bone disease
any of the diseases and injuries that
affect human bones.
Diseases and injuries of bones are major causes of abnormalities of the locomotor system. Although physical injury, causing fracture, dominates over disease, fracture is but one of several common causes of bone disease, and disease, in fact, is a common cause of fracture.
Bone diseases and injuries were formerly regarded as conditions that were more mechanical than metabolic. An improved understanding of the dual mechanical and chemical function of bone, however, has permitted a more integrated biological view.
In congenital dislocation of the hip, the socket part of the joint, the acetabulum, loses the mechanical stimulus to normal growth and development because the ball part of the joint, the head of the femur, does not rest in the joint. The acetabulum and a large part of the pelvis develop poorly or not at all, whereas the femoral head, if it makes contact higher up on the pelvis, may stimulate development of a new joint structure. Poliomyelitis affecting the lower extremity in children results in short, thin bones with sometimes severe leg-length discrepancy. In adults, an extremity affected by nerve injury gradually develops osteopenia (a reduced amount of bone tissue), so that it fractures easily. In the elderly, bed rest is regarded as a cause of increased osteopenia with vertebral fractures.
The bone tissue's capacity for remodelling in
response to mechanical demand is retained even in the aged. In osteoarthritis,
because the weight distribution across the knee or hip joints is uneven, the
bone beneath the cartilage hypertrophies on the compression side of the joint
and atrophies on the extension side.
The normal function of bone requires an adequate supply of amino acids (building blocks for proteins) for synthesis of collagen, the chief component for the organic matrix; of calcium and phosphate for mineralization of the organic matrix; and of other organic compounds and mineral elements. Also, growth, repair, and remodelling of the bone tissue require a precisely regulated supply of hormones, vitamins, and enzymes. Skeletal disease, when it is due to inadequacies in the supply or action of the above essentials, associated with abnormalities outside the skeleton, is termed metabolic. Examples of such abnormalities are dietary deficiency and gastrointestinal, liver, kidney, and hormonal diseases. In addition, osteoporosis (age-related loss of bone with tendency to fractures) is traditionally included among the metabolic conditions even though its cause is not known.
Changes in bone tissue due to metabolic abnormalities are classified with regard to the amount and composition of the bone tissue. When the amount of bone is lower or higher than normal, the conditions are termed, respectively, osteopenia and osteosclerosis. These terms do not imply any specific disease but simply describe the amount of bone. Osteopenia is common both locally and generally throughout the skeleton. Localized osteopenia is evident in X rays of tumours or infections of bone, in osteonecrosis (death of bony tissue), in fracture, and in conditions of diminished mechanical demand. Osteopenia may thus be associated both with atrophy from disuse and with active remodelling of bone; it occurs when bone resorption occurs faster than bone formation. Generalized osteopenia occurs in osteomalacia, osteoporosis, and osteogenesis imperfecta. Osteosclerosis occurs locally in osteoarthritis, osteonecrosis, and osteomyelitis; it represents an attempt at structural strengthening by thickening of bony trabeculae, but its X-ray appearance may be confused with that of dead bone, retaining its density while adjacent normal bone has become osteopenic. Widespread, but hardly ever truly generalized, osteosclerosis occurs in marble bone disease and in Paget's disease. Except in the latter condition, however, osteopenia and osteosclerosis are not associated with detectable biochemical abnormalities. (These diseases are characterized below.)
When the normal composition of bone tissue is altered by deficient mineralization of the organic matrix, the condition is called rickets, if in children and osteomalacia if in adults. The mineralization deficiency is due in part to a lower than normal calcium-phosphate ion product in the body fluids. In rickets the bones become tender, soft, and deformed; X rays show characteristic abnormalities at the growth zones, especially evident at the wrist, knee, and ankle joints. In osteomalacia, bone tenderness and pain accompany the slow development of spontaneous, often symmetric fractures characteristically present in the pelvis and the thigh bones. The X-ray appearance of osteomalacia is rather normal until visible fracture has developed. Biochemical abnormalities usually present in rickets and osteomalacia are increased blood concentration of the enzyme alkaline phosphatase, believed to be important for bone formation or resorption, and decreased blood concentrations of calcium or phosphate or both; the calcium concentration may fall to levels so low that muscle and nerve function are impaired (tetany). Microscopic examination of the bone tissue reveals the deficient mineralization of the organic matrix. The entire skeleton is affected in both rickets and osteomalacia, though abnormalities are more evident in growth centres in children and areas of maximal mechanical load in adults.
