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Mouse with spinal muscular atrophy.jpg
Mouse (right) with spinal muscular atrophy
Specialty Pathology
Symptoms Loss of body cells, signs of ageing
Types Muscular atrophy, gland atrophy
CausesPoor nourishment, poor circulation, loss of hormonal support, loss of nerve supply to target organ(s), excessive apoptosis of cells, insufficient exercise, ageing
Risk factors Old age, sedentary lifestyle
Prognosis Depends on the cause

Atrophy is the partial or complete wasting away of a part of the body. Causes of atrophy include mutations (which can destroy the gene to build up the organ), poor nourishment, poor circulation, loss of hormonal support, loss of nerve supply to the target organ, excessive amount of apoptosis of cells, and disuse or lack of exercise or disease intrinsic to the tissue itself. In medical practice, hormonal and nerve inputs that maintain an organ or body part are said to have trophic effects. A diminished muscular trophic condition is designated as atrophy. Atrophy is reduction in size of cell, organ or tissue, after attaining its normal mature growth. In contrast, hypoplasia is the reduction in the cellular numbers of an organ, or tissue that has not attained normal maturity.


Atrophy is the general physiological process of reabsorption and breakdown of tissues, involving apoptosis. When it occurs as a result of disease or loss of trophic support because of other diseases, it is termed pathological atrophy, although it can be a part of normal body development and homeostasis as well.

Normal development

Examples of atrophy as part of normal development include shrinking and the involution of the thymus in early childhood, and the tonsils in adolescence. In old age, effects include, but are not limited to, loss of teeth, hair, thinning of skin that creates wrinkles, weakening of muscles, loss of weight in organs and sluggish mental activity. [1]

Muscle atrophies

Disuse atrophy of muscles and bones, with loss of mass and strength, can occur after prolonged immobility, such as extended bedrest, or having a body part in a cast (living in darkness for the eye, bedridden for the legs etc.). This type of atrophy can usually be reversed with exercise unless severe.

There are many diseases and conditions which cause atrophy of muscle mass. For example, diseases such as cancer and AIDS induce a body wasting syndrome called cachexia , which is notable for the severe muscle atrophy seen. Other syndromes or conditions which can induce skeletal muscle atrophy are congestive heart failure and liver disease.

During aging, there is a gradual decrease in the ability to maintain skeletal muscle function and mass. This condition is called sarcopenia , and may be distinct from atrophy in its pathophysiology. While the exact cause of sarcopenia is unknown, it may be induced by a combination of a gradual failure in the satellite cells which help to regenerate skeletal muscle fibers, and a decrease in sensitivity to or the availability of critical secreted growth factors which are necessary to maintain muscle mass and satellite cell survival. [2]

Dystrophies, myositis, and motor neuron conditions

Pathologic atrophy of muscles can occur with diseases of the motor nerves or diseases of the muscle tissue itself. Examples of atrophying nerve diseases include Charcot-Marie-Tooth disease, poliomyelitis, amyotrophic lateral sclerosis (ALS or Lou Gehrig's disease), and Guillain–Barré syndrome. Examples of atrophying muscle diseases include muscular dystrophy, myotonia congenita, and myotonic dystrophy.

Changes in Na+ channel isoform expression and spontaneous activity in muscle called fibrillation can also result in muscle atrophy.

A flail limb is a medical term which refers to an extremity in which the primary nerve has been severed, resulting in complete lack of mobility and sensation. The muscles soon wither away from atrophy.

Gland atrophy

The adrenal glands atrophy during prolonged use of exogenous glucocorticoids like prednisone. Atrophy of the breasts can occur with prolonged estrogen reduction, as with anorexia nervosa or menopause. Testicular atrophy can occur with prolonged use of enough exogenous sex steroids (either androgen or estrogen) to reduce gonadotropin secretion.

Vaginal atrophy

In post-menopausal women, the walls of the vagina become thinner (atrophic vaginitis). The mechanism for the age-related condition is not yet clear, though there are theories that the effect is caused by decreases in estrogen levels. [3] This atrophy, occurring concurrently with breast atrophy, is consistent with the homeostatic (normal development) role of atrophy in general, as after menopause the body has no further functional biological need to maintain the reproductive system which it has permanently shut down.


One drug in test seemed to prevent the type of muscle loss that occurs in immobile, bedridden patients. [4] Testing on mice showed that it blocked the activity of a protein present in the muscle that is involved in muscle atrophy. [5] However, the drug's long-term effect on the heart precludes its routine use in humans, and other drugs are being sought. [4]

See also

Related Research Articles

<span class="mw-page-title-main">Cachexia</span> Medical condition

Cachexia is a complex syndrome associated with an underlying illness, causing ongoing muscle loss that is not entirely reversed with nutritional supplementation. A range of diseases can cause cachexia, most commonly cancer, congestive heart failure, chronic obstructive pulmonary disease, chronic kidney disease, and AIDS. Systemic inflammation from these conditions can cause detrimental changes to metabolism and body composition. In contrast to weight loss from inadequate caloric intake, cachexia causes mostly muscle loss instead of fat loss. Diagnosis of cachexia can be difficult due to the lack of well-established diagnostic criteria. Cachexia can improve with treatment of the underlying illness but other treatment approaches have limited benefit. Cachexia is associated with increased mortality and poor quality of life.

