Human Anatomy Chapter 6 Textbook

The 6 Functions of the Skeletal System
1. Support
2. Protection
3. Assistance in Movement
4. Mineral Homeostasis (Storage and Release)
5. Blood cell production
6. Triglyceride Storage
Skeletal System Function in Support
The skeleton serves as the structural framework for the body by supporting soft tissues and providing attachment points for tendons of most skeletal muscles.
Skeletal System Function in Protection
The skeleton protects the most important internal organs from injury. For example, cranial bones protect the brain, and the rib cage protects the heart and lungs.
Skeletal System Function in Assistance and Movement
Most skeletal muscles attach to bones; when they contract, they pull on bones to produce movement.
Skeletal System Function in Mineral Homeostasis (Storage and Release)
Bone tissue makes up about 18% of the weight of the human body. It stores several minerals, especially calcium and phosphorus, which contribute to the strength of the bone. Bone tissue stores about 99% of the bodies calcium. On demand, bone releases minerals into the blood to maintain critical mineral balances (homeostasis) and to distribute the minerals to other parts of the body.
Skeletal System Function in Blood Cell Production
Within certain bones, a connect tissue called red bone marrow produces red blood cells, white blood cells and platelets, a process called hemopoiesis.
Red Bone Marrow
Consists of developing blood cells, adipocytes, fibroblasts, and macrophages within a network of reticular fibres. It is present in developing bones of the fetus and in some adult bones, such as the hip (pelvic) bones, ribs, sternum (breastbone), vertebrae (backbone), skull, and ends of bones of the humerus (arm bone) and femur (thigh bone). In a new born, all bone marrow is red and is involved in hemopoiesis. With increasing age, much of the bone marrow changes from red to yellow.
Skeletal System Function in Triglyceride Storage
Yellow bone marrow consists mainly of adipose cells, which store triglycerides. The stored triglycerides are a potential chemical energy reserve.
Long Bone
Greater in length than in width. A typical long bone consists of a diaphysis, epiphyses, metaphyses, articular cartilage, periosteum, medullary cavity, and endosteum.
Diaphysis
The bones shaft or body- the long cylindrical, main portion of the bone.
Epiphyses
The proximal and distal ends of the bone
Metaphyses
The regions between the diaphyses and the epiphyses. In a growing bone, each metaphysis contains and epiphyseal growth plate.
Epiphyseal Growth Plate
A layer of hyaline cartilage that allows the diaphyses of the bone to grow in length. When a bone ceases to growth in length at about ages 14-24, the cartilage in the epiphyseal plate is replaced by bone; the resulting bony structure is known as the epiphyseal line.
Articular Cartilage
A thin layer of hyalin cartilage covering part of the epiphysis where the bone forms an articulation (joint) with another bone. It reduces friction and absorbs shock at freely moveable joints. Because articular cartilage lacks a perichondrium and lacks blood vessels, repair of damage is limited.
Periosteum
A tough connective tissue sheath and its associated blood supply that surrounds the bone surface wherever it is not covered by articular cartilage. It is composed of an outer fibrous layer of dense irregular connective tissue and an inner osteogenic layer that consists of cells. Some of the cells enable the bone to grow in thickness, but not in length. The periosteum also protects the bone, assists in fracture repair, helps nourish bone tissue, and serves as an attachment point for ligaments and tendons. The periosteum is attached to the underlying bone by perforating fibres.
Perforating Fibres
Thick bundles of collagen that extend from the periosteum into the bone of the extracellular matrix.
Medullary (Marrow) Cavity
A hollow cylindrical space within the diaphyses that contains fatty yellow bone marrow and numerous blood vessels in adults. This cavity minimizes the weight of the bone by reducing the dense bony material where it is least needed. The long bones tubular design provides maximum strength with minimum weight.
Endosteum
A thin membrane that lines the medullary cavity. It contains a single layer of bone forming cells and a small amount of connective tissue.
Osseous Tissue
Contains an abundant extracellular matrix that surrounds widely separated cells. The extracellular matrix is about 15% water, 30% collagen fibres, and 55% crystallized mineral salts. The most abundant mineral salt is calcium hydroxide, to form crystals of hydroxyapatite.
Calcification
As crystals form, they combine with still other mineral salts, such as calcium carbonate, and ions such as magnesium, fluoride, potassium, and sulfate. As these minerals are deposited in the framework formed by the collagen fibres of the extracellular matrix, they crystallize and tissue hardens. This process of calcification is initiated by bone-building cells called osteoblasts. Requires the presence of collagen fibres.
Bone Hardness
Depends on the crystallized inorganic mineral salts
Bone Flexibility
Depends on its collagen fibres
Collagen Fibres in Bone
They provide tensile strength, resistance to being stretch or pulled apart.
4 Cells Present in Bone Tissue
1. Osteogenic Cells
2. Osteoblasts
3. Osteocytes
4. Osteoclasts
Osteoprogenitor Cells
Unspecialized bone stem cells derived from mesenchyme, the tissue from which almost all connective tissues are formed. They are the only bones cells to undergo cell division; the resulting cells develop into osteoblasts. They are found along the inner lining portion of the periosteum, in the endosteum, and in the canals within bone that contain blood vessels.
