Atrophy

Atrophia

For medical students2 min readUpdated 2026-10-10

Atrophy is an adaptive process characterized by a decrease in the size and volume of an organ or tissue, leading to a reduction or complete loss of its function. In most cases, these changes are reversible, and the stroma of the organ often retains its volume while undergoing sclerosis.

Essence of the processA typical example of the body's adaptation to changing conditions in health and disease.

ReversibilityIn most cases, atrophic changes are reversible once the underlying cause is removed.

Stroma changesThe stroma retains its volume but frequently undergoes sclerosis (proliferation of connective tissue).

Aging pigmentDuring senile atrophy, lipofuscin accumulates within cells, causing 'brown atrophy'.

Physiological Atrophy

Physiological atrophy occurs continuously throughout the body and acts as a natural mechanism of adaptation to changing life conditions. A prominent example includes age-related changes (aging). During this period, the number of functionally active cells and the volume of intracellular organelles naturally decrease, leading to a general decline in organ function.

A characteristic sign of aging at the cellular level is the accumulation of the pigment lipofuscin, leading to the development of so-called "brown atrophy". Microscopically (e.g., in brown atrophy of the liver), hepatocytes appear reduced in size, and clusters of brown pigment granules are clearly visible in their cytoplasm.

Tactical examples of physiological involution include:

Atrophy of endocrine glands.
Atrophy of the ovaries, mammary glands, and thymus.
Atrophy of the spermatogenic epithelium of the testes.

The extreme degree of age-related changes is senile (involutional) cachexia—a generalized atrophy of the entire body resulting from a global decrease in metabolic rate and the shutdown of many body functions.

General Pathological Atrophy

Pathological atrophy develops against the background of various diseases and is always an important link in their pathogenesis. It is traditionally subdivided into general and local.

General pathological atrophy manifests as pathological cachexia (wasting). Depending on the leading cause, several types of this condition are distinguished:

Inanition (starvation) — occurs with prolonged fasting and inadequate nutrient intake.
Cerebral and pituitary cachexia — develops in severe brain diseases when central regulation is disrupted.
Post-traumatic cachexia — severe wasting accompanying massive bodily injuries.

Local Pathological Atrophy

Local pathological atrophy is significantly more common in clinical practice than general atrophy. Depending on the mechanism of development (pathogenesis), five main types are distinguished:

Disuse atrophy. Occurs due to the absence of function in an organ or tissue. A classic example is skeletal muscle atrophy of a limb following a bone fracture due to enforced immobilization.
Neurotrophic atrophy. Associated with impaired tissue innervation. For example, in poliomyelitis, motor neurons are destroyed, leading to severe atrophy of the corresponding skeletal muscles.
Pressure atrophy. Develops when tissue is compressed by accumulated fluid or a growing tumor. A characteristic example is brain tissue atrophy in hydrocephalus, where cerebrospinal fluid accumulates in the ventricles and presses on the parenchyma.
Ischemic atrophy (insufficient blood supply). Caused by narrowing of the lumen of arteries supplying an organ. For instance, renal artery stenosis (e.g., due to an atherosclerotic plaque) leads to marked renal atrophy.
Atrophy from physical or chemical agents. Arises under the influence of physical or chemical agents. An example is bone marrow atrophy developing due to radiation exposure.

Mnemonic

To remember the five types of local pathological atrophy, use the phrase "Poor Grandpa Never Remembers Names": Poor (Pressure), Grandpa (General/Disuse), Never (Neurotrophic), Remembers (Radiation/Damaging agents), Names (Ischemia / vascular restriction). Alternative clinical mnemonic: DINPI: Disuse, Ischemia, Neurotrophic, Pressure, Injurious agents.

Frequently asked questions

What types of general pathological atrophy (cachexia) exist?

The following types of general pathological atrophy (cachexia) exist:

Inanition (starvation) — develops during starvation (absence or deficiency of food).
Cerebral and pituitary cachexia — occurs in brain diseases.
Post-traumatic cachexia — develops as a consequence of sustained injuries.

Senile (involutional) cachexia is also distinguished, although it refers to manifestations of physiological atrophy occurring in connection with a decreased metabolic rate.

Which organs and structures undergo physiological atrophy?

Various organs and structures undergo physiological atrophy during normal life activity and aging:

Umbilical vessels and ductus arteriosus — atrophy after birth.
Thymus — undergoes age-related involution.
Endocrine glands — including gonads (ovaries, spermatogenic epithelium of the testes) in old age.
Mammary glands — undergo involution.
Bones and muscles — atrophy in elderly individuals (senile atrophy).

In senile cachexia, physiological atrophy of the entire human body is observed.

How does atrophy differ from hypoplasia and aplasia?

Atrophy differs from hypoplasia in the time of onset and the initial state of the organ.

Feature	Atrophy	Hypoplasia
Definition	Reduction in the volume of an organ that previously reached normal dimensions	Congenital underdevelopment of an organ
Initial volume	Was normal prior to the process	Never initially achieves normal volume

Aplasia is mentioned as a developmental malformation (e.g., of the salivary glands), but its detailed differences from atrophy are separate entities.

What macroscopic features characterize an atrophied organ?

An atrophied organ is characterized by the following macroscopic features:

Size and shape — the organ is usually reduced in size but retains its original shape (with uniform atrophy).
Consistency — becomes firmer due to stromal sclerosis (proliferation of connective tissue) or replacement by proliferating adipose tissue.
Surface — may become pebbled or granular upon uneven parenchymal loss (e.g., in granular contracted kidney).
Color — upon accumulation of lipofuscin pigment, the organ acquires a brown coloration (brown atrophy).

What is the mechanism of lipofuscin formation in cells during atrophy?

The mechanism of lipofuscin ("aging pigment") formation is associated with damage to cellular organelles and impaired degradation processes.

Pigment accumulates in the cytoplasm due to a deficiency of intracellular antioxidants, leading to lipid peroxidation of membrane lipids. As a result, autolysosomes form containing undigested cellular debris (fragments of mitochondria, endoplasmic reticulum). These structures form residual bodies, which constitute lipofuscin granules—an insoluble pigment composed of lipid and phospholipid polymers bound to protein.

What ultrastructural changes occur in a cell during atrophy?

Using neurotrophic muscle atrophy as an example, the following ultrastructural changes are described:

Reduction of organelles — the number of mitochondria and myofilaments decreases, and the volume of the endoplasmic reticulum drops.
Autophagy — the number of autophagic vacuoles containing fragments of mitochondria and endoplasmic reticulum increases.
Accumulation of lipofuscin — residual bodies containing undigested cellular debris are formed, exemplified by lipofuscin granules.

What is brown atrophy and why is it called that?

It is a type of age-related physiological atrophy in which granules of the pigment lipofuscin accumulate in reduced cells (such as hepatocytes), imparting a characteristic brown color to the tissue.

What happens to the stroma of an organ during atrophy?

The stroma typically retains its original volume, but often undergoes sclerosis—the proliferation of connective tissue that fills the space.

Is atrophy reversible?

Yes, in most cases it is a reversible adaptive process. The function and volume of the tissue can recover if the cause of the pathology is eliminated in time.

Go deeper

Morphological picture of brown atrophy of the liver
Pathogenesis of senile (involutional) cachexia
Types of pathological cachexia (alimentary, cerebral, post-traumatic)
Mechanisms of stromal sclerosis during parenchymal atrophy
Differences between atrophy and necrosis at the tissue level