Myotonia is a symptom of a small handful of certain neuromuscular disorders characterized by delayed relaxation of the skeletal muscles after voluntary contraction or electrical stimulation.

Weakness is a symptom of a number of different conditions. The causes are many and can be divided into conditions that have true or perceived muscle weakness. True muscle weakness is a primary symptom of a variety of skeletal muscle diseases, including muscular dystrophy and inflammatory myopathy. It occurs in neuromuscular junction disorders, such as myasthenia gravis.

<span class="mw-page-title-main">Mucopolysaccharidosis</span> Medical condition

Mucopolysaccharidoses are a group of metabolic disorders caused by the absence or malfunctioning of lysosomal enzymes needed to break down molecules called glycosaminoglycans (GAGs). These long chains of sugar carbohydrates occur within the cells that help build bone, cartilage, tendons, corneas, skin and connective tissue. GAGs are also found in the fluids that lubricate joints.

<span class="mw-page-title-main">Striated muscle tissue</span> Muscle tissue with repeating functional units called sarcomeres

Striated muscle tissue is a muscle tissue that features repeating functional units called sarcomeres. The presence of sarcomeres manifests as a series of bands visible along the muscle fibers, which is responsible for the striated appearance observed in microscopic images of this tissue. There are two types of striated muscle:

<span class="mw-page-title-main">Neuromuscular junction</span> Junction between the axon of a motor neuron and a muscle fiber

A neuromuscular junction is a chemical synapse between a motor neuron and a muscle fiber.

<span class="mw-page-title-main">Myostatin</span> Mammalian and avian protein

Myostatin is a protein that in humans is encoded by the MSTN gene. Myostatin is a myokine that is produced and released by myocytes and acts on muscle cells to inhibit muscle growth. Myostatin is a secreted growth differentiation factor that is a member of the TGF beta protein family.

<span class="mw-page-title-main">Endocrine gland</span> Glands of the endocrine system that secrete hormones to blood

Endocrine glands are ductless glands of the endocrine system that secrete their products, hormones, directly into the blood. The major glands of the endocrine system include the pineal gland, pituitary gland, pancreas, ovaries, testes, thyroid gland, parathyroid gland, hypothalamus and adrenal glands. The hypothalamus and pituitary glands are neuroendocrine organs.

<span class="mw-page-title-main">Hyperplasia</span> Increase in the amount of organic tissue that results from cell proliferation

Hyperplasia, or hypergenesis, is an enlargement of an organ or tissue caused by an increase in the amount of organic tissue that results from cell proliferation. It may lead to the gross enlargement of an organ, and the term is sometimes confused with benign neoplasia or benign tumor.

<span class="mw-page-title-main">Cockayne syndrome</span> Medical condition

Cockayne syndrome (CS), also called Neill-Dingwall syndrome, is a rare and fatal autosomal recessive neurodegenerative disorder characterized by growth failure, impaired development of the nervous system, abnormal sensitivity to sunlight (photosensitivity), eye disorders and premature aging. Failure to thrive and neurological disorders are criteria for diagnosis, while photosensitivity, hearing loss, eye abnormalities, and cavities are other very common features. Problems with any or all of the internal organs are possible. It is associated with a group of disorders called leukodystrophies, which are conditions characterized by degradation of neurological white matter. The underlying disorder is a defect in a DNA repair mechanism. Unlike other defects of DNA repair, patients with CS are not predisposed to cancer or infection. Cockayne syndrome is a rare but destructive disease usually resulting in death within the first or second decade of life. The mutation of specific genes in Cockayne syndrome is known, but the widespread effects and its relationship with DNA repair is yet to be well understood.

Sarcopenia is a type of muscle loss that occurs with aging and/or immobility. It is characterized by the degenerative loss of skeletal muscle mass, quality, and strength. The rate of muscle loss is dependent on exercise level, co-morbidities, nutrition and other factors. The muscle loss is related to changes in muscle synthesis signalling pathways. It is distinct from cachexia, in which muscle is degraded through cytokine-mediated degradation, although both conditions may co-exist. Sarcopenia is considered a component of frailty syndrome. Sarcopenia can lead to reduced quality of life, falls, fracture, and disability.

Hypoestrogenism, or estrogen deficiency, refers to a lower than normal level of estrogen. It is an umbrella term used to describe estrogen deficiency in various conditions. Estrogen deficiency is also associated with an increased risk of cardiovascular disease, and has been linked to diseases like urinary tract infections and osteoporosis.