Osteoblasts
Bone building cells. They synthesize and secrete collagen fibres and other organic components needed to build to extracellular matrix of bone tissue, and they initiate calcification. As osteoblasts surround themselves with extracellular matrix, they become trapped in their secretions and become osteocytes.
Osteocytes
Mature bone cells. The main cells of bone tissue and maintain its daily metabolism, such as exchange of nutrients and wastes with blood. Like osteoblasts, osteocytes do no undergo cell division.
Osteoclasts
Huge cells derived from as many as 50 monocytes ( a type of white blood cell) and are concentrated in the endosteum. On the side of the cell that faces the bones surface, the osteoclasts plasma membrane is deeply folded into a ruffled border. Here the cell releases powerful lysosomal enzymes and acids that digest the protein and mineral components of the underlying extracellular bone matrix.
Resorption
The breakdown of the bone extracellular matrix. It is part of the normal development, maintenance, and repair of bone. They help regulate blood calcium level and are target cells for drug therapy, used to treat osteoporosis.
Bone
Not completely solid but has many small spaces between its cells and extracellular matrix components. Some spaces serve as channels for blood vessels that supply bone cells with nutrients. Other spaces act as storage areas for red bone marrow. Depending on the size and distribution of the spaces, the regions of a bone may be categorized and compact or spongy. Overall, about 80% of the skeleton is compact bone and 20% is spongy bone.
Compact Bone
Contains few spaces and is the strongest form of bone tissue. It is found beneath the periosteum of all bones and makes up the bulk of the diaphyses of long bones. Compact bone tissue provides protection and support and resists the stresses produced by weight and movement. Composed of repeating structural units called osteons or haversion systems. Each osteon consists of concentric lamellae or haversion canal.
Concentric lamellae
Resemble the growth rings of a tree. They are circular plates of mineralized plates of extracellular matrix of increasing diameter, surrounding a small network of blood vessels and nerves located in the central canal. These tubelike units of bone generally form a series of parallel cylinders that, in long bones, tend to run parallel to the long axis of the bone.
Lacunae
Small spaces between concentric lamellae, which contain osteocytes.
Canaliculi
Radiate in all directions from the lacunae and are filled with extracellular fluid. Inside the canaliculi are slender fingerlike processes of osteocytes. Neighbouring osteocytes communicate via gap junctions. The cansliculi connect lacunae with one another and with the central canals, forming an intricate, miniature system of interconnected canals throughout the bone. This system provides many routes for nutrients and oxygen to reach the osteocytes and for removal of wastes.
Osteons in Compact Bone Tissues
They are aligned in the same direction and are parallel to the length of the diaphysis. As a result, the shaft of a long bone resists bending or fracturing even when considerable force is applied from either end.
Lines of Stress in Bone
The lines of stress in a bone are not static. They change as a person learns to walk and in response to repeated strenuous physical activity, such as weight training. These lines of stress in bone can also change because of fracture or physical deformity. Thus, the organization of osteons is not static but changes over time in response to the physical demands placed on the skeleton.
Interstitial Lamellae
The areas between neighbouring osteons contain this lamellae, which also have lacunae with osteocytes and canaliculi. Interstitial lamellae are fragments of older osteons that have been partially destroyed during bone rebuilding or growth.
Perforating (Volkmann’s) Canals
Transverse canals where blood vessels and nerves from the periosteum penetrate the compact bone. These vessels and nerves of the perforating canals connect those of the medullary cavity, periosteum and central canals.
Circumferential Lamellae
Lamellae arranged around the entire outer and inner circumference of the shaft of a long bone. They develop during initial bone formation.
Outer Circumferential Lamellae
The circumferential lamellae directly deep to the periosteum. They are connected to the periosteum by perforating (Sharpey’s) fibres.
Inner Circumferential Lamellae
The circumferential lamellae that line the medullary cavity.
Spongy Bone Tissue
Also referred to as trabecular or cancellous bone tissue. Does not contain osteons and is always located in the interior of a bone, protected by a covering of compact bone. It consists of lamellae arranged in an irregular pattern of thin columns called trabeculae. Between the trabeculae are spaces that are visible to the unaided eye. These macroscopic spaces are filled with red bone marrow in bones that produce blood cells, and yellow bone marrow (adipose tissue) in other bones. Both types of bone marrow contain numerous small blood vessels that provide nourishment to the osteocytes. Each trabeculae consists of concentric lamellae, osteocytes that lie in lacunae, and canaliculi that radiate outward from lacunae.
Spongy Bone In Specific Bones
Spongy bone makes up most of the interior bone tissue of short flat sesamoid, and irregularly shaped bones. In long bones it forms the core of the epiphyses beneath the paper thin layer of compact bone, and forms a variable narrow rim bordering the medullary cavity of the diaphyses. Spongy bone is always covered by a layer of compact bone for protection.
