Musculoskeletal System

佚名

T he musculoskeletal system is a complex system of bones, muscles, ligaments, tendons, and other tissues that gives the body form and shape. It also protects vital organs, makes movement possible, stores calcium and other minerals in the bony matrix for mobilization if deficiency occurs, and provides sites for hematopoiesis (blood cell production) in the marrow.

BONES

The human skeleton contains 206 bones, which are composed of inorganic salts (primarily calcium and phosphate), embedded in a framework of collagen fibers.

Bone shape and structure

Bones are classified by shape as either long, short, flat, or irregular. Long bones are found in the extremities and include the humerus, radius, and ulna of the arm; the femur, tibia, and fibula of the leg; and the phalanges, metacarpals, and metatarsals of the hands and feet (See Structure of long bones .) Short bones include the tarsal and carpal bones of the feet and hands, respectively. Flat bones include the frontal and parietal bones of the cranium, ribs, sternum, scapulae, ilium, and pubis. Irregular bones include the bones of the spine (vertebrae, sacrum, coccyx) and certain bones of the skull ― the temporal, sphenoid, ethmoid, and mandible.

Classified according to structure, bone is either cortical (compact) or cancellous (spongy or trabecular). Adult cortical bone consists of networks of interconnecting canals, or canaliculi. Each of these networks, or haversian systems, runs parallel to the bone's long axis and consists of a central haversian canal surrounded by layers (lamellae) of bone. Between adjacent lamellae are small openings called lacunae, which contain bone cells or osteocytes. The canaliculi, each containing one or more capillaries, provide a route for tissue fluids transport; they connect all the lacunae.

Cancellous bone consists of thin plates (trabeculae) that form the interior meshwork of bone. These trabeculae are arranged in various directions to correspond with the lines of maximum stress or pressure. This gives the bone added structural strength. Chemically, inorganic salts (calcium and phosphate, with small amounts of sodium, potassium carbonate, and magnesium ions) comprise 70% of the mature bone. The salts give bone its elasticity and ability to withstand compression.

Bone growth

Bone formation is ongoing and is determined by hormonal stimulation, dietary factors, and the amount of stress put on the bone. It is accomplished by the continual actions of bone-forming osteoblasts and bone-reabsorbing cells osteoclasts. Osteoblasts are present on the outer surface of and within bones. They respond to various stimuli to produce the bony matrix, or osteoid. As calcium salts precipitate on the organic matrix, the bone hardens. As the bone forms, a system of microscopic canals in the bone form around the osteocytes. Osteoclasts are phagocytic cells that digest old, weakened bone section by section. As they finish, osteoblasts simultaneously replace the cleared section with new, stronger bone.

Vitamin D supports bone calcification by stimulating osteoblast activity and calcium absorption from the gut to make it available for bone building. When serum calcium levels fall, the parathyroid gland releases parathyroid hormone, which then stimulates osteoclast activity and bone breakdown, freeing calcium into the blood. Parathyroid hormone also increases serum calcium by decreasing renal excretion of calcium and increasing renal excretion of phosphate ion.

Phosphates are essential to bone formation; about 85% of the body's phosphates are found in bone. The intestine absorbs a considerable amount of phosphates from dietary sources, but adequate levels of vitamin D are necessary for their absorption. Because calcium and phosphates interact in a reciprocal relationship, renal excretion of phosphates increases or decreases in inverse proportion to serum calcium levels. Alkaline phosphatase (ALP) influences bone calcification and lipid and metabolite transport. Osteoblasts contain an abundance of ALP. A rise in serum ALP levels can identify skeletal diseases primarily those characterized by marked osteoblastic activity such as bone metastases or Paget's disease. It can also identify biliary obstruction or hyperparathyroidism, or excessive ingestion of Vitamin D.

In children and young adults, bone growth occurs in the epiphyseal plate, a layer of cartilage between the diaphysis and epiphysis of long bones.

Osteoblasts deposit new bone in the area just beneath the epiphysis, making the bone longer, and osteoclasts model the new bone's shape by resorbing previously deposited bone. These remodeling activities promote longitudinal bone growth, which continues until the epiphyseal growth plates, located at both ends, close during adolescence. In adults, bone growth is complete, and this cartilage is replaced by bone, becoming the epiphyseal line.

JOINTS

The tendons, ligaments, cartilage, and other tissues that connect two bones comprise a joint. Depending on their structure, joints either predominantly permit motion or provide stability. Joints, like bones, are classified according to structure and function.

Classification of joints

The three structural types of joints are fibrous, cartilaginous, and synovial.

• Fibrous joints, or synarthroses , have only minute motion and provide stability when tight union is necessary, as in the sutures that join the cranial bones.
• Cartilaginous joints, or amphiarthroses , allow limited motion, as between vertebrae.
• Synovial joints, or diarthroses , are the most common and permit the greatest degree of movement. These joints include the elbows and knees. (See Structure of a synovial joint .)

