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In cell biology and pathophysiology, cellular adaptation refers to changes made by a cell in response to adverse environmental changes. The adaptation may be physiologic(al) (normal) or pathologic(al) (abnormal). Five minor types of adaptation include atrophy, hypertrophy, hyperplasia, dysplasia, and metaplasia.
Atrophy is a decrease in cell size. If enough cells in an organ atrophy the entire organ will decrease in size. Thymus atrophy during early human development (childhood) is an example of physiologic atrophy. Skeletal muscle atrophy is a common pathologic adaptation to skeletal muscle disuse (commonly called "disuse atrophy"). Tissue and organs especially susceptible to atrophy include skeletal muscle, cardiac muscle, secondary sex organs, and the brain.
Hypertrophy is an increase in cell size. If enough cells of an organ hypertrophy so will the whole organ. The heart and kidneys have increased susceptibility to hypertrophy. Hypertrophy involves an increase in intracellular protein rather than cytosol (intracellular fluid). Hypertrophy may be caused by mechanical signals (e.g., stretch) or trophic signals (e.g., growth factors). An example of physiologic hypertrophy is in skeletal muscle with sustained weight bearing exercise. An example of pathologic hypertrophy is in cardiac muscle as a result of hypertension.
Hyperplasia is an increase in the number of cells. It is the result of increased cell mitosis, or division. The two types of physiologic hyperplasia are compensatory and hormonal. Compensatory hyperplasia permits tissue and organ regeneration. It is common in epithelial cells of the epidermis and intestine, liver hepatocytes, bone marrow cells, and fibroblasts. It occurs to a lesser extent in bone, cartilage, and smooth muscle cells. Hormonal hyperplasia occurs mainly in organs that depend on estrogen. For example, the estrogen-dependent uterine cells undergo hyperplasia and hypertrophy following pregnancy. Pathologic hyperplasia is an abnormal increase in cell division. A common pathologic hyperplasia in women occurs in the endometrium and is called endometriosis.
Metaplasia occurs when a differentiated cell of a certain type is replaced by another cell type, which may be less differentiated. It is a reversible process thought to be caused by stem cell reprogramming. Stem cells are found in epithelia and embryonic mesenchyme of connective tissue. A prominent example of metaplasia involves the changes associated with the respiratory tract in response to inhalation of irritants, such as smog or smoke. The bronchial cells convert from mucus-secreting, ciliated, columnar epithelium to non-ciliated, squamous epithelium incapable of secreting mucus. These transformed cells may become dysplasic or cancerous if the stimulus (e.g., cigarette smoking) is not removed. The most common example of metaplasia is Barrett's esophagus, when the non-keratinizing squamous epithelium of the esophagus undergoes metaplasia to become mucinous columnar cells, ultimately protecting the esophagus from acid reflux originating in the stomach. If stress persists, metaplasia can progress to dysplasia and eventually carcinoma; Barrett's esophagus, for example, can eventually progress to adenocarcinoma of the esophagus if not treated.
Dysplasia refers to abnormal changes in cellular shape, size, and/or organization. Dysplasia is not considered a true adaptation; rather, it is thought to be related to hyperplasia and is sometimes called "atypical hyperplasia". Tissues prone to dysplasia include cervical and respiratory epithelium, where it is strongly associated with the development of cancer; it may also be involved in the development of breast cancer. Although dysplasia is reversible, if stress persists, then dysplasia progresses to irreversible carcinoma.
Notes and references
- Huether, S. E. & McCance, K. L. (2008). Understanding Pathophysiology, Ed 4, p. 62-65.
- Porth, Carol Mattson (2005). Pathophysiology : Concepts of Altered Health States (PDF) (7th ed.). Philadelphia, Pa: Lippencott, Williams & Wilkins. p. 105. ISBN 0-7817-4988-3. Retrieved 28 December 2016.