Insufficient protein, caloric, and vitamin intake interferes with bone formation during growth and remodelling, directly because of an inadequate supply for matrix formation and indirectly because of a deficient production of crucial hormones and enzymes. The effect in the young is stunted growth and in adults is osteopenia.
Deficient intake of calcium or phosphate or both, unassociated with vitamin D deficiency, causes a compensatory action of parathyroid hormone whereby the mineral is mobilized from the skeleton with eventual development of osteopenia. Deficient calcium intake (milk) and excessive phosphate intake (meat) causes osteopenia, fractures, and loss of teeth in dogs, cats, and other animals by excessive compensatory parathyroid hormone action.
Insufficient intake of vitamin D is one of many ways in which rickets may develop. The condition, once universally prevalent, is now rare in countries that ensure adequate supply of vitamin D in fortified milk and healthy living habits including adequate exposure to sunshine. Malabsorption of calcium and vitamin D causes a mixture of osteopenia and osteomalacia and requires high intake of calcium and vitamin D.
Parathyroid hormone is concerned with the maintenance of calcium concentration at the cell membranes. It functions by increasing the passage of calcium through the lining of the intestine, by increasing the resorption of bone tissue, and by increasing the reabsorption of calcium in the renal tubuli. Overactive parathyroid hormone causes osteopenia by excessive resorption of bone; in extreme cases spontaneous fractures may occur. Excessive secretion of parathyroid hormone may be due to a tumour of the parathyroid glands, may be secondary to dietary deficiency or malabsorption of calcium and vitamin D, or may be due to renal osteodystrophy (see below).
Adrenal corticosteroid hormone is associated with skeletal abnormalities, osteopenia, and osteonecrosis. Osteopenia develops because increased levels of corticosteroids, caused by disease (pituitary or adrenal tumour) or by long-term medication (e.g., for asthma), depress the rate of formation of bone tissue. Osteonecrosis is associated with even short-term intake of large doses of high corticosteroid medication.
The effects of kidney disease on bone reflect the role of the kidney in maintaining calcium and phosphate balance, mediated by parathyroid hormone. The two main units of the kidney, the tubules and the glomerulus, are associated with two groups of bone diseases: the former with a low level of phosphate in the blood (hypophosphatemia) and the latter with renal osteodystrophy (see below), both characterized by rickets and osteomalacia. In addition, kidney transplantation is associated with overactivity of the parathyroid glands and osteonecrosis.
Reabsorption of phosphate by the kidney tubules is deficient in a hereditary disorder, familial hypophosphatemia; the phosphate leak causes low concentration of blood phosphate and, in turn, deficient mineralization of bone tissue, rickets, and osteomalacia. Familial hypophosphatemia is the most common cause of rickets in Europe and the United States. The basic deficiency is treated with high oral doses of phosphate. Advanced forms of the disease still result in stunted growth and skeletal deformity, often necessitating repeated surgery. More complex tubular reabsorption defects are also the cause of bicarbonate, amino acid, and glucose losses; the resulting disease is so severe that the bony abnormalities usually become less important.
Renal glomerular disease with high levels of urea in the blood--uremia--is associated with renal osteodystrophy. The condition leads to severe rickets or osteomalacia associated with compensatory secondary hyperparathyroidism. In children, stunted growth may be the first symptom that leads to detection of the kidney disease; the skeletal abnormality cannot be ascribed solely to an abnormal mineral balance but is probably due also to an adverse effect of uremia on protein metabolism. Growth may resume after successful kidney transplantation, and gross deformity of the extremities may be corrected surgically. Chronic uremia in adults, even when treated by use of the artificial kidney, causes osteoporosis and deposition of calcium apatite in arterial walls and tendon sheaths, probably associated with hyperparathyroidism.