Synovial joints have distinguishing characteristics:

• The two articulating surfaces of the bones have a smooth hyaline covering (articular cartilage) that is resilient to pressure.
• Their opposing surfaces are congruous and glide smoothly on each other.
• A fibrous (articular) capsule holds them together.
• Beneath the capsule, lining the joint cavity, is the synovial membrane, which secretes a clear viscous fluid called synovial fluid. This fluid lubricates the two opposing surfaces during motion and also nourishes the articular cartilage.
• Surrounding a synovial joint are ligaments, muscles, and tendons, which strengthen and stabilize the joint but allow free movement.

Joint movement

The two types of synovial joint movement are angular and circular.

Angular movement

Joints of the knees, elbows, and phalanges permit the following angular movements:

• flexion (closing of the joint angle)
• extension (opening of the joint angle)
• hyperextension (extension of the angle beyond the usual arc).

Other joints, including the shoulders and hips, permit:

• abduction (movement away from the body's midline)
• adduction (movement toward the midline).

Circular movements

Circular movements include:

• rotation (motion around a central axis), as in the ball and socket joints of the hips and shoulders
• pronation (downward wrist or ankle motion)
• supination (upward wrist motion to begging position).

Other kinds of movement are inversion (inward turning, as of foot), eversion (outward turning, as of foot), protraction (as in forward motion of the mandible), and retraction (returning protracted part into place).

MUSCLES

The most specialized feature of muscle tissue ― contractility ― makes the movement of bones and joints possible. Normal skeletal muscles contract in response to neural impulses. Appropriate contraction of muscle usually applies force to one or more tendons. The force pulls one bone toward, away from, or around a second bone, depending on the type of muscle contraction and the type of joint involved. Abnormal metabolism in the muscle may result in inappropriate contractility. For example, when stored glycogen or lipids cannot be used because of the lack of an enzyme necessary to convert energy for contraction, the result may be cramps, fatigue, and exercise intolerance.

Muscles permit and maintain body positions, such as sitting and standing. Muscles also pump blood through the body (cardiac contraction and vessel compression), move food through the intestines (peristalsis), and make breathing possible. Skeletal muscular activity produces heat; it is an important component in temperature regulation. Deep body temperature regulators are found in the abdominal viscera, spinal cord, and great veins. These receptors detect changes in the body core temperature and stimulate the hypothalamus to institute appropriate temperature changing responses, such as shivering in response to cold. Muscle mass accounts for about 40% of an average man's weight.

Muscle classification

Muscles are classified according to structure, anatomic location, and function:

• Skeletal muscles are attached to bone and have a striped (striated) appearance that reflects their cellular structure.
• Visceral muscles move contents through internal organs and are smooth (nonstriated).
• Cardiac muscles (smooth) comprise the heart wall.

When muscles are classified according to activity, they are called either voluntary or involuntary. (See Chapter 8 , “Nervous system.”) Voluntary muscles can be controlled at will and are under the influence of the somatic nervous system; these are the skeletal muscles. Involuntary muscles, controlled by the autonomic nervous system, include the cardiac and visceral muscles. Some organs contain both voluntary and involuntary muscles.

Muscle contraction

Each skeletal muscle consists of many elongated muscle cells, called muscle fibers, through which run slender threads of protein, called myofibrils. Muscle fibers are held together in bundles by sheaths of fibrous tissue, called fascia. Blood vessels and nerves pass into muscles through the fascia to reach the individual muscle fibers. Motor neurons synapse with the motor nerve fibers of voluntary muscles. These fibers reach the membranes of skeletal muscle cells at neuromuscular (myoneural) junctions. When an impulse reaches the myoneural junction, the junction releases the neurotransmitter, acetylcholine, which releases calcium from the sarcoplasmic reticulum, a membranous network in the muscle fiber, which, in turn, triggers muscle contraction. The energy source for this contraction is adenosine triphosphate (ATP). ATP release is also triggered by the impulse at the myoneural junction. Relaxation of a muscle is believed to take place by reversal of these mechanisms.

Muscle fatigue results when the sources of ATP in a muscle are depleted. If a muscle is deprived of oxygen, fatigue occurs rapidly. As the muscle fatigues, it switches to anaerobic metabolism of glycogen stores, in which the stored glycogen is split into glucose (glycolysis) without the use of oxygen. Lactic acid is a by-product of anaerobic glycolysis and may accumulate in the muscle and blood with intense or prolonged muscle contraction.

TENDONS AND LIGAMENTS

Skeletal muscles are attached to bone directly or indirectly by fibrous cords known as tendons. The least movable end of the muscle attachment (generally proximal) is called the point of origin; the most movable end (generally distal) is the point of insertion.

Ligaments are fibrous connections that control joint movement between two bones or cartilages. Their purpose is to support and strengthen joints.

PATHOPHYSIOLOGIC MANIFESTATIONS

Alterations of the normal functioning of bones and muscles are described next. Most musculoskeletal disorders are caused by or profoundly affect other body systems.

Alterations in bone

Disease may alter density, growth, or strength of bone.

