atrophy, © International Osteoporosis Foundation decrease in size of a body part, cell, organ, or tissue. The term implies that the atrophied part was of a size normal for the individual, considering age and circumstance, prior to the diminution. In atrophy of an organ or body part, there may be a reduction in the number or in the size of the component cells, or in both.
Certain cells and organs normally undergo atrophy at certain ages or under certain physiologic circumstances. In the human embryo, for example, a number of structures are transient and at birth have already undergone atrophy. The adrenal glands become smaller shortly after birth because an inner layer of the cortex has shrunk. The thymus and other lymphoid tissues atrophy at adolescence. The pineal organ tends to atrophy about the time of puberty; usually calcium deposits, or concretions, form in the atrophic tissue. The widespread atrophy of many tissues that accompanies advanced age, although universal, is influenced by changes of nutrition and blood supply that occur during active mature life.
The normal cyclic changes of female reproductive organs are accompanied by physiologic atrophy of portions of these organs. During the menstrual cycle, the corpus luteum of the ovary atrophies if pregnancy has not occurred. The muscles of the uterus, which enlarge during pregnancy, rapidly atrophy after the delivery of the child; and after completion of lactation the milk-producing acinar structures of the breast diminish in size. After the menopause the ovaries, uterus, and breasts normally undergo a degree of atrophic change.
Atrophy in general is related to changes in nutrition and metabolic activity of cells and tissues. A widespread or generalized atrophy of body tissues occurs under conditions of starvation, whether because food is unavailable or because it cannot be taken and absorbed due to the presence of disease. The unavailability of certain essential protein components and vitamins disturbs the metabolic processes and leads to atrophy of cells and tissues. Under conditions of protein starvation, the body protein is broken down into constituent amino acids, which serve to provide energy and help maintain the structure and cells of the most essential organs. The brain, heart, adrenals, thyroid, pituitary, gonads, and kidneys show less atrophy, relatively, than the body as a whole; whereas the fatty stores of the body, liver, spleen, and lymphoid tissues diminish relatively more than the body as a whole. The brain, heart, and kidneys, organs with abundant blood supply, appear to be the least subject to the wasting effects of starvation.
Associated with the widespread atrophy due to lack of protein is the atrophy of certain tissues that is due to deficiencies of specific vitamins. Atrophic changes of the skin increase because of the lack of vitamin A, and atrophy of muscle increases because of the unavailability of vitamin E.
After a growth period of human metabolism, there sets in a gradual decline: slow structural changes other than those due to preventable diseases or accidents occur. Aging eventually is characterized by marked atrophy of many tissues and organs, with both a decline in the number of cells and an alteration in their constitution. This is reflected eventually in the changed, diminished, or lost function characteristic of old age and eventuates in death. The changes in senescence are affected by both inherited constitution and environmental influences, including disease and accident.
Atrophic changes of aging affect almost all tissues and organs, but some changes are more obvious and important. Arteriosclerosis—the thickening and hardening of arterial walls—decreases the vascular supply and usually accentuates aging processes.
Atrophy in old age is especially noticeable in the skin, characteristically flat, glossy or satiny, and wrinkled. The atrophy is due to aging changes in the fibres of the true skin, or dermis, and in the cells and sweat glands of the outer skin. Wasting of muscle accompanied by some loss of muscular strength and agility is common in the aged. In a somewhat irregular pattern, there is shrinkage of many individual muscle fibres as well as a decrease in their number. Other changes have been observed within the muscle cells.
Increase of the pigment lipofuscin is also characteristic in the muscle fibres of the heart in the aged in a condition known as brown atrophy of the heart. Wasting of the heart muscle in old age may be accompanied by increase of fibrous and fatty tissue in the walls of the right side of the heart and by increased replacement of elastic tissue with fibrous tissue in the lining and walls of coronary arteries within the heart muscle. Abnormal deposits of the protein substance amyloid also occur with greater frequency in the atrophic heart muscle in old age.
Atrophy of the liver in the aged is also accompanied by increased lipochrome pigment in the atrophied cells.
The bones become progressively lighter and more porous with aging, a process known as osteoporosis. The reduction of bone tissue is most marked in cancellous bone—the open-textured tissue in the ends of the long bones—and in the inner parts of the cortex of these bones. In addition to changes in and loss of osteocytes, or bone cells, there is decreasing mineralization, or calcium deposit, with enhanced fragility of the bones.