Kidney transplantation is occasionally followed by hyperparathyroidism and osteonecrosis. The overactivity of the parathyroids is ascribed to the fact that, prior to correction of the kidney disease, the glands have had to function at an abnormally high level for such a long time that the mechanisms for shutting them off have become deficient. The cause of osteonecrosis after kidney transplantation is at least partly the high doses of corticosteroid treatment used to prevent rejection of the transplant. Osteonecrosis of the hip or knee joints may cause residual disability after successful kidney transplantation.
Generalized osteopenia without evidence of osteomalacia is termed osteoporosis. It may be secondary to metabolic abnormalities discussed above or may be without known cause. Osteoporosis from unknown cause is by far the most common bone disease; it probably occurs in all aged individuals and may sometimes become evident as early as age 30-40. The spine is particularly affected.
Diagnosis of less severe stages of osteoporosis is a complicated matter because the condition is not associated with measurable chemical abnormalities or with observable tissue abnormality other than a decrease in bone mass. It is generally believed that the commonly occurring fractures in old age, those of the hip, knee, and wrist, are due to osteoporosis. Unlike vertebral fractures in osteoporosis, fractures of the limbs hardly ever occur without a distinct accident, and they are never preceded by bone pain or tenderness. The diminished quantity of bone tissue, the characteristic feature of osteoporosis, is clearly implicated in the diminished resistance of the bones to fracture, but there may also be a change in the quality of the bone tissue.
In women osteoporosis is caused by a change in the hormonal pattern, and hormonal substitution therapy is sometimes used. Except for the occurrence of extremity fractures, the outlook in osteoporosis is on the whole good. Active muscle exercises are advocated both as prevention and as therapy in osteoporosis.
Paget's disease, increasingly common after middle age, is
characterized by widespread areas of osteosclerosis; the cause is unknown.
The cells of the bone tissue die if deprived of arterial blood supply for more than a few hours. The condition is called necrosis of bone or osteonecrosis. Osteonecrosis may be caused by injury to blood vessels, associated with dislocation or fracture of bone; by blood clots or gas bubbles in the blood vessels; by invasion of foreign tissue; and by metabolic disease.
Osteonecrosis may involve the shaft (diaphysis) or the ends (epiphyses) of the long bones. Sometimes the bone marrow of the diaphysis is primarily involved, and in osteomyelitis it is usually the compact (cortical) bone of the shaft that undergoes necrosis. For mechanical reasons, and because there is a poorer blood supply to cortical bone than to the cancellous bone of the epiphyses, the course of events following osteonecrosis differs in the two types of bone. When cortical bone is involved, the dead bone may prevent healing of osteomyelitis by mechanical irritation. When the cancellous bone of the epiphyses is involved, the lesion is invaded by blood vessels from adjacent bone, and a vigorous repair process ensues, characterized by removal of dead, and the formation of new, bone. The lesion may heal with reconstitution of both structural and mechanical properties, or the process of rebuilding may weaken the bone structure so that it collapses from the mechanical forces across the joint. In these circumstances the joint cartilage is damaged, and osteoarthritis eventually develops. It is for this reason that treatment of osteonecrosis in the early stage consists of protecting the joint from weight bearing; the condition is most often encountered in the hip and the knee.
It has only recently been recognized that osteonecrosis may
often develop spontaneously or in association with the use of corticosteroid
hormone and in pancreatic disease. In these conditions the immediate cause of
impaired blood supply is not clear.