Trabeculae of Spongy Bone
At first glance, trabeulae of spongy bone may appear to be less organized than the osteons of compact bone tissue. However they are precisely oriented along lines of stress, a characteristic that helps bones resist stresses and transfer forces without breaking. Spongy bone tissue tends to be located where bones are not heavily stressed or where stresses are applied from many directions. The trabeculae do not achieve their final arrangement until locomotion is completely learned. In fact, the arrangement can even be altered as lines of stress change due to a poorly healed fracture or deformity.
Spongy Bone Differences From Compact Bone
Spongy bone tissue is different from compact bone in two respects. First, spongy bone tissue is light, which reduces the overall weight of a bone. This reduction allows the bone to move more readily when pulled by a skeletal muscle. Second, the trabeculae of spongy bone tissue support and protect the red bone marrow. Spongy bone in the hips, ribs, sternum, vertebrae and the proximal end of the humerus and femur is the only site where red bone marrow is stored and, thus, the site where hemopoiesis (red blood cell production) occurs in adults.
Blood supply to bones
Bone is richly supplied with blood. Blood vessels, which are especially abundant in portions of bone containing bone marrow, pass into bones from the periosteum.
Periosteal Arteries
Small arteries accompanied by nerves, enter the diaphysis through many perforating (Volkmann’s) canals and supply the periosteum and outer part of the compact bone.
Nutrient artery
Located near the centre of the diaphysis, it is large and passes through a hole in compact bone called the nutrient foramen. On entering the medullary cavity, the nutrient artery divides into proximal and distal branches that course toward each end of the bone. These branches supply both the inner part of compact bone tissue of the diaphysis and the spongy bone tissue and red bone marrow as far as the epiphyseal plates (or lines). Some bones, like the tibia, have only one nutrient artery; others like the femur (thigh bone), have several. The ends of long bones are supplied by the metaphyseal and epiphyseal arteries, which arise from arteries that supply the associated joint.
Metaphyseal Arteries
Enter the metaphyses of a long bone and, together with the nutrient artery, supply the red bone marrow and one tissue of the metaphyses.
Epiphyseal Arteries
Enter the epiphyses of a long bone and supply the red bone marrow and bone tissue of the epiphyses.
Nerve supply to bones
nerves accompany the blood vessels that supply bones. The periosteum is rich in sensory nerves, some of which carry pain sensations. These nerves are especially sensitive to tearing or tension , which explains the severe pain the results from a fracture or bone tumor.
Bone Marrow Needle Biopsy
In this procedure, a needle is inserted into the middle of the bone to withdraw a sample of red bone marrow to examine it for conditions such as leukemias, metastatic neoplasms, lymphoma, Hodgkins disease and aplastic anemia. As the needle penetrates the periosteum, pain is felt. Once it passes through, there is little pain.
Ossification / Osteogenesis
The process by which bone forms. Bone formation occurs in four principal situations:
1. The initial formation of bones in an embryo and fetus.
2. The growth of bones during infancy, childhood, and adolescence until their adult size is reached.
3. The remodelling of bone (replacement of old bone tissue by new bone tissue throughout life).
4. The repair of fractures (breaks in bones) throughout life.
Initial Bone Formation in an Embryo and Fetus
The embryonic “skeleton,” initially composed of mesenchyme in the general shape of bones, is the site where cartilage formation and ossification occur during the 6th week of embryonic development. Bone formation follows one of two patterns; Intramembranous Ossification, Endochondral Ossification.The two patterns of bone formation, which involve the replacement of preexisting connective tissue with bone, do not lead to differences in the structure of mature bones, but are simply different methods of bone development.
Intramembranous Ossification
Bone forms directly with mesenchyme, which is arranged in sheet like layers that resemble membranes. It is the simpler of the two methods of bone formation. The flat bones of the skull, most of the facial bones, mandible, and the medial part of the clavicle are formed this way. Also, the fontanels that help the fetal skull pass through the birth canal later harden as they undergo intramembranous ossification which occurs in 4 stages:
1. Development of ossification centre.
2. Calcification.
3. Formation of Trabeculae.
4. Development of the Periosteum.
Development of the Ossification Center (Intra. Ossification)
At the site where the bones will develop, specific channel messages cause the cells of the mesenchyme to cluster together and differentiate, first into osteoprogenitor cells and then into osteoblasts. The site of such a cluster is called an ossification center. Osteoblasts secrete the organic extracellular matrix of bone until they are surrounded by it.
Calcification (Intra. Ossification)
Next the secretion of the extracellular matrix stops, and the cells, now called osteocytes, lie in lacunae and extend their narrow cytoplasmic processes into canaliculi that radiate in all directions. Within a few days, calcium and other mineral salts are deposited and the extracellular matrix hardens or calcifies (calcification).
Formation of Trabeculae (Intra. Ossification)
As the bone extracellular matrix forms, it develops into trabeculae that fuse with one another to form spongy bone and around the network of blood vessels in the tissue. Connective tissues associated with the blood vessels in the trabeculae differentiates into red bone marrow.
