, the chondrocytes that are farthest from the epiphysis begin to starve, and in response, they swell up. (Recall that this is the fate suffered by the chondrocytes in the diaphysis of a long bone during endochondral ossification.) During this transformation, the swollen chondrocytes release alkaline substances into the surrounding matrix, which causes the pH of the matrix to rise. Mineral salts precipitate into the cartilage, causing it to calcify.
- Osteogenic zone: the calcified cartilage ossifies: Eventually, the chondrocytes farthest from the epiphysis die within their lacunae. Osteoclasts digest some of the calcified cartilage, leaving behind long finger-like projections of calcified cartilage that point toward the medullary cavity of the diaphysis. New blood vessels grow between these projections, bringing with them osteoblasts that deposit layers of spongy bone; hence, the projections of calcified cartilage ossify.
- Remodeling zone: the medullary cavity expands: The spongy bone that is deposited in the osteogenic zone doesn’t last very long. Osteoclasts resorb the spongy bone and digest the remaining calcified cartilage at the tips of the projecting calcified cartilage. This action causes the medullary cavity to grow longer as the bone grows longer. Notice, too, that the thickness of the epiphyseal plate remains fairly constant as the bone grows longer; cartilage is piled up on the epiphysis side of the plate while bone disappears from the diaphysis side. In essence, the medullary cavity “chases after” the epiphysis that is being pushed away from the diaphysis.
As a person nears adulthood, cartilage formation at the growth zone slows while activity within the other zones continues at a steady pace. When this occurs, ossification on the diaphysis side of the epiphyseal plate eventually “overtakes” the growth zone. When the growth zone ossifies, the epiphyseal plate is “fused” and longitudinal growth ceases. Most epiphyseal plates fuse by age 20, and after fusion, they are called epiphyseal lines. Table 9-2 shows the approximate ages that epiphyseal plates become epiphyseal lines in different bones.
Table 9-2. Age at time of growth plate fusion
Appositional Growth
Although fusion of an epiphyseal plate means a bone cannot get longer, the bone can still grow wider, a process called appositional growth (ap-ō-ZISH-un-al; to place at). This type of growth occurs whenever osteoblasts add matrix to the bone’s outer surface faster than osteoclasts can remove it. Appositional growth occurs fastest during childhood and adolescence but continues at a very slow pace through most of adulthood. For a growing child, appositional growth is especially important in developing the weight-bearing bones of the lower limbs. Without appositional growth to accompany longitudinal growth, these long bones would likely bend and break.
Of course, thicker bones can better support the body’s weight. But wouldn’t appositional growth cause bones to be significantly more dense and heavier? Interestingly, the answer is no. As osteoblasts add bone matrix to the periosteal side of the bone, osteoclasts remove bone matrix from the endosteal side; therefore, as a long bone’s outside diameter widens, its medullary cavity also widens. However, the rate of bone deposition along the periosteum slightly exceeds the rate of bone resorption along the endosteum. The result is a thickening of the compact bone in the diaphysis region as the overall diameter of this region increases. But the medullary cavity’s diameter also increases, which allows the bone to remain lightweight while providing additional room for bone marrow (see Figure 9-6).
During appositional growth, new osteons develop as infoldings of the periosteum and circumferential lamellae. The growth process takes place in four steps:
- Formation of bone ridges. Osteoblasts in the periosteum deposit bone matrix that forms a bony ridge on either side of a periosteal artery, vein, and nerve.
- Fusion of bone ridges. Osteoblasts continue to deposit bone matrix, causing the ridges to rise above and over the vessel. Eventually, the ridges fuse, enclosing the vessel within a tunnel. The enclosed vessels and nerve maintain connections with surface vessels and nerves by way of branches within perforating (Volkmann’s) canals.
- Formation of concentric lamellae. Osteoblasts lining the inside of the tube deposit bone matrix in a series of circular layers (concentric lamellae). As each new lamella is added, the tunnel around the vessel gets smaller. The lining of this tunnel was derived from the periosteum but is now called endosteum.
- Completion of osteon. In time, a final, innermost lamella forms around the vessel and the central (Haversian) canal is complete. Several layers of circumferential lamellae are laid down on the bone’s surface, while new osteons begin forming. The entire process repeats at another vessel nearby, forming another osteon.
From beginning to end, construction of an osteon takes about 100 days. Periodically, osteoclasts erode grooves in the surfaces of a bone and in the process cut into old osteons. When new osteons form in these regions, the remnants of the old osteons remain as interstitial lamellae. The average life expectancy of an osteon in a middle aged man is about 15 years.