Atrophy of the brain in old age is shown by narrowing of the ridges, or gyri, on the surface of the brain and by increased fluid in the space beneath the arachnoid membrane, the middle layer of the brain covering. There is shrinkage of individual nerve cells, with an increase in their lipochrome pigment content, as well as a decrease in their number. Sometimes the nerve fibrils have degenerated, and deposits called senile plaques may be found between the nerve cells, particularly in the frontal cortex and hippocampus (a ridge in the wall of an extension, or horn, of the lateral ventricle, or cavity, of the brain). Similar atrophic changes are seen in the brain in Alzheimer’s disease, a condition of unknown cause most likely to occur in older patients. The mental deterioration (senile dementia) of the aged is the clinical manifestation of these changes. Senile atrophy may be increased and complicated by the presence of arteriosclerosis.
A destructive or atrophic lesion affecting the pituitary glands with loss of hormones leads to atrophy of the thyroid, adrenal glands, and gonads and in turn brings atrophic changes to their target organs and the viscera. The decrease in size of the endocrine glands may be extreme.
Local atrophy of muscle, bone, or other tissues results from disuse or diminished activity or function. Although the exact mechanisms are not completely understood, decreased blood supply and diminished nutrition occur in inactive tissues. Disuse of muscle resulting from loss of motor nerve supply to the muscle (e.g., as a result of poliomyelitis) leads to extreme inactivity and corresponding atrophy. Muscles become limp and paralyzed if there is destruction of the nerve cells in the spinal cord that normally activate them. The shrinkage of the paralyzed muscle fibres becomes evident within a few weeks. After some months, fragmentation and disappearance of the muscle fibres occurs with some replacement by fat cells and a loose network of connective tissue. Some contracture may result.
The skeletal tissues forced to inactivity by paralysis (e.g., of a limb as a result of poliomyelitis) also undergo disuse atrophy. If there is a tendency for bone to become lighter and more porous in some particular area, a condition known as local osteoporosis, this can be recognized by X-rays within a few weeks. The cortex of the long bones becomes considerably thinned or atrophic, with decreased mineral content. Disuse as a result of painfully diseased joints, as in rheumatoid arthritis, results in a similar but lesser degree of atrophy of muscles concerned with movement of the involved joint; and local atrophy may also occur in the bone in the neighbourhood of the joint. A local osteoporosis of bone known as Sudeck’s atrophy sometimes develops rapidly in the area of an injury to bone.
Severe or prolonged deficits of blood sugar deprive the nervous system of needed sources of energy and as a rare event result in degeneration of cells of the brain and peripheral nerves. The disuse atrophy of muscle or bone that may result is fundamentally similar to the other disuse atrophies of these tissues.
Persistent pressure will cause atrophy of a compressed cell, organ, or tissue, presumably because of interference with the nutrition and metabolic activity of the affected part. Cells in a local area (e.g., in the liver) atrophy from the pressure of materials such as amyloid deposited around them. The pressure of an expanding benign tumour causes atrophy of adjacent normal structures. The pressure of a localized dilatation of an artery (aneurysm) will cause atrophy of tissues, even bone, on which it impinges.
Bulging of an intervertebral disk or growth of a tumour sometimes brings pressure on nerves near their point of exit from the spinal cord; if the pressure is prolonged, the muscles normally controlled by these nerves may atrophy. Most often the calf muscles are affected. Pressure as a result of involvement of the vertebrae at the level of the neck, or from compression of the network of nerves called the brachial plexus by the scalenus anticus muscle, produces similar effects in the upper chest and arms.
Simple disuse of muscle or bone, as, for example, from the immobilization produced when a limb is put in a cast or sling, results in atrophy of these tissues. In the case of muscle, the degree of atrophy is generally less severe than that caused by injury to a nerve, although the nature of the change is similar.
Localized atrophies of leg and arm muscles may result from hereditary or familial diseases in which the nerves of the spinal cord that supply them are inactivated or destroyed. In Charcot-Marie-Tooth disease, the atrophy involves mainly the peroneal muscles, at the outer side of the lower legs, and sometimes the muscles of the hand as well. It commonly begins in childhood or adolescence. Peroneal muscle atrophy is also seen in the hereditary spinal cord degenerative disease known as Friedreich’s ataxia.