Development of the Periosteum (Intra. Ossification)
In conjunction with the formation of trabeculae, the mesenchyme condenses at the periphery of the bone and develops into the periosteum. Eventually a thin layer of compact bone replaces the surface layers of the spongy bone, but spongy bone remains in the centre. Much of the newly formed bone is remodelled (destroyed and reformed) as the bone is transformed into its adult size and shape.
Endochondral Ossification
The replacement of cartilage by bone. Although the bone of the body are formed in this way, the process is best observed in a long bone. It proceeds in 6 stages:
1. Development of the Cartilage Model.
2. Growth of the Cartilage Model.
3. Development of the primary ossification center.
4. Development of the Medullary (Marrow) Cavity.
5. Development of the Secondary Ossification Centers.
6. Formation of Articular Cartilage and the Epiphyseal (growth) Plate.
Development of the Cartilage Model (Endo. Ossification)
At the site where the bone is going to form, specific chemical messages cause the cells in mesenchyme to crowd together in the general shape of the future bone, and then develop into chondroblasts. The chondroblasts secrete cartilage extracellular matrix, producing a carriage model consisting of hyaline cartilage. A covering called the perichondrium develops around the cartilage model.
Growth of the Cartilage Model (Endo. Ossification)
Once chondroblasts become deeply buried in the cartilage extracellular matrix, they are called chondrocytes. The cartilage model grows in length bby continual cell division of chondrocytes, accompanied by further secretion of cartilage extracellular matrix. This type of cartilaginous growth is called interstitial (endogenous) growth (growth from within), results in an increase in length. As the cartilage model continues to grow, chondrocytes in its midregion hypertrophy (increase in size) and the surrounding cartilage extracellular matrix begins to calcify.
Appositional (Exogenous) Growth
Growth at the outer surface. Growth of cartilage is due mainly to the disposition of extracellular matrix material on the cartilage surface of the new model by new chondroblasts that develop from the perichondrium.
Development Of The Primary Ossification Center (Endo. Ossification)
Primary ossification proceeds inward from the external surface of the bone. A nutrient artery penetrates the perichondrium and the calcifying cartilage model through a nutrient foramen in the mid region of the cartilage model, stimulating osetoprogenitor cells in the perichondrium to differentiate into osteoblasts.
Periosteum
Once the perichondrium starts to form bone, it is known as the periosteum.
Primary Ossification Center
Near the middle of the cartilage model, periosteal capillaries grow into the disintegrating calcified cartilage, including growth of the primary ossification center, a region where bone tissue will replace most of the cartilage. Osteoblasts then begin to deposit bone extracellular matrix over the remnants of calcified cartilage, forming spongy bone trabeculae. Primary ossification spreads from this central location toward both ends of the cartilage model.
Development of the Medullary (Marrow) Cavity (Endo. Ossification)
As the primary ossification center grows toward the ends of the bone, osteoclasts break down some of the newly formed spongy bone trabeculae. This activity leaves a cavity, the medullary (marrow) cavity, in the diaphysis (shaft). Eventually, most of the wall of the diaphysis is replaced by compact bone.
Development of the Secondary Ossification Centers (Endo. Ossification)
When branches of the epiphyseal artery enter the epiphyses, secondary ossification centres develop, usually around the time of birth. Bone formation is similar to what occurs in primary ossification centers. However, in secondary ossification centers spongy bone remains in the interior of the epiphyses (no medullary cavities are formed here). In contrast to primary ossification, secondary ossification proceeds outward from the center of the epiphysis toward the outer surface of the bone.
Formation of Articular Cartilage and the Epiphyseal (Growth) Plate (Endo. Ossification)
The hyaline cartilage that covers the epiphysis becomes the articular cartilage. Prior to adulthood, hyaline cartilage remains between the diaphysis and epiphysis as the epiphyseal growth plate, the region responsible for the lengthwise growth of longs bones.
Bone Growth
During infancy, childhood, and adolescence, bones throughout the body grow in thickness by appositional growth, and long bones lengthen by the addition of bone material on the diaphyseal side of the epiphyseal plate by interstitial growth.
Bone Growth in Length
The growth in the length of bones involves the two following major events:
1. Interstitial growth of cartilage on the epiphyseal side of the epiphyseal plate
2. Replacement of cartilage on the diaphyseal side of the epiphyseal plate with the bone by endochondral ossification.
Epiphyseal Growth Plate 4 Zones
A layer of hyaline cartilage in the metaphysis of a growing bone.
1. Zone of resting cartilage
2. Zone of perforating cartilage
3. Zone of hypertrophic cartilage
4. Zone of calcified cartilage
Zone of resting Cartilage
This layer is nearest the epiphysis and consists of small, scattered chondrocytes. The cells do not function in the bone growth, they anchor the epiphyseal plate to the epiphysis of the bone.
Zone of Proliferating Cartilage
Slightly larger chondrocytes in this zone are arranged like stacks of coins. These chondrocytes undergo interstitial growth as they divide and secrete extracellular matrix. The chondrocytes in this zone divide to replace those that die at the diaphyseal side of the epiphyseal plate.