Now that you know how a long bone grows in length and width, you may be wondering how short bones, flat bones, and irregular bones grow. While a bone must have an epiphyseal plate in order to have longitudinal growth as described earlier, bones of all shapes can experience appositional growth in the manner just described.
Now that you know how a long bone grows in length and width, you may be wondering how short bones, flat bones, and irregular bones grow. While a bone must have an epiphyseal plate in order to have longitudinal growth as described earlier, bones of all shapes can experience appositional growth in the manner just described.
Figure 9-6. Appositional bone growth
FACTORS AFFECTING BONE DEVELOPMENT
Although all tissues need an assortment of nutrients to stay healthy, a few nutrients are especially important to bone health.
- Proteins: Strong, resilient bones and cartilages contain a significant amount of collagen protein. Proteins in the diet are broken down in the intestines to their basic building blocks, amino acids. In turn, osteoblasts and chondroblasts use amino acids to make collagen.
- Minerals: In particular, calcium and phosphorus are needed to form the inorganic mineral salts that harden the bone matrix. Chondrocytes use sulfur to make chondroitin sulfate, which stiffens the hyaline cartilage located on the ends of bones and in epiphyseal plates. Sulfur also forms sulfide bonds in collagen, increasing its durability and providing flexibility to the collagen fibers.
- Vitamins: Two vitamins that play noteworthy roles in bone growth and maintenance are vitamins C and D. Vitamin C promotes the formation of cross-links between adjacent collagen fibers. The cross-links hold the fibers together and contribute to a bone’s tensile (pulling) strength. Calcitriol (kal si-TRĪ-ol), or active vitamin D, promotes bone deposition by stimulating osteoblasts to secrete more osteoid. It also stimulates cells in the intestine to make a protein called calbindin, which binds to calcium in food, thereby allowing the calcium to enter the blood. Without calbindin, most of the calcium a person might eat would pass right through the intestines and never reach the bones.
Although calcitriol functions as a hormone, other hormones that play significant roles in bone development include growth hormone, thyroxine, and the sex hormones.
- Growth hormone (GH): The pea-sized pituitary gland at the base of the brain releases this hormone that stimulates cells to absorb amino acids and other chemicals from the blood, and it promotes protein synthesis. As the name suggests, growth hormone promotes growth; however, it does this in a roundabout way. Growth hormone causes the liver and muscles to secrete a group of proteins called insulin-like growth factors – IGFs, or somatomedins. The IGFs promote bone growth by stimulating chondrocytes to make cartilage at epiphyseal disks.
- Thyroxine (thī-ROK-sēn): The thyroid gland in the neck releases this hormone, also called thyroid hormone (TH), which increases the metabolic activity of cells. Thyroxine also enhances growth hormone’s effect on chondrocytes and osteoblasts.
- Sex hormones: The gonads (ovaries and testes) and the adrenal glands near the kidneys release sex hormones, including estrogen and testosterone. Sex hormones stimulate longitudinal bone growth, as evidenced by the dramatic growth spurt that occurs at the time of puberty. However, sex hormones also promote the calcification of epiphyseal disks. Females usually stop growing sooner than males due to the effect of high estrogen levels at puberty. Estrogen has a greater effect than testosterone in causing the fusion of epiphyseal plates.
BONE REMODELING
Having learned about how bones develop, it might seem logical to compare bones to concrete. Concrete begins as a soft mixture that becomes extremely hard over time. Likewise, bones begin as either a soft membrane or a cartilage model that hardens over time, but there the analogy ends. Unlike concrete, which may not change for decades, bones are always changing. New bone matrix is constantly added to bones, and at the same time, old matrix is constantly removed from them. This simultaneous bone deposition and bone resorption is called bone remodeling. First, we will discuss the importance of remodeling as part of a bone’s response to physical stress. Next we will discuss how remodeling is important to calcium homeostasis, and then we conclude with a look at how bones repair themselves after injury.
BONE REMODELING AND BONE DENSITY
Bone density is a measure of a bone’s mineral (mainly calcium salt) content, and it has a positive effect on the bone’s structural strength. In other words, as a bone’s mineral content increases, so does the bone’s density and strength. Bone remodeling can significantly alter bone density, but in most young and middle-aged adults, the rates of bone deposition and bone resorption are roughly equal. The result is that most bones in these individuals maintain a nearly constant shape and size. However, if a bone experiences higher than-normal physical stress, such as compression or bending, the rate of bone deposition can exceed that of bone resorption. This explains why leg bones of a long-distance runner may be significantly more dense and stronger than leg bones of a sedentary person.