<span class="mw-page-title-main">Neuromuscular disease</span> Medical condition

A neuromuscular disease is any disease affecting the peripheral nervous system (PNS), the neuromuscular junction, or skeletal muscle, all of which are components of the motor unit. Damage to any of these structures can cause muscle atrophy and weakness. Issues with sensation can also occur.

<span class="mw-page-title-main">Muscle atrophy</span> Medical condition

Muscle atrophy is the loss of skeletal muscle mass. It can be caused by immobility, aging, malnutrition, medications, or a wide range of injuries or diseases that impact the musculoskeletal or nervous system. Muscle atrophy leads to muscle weakness and causes disability.

Starvation response in animals is a set of adaptive biochemical and physiological changes, triggered by lack of food or extreme weight loss, in which the body seeks to conserve energy by reducing the amount of calories it burns.

<span class="mw-page-title-main">Orthopedic pathology</span>

Orthopedic pathology, also known as bone pathology is a subspecialty of surgical pathology which deals with the diagnosis and feature of many bone diseases, specifically studying the cause and effects of disorders of the musculoskeletal system. It uses gross and microscopic findings along with the findings of in vivo radiological studies, and occasionally, specimen radiographs to diagnose diseases of the bones.

In cell biology and pathophysiology, cellular adaptation refers to changes made by a cell in response to adverse or varying environmental changes. The adaptation may be physiologic (normal) or pathologic (abnormal). Four types of morphological adaptations include atrophy, hypertrophy, hyperplasia, and metaplasia.

<span class="mw-page-title-main">Denervation</span> Loss of nerve supply

Denervation is any loss of nerve supply regardless of the cause. If the nerves lost to denervation are part of the neuronal communication to a specific function in the body then altered or a loss of physiological functioning can occur. Denervation can be caused by injury or be a symptom of a disorder like ALS, post-polio syndrome, or POTS. Additionally, it can be a useful surgical technique to alleviate major negative symptoms, such as in renal denervation. Denervation can have many harmful side effects such as increased risk of infection and tissue dysfunction.

Electrical impedance myography, or EIM, is a non-invasive technique for the assessment of muscle health that is based on the measurement of the electrical impedance characteristics of individual muscles or groups of muscles. The technique has been used for the purpose of evaluating neuromuscular diseases both for their diagnosis and for their ongoing assessment of progression or with therapeutic intervention. Muscle composition and microscopic structure change with disease, and EIM measures alterations in impedance that occur as a result of disease pathology. EIM has been specifically recognized for its potential as an ALS biomarker by Prize4Life, a 501(c)(3) nonprofit organization dedicated to accelerating the discovery of treatments and cures for ALS. The $1M ALS Biomarker Challenge focused on identifying a biomarker precise and reliable enough to cut Phase II drug trials in half. The prize was awarded to Dr. Seward Rutkove, chief, Division of Neuromuscular Disease, in the Department of Neurology at Beth Israel Deaconess Medical Center and Professor of Neurology at Harvard Medical School, for his work in developing the technique of EIM and its specific application to ALS. It is hoped that EIM as a biomarker will result in the more rapid and efficient identification of new treatments for ALS. EIM has shown sensitivity to disease status in a variety of neuromuscular conditions, including radiculopathy, inflammatory myopathy, Duchenne muscular dystrophy, and spinal muscular atrophy.

<span class="mw-page-title-main">Acquired non-inflammatory myopathy</span> Medical condition

Acquired non-inflammatory myopathy (ANIM) is a neurological disorder primarily affecting skeletal muscle, most commonly in the limbs of humans, resulting in a weakness or dysfunction in the muscle. A myopathy refers to a problem or abnormality with the myofibrils, which compose muscle tissue. In general, non-inflammatory myopathies are a grouping of muscular diseases not induced by an autoimmune-mediated inflammatory pathway. These muscular diseases usually arise from a pathology within the muscle tissue itself rather than the nerves innervating that tissue. ANIM has a wide spectrum of causes which include drugs and toxins, nutritional imbalances, acquired metabolic dysfunctions such as an acquired defect in protein structure, and infections.


  1. W. T. Councilman (1913). "Chapter Two". Disease and Its Causes. New York Henry Holt and Company London Williams and Norgate The University Press, Cambridge, U.S.
  2. Campellone, Joseph V. (2007-05-22). "Muscle atrophy". MedlinePlus. Archived from the original on 13 October 2007. Retrieved 2007-10-02.
  3. "Types of Atrophy". Archived from the original on 28 September 2007. Retrieved 2007-10-02.
  4. 1 2 "Drug could stop muscle wasting'". 2006-05-25. Archived from the original on 2007-09-11. Retrieved 2006-05-27.
  5. Wang X, Hockerman GH, Green Iii HW, Babbs CF, Mohammad SI, Gerrard D, Latour MA, London B, Hannon KM, Pond AL (May 24, 2006). "Merg1a K+ channel induces skeletal muscle atrophy by activating the ubiquitin proteasome pathway". FASEB J. 20 (9): 1531–3. doi:10.1096/fj.05-5350fje. PMID   16723379. S2CID   15763153.