Zone of Hypertrophic Cartilage
This layer consists of large, maturing chondrocytes arranged in columns.
Zone of Calcified Cartilage
The final zone of the epiphyseal plate is only a few cells thick and consists mostly of chondrocytes that are dead because the extracellular matrix around them has calcified. Osteoclasts dissolve the calcified cartilage, and osteoblasts and capillaries from the diaphyses invade the area. The osteoblasts lay down bone extracellular matrix, replacing the calcified cartilage by endochondral ossification. As a result the zone of calcified cartilage becomes the “new diaphysis” that is firmly cemented to the rest of the diaphysis of the bone.
Epiphyseal (Growth) Plate
The activity of the epiphyseal plate is the only way that the diaphysis can increase in length. As a bone grows the chondrocytes proliferate on the epiphyseal side of the plate. New chondrocytes replace older ones, which are destroyed by calcification. Thus, the cartilage is replaced by bone on the diaphyseal side of the plate. In this way, the thickness of the of the epiphyseal plate remains relatively constant, but the bone on the diaphyseal side increases in length.
Damage to cartilage of epiphyseal plate
If a bone fracture damages the epiphyseal plate, the fractured bone may be shorter than normal once adult stature is reached. This is because damage to cartilage, which is avascular, accelerates closure of the epiphyseal plate due to the cessation of cartilage cell division, thus inhibiting lengthwise growth of bone.
Epiphyseal Line
When adolescents comes to an end (18 in females, 21 in males), the epiphyseal plate closes; that is, the epiphyseal cartilage cells stop dividing and bone replaces all remaining cartilage. With the appearance of the epiphyseal line, bone growth in length stops completely.
Closure of the Epiphyseal Plate
A gradual process and the degree to which it occurs is useful in determining bone age, predicting adult height, and establishing age at death from skeletal remains.
Bone Growth in Thickness
Like cartilage, bone can grow in thickness (diameter) only by appositional growth. Bone tissue is being deposited on the outer surface of bone, the bone lining the medullary cavity is destroyed by osteoclasts in the endosteum. In this way, the medullary cavity enlarges as the bone increases in thickness.
Appositional Growth of Bone
1. At the bone surface, periosteal cells differentiate into osteoblasts, which secrete the collagen fibres and other organic materials that form the bone extracellular matrix. The osteoblasts become surrounded by extracellular matrix and develop into osteocytes. This process forms bone ridges on either side of the peristeal blood vessel. The ridge slowly enlarge and create a groove for the periosteal blood vessel.
2. Eventually, the ridges fold together and fuse, and the groove becomes a tunnel that encloses the blood vessel. The former periosteum now becomes the endosteum that lines the tunnel.
3. Osteoblasts in the endosteum deposit bone extracellular matrix, forming new concentric lamellae. The formation of additional concentric lamellae proceeds inward toward the periosteal blood vessel. In this way, the tunnel fills in, and a new osteon is created.
4. As an asteon is forming, osteoblasts under the periosteum deposit new circumferential lamellae, further increasing the thickness of the bone. As additional periosteal blood vessels become enclosed as in step 1, the growth process continues.
Bone Remodelling
The ongoing replacement of old bone tissue by new bone tissue. It involves bone reabsorption, the removal of minerals and collagen fibres from bone by osteoclasts, and bone disposition, the addition of minerals and collagen fibres by osteoblasts. Since the strength of bone is related to he degree to which it is stressed, if newly formed bone is subjected to heavy loads, it will grow thicker and therefore be stronger than old bone. Also, the shape of a bone can be altered for proper support based on the stress patterns experienced during the remodelling process. Finally, new bones more resistant to fracture than old bone.
Orthodontics
The branch of dentistry concerned with the prevention and correction of poorly aligned teeth. The movement of teeth by braces places a stress on the bone that forms the socket that anchors the teeth. In response to this artificial stress, osteoblasts and osteoclasts remodel the socket so that the teeth align properly.
The balance between osteoclasts and osteoblasts
A delicate balance exists between the actions of osteoclasts and osteoblasts. Should too much new tissue be formed, the bone becomes abnormally thick and heavy. If too much mineral material is deposited in the bone, the surplus may form thick bumps, called spurs, on the bone that interfere with movement at joints.
Excessive Loss of Calcium in Bone
Weakens the bones, and they may break, as what occurs in osteoporosis, or they may become to flexible as in rickets and osteomalacia.
Paget’s Disease
There is an excessive proliferation of osteoclasts so that bone resorption occurs faster than bone disposition. In response, osteoblasts attempt to compensate, but the new bone is weaker because it has a higher proportion of spongy to compact bone, mineralization is decreased, and the newly synthesized extracellular matrix contains abnormal proteins. The newly formed bone, especially that of the pelvis, limbs, lower vertebrae, and skull, become enlarged, hard and brittle and easily fracture.