While physical stress increases the rate of bone deposition, a lack of physical stress increases the rate of bone resorption. You can see this effect in a person who has had a broken leg immobilized by a cast. During the healing process, a broken leg bone may become significantly less dense than the similar bone in the healthy leg. In addition, bone density in the healthy leg may increase if those bones have to support more body weight while the broken bone heals. Applying stress to the healed bone increases bone deposition and can return the bone’s density to normal.
So how does a bone “know” when it is being stressed? There are various hypotheses that attempt to answer this question. Osteocytes within lacunae may react to minute electrical currents generated when the bone’s mineral salts are compressed. Geologists have noted that mineral salts, such as quartz, generate minute electrical currents when compressed, a response called the piezoelectric effect (pī-zō-ē-LEK-trik; piezo, squeeze). The minerals in bone matrix also exhibit a piezoelectric effect when compressed. Simply standing up could stress a leg bone enough to “shock” its osteocytes. In response, the osteocytes can stimulate osteoblasts on the bone’s surface (by way of gap junctions), which respond by secreting more osteoid. The response of immobilized bones to artificially produced electric fields supports the piezoelectric hypothesis. Exposing an immobilized bone to electrical fields, which are the same intensity as those generated naturally under stress, can cause bone deposition to increase.
A second hypothesis for how bones detect mechanical stress relates to changes in hydrostatic pressure. When osseous tissue is squeezed, the pressure of liquids inside lacunae and canaliculi increases. Osteocytes may respond to this change in hydrostatic pressure by stimulating the osteoblasts as described previously. Osteoblasts may also be responding to increasing temperature that bones experience when under physical stress. It is likely that bones may respond to all of these factors.
So why don’t all bones respond the same way to stress? Some bones, such as those on top of the skull are rarely stressed. According to hypotheses, these bones should disappear because of resorption. Since this does not happen, it is apparent that not all bones respond to stress in the same way. While bones generally respond to periodic changes in stress by increasing deposition, some bones respond to constant stress by increasing resorption. Orthodontists take advantage of this fact when using braces to straighten protruding teeth. Applying constant pressure to the anterior side of a tooth causes resorption on the posterior side of the tooth’s socket. This allows room for the tooth to move posteriorly.
BONE REMODELING AND Ca2+ HOMEOSTASIS
Not only does bone remodeling reshape bones to adapt them to the demands of physical stress, it is also important in maintaining optimum calcium concentration in the blood. Calcium is required for muscle contraction, transmission of nerve signals, blood clotting, and many other processes. There fore, the role of the skeletal system in supplying calcium to the blood cannot be understated. Bones store 99% of the body’s calcium, and remodeling causes about 25% of the calcium in the blood to exchange with calcium in bones every minute. All in all, remodeling accounts for about 10% of the skeleton being recycled each year. Two hormones, parathyroid hormone and calcitonin, regulate blood calcium levels, and they do this, in part, by affecting bone remodeling (Figure 9-7).
Parathyroid hormone (PTH) is made in four small parathyroid glands on the posterior surface of the thyroid gland. PTH increases blood calcium concentration (Ca2+) in several ways, but one way is by increasing bone resorption. The parathyroid glands secrete PTH into the blood when the blood calcium concentration (Ca2+) is lower than optimum. When PTH reaches the bones, it stimulates osteoclasts. The osteoclasts respond by releasing more acids that dissolve the mineral salts in bone matrix. Some of the liberated calcium ions diffuse into nearby blood vessels, thereby increasing blood Ca2+.
Figure 9-7. Calcium homeostasis
REPAIR OF FRACTURES
In order for bones to function in the ways described at the beginning of the chapter, it is essential that they be repaired when damaged. Therefore, it is appropriate to conclude this chapter with a discussion of how broken bones heal. A break in a bone is called a fracture, and the healing of a fracture involves four stages: hematoma, fibrocartilage callus, bony callus, and remodeling.
