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 network, or haversian system, 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 capillary or more, 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 formation is ongoing and is determined by hormonal stimulation, dietary factors, and the amount of stress put on the bone. It’s accomplished by the continual actions of bone-forming osteoblasts and bone-reabsorbing cells called 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 forms 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 the serum calcium level falls, 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 inversely proportional to the serum calcium level. Alkaline phosphatase (ALP) influences bone calcification and lipid and metabolite transport. Osteoblasts contain an abundance of ALP. A rise in the serum ALP level can indicate the presence of a skeletal disease, primarily one characterized by marked osteoblastic activity, such as bone metastases or Paget’s disease. It can also point to biliary obstruction, 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 reabsorbing previously deposited bone. These remodeling activities promote longitudinal bone growth, which continues until the epiphyseal growth plates, located at both ends, close during adolescence. Human growth factor and sex hormones influence the rate of ossification. In adults, bone growth is complete, and cartilage is replaced by bone, becoming the epiphyseal line.

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

♦ Fibrous joints, or synarthroses, permit only slight movement 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.

Synovial joints have distinguishing characteristics:

♦ The two articulating surfaces of the bones have a smooth hyaline covering (articular cartilage) that’s 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.

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

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

♦ Skeletal muscles are attached to bone and have striped (striated) appearances that reflect their cellular structures.

♦ Visceral muscles move contents through internal organs and are smooth (nonstriated).

♦ Cardiac muscles (smooth) constitute the heart wall.

When muscles are classified according to activity, they’re 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 voluntary and involuntary muscles.

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 tissues called fascia. Blood vessels and nerves pass into muscles through the fascia to reach the individual muscle fibers. Motoneurons 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. Muscle contraction is isometric or isotonic. Isometric contraction results in an increase in tension without change in length. Isotonic contraction occurs when the muscle shortens as weight is lifted. 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.

Disease may alter bone density, growth, or strength.

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

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, page 372.)

Each year, an estimated 25% of the population has traumatic musculoskeletal injury, 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.

Children’s bones usually heal rapidly and without deformity. However, epiphyseal plate fractures in children are likely to cause deformity because they interfere with normal bone growth. In elderly people, underlying systemic illness, impaired circulation, or poor nutrition may cause slow or poor healing.

Carpal tunnel syndrome, a form of repetitive stress injury, is the most common nerve entrapment syndrome. Carpal tunnel syndrome usually occurs in women between ages 30 and 60 (posing a serious occupational health problem). However, men who are also employed as assembly-line workers and packers and who repeatedly use poorly designed tools are just as likely to develop this disorder. Any strenuous use of the hands—sustained grasping, twisting, or flexing—aggravates this condition.

Clubfoot, also called talipes, is the most common congenital disorder of the lower extremities. It’s marked primarily by a deformed talus and shortened Achilles tendon, which give the foot a characteristic clublike appearance. In talipes equinovarus, the foot points downward (equinus) and turns inward (varus), and the front of the foot curls toward the heel (forefoot adduction).

Clubfoot occurs in about 1 per 1,000 live births, is bilateral in about half of all cases, and is twice as common in boys as in girls. It may be associated with other birth defects, such as myelomeningocele, spina bifida, and arthrogryposis. Clubfoot is correctable with prompt treatment.

Developmental dysplasia of the hip (DDH), an abnormality of the hip joint present from birth, is the most common disorder affecting the hip joints in children younger than 3 years. About 85% of affected infants are females.

DDH can be unilateral or bilateral and can affect the femoral head, the acetabulum, or both. This abnormality occurs in three forms of varying severity:

♦ Unstable dysplasia—the hip is positioned normally but can be dislocated by manipulation.

♦ Subluxation or incomplete dislocation—the femoral head rides on the edge of the acetabulum.

♦ Complete dislocation—the femoral head is totally outside the acetabulum.