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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]


Atrophy is the partial or complete wasting away of a part of the body. Causes of atrophy include poor nourishment, poor circulation, loss of hormonal support, loss of nerve supply to the target organ, disuse or lack of exercise or disease intrinsic to the tissue itself. Hormonal and nerve inputs that maintain an organ or body part are referred to as trophic. Atrophy is a general physiological process of reabsorption and breakdown of tissues, involving apoptosis on a cellular level. When it occurs as a result of disease or loss of trophic support due to other disease, it is termed pathological atrophy, although it can be a part of normal body development and homeostasis as well.

Types of Atrophy

Normal Development

Examples of atrophy as part of normal development include shrinkage and involution of the thymus in early childhood and the tonsils in adolescence.

Breast Atrophy

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

Muscle Atrophy

Disuse atrophy of muscles (muscle atrophy) 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. Astronauts must exercise regularly to minimize atrophy of their limb muscles while they are in microgravity.

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.[1]

Dystrophies, Myosities, and Motor Neuron Conditions

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

Vaginal Atrophy

In post-menopausal women, the walls of the vagina atrophy and become thinner. 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.[2]


It has been reported that Astemizole might prevent 97% of the muscle wasting that occurs in immobile, bedridden patients.[3]Testing upon mice showed that it blocked the activity of a protein present in the muscle that is involved in muscle atrophy.[4] However the concerns for the drug's longterm effects on the heart preclude its routine use in humans for this indication and further alternative drugs are being sought.[3]

Related Chapters


  1. Campellone, Joseph V. (2007-05-22). "Muscle atrophy" (html). MedlinePlus. Retrieved 2007-10-02.
  2. "Types of Atrophy" (html). Retrieved 2007-10-02.
  3. 3.0 3.1 "Drug could stop muscle wasting'". 25 May,2006. Retrieved 2006-05-27. Check date values in: |date= (help)
  4. Wang X, Hockerman GH, Green Iii HW, Babbs CF, Mohammad SI, Gerrard D, Latour MA, London B, Hannon KM, Pond AL (2006). "Merg1a K+ channel induces skeletal muscle atrophy by activating the ubiquitin proteasome pathway". FASEB J. PMID 16723379. Unknown parameter |month= ignored (help)

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