Bone tissue and the metaphyseal growth cartilage (the
cartilage, between the end of the bone and the shaft, that later becomes bone)
may be injured during the course of X-ray treatment of tumours. The risk is well
recognized but cannot always be avoided. The most common radiation injury to
bone is fracture of the neck of the thigh bone (the femur) following radiation
treatment of cancer of the uterus or the bladder. There is pain in the bone
before this type of fracture can be seen by X ray; the fracture usually heals
without displacement. In children, the X-ray treatment of certain kidney tumours
may cause growth abnormalities of the spine with development of lateral
curvature (scoliosis); and radium treatment of hemangioma (a tumour made up of
blood vessels) of the knee region may cause growth retardation in parts of the
metaphyseal cartilages with knock-knee or bowleg deformity. X-ray treatment of
certain premalignant bone tumours may make them fully malignant. Intense
radiation may cause osteonecrosis, sometimes associated with secondary
osteomyelitis.
Infection of bone tissue by microorganisms is termed osteomyelitis. Microorganisms may gain access to bone either by spreading in the bloodstream in an infectious lesion elsewhere in the body (hematogenous osteomyelitis) or through a skin wound.
The incidence of hematogenous osteomyelitis reflects the fact that the body is more susceptible to invasion by microorganisms when nutrition and hygiene are poor. Thus, hematogenous osteomyelitis is common in South America, Asia, and Africa, but in the developed countries the incidence has declined sharply during the last 50 years. In these latter countries hematogenous osteomyelitis is often associated with slum conditions or systemic disease. High-energy fractures, notably motor or missile accidents, and extensive surgery, associated with the direct introduction of microorganisms into bone, however, are increasingly common causes of osteomyelitis worldwide.
Osteomyelitis is commonly caused by pus-forming (pyogenic) microorganisms, usually Staphylococcus aureus or Mycobacterium tuberculosis. Pyogenic osteomyelitis occurs both by direct routes and by hematogenous spread from an infection of the skin, urogenital tract, lung, or upper respiratory tract. Tuberculosis of the bone is always hematogenous in origin, usually disseminated from lesions in the lungs or the kidneys.
Hematogenous osteomyelitis is more common in children than in adults. In children it is usually located in the growing end of the long bones, at the hip, for example. In adults, hematogenous osteomyelitis is commonly located in the vertebrae of the spine (tuberculous or septic spondylitis). Osteomyelitis caused by direct invasion of microorganisms often complicates open fractures and operations for fracture or for degenerative joint disease.
Osteomyelitis is associated with the cardinal symptoms of inflammation: complaints of illness, fever, local redness, swelling, warmth, pain, and tenderness. In the early stages the X-ray appearance may be normal; later, signs of destruction and repair of bone ensue. Untreated, the condition may cause extensive destruction of bone, blocking of the nutrient blood vessels with death of bone tissue, extension to an adjacent joint with development of arthritis, and eventually a break through the skin with the evacuation of pus. It may heal, but occasional flare-ups usually occur, with evacuation of pus and small pieces of dead bone (sequestra) through a persistent communication from skin to bone (a chronic sinus).
The treatment of osteomyelitis is primarily aimed at
killing microorganisms with antibiotics and, in later stages, removing pus and
sequestra by surgery.
Primary tumours, more common in children than in adults, are classified as malignant or benign; intermediary forms exist, however, and benign bone tumour may present therapeutic problems because of its location. Primary bone tumours are characterized by their origin in the skeletal tissue elements, for example, bone tissue tumours (the malignant osteogenic sarcoma and the benign osteoma), cartilage tumours (the malignant chondrosarcoma and the benign chondroma), bone marrow tumours (the malignant myeloma and the benign eosinophilic granuloma). Metastatic (secondary) tumours are malignant by definition and are characterized by their site of origin.
Common symptoms of bone tumour are pain, swelling, and fracture that is spontaneous or is caused by only trivial forces. Most bone tumours cause abnormalities observable in X rays--defects in the bone tissue can be seen or bone that has formed in reaction to the tumour or, in some types of tumour, the tumours themselves, which consist of bone. Some bone tumours cause biochemical abnormalities detectable by examination of blood samples: myeloma (production of characteristic protein, a globulin) or metastatic cancer of the prostate (production of the enzyme acid phosphatase). The ultimate identification of bone tumour rests on examination of tissue samples.