Bone Resorption
An osteoclasts attaches tightly t the bone surface at she endosteum or periosteum and forms a leakproof seal at the edges of its ruffled border. Then it releases protein digesting lysosomal enzymes and several acids into the sealed pocket. The enzymes digest collagen fibres and other organic substances while the acids dissolve the bone minerals. Once a small area of bone has been resorbed, osteoclasts depart and osteoblasts move in to rebuild the bone in that area.
Minerals
Large amounts of calcium and phosphorus are needed while bones are growing, as are smaller amounts of magnesium, fluoride, and manganese. These minerals are also necessary during bone remodelling.
Vitamins
Vitamin A stimulates activity of osteoblasts. Vitamin C is needed for synthesis of collagen, the main bone protein. Vitamin D helps bone by increasing the absorption of calcium from foods in the gastrointestinal tract into the blood. Vitamin K and B12 are also needed for the synthesis of bone proteins.
Insulinlike Growth Factor Hormones
During childhood, the hormones most important to bone growth are the insulin like growth factors (IGFs), which are produced in the liver and bone tissues. IGFs stimulate osteoblasts, promote cell division at the epiphyseal plate and in the periosteum, and enhance the synthesis of proteins needed to build new bone. IGFs are produced in response to the secretion of the human growth hormone (hGH), from the anterior lobe of the pituitary gland.
Thyroid Hormones (T3 and T4)
From the thyroid gland also promote bone growth by stimulating osteoblasts.
Insulin
The hormone insulin from the pancreas promotes bone growth by increasing the synthesis of bone proteins.
Sex Hormones
At puberty, the secretion of sex horses causes a dramatic effect on bone growth. They include estrogens (produced in the ovaries) and androgens such as testosterone (produced in the testes). The adrenal glands of both sexes produce androgens, and other tissues, such as adipose tissues, can convert androgens to estrogens. These hormones are responsible for increased osteoblastic activity, synthesis of bone extracellular matrix, and a sudden “growth spurt” that occurs during teenage years. Estrogens also promote changes in the skeleton that are typical of females, such as widening of the pelvis. They also shut down the epiphyseal growth plate causing elongation of bones to cease.
Sex Hormones in adults
During adulthood, sex hormones contribute to bone remodelling by slowing separation of old bone and promoting new deposition of new bone. One way estrogens slow resorption is promoting apoptosis (programmed death) of osteoclasts.
Calcitriol
(The active form of Vitamin D). Parathyroid Hormone that has an effect on bone remodelling.
Moderate weight bearing exercises
Maintain sufficient strain on bones to increase and maintain their bone density.
Fracture
Any break in bone. They are named according to their severity, the shape or position of the fracture line, or even the physician who first described them.
Stress Fracture
A series of microscopic fissures in bone that forms without any evidence of injury to other tissues. IN healthy adults, stress fractures result form repeated, strenuous activities, such as running, jumping, or aerobic activity. They are quite painful and also result from decrease processes that disrupt normal bone calcification such as osteoporosis. About 25% of stress fractures involve the tibia. Although standard x-ray images often fail to reveal the presence of stress fractures, they show up clearly in a bone scan.
Repair of Bone Fracture
Involves 3 stages:
1. Reactive Phase
2. Reparative Phase: Fibrocartilage callus formation and bony callus formation
3. Bone remodelling phase
4.
1. Reactive Phase
This phase is an early inflammatory phase. Blood vessels crossing the fracture line are broken. As blood leaks front he torn end of the vessels, a mass of blood (usually clotted) forms around the site of the fracture.
Fracture Hematoma
A mass of blood that forms by the site of a fracture as a result form the blood vessels being torn. It usually forms 6 to 8 hours after injury. Because the circulation of blood stops at the site where the blood fracture hematoma forms, nearby bone cells die. Swelling and inflammation occur in response to dead bone cells, prodding additional cellular debris.
Phagocytes and Osteoclasts
(Neutrophils and Macrophages) and Osteoclasts begin to remove the dead and damaged tissue in and around the fracture hematoma. This stage may last up to several weeks.
2. a.) Reparative Phase: Fibrocartilaginous Callus Formation
The reparative phase is characterized by two events: the formation of a fibrocartilaginous callus and a bony callus bridge the gap between the broken ends of the bones. Blood vessels grow into the fracture hematoma and phagocytes begin to clean up dead bone cells. Fibroblasts from the periosteum invade the fracture site and produce collagen fibres. In addition, cells from the periosteum develop into chondroblasts and begin to produce fibrocartilage in this region.
Fibrocartilaginous (soft) Callus
A mass of repair tissue consisting of collagen fibers and cartilage that bridges the broken ends of bone. Formation of this callus takes about 3 weeks.
2. b.) Reparative Phase: Bony Callus Formation
In areas closer to well vascularized healthy bone tissue, osteoprogenitor cells develop into osteoblasts, which begin to produce spongy bone trabeculae. The trabeculae join living and dead portions of the original bone fragments. In time, the fibrocartilage is converted to spongy bone, and the callus is often referred to as a bony (hard) callus. The bony callus lasts about 3 to 4 months.