- Hematoma stage: When a bone breaks (fractures), blood vessels rupture and blood spills out into the surrounding tissues. Blood loss from the vessel is called hemorrhage. Chemical reactions in the blood cause numerous protein fibers to form at the injury site. The fibers trap blood cells to form a mass called a hematoma (hē-ma-TŌ-ma; hema, blood; oma, tumor), or blood clot. This process is called coagulation (kō-ag-ū-LĀ-shun; curdle). The hematoma helps prevent further loss of blood from the broken blood vessels. At this time, the damaged tissues release a variety of chemicals that promote inflammation. Signs of inflammation include swelling, redness, and heat. Specialized white blood cells called macrophages move through the wound removing dead tissue, any bacteria that might be present, and generally “cleaning up” the wound.
- Fibrocartilage callus stage: A few days after the fracture, blood vessels grow into the area and mesenchyme cells differentiate to become fibroblasts. Fibroblasts secrete collagen proteins that form a network of collagen fibers in the interstitial spaces. At the same time, other mesenchyme cells become chondroblasts that secrete cartilage matrix. The cartilage matrix hardens around the collagen fibers creating a mass called a fibrocartilage callus. The fibrocartilage callus acts like a “bridge” to hold the broken ends of the bone together. In time the fibrocartilage callus calcifies, which sets the stage for the deposition of bone matrix. The wound now looks similar to the early stages of endochondral ossification (described earlier).
- Bony callus stage: Eventually, the calcified fibrocartilage callus is replaced by osseous tissue to form a bony callus. This happens after osteogenic cells and osteoclasts migrate into the fibrocartilage callus. Osteoclasts begin digesting the calcified cartilage, while osteogenic cells differentiate to become osteoblasts. Within a month after the fracture, osteoblasts begin secreting osteoid within the fibrocartilage callus. The initial osseous tissue that forms in the wound is woven bone, which is similar to that formed in the medullary cavity during endochondral ossification. In time, more layers of bone matrix are added to the trabeculae, converting the woven bone to lamellar bone.
- Remodeling stage: Normally, more bone matrix is deposited during the healing process than is needed, so resorption by osteoclasts removes excess osseous material. Ultimately, the final shape of the bone will be influenced by patterns of stress.
TOPICS TO KNOW FOR CHAPTER 9
(Osseous Tissue)
accessory parts of the skeletal system
alkaline phosphatase
anatomy of a long bone
anatomy of non-long bones
antagonists
appendicular skeleton
appositional growth
articular cartilage
articulations
axial skeleton
blood clot
bone collar
bone density
bone deposition
bone deposition by osteoblasts
bone marrow
bone matrix
bone models
bone remodeling
Ca2+ homeostasis
bone repair
bone resorption
bony callus stage
calbindin
calcification
calcitonin (CT)
calcitriol
canaliculi
cancellous bone
cartilage
central canal
chondroitin sulfate
circumferential lamellae
classification of bone matrix
classification of bones
coagulation
collagen fibers
compact bone
comparison of trabeculae and
osteons
compression strength
concentric lamellae
cortical bone
development and growth of
bones
diaphysis
endochondral ossification
endosteum
epiphyseal lines
epiphyseal plate
epiphysis
estrogen
factors affecting bone
development
fibrocartilage callus stage
fibrous periosteum
flat bones
fontanels
function of periosteum
functions of skeletal cartilages
functions of the skeletal system
growth hormone
growth zone
Haversian canal
Haversian systems
hematoma
hematoma stage
hemopoiesis
hemopoietic stem cells
hemopoietic tissue
Howship’s lacuna
hyaluronic acid
hydroxyapatite
inflammation
inorganic matrix
insulin-like growth factors
interstitial lamellae
intramembranous ossification
irregular bones
joints
lacunae
lamellae
lamellar bone
ligament
long bones
longitudinal growth
lymphatics of bone
macrophages
medullary cavity
mesenchyme membranes
metaphysis
mineral salts
monocytes
nutrient artery
nutrient foramen
organic matrix
osseous tissue
ossification
ossification center
osteoblasts
osteoclasts
osteocytes
osteogenesis
osteogenic cells
osteogenic layer
osteogenic zone
osteoid
osteons
parathyroid hormone (PTH)
patterns of bone growth
perforating canals
perforating fibers
primary ossification center
proteoglycans
red marrow
remodeling stage
remodeling zone
repair of fractures
resorption pit
ruffled membrane
secondary ossification centers
sesamoid bones
sex hormones
Sharpey’s fibers
short bones
skeletal system
skeleton
somatomedins
spongy bone
suture bones
tension strength
testosterone
the periosteum
thyroxine
torsion strength
trabeculae
transformation zone
vessels in bone
vitamin C
vitamin D
Volkmann’s canals
Wormian bones
woven bone
yellow marrow
EOC Questions