Benign tumours may be excised and the defect filled with a
bone transplant for structural support. Malignant tumours may be treated by
ionizing radiation, chemical agents, or surgery. Treatment of metastatic bone
tumour is aimed at suppression of pain and prevention or repair of fracture by
external support or, occasionally, by internal fixation. Treatment of malignant
primary bone tumour is aimed at destruction of the tumour either by segmental
resection of the involved region or by amputation.
A fracture occurs when the bone tissue is subjected to tensile, compressive, or shear forces in excess of its strength. Both the strength of the bone tissue and the nature of the forces acting on bone change from infancy to old age, both normally and as a result of disease. Therefore, the incidence and type of fractures changes with age.
The bone tissue in young adults has high resistance to mechanical deformation. Fractures of cortical bone in adults require tremendous forces, such as those encountered in motor accidents, and are therefore often associated with severe skin injuries and other lesions of soft tissue. Bones in children are springy and resilient, and the membrane enclosing the bones--the periosteum--is thick. Angular deformation of long bones in children therefore often results in incomplete or "greenstick" fractures. In the elderly the bone tissue becomes more brittle, especially the cancellous bone in vertebrae and in shoulder, wrist, hip, and knee joints.
The forces acting on the skeleton of a child normally are defined by body size and weight. Fractures in children are therefore rarely severely displaced or associated with severe soft tissue injury. In adults age 20-50, fractures are often caused by direct, high-energy forces that have an explosive effect on bone and soft tissues and may cause severely displaced open fractures. In the aged, fracture is usually caused by mild forces acting on brittle bone. Such fractures are rarely associated with soft tissue injury and often involve cancellous rather than cortical bone.
Many diseases decrease the strength of the bone tissue, and some expose the body to increased mechanical forces. Osteoporosis, which is prevalent in women over 50, is the major cause of fractures in old age. Less common causes of decreased bone strength are osteogenesis imperfecta, long-term corticosteroid treatment, and osteomalacia. Common causes of locally decreased bone strength are injury of peripheral nerves and tumour.
The existence of a fracture is often deduced from a history of injury and observation of swelling, tenderness, faulty alignment, the sound that the broken ends make, loss of function, and associated injuries. Precise diagnosis is made by X-ray examination.
Most fractures occur without skin injury (closed fractures). The skin wound in open fractures is caused either by severe direct violence or by a sharp bone fragment that pierces the skin from within.
Fracture sometimes develops slowly rather than suddenly. These fatigue, or stress, fractures occur either because the bone tissue is exposed to forces that overwhelm its capacity for structural adaptation or because there is pre-existing disease. Examples of the former are fracture of the thigh bone and fracture of the bones of the foot (march fracture) in soldiers during their initial months of physical training. Bone diseases associated with fatigue fracture are osteomalacia, Paget's disease, and radiation injury to bone. Fatigue fracture usually produces pain even before bone abnormality can be seen in the X rays.
Except when forces act with explosive suddenness, vessels and nerves usually escape injury because of their elasticity and resilience. For anatomic reasons, nerve injury may occur in fracture-dislocation of the hip and in fracture of the long bone of the upper arm (the humerus) through the diaphysis in adults and just above the elbow in children; the latter fracture is associated with compression of the accompanying artery. Fracture and dislocation of the vertebrae caused by severe forces may be associated with spinal cord injury. Certain fractures injure the nutrient blood vessels of the bone tissue with osteonecrosis as a result.
The bone blood vessels rupture when there is fracture. The resultant bleeding causes swelling at the site of fracture (fracture hematoma) and later discoloration of the skin. Occasionally the bleeding is so severe that the circulating blood volume is significantly diminished and shock ensues. The nerve endings of the periosteum are distended by the bleeding caused by fracture, and motion or pressure at the fracture site is painful.