3. Bone Remodelling phase
The final phase of fracture repair is bone remodelling of the callus. Dead portions of the original fragments of bone are gradually resorbed by osteoclasts. Compact bone replaces spongy bone around the periphery of the fracture. Sometimes the repair process is so thorough that the fracture is undetectable. However, a thickened area on the surface of the bone remains as evidence of a healed fracture.
Giantism
Caused by the oversecretion of the Human growth hormone during childhood, in which a person becomes much taller and heavier than normal.
Pituitary Dwarfism
Caused by the undersecretion of the human growth hormone, in which a person has a short stature. Although the head, trunk and limbs of a pituitary dwarf are smaller than normal, they are proportionate. The condition can be treated medically with the human growth hormone until the epiphyseal plate is closed.
Acromegaly
Oversecretion of the human growth hormone during adulthood. Although hGH cannot produce further lengthening of the long bones because the epiphyseal plates are already closed, the bone of the hands, feet, jaws thicken and other tissues enlarge. In addition, the eyelids, lips, tongue, and nose enlarge, and the skin thickens and develops furrows, especially on the forehead and soles.
Achondroplasia
An inherited condition in which the conversion of cartilage to bone is abnormal. It results in the most kind of dwarfism, called anchondroplastic dwarfism. These individuals are typically about 4 feet tall as adults. They have an oversized trunk, short limbs, and a slightly enlarged head with a prominent forehead and flattened nose at the bridge. The condition is essentially untreatable, although some individuals opt for limb-lengthening surgery.
Treatments for fractures
Vary according to age, type of fracture, and the bone involved. The ultimate goals of fracture treatment are realignment of the bone fragments, immobilization to maintain realignment, and restoration of function. For bones to unite properly, the fractured end must be brought into alignment. This process, called reduction, is commonly referred to as setting a fracture.
Closed Reduction
The fractured end of a bone are brought into alignment by manual manipulation, and the skin remains intact.
Open Reduction
The fractured end of a bone are brought into alignment by a surgical procedure using internal fixation devices such as screws, plates, pins, rods, and wires. Following reduction, a fractured bone may be kept immobilized by a cast, sling, splint, elastic bandage, external fixation device, or combination of these devices.
Open (Compound) Fracture
The broken ends of the bone protrude through the skin.
Closed (Simple) Fracture
The broken end of the bone does not protrude through the skin.
Comminuted Fracture
The bone is splintered, crushed or broken into pieces at the site of impact, and the smaller bone fragments lie between the two main fragments.
Greenstick Fracture
A partial fracture in which one side of the bone is broken and the other side bends; similar to the way a greenstick breaks on one side while the other stays whole, but bends; occurs only in children, whose bones are not fully ossified and contain more organic material than inorganic material.
Impacted Fracture
One end of the fractured bone is forcefully driven into the interior of the other.
Pott Fracture
Fracture of the distal end of the lateral led bone (fibula), with serious injury of the distal tibial articulation.
Colles Fracture
Fracture of the distal end of the lateral foramen bone (radius) in which the distal fragment is placed posteriorly.
Bone’s Role in Calcium Homeostasis
Bone is the bodies major calcium reservoir, storing 99% of total body calcium. One way to maintain the level of calcium in the blood is the control the rates of calcium resorption from bone into blood and from calcium deposition from blood into bone. Both nerve and muscle cells depend on a stable level of calcium ions in the extracellular fluid to function properly. Also blood clotting. The role of bone in calcium homeostasis is t help buffer the blood calcium level, releasing calcium into blood plasma when the level decreases using osteoclasts, and absorbing calcium when the level rises using osteoblasts.
Parathyroid Hormone (PTH)
Calcium exchange is regulated by hormones. The parathyroid hormone secreted by the thyroid glands increases the blood calcium levels. Operates via negative feedback system. If some stimulus causes the blood calcium levels to drop, parathyroid gland cells (receptors) detect this change and increase their production of a molecule known as cyclic adenosine monophosphate. The PTH also acts on the kidneys (effectors) to decrease loss of calcium in the urine, so more is retained in the blood. And PTH stimulates the formation of calcitrol (active form of vitamin D), a hormone that promotes absorption of calcium from foods in the GI tract into the blood. Both of these actions also help elevate blood calcium levels.
Calcitonin (CT)
Works to decrease calcium levels in the blood. When blood calcium levels rise about normal, parafollicular cells in the thyroid releases this hormone. It inhibits activity of the osteoclasts, speeds blood calcium uptake by bone, and accelerates calcium disposition into bones. Promotes formation and decreases blood calcium level. Calcitonin harvest from salmon (Miacalcin) is an effective drug for treating osteoporosis because it slows bone resorption.
Mechanical Stress on Bone
Those that result from the pull of skeletal muscles and the pull of gravity. Weight bearing activities help build and retain bone mass.