Density

In healthy young adults, the resorption and formation phases are tightly coupled to maintain bone mass in a steady state. Bone loss occurs when the two phases become uncoupled, and resorption exceeds formation. Estrogen not only regulates calcium uptake and release, it also regulates osteoblastic activity. Decreased estrogen levels may lead to diminished osteoblastic activity and loss of bone mass, called osteoporosis. In children, vitamin D deficiency prevents normal bone growth and leads to rickets.

Growth

The osteochondroses are a group of disorders characterized by avascular necrosis of the epiphyseal growth plates in growing children and adolescents. In these disorders, a lack of blood supply to the femoral head leads to septic necrosis, with softening and resorption of bone. Revascularization then initiates new bone formation in the femoral head or tibial tubercle, which leads to a malformed femoral head.

Bone strength

Both cortical and trabecular bone contribute to skeletal strength. Any loss of the inorganic salts that comprise the chemical structure of bone will weaken bone. Cancellous bone is more sensitive to metabolic influences, so conditions that produce rapid bone loss tend to affect cancellous bone more quickly than cortical bone.

Alterations of muscle

Pathologic effects on muscle include atrophy, fatigue, weakness, myotonia, and spasticity.

Atrophy

Atrophy is a decrease in the size of a tissue or cell. In muscles, the myofibrils atrophy after prolonged inactivity from bed rest or trauma (casting), when local nerve damage makes movement impossible, or when illness removes needed nutrients from muscles. The effects of muscular deconditioning associated with lack of physical activity may be apparent in a matter of days. An individual on bed rest loses muscle strength, as well as muscle mass, from baseline levels at a rate of 3% a day.

Conditioning and stretching exercises may help prevent atrophy. If reuse isn't restored within 1 year, regeneration of muscle fibers is unlikely.

Fatigue

Pathologic muscle fatigue may be the result of impaired neural stimulation of muscle or energy metabolism or disruption of calcium flux. See Chapter 5 , Fluid and electrolytes, for a detailed discussion of these events.

Weakness

Periodic paralysis is a disorder that can be triggered by exercise or a process or chemical (such as medication) that increases serum potassium levels. This hyperkalemic periodic paralysis may be caused by a high-carbohydrate diet, emotional stress, prolonged bed rest, or hyperthyroidism. During an attack of periodic paralysis, the muscle membrane is unresponsive to neural stimuli, and the electrical charge needed to initiate the impulse (resting membrane potential) is reduced from �90 mV to �45 mV.

Myotonia and spasticity

Myotonia is delayed relaxation after a voluntary muscle contraction ― such as grip, eye closure, or muscle percussion ― accompanied by prolonged depolarization of the muscle membrane. Depolarization is the reversal of the resting potential in stimulated cell membranes. It is the process by which the cell membrane “resets” its positive charge with respect to the negative charge outside the cell. Myotonia occurs in myotonic muscular dystrophy and some forms of periodic paralysis.

Stress-induced muscle tension, or spasticity, is presumably caused by increased activity in the reticular activating system and gamma loop in the muscle fiber. The reticular activating system consists of multiple diffuse pathways in the brain that control wakefulness and response to stimuli. A pathologic contracture is permanent muscle shortening caused by muscle spasticity, seen in central nervous system injury or severe muscle weakness.

DISORDERS

Bone fracture

When a force exceeds the compressive or tensile strength (the ability of the bone to hold together) of the bone, a fracture will occur. (For an explanation of the terms used to identify fractures, see Classifying fractures .)

An estimated 25% of the population has traumatic musculoskeletal injury each year, and a significant number of these involve fractures.

The prognosis varies with the extent of disablement or deformity, amount of tissue and vascular damage, adequacy of reduction and immobilization, and patient's age, health, and nutritional status.

Causes

Risk factors for fractures are those that involve force to bone, such as:

• falls
• motor vehicle accidents
• sports
• use of drugs that impair judgment or mobility
• young age (immaturity of bone)
• bone tumors
• metabolic illnesses(such as hypoparathyroidism or hyperparathyroidism)
• medications that cause iatrogenic osteoporosis, such as steroids.

Pathophysiology

When a bone is fractured, the periosteum and blood vessels in the cortex, marrow, and surrounding soft tissue are disrupted. A hematoma forms between the broken ends of the bone and beneath the periosteum, and granulation tissue eventually replaces the hematoma.

Damage to bone tissue triggers an intense inflammatory response in which cells from surrounding soft tissue and the marrow cavity invade the fracture area, and blood flow to the entire bone is increased. Osteoblasts in the periosteum, endosteum, and marrow produce osteoid (collagenous, young bone that has not yet calcified, also called callus), which hardens along the outer surface of the shaft and over the broken ends of the bone. Osteoclasts reabsorb material from previously formed bones and osteoblasts to rebuild bone. Osteoblasts then transform into osteocytes (mature bone cells).

Signs and symptoms

Signs and symptoms of bone fracture may include:

• deformity due to unnatural alignment
• swelling due to vasodilation and infiltration by inflammatory leukocytes and mast cells
• muscle spasm
• tenderness
• impaired sensation distal to the fracture site due to pinching or severing of neurovascular elements by the trauma or by bone fragments
• limited range of motion
• crepitus, or “clicking” sounds on movement caused by shifting bone fragments.