A fracture starts to heal at the very moment that it occurs. The fracture hematoma is invaded by cellular elements; these form organic matrix and mineral into bone (callus) that bridges the fracture. Formation of callus is faster in children than in adults and in cancellous bone than in cortical bone. Fracture of the thigh, which may heal in four to six weeks in a toddler, may require as many months in an adult. Similarly, fracture of the cancellous bone of the upper end of the humerus usually requires one-third or less of the time required for healing of a fracture of the cortical shaft of the same bone. Bridging of the fracture is hindered by separation and motion of the bone fragments, poor blood supply, and infection. After the fracture has healed, the region is remodelled by resorption and formation of bone so as to accommodate the microstructure of the bone tissue to precise mechanical demands. This remodelling is most effective in children; in adults gross deformity may exceed the remodelling capacity.
The most severe and most common cause of deficient healing is infection, osteomyelitis, associated with open fractures, which permit direct access for disease-causing organisms. The condition is prevented by treatment of open fractures with antibiotics and closure of the skin. A fracture may also unite slowly or not at all because of deficient blood supply to one or more of the bone fragments, separation of the fragments by distention or interposition of a tendon or ligament, or excessive motion at the fracture site.
The guiding principle in treatment of fractures is restoration of normal length and alignment when necessary and avoidance of motion between the fracture fragments. Some fractures, notably compression fractures of cancellous bone, are inherently stable (remain in normal alignment) and require temporary immobilization by bed rest or a sling only because of pain. Most fractures are stable in acceptable position only after reduction of dislocation and immobilization by fixation, externally by traction or plaster or internally by introduction of metallic screws, plates, nail, or wire (internal fixation).
Nonunion results in a false joint--pseudarthrosis--characterized by pain and motion at the fracture site. Healing may be achieved by immobilization with or without internal fixation and by transplantation of bone to bridge the defect.
Fracture may cause permanent deformity by residual
angulation or by shortening owing to overlap of cortical bone fragments,
compression of cancellous bone, or, in children, arrest of metaphyseal cartilage
growth. Osteoarthritis is a late complication of fracture at a joint when the
joint cartilage surfaces are disturbed and the joint is unstable.
Many important diseases of the locomotor system are congenital in the sense that they become evident at or soon after birth. This does not imply that they all are genetically determined. Most are caused by factors operating during pregnancy, delivery, or early infancy.
Intrauterine injuries of the locomotor system are dramatically exemplified by the thalidomide catastrophe: children born of some women who received this drug during the initial three months of pregnancy had severe extremity defects (phocomelia). Most intrauterine injuries are probably not caused by drugs, however, but perhaps by viral, hormonal, or mechanical factors. Intrauterine amputations, clubfeet, and congenital dislocation of the hip probably belong to this group. Birth injuries with fracture of the collarbone or humerus occur because of mechanical difficulties during delivery. These fractures heal extremely fast.
Developmental abnormalities may affect isolated or multiple
regions of the skeleton, or they may involve a specific tissue system; the
latter are often heritable. Examples of isolated abnormalities are partial or
total absence of the collarbone, radius (the long bone on the thumb side of the
lower arm), and the thigh bone; congenital false joint in the shin bone (tibia);
and absence of a middle segment of a limb (phocomelia; see below). Treatment of
these conditions is difficult, often requiring advanced transplantation or
orthopedic devices and sometimes necessitating amputation in childhood. Multiple
abnormalities are represented by polyostotic fibrous dysplasia, in which
affected bone is replaced by connective-tissue matrix of obscure origin. The
condition may cause multiple deformities that require surgical correction.
Heritable disorders of the skeleton include osteogenesis imperfecta, the Hurler and Marfan syndromes and several disorders of epiphyseal and metaphyseal growth centres. (For a detailed treatment of these heritable disorders, see the article connective tissue disease.)
Heritable metaphyseal dysplasias, causing bone deformities
near the joints, exist in several forms. The primary defect lies in the growth
zone of the long bones. One of these conditions (hypophosphatasia) results from
a deficiency in the enzyme alkaline phosphatase and is one of the few hereditary
generalized disorders of the bony skeleton in which an enzyme defect has been
identified. Multiple defects in the growth zones of the skeleton are distinct
from familial hypophosphatemia, a condition characterized by low phosphate
levels in the blood; it affects the kidney primarily and the skeleton only
secondarily. Hemophilia, finally, is a generalized heritable condition that
affects the locomotor system only secondarily by bleeding in bones and joints.
