|Classification and external resources|
Hyperplasia (from ancient Greek ὑπέρ huper, "over" + πλάσις plasis, "formation") or hypergenesis, means increase in number of cells/proliferation of cells. It may result in the gross enlargement of an organ and the term is sometimes confused with benign neoplasia / benign tumor.
Hyperplasia is a common preneoplastic response to stimulus. Microscopically cells resemble normal cells but are increased in numbers. Sometimes cells may also be increased in size (hypertrophy). Hyperplasia is different from hypertrophy in that the adaptive cell change in hypertrophy is an increase in cell size, whereas hyperplasia involves an increase in the number of cells.
Difference from neoplasia
Hyperplasia is considered to be a physiological (normal) response to a specific stimulus, and the cells of a hyperplastic growth remain subject to normal regulatory control mechanisms. This stands in contrast to neoplasia (the process underlying cancer and benign tumors), in which genetically abnormal cells proliferate in a non-physiological manner which is unresponsive to normal stimuli.
As seen in examples below, such physiological proliferation of cells may in fact be secondarily due to a pathological cause. Still, the proliferation itself is a normal response to another abnormal condition, in contrast to neoplasia, where the proliferation in itself is abnormal.
Hyperplasia may be due to any number of causes, including increased demand (for example, proliferation of basal layer of epidermis to compensate skin loss), chronic inflammatory response, hormonal dysfunctions, or compensation for damage or disease elsewhere. Hyperplasia may be harmless and occur on a particular tissue. An example of a normal hyperplastic response would be the growth and multiplication of milk-secreting glandular cells in the breast as a response to pregnancy, thus preparing for future breast feeding.
Hyperplasia may also be induced artificially by injecting hormones such as IGF-1 and human growth hormone. Perhaps the most interesting and potent effect IGF has on the human body is its ability to cause hyperplasia, which is an actual splitting of cells.[original research?] By contrast, hypertrophy is what occurs, for example, to skeletal muscle cells during weight training and steroid use and is simply an increase in the size of the cells. With IGF use, one is able to cause hyperplasia which actually increases the number of muscle cells present in the tissue. Weight training with or without anabolic steroid use enables these new cells to mature in size and strength. In addition, animal tests have shown that stretching a muscle can trigger hyperplasia, though this phenomenon has yet to be confirmed in humans. It is theorized that hyperplasia may also be induced through specific power output training for athletic performance, thus increasing the number of muscle fibers instead of increasing the size of a single fiber. This mechanism has thus far only been observed in birds.
Hyperplasia may also occur abnormally, and is associated with a variety of clinical diseases.
Examples in human biology and disease
Some of the more commonly known clinical forms of hyperplasia, or conditions leading to hyperplasia, are:
- Benign prostatic hyperplasia, also known as prostate enlargement.
- Cushing's disease – Physiopathology of hyperplasia of adrenal cortex due to increased circulating level of ACTH (adrenocorticotropic hormone).
- Congenital adrenal hyperplasia
- Endometrial hyperplasia – Hyperproliferation of the endometrium, usually in response to unopposed estrogen stimulation in the setting of polycystic ovary syndrome or exogenous administration of hormones. Atypical endometrial hyperplasia may represent an early neoplastic process which can lead to endometrial adenocarcinoma.
- Hemihyperplasia when only half (or one side) of the body is affected, sometimes generating limbs of different lengths.
- Hyperplasia of the breast – "Hyperplastic" lesions of the breast include usual ductal hyperplasia, a focal expansion of the number of cells in a terminal breast duct, and atypical ductal hyperplasia, in which a more abnormal pattern of growth is seen, and which is associated with an increased risk of developing breast cancer. The biology of these lesions is the subject of dispute, with some authorities arguing that both of these lesions are the result of neoplasia, and that the application of the term "hyperplasia" in this instance is "inaccurate."
- Intimal hyperplasia – The thickening of the Tunica intima of a blood vessel as a complication of a reconstruction procedure or endarterectomy. Intimal hyperplasia is the universal response of a vessel to injury and is an important reason of late bypass graft failure, particularly in vein and synthetic vascular grafts.
- Focal epithelial hyperplasia (also known as Heck's disease) – This is a wart-like growth in the mucous tissues of the mouth or, rarely, throat that is caused by certain sub-types of the human papillomavirus (HPV). Heck's disease has not been known to cause cancer.
- Sebaceous hyperplasia – In this condition, small yellowish growths develop on the skin, usually on the face. This condition is neither contagious nor dangerous.
- Compensatory liver hyperplasia – The liver undergoes cellular division after acute injury, resulting in new cells that restore liver function back to baseline. Approximately 75% of the liver can be acutely damaged or resected with seemingly full regeneration through hepatocyte division, i.e., hyperplasia. This is what makes living-donor liver transplants possible.
- M. Donald McGavin, James F. Zachary (2007). Pathologic Basis of Veterinary Disease, Fourth Edition. Mosby Elsevier.
- Ramzi Cotran et al (1999). Robbins pathologic basis of disease (6th ed.). W.B. Saunders. ISBN 0-7216-7335-X. OCLC 222671811.
- Antonio J, Gonyea WJ (Aug 1994). "Muscle fiber splitting in stretch-enlarged avian muscle". Med Sci Sports Exerc. 26 (8): 973–977. PMID 7968431.
- Tavassoli FA (2005). "Breast pathology: rationale for adopting the ductal intraepithelial neoplasia (DIN) classification". Nature Clinical Practice Oncology 2 (3): 116–117. doi:10.1038/ncponc0109. PMID 16264885.