Hyperplasia
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Hyperplasia (or "hypergenesis") is a general term referring to the proliferation of cells within an organ or tissue beyond that which is ordinarily seen in e.g. constantly dividing cells. Hyperplasia may result in the gross enlargement of an organ, the formation of a benign tumor, or may be visible only under a microscope. Hyperplasia is considered to be a physiological 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 some benign tumors), in which genetically abnormal cells proliferate in a non-physiological manner which is unresponsive to normal stimuli.[1]
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[edit] Causes
Hyperplasia may be due to any number of causes, including increased demand, 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. Hypertrophy, on the other hand, is what occurs during weight training and steroid use and is simply an increase in the size of muscle cells. With IGF use, one is able to cause this 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.[2]
Hyperplasia may also occur abnormally, and is associated with a variety of clinical diseases.
[edit] Examples in human biology and disease
Some of the more commonly-known clinical forms of hyperplasia, or conditions leading to hyperplasia, are:
- 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.
- Benign prostatic hyperplasia, also known as prostate enlargement.
- 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."[3]
- 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 the basis for living-donor liver transplants.
[edit] References
- ^ Ramzi Cotran, Vinay Kumar, Tucker Collins (1999). Robbins Pathologic Basis of Disease, Sixth Edition. W.B. Saunders. ISBN 072167335X.
- ^ Antonio, J, et al. (1994) "Muscle fiber splitting in stretch-enlarged avian muscle". Medicine & Science in Sports & Exercise, 26:8, 973-7.
- ^ Tavassoli FA (2005). "Breast pathology: rationale for adopting the ductal intraepithelial neoplasia (DIN) classification". Nature clinical practice. Oncology 2 (3): 116-7. doi:. PMID 16264885.
[edit] External links
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