Traction counteracts muscle pull on the skeleton and is used to reduce and stabilize fractures and to prevent muscle shortening. Traction is applied by ropes and pulleys fastened to the skin by adhesive tape or directly to the skeleton with the aid of metal pins drilled into bone.
Internal fixation (osteosynthesis) of bone is aimed at restoration of continuity and stability during healing of a fracture, arthrodesis, or osteotomy (see below). For this purpose a variety of metal screws, pins, plates, and wires have been developed. The metal used is either stainless steel or a chromium-cobalt-molybdenum alloy that resists the corrosive action of the body fluids.
Arthroplasty, aimed at restoration of normal joint motion, is usually performed because of pain and restricted motion--for example, in rheumatoid arthritis of the elbow or the hip--but occasionally to restrict mobility--for example, in recurrent dislocation of the shoulder. Structural support and smooth gliding surfaces can be obtained by insertion of metallic devices; in the hip, for example, both the ball and the socket of the joint can be replaced. Osteotomy is aimed at correction of bony or articular deformity by cutting through bone and letting the fracture heal in the desired position, usually with the aid of internal fixation.
Arthrodesis is aimed at elimination of motion in a joint (fusion) in order to eliminate pain in osteoarthritis and rheumatoid arthritis, stabilize a joint that is either unstable or lacks useful muscle power, and remove an infectious lesion in arthritis. The operation involves removal of joint cartilage and immobilization; a bone transplant is sometimes used for more rapid restoration of continuity.
Bone resection implies surgical removal of bone and is performed either in the course of an arthroplasty or independently. The operation is performed in certain fractures and for removal of tumour.
Epiphysiodesis (the fixing of the epiphysis to the bone shaft) is aimed at temporary or permanent cessation of growth in a metaphyseal cartilage. The operation is performed at the knee for compensation of growth in the other leg--for example, because of poliomyelitis--or in one of the other growth cartilages in the same knee.
Tendon transfer is aimed at changing the mechanical effect of the corresponding muscle. The operation is performed to restore function lost by paralysis and to correct an abnormality in the motion of a joint.
Transplantation of bone is aimed at stimulation of bone formation and giving structural support until a defect has been bridged by new bone. If the bone cells of the transplant survive, they can continue to form bone and can stimulate adjacent tissue to formation of bone. Without survival, the transplant may function as a scaffold for invasion by tissue from adjacent bone, guided by the microstructure of the dead transplant. Cell-rich cancellous bone stimulates bone formation more effectively than does cortical bone, which gives better structural support.
The fundamental problems in transplantation of bone, as with other tissues, are cell death because of deficient blood supply and a tendency toward rejection. The smaller the transplant, the better are the possibilities that blood vessels will reach the cells in time; this is why many small chips are used for stimulation of bone formation. Another possibility is to transplant bone in continuity with attached vessels in order to preserve the blood supply of the transplant. The immunologic problem is usually circumvented by use of bone from the individual himself (autotransplantation). In children sufficient bone for autotransplantation is often not available; bone from another individual will then be used. An attempt to modify the immunologic reaction to such a transplant is usually made by radiation and by storage in a bone bank.
Common indications for transplantation of bone are nonunion of a fracture, a bone cyst, arthrodesis, and structural defects in cancellous bone caused by compression fracture--for example, the heel bone.
Amputation is performed for four reasons: arterial disease,
gross injury, tumour, and developmental abnormality, all more common in the legs
than in the arms. Arterial disease, arteriosclerosis ("hardening of the
arteries"), often associated with diabetes, is common in the aged. Gross
injury to nerves, vessels, and soft tissues and primary tumours of bone or other
connective tissue usually involve relatively young individuals. Developmental
abnormalities--for example, congenital false joint in the tibia--may occasion
amputation in childhood. (G.C.H.B.) (Ed.)