Aging and Bone Tissue
from birth through adolescence, more bone tissue is produced than is lost during bone remodelling. In young adults the rates of bone disposition and resorption are about the same. As the levels of sex hormones diminishes during middle age, especially in women after menopause, a decrease in bone mass occurs because bone resorption by osteoclasts outpaces bone disposition by osteoblasts. In old age, loss of bone through resorption occurs more rapidly than bone gain. Because women’s bones are generally smaller and less massive then mens bones, loss of bone mass in old age usually has a greater effect in females. These factors contribute to the higher incidence of osteoporosis in females.
Demineralization
Results in loss of bone mass. The loss of calcium and other minerals from bone extracellular matrix. The loss usually begins after age 30 in females, and accelerates at 45 when estrogen levels greatly decrease.
Brittleness
Results from a decreased rate of protein synthesis. The organic part of bone extracellular matrix, collagen fibres gives bone its tensile strength. The loss of tensile strength causes the bones to become very brittle and susceptible to fracture. In some very elderly, collagen fibre synthesis slows, in part due to the diminished production of human growth hormone. In addition to increasing susceptibility to fractures, loss of bone mass also leads to deformity, pain, loss of height, and loss of teeth.
Calcium and Phosphorus
Make bone extracellular matrix hard
Magnesium
Helps form bone extracellular matrix
Fluoride
Helps strengthen bone extracellular matrix
Manganese
Activates enzymes involved in synthesis of bone extracellular matrix
Vitamin A
Needed for the activity of osteoblasts during remodelling of bone; deficiency stunts bone growth; toxic in high doses.
Vitamin C
Needed for synthesis of collagen, the main bone protein; deficiency leads to decreased collagen production, which slows down bone growth and delays repair of broken bones.
Vitamin D
Active from (calcitrol) is produced by the kidneys; helps build bone by increasing absorption of calcium from GI tract into blood; deficiency causes faulty calcification and slows down bone growth; may reduce risk of osteoporosis but is toxic if taken in high doses.
Vitamin K and B12
Needed for synthesis of bone proteins; deficiency leads to abnormal protein production in bone extracellular matrix and decreased bone density.
Bone Scan
A diagnostic procedure that takes advantage of the fact that bone is living tissue. A small amount of a radioactive tracer compound that is readily absorbed by bone is injected intravenously. The degree of uptake by the tracer is related to the amount of blood flow to the bone. A scanning device (gamma camera) measures the radiation emitted from the bones, and the information is translated into a photograph that can be read like an x-ray on a computer. Darker or lighter areas indicate bone abnormalities. Darker sport or “hot spots” are areas of increased bone metabolism that may indicate cancer, abnormal healing of fractures, or abnormal bone growth. “Cold Spot” indicate decreased metabolism which may indicate bone degeneration, decalcified bone, fractures, bone infections, Paget’s Disease, and rheumatoid arthritis. Detects 3-6 months sooner than an x ray. The standard test for bone density.
Osetoporosis
A condition of porous bones. Bone resorption (breakdown) outpaces bone deposition (formation). Largely due to depletion of calcium. Bone mass becomes so depleted that bone fractures occur easily.
Rickets and Osteomalacia
Two forms of the same disease that result from inadequate calcification of the extracellular bone matrix, usually cause by a vitamin D deficiency.
Rickets
A disease of children in which the growing bone become “soft” or rubbery and are easily deformed. Because new bone formation at the epiphyseal plate fails to ossify, bowed legs and deformities in the skull, rib cage, and pelvis are common.
Osteomalacia
The adult counterpart of rickets. New bone formed during remodelling fails to calcify, and the person experiences varying degrees of pain and tenderness in bones, especially the hips and legs. Bone fractures also result from minor trauma. Prevention and treatment from rickets and osteomalacia consists of administration of adequate vitamin D and exposure to moderate amounts of sunlight.
Osteoarthritis
The degeneration of articular cartilage such that the bony ends touch; the resulting friction of bone against bone worsens the condition. Usually associated with the elderly.
Osteomyelitis
An infection of bone characterized by high fever, swelling, chills, pain, nausea, pus formation, edema, and warmth over the effected bone and rigid overlying muscles. It is often caused by bacteria, usually staphylococcus aureus. The bacteria may reach the bone from the outside of the body (through open fractures, penetrating wounds, urinary tract infection, or orthopaedic surgical procedures)
Osteopenia
Reduced bone mass due to a decrease in the rate of bone synthesis to a level too low to compensate for normal bone resorption; any decrease in bone mass below normal. example is osteoporosis.
Osteosarcoma
Bone cancer that primarily affects osteoblasts and occurs most often in teenagers during their growth spurt; the most common sites are the metaphyses of the thigh bone (femur), shin bone (tibia), and arm bone (humerus). Metastases occur most often in lungs; treatment consist of multi drug chemotherapy and removal of the malignant growth, or amputation of the limb.

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Functions of the Integumentary System -Resistance to trauma and infection -Prevents loss or gain of water -Vitamin D synthesis -Sensory receptors for heat, cold, touch, texture, pressure, vibration, and tissue injury -Thermoregulation How does skin resist trauma and infection? -Skin …

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