Atrophy of brain or spinal cord tissue may be brought about by injuries that directly affect a localized area or that interfere with the blood supply to an area. When peripheral nerves are severed, degenerative and eventually atrophic changes ensue in the part beyond the injury. This type of atrophy is known as Wallerian degeneration. If conditions do not allow regeneration of nerve fibres from the proximal fragment of the cut nerve, atrophy is the eventual fate of the nerve tissue distal to the injury. Retrograde atrophy also occurs from disuse and affects the ganglion cells of the injured nerve.
Prolonged pressure brings about atrophy in the central nervous system as elsewhere. The pressure of an expanding tumour of the membranes covering the brain results in localized atrophy of the adjacent brain substance on which it impinges. In hydrocephalus more widespread atrophy of brain tissue results from the abnormal amounts of fluid confined within the rigid bony compartment of the skull. Increased pressure within the skull may force a portion of the brain through the foramen magnum, the bony opening at the base of the skull, and, if prolonged, results in a localized atrophy of cerebellar tissue pressed against the bony wall.
The late stages of chronic infections may be characterized by atrophy of the brain. A striking example of this is the variety of syphilitic infection of the nervous system known as general paresis in which the brain is shrunk and reduced in weight, the atrophy affecting mainly the cortex of the brain, particularly or most markedly in the frontal area. Occasionally the atrophy is local or affects only one side of the brain. The shrinkage of the brain tissue is mainly due to loss of many nerve cells of the cortex.
Atrophy of adipose tissue of the body occurs as a part of the generalized atrophy of prolonged undernutrition. Localized atrophy of adipose tissue—lipodystrophy—may be the result of injury to the local area; e.g., repeated insulin injections cause atrophy of fatty tissue at the site of the injections. Progressive lipodystrophy is a disease of unknown cause in which the fatty tissue atrophies only in certain regions of the body. It occurs mainly in women and often begins in childhood; the progressive wasting of adipose tissue affects mainly the face, arms, and trunk. In the affected areas, the specialized fat-holding cells of adipose tissue disappear.
A widespread atrophic change in the skin has been noted as a prominent part of the aging process. Similar atrophic changes in the skin appear to be brought about or enhanced by excessive exposure to sunlight. While a number of abnormal conditions of the skin may include localized atrophic changes in the epidermis or dermis as a part of their lesions, certain generalized diseases of the skin are particularly characterized by such changes. The hardening of the skin known as scleroderma may occur in a localized, or circumscribed, form called morphea or as a more diffuse and severe disease. Advanced stages of scleroderma are characterized by marked atrophy of the tissue and appendages of the true skin. Atrophic thinning of the overlying epidermis also may occur, and the underlying fatty tissue and muscle may atrophy as well. The chronic form of the disease discoid lupus erythematosus also is characterized by atrophy. In advanced stages atrophy occurs particularly in the epidermis in focal areas. The thinned layer of epidermis may be a prominent feature of the microscopic appearance of the skin.
Endocrine glandular tissues may undergo atrophy when an excess of their hormonal product is present as a result of disease. An example is seen in connection with a hormone-producing tumour of the cortical tissue of one adrenal gland, which may be accompanied by marked atrophy of the cortical tissue of the opposite adrenal gland. This probably results from disturbance of the delicate mechanism of hormonal stimulation via the pituitary gland.
Various endocrine organs (thyroid, adrenals, gonads) depend for their activity on endocrine stimulation by hormones of the pituitary gland. A severe general failure of production of the pituitary hormones results in the widespread endocrine atrophy of Simmonds’ disease, as has been noted. Lesser degrees of pituitary functional disturbance may disturb a delicate balance, involving mainly one type of stimulating hormone of the pituitary, and may result in selective atrophy of the adrenal cortical tissue or of the gonads.
Glands that release their secretions through a duct (e.g., salivary glands, pancreas) may become atrophic as a result of obstruction of the duct. In the pancreas, a complete obstruction of its duct results in atrophy of the glandular tissue, except for the insulin-producing islets of Langerhans, the secretion of which is absorbed into the bloodstream. Factors of both disuse and increased pressure may be present in the atrophy resulting from obstruction of the outlet channel. Similarly, rapid and complete obstruction of a ureter is followed by atrophy of the corresponding kidney.
Cases of atrophy resulting from chemical injury are not common. In chronic arsenic poisoning, however, degenerative changes occur in peripheral nerves, resulting in weakness and atrophy in the tissues (usually legs or arms) to which the nerves are distributed. Similar results may follow the peripheral neuropathy of chronic lead poisoning.