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Copyright © May 20, 2008 6:25 AM by Karl Loren on behalf of Vibrant Life, ALL RIGHTS RESERVED. Permission is granted for non-commercial downloading, copying, distribution or redistribution on two conditions: One, that some form of copyright notice is included in every copy distributed or copied, showing the copyright belonging to Vibrant Life, Burbank, CA, at www.oralchelation.com . The second condition is that the material is not to be used for any purpose contrary to the purposes and objectives of this site. This permission does not extend to materials on this site which are copyrighted by others.
Click here to add the Wednesday Letter as a Channel on your desktop. If your browser is so-equipped, you will be guided through a series of simple questions (about subscription information). Depending on your choices you can show the Vibrant Life Wednesday Letter as one of your "active channels" which will automatically download the new Wednesday Letter every month. In this way you can have the Wednesday Letter delivered to your desktop during the night (or your schedule) for immediate viewing in your browser. You can turn on or off this channel, at will, and delete the channel from your desktop at any time. With this feature operating you can click on the Wednesday Letter channel at any time to read the most recent copy of this electronic letter.
You can reach Vibrant Life in many ways, including by mail to Vibrant Life, 2808 N. Naomi St., Burbank, CA 91504. Within the US and Canada, use the toll free number: (800) 523-4521, the local number: (818) 558-1799, the FAX: (818) 558-7299, eMail to kimberly@oralchelation.com or any one of the hundreds of message forms throughout the 50 web sites. Vibrant Life normally ships the same day we get an order. There are message forms on each of the 100,000+ pages on this and other sites where you can communicate with Vibrant Life. Check out our companion site, at: http://www.oralchelation.net where Karl's 2000 page book is published. Karl Loren is the author and webmaster for this BOOK, as well as for another web site about ORAL CHELATION. His personal philosophical articles are at PHILOSOPHY.
Copyright © May 20, 2008 6:25 AM by Karl Loren on behalf of Vibrant Life, ALL RIGHTS RESERVED. Permission is granted for non-commercial downloading, copying, distribution or redistribution on two conditions: One, that some form of copyright notice is included in every copy distributed or copied, showing the copyright belonging to Vibrant Life, Burbank, CA, at www.oralchelation.com . The second condition is that the material is not to be used for any purpose contrary to the purposes and objectives of this site. This permission does not extend to materials on this site which are copyrighted by others.
Click here to add the Wednesday Letter as a Channel on your desktop. If your browser is so-equipped, you will be guided through a series of simple questions (about subscription information). Depending on your choices you can show the Vibrant Life Wednesday Letter as one of your "active channels" which will automatically download the new Wednesday Letter every month. In this way you can have the Wednesday Letter delivered to your desktop during the night (or your schedule) for immediate viewing in your browser. You can turn on or off this channel, at will, and delete the channel from your desktop at any time. With this feature operating you can click on the Wednesday Letter channel at any time to read the most recent copy of this electronic letter.
You can reach Vibrant Life in many ways, including by mail to Vibrant Life, 2808 N. Naomi St., Burbank, CA 91504. Within the US and Canada, use the toll free number: (800) 523-4521, the local number: (818) 558-1799, the FAX: (818) 558-7299, eMail to kimberly@oralchelation.com or any one of the hundreds of message forms throughout the 50 web sites. Vibrant Life normally ships the same day we get an order. There are message forms on each of the 100,000+ pages on this and other sites where you can communicate with Vibrant Life. Check out our companion site, at: http://www.oralchelation.net where Karl's 2000 page book is published. Karl Loren is the author and webmaster for this BOOK, as well as for another web site about ORAL CHELATION. His personal philosophical articles are at PHILOSOPHY.
Copyright © May 20, 2008 6:25 AM by Karl Loren on behalf of Vibrant Life, ALL RIGHTS RESERVED. Permission is granted for non-commercial downloading, copying, distribution or redistribution on two conditions: One, that some form of copyright notice is included in every copy distributed or copied, showing the copyright belonging to Vibrant Life, Burbank, CA, at www.oralchelation.com . The second condition is that the material is not to be used for any purpose contrary to the purposes and objectives of this site. This permission does not extend to materials on this site which are copyrighted by others.
