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Hyperplasia

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(Redirected from Oral verrucous hyperplasia)
Hyperplasia
Whereas hypertrophy stems from an increase in cell size, hyperplasia results from an increase in cell number.
SpecialtyPathology
TypesBenign prostatic hyperplasia, Hyperplasia of the breast(many more)[1][2]
Diagnostic methodBiopsy[3]
TreatmentDepends which type (see types)

Hyperplasia (from ancient Greek ὑπέρ huper 'over' + πλάσις plasis 'formation'), or hypergenesis, is an enlargement of an organ or tissue caused by an increase in the amount of organic tissue that results from cell proliferation.[4] It may lead to the gross enlargement of an organ, and the term is sometimes confused with benign neoplasia or benign tumor.[5]

Hyperplasia is a common preneoplastic response to stimulus.[6] Microscopically, cells resemble normal cells but are increased in numbers. Sometimes cells may also be increased in size (hypertrophy).[7] Hyperplasia is different from hypertrophy in that the adaptive cell change in hypertrophy is an increase in the size of cells, whereas hyperplasia involves an increase in the number of cells.[8]

-plasia and -trophy
  • Abiotrophy (loss in vitality of organ or tissue)
  • Atrophy (reduced functionality of an organ, with decrease in the number or volume of cells)
  • Hypertrophy (increase in the volume of cells or tissues)
  • Hypotrophy (decrease in the volume of cells or tissues)
  • Dystrophy (any degenerative disorder resulting from improper or faulty nutrition)

Causes

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Hyperplasia may be due to any number of causes, including proliferation of basal layer of epidermis to compensate skin loss, chronic inflammatory response, hormonal dysfunctions, or compensation for damage or disease elsewhere.[9] 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.[10]

Perhaps the most interesting and potent[editorializing] effect insulin-like growth factor 1 (IGF) has on the human body is its ability to cause hyperplasia, which is an actual splitting of cells.[11] By contrast, hypertrophy is what occurs, for example, to skeletal muscle cells during weight training and is simply an increase in the size of the cells.[12] With IGF use, one is able to cause hyperplasia which actually increases the number of muscle cells present in the tissue.[13] Weight training enables these new cells to mature in size and strength. 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.[14]

Mechanism

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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.[5] However, hyperplasia can also occur as a pathological response, if an excess of hormone or growth factor is responsible for the stimuli. Similarly to physiological hyperplasia, cells that undergo pathologic hyperplasia are controlled by growth hormones, and cease to proliferate if such stimuli are removed.[15] This differs from neoplasia (the process underlying cancer and benign tumors), in which genetically abnormal cells manage to proliferate in a non-physiological manner which is unresponsive to normal stimuli.[16] That being said, the effects caused by pathologic hyperplasia can provide a suitable foundation from which neoplastic cells may develop.[15]

Role in disease

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Hyperplasia of certain tissues may cause disease. Pathologic hyperplasia in these tissues may occur due to infection, physiological stress or trauma, or abnormal levels of particular hormones, such as estrogen, ACTH, or cortisol.[17]

Types

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Some of the more commonly known clinical forms of hyperplasia, or conditions leading to hyperplasia, include:

Patient with hemihyperplasia involving the upper and lower left extremities. The leg length discrepancy can be noted by the pelvic tilt.
  • Hemihyperplasia – When only half (or one side) of the body is affected, sometimes generating limbs of different lengths.[21]
  • 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.[2]
  • 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.[22]
  • 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.[23]
  • Myofibre hyperplasia (also known as double-muscling) – seen in cattle, genetic mutations cause large muscles due to increased proliferation of myofibres and decreased adipose tissue.[24]
  • Sebaceous hyperplasia – In this condition, small yellowish growths develop on the skin, usually on the face. This condition is neither contagious nor dangerous.[25]
  • 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.[26]
  • Epidermal hyperplasia of the skin[citation needed]

See also

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References

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  1. ^ a b "Prostate Enlargement (Benign Prostatic Hyperplasia)". National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK). U.S. Department of Health and Human Services National Institutes of Health. Retrieved 2015-05-30.
  2. ^ a b Koerner FC (2009). Diagnostic Problems in Breast Pathology. Elsevier Health Sciences. ISBN 978-1-4160-2612-9.
  3. ^ Dunphy LM, Winland-Brown JE (April 2011). Primary Care: The Art and Science of Advanced Practice Nursing. F.A. Davis. ISBN 978-0-8036-2647-8.
  4. ^ "Hyperplasia". MedlinePlus Medical Encyclopedia. National Library of Medicine, U.S. Department of Health and Human Services National Institutes of Health. Retrieved 2015-05-30.
  5. ^ a b Sembulingam K, Sembulingam P (September 2012). Essentials of Medical Physiology. JP Medical Ltd. ISBN 9789350259368.
  6. ^ Zachary JF, McGavin MD (December 2013). Pathologic Basis of Veterinary Disease. Elsevier Health Sciences. ISBN 978-0-323-29172-9.
  7. ^ Braun CA, Anderson CM (2007). Pathophysiology: Functional Alterations in Human Health. Lippincott Williams & Wilkins. p. 17. ISBN 978-0-7817-6250-2.
  8. ^ Rubin E, Reisner HM (2009). Essentials of Rubin's Pathology. Lippincott Williams & Wilkins. ISBN 978-0-7817-7324-9.
  9. ^ Porth C (2011). Essentials of Pathophysiology: Concepts of Altered Health States. Lippincott Williams & Wilkins. ISBN 978-1-58255-724-3.
  10. ^ Dirbas F, Scott-Conner C (January 2011). Breast Surgical Techniques and Interdisciplinary Management. Springer Science & Business Media. ISBN 978-1-4419-6076-4.
  11. ^ Gardiner P. Advanced Neuromuscular Exercise Physiology. Human Kinetics. ISBN 978-1-4504-1227-8.
  12. ^ Metzl JD, Shookhoff C (October 2009). The Young Athlete: A Sports Doctor's Complete Guide for Parents. Little, Brown. ISBN 978-0-316-08673-8.
  13. ^ Rodgers K, ed. (November 2011). The Endocrine System. Britannica Educational Publishing. ISBN 978-1-61530-731-9.
  14. ^ Kisner C, Colby LA (December 2012). Therapeutic Exercise: Foundations and Techniques. F.A. Davis. ISBN 978-0-8036-3897-6.
  15. ^ a b c Kumar V, Abbas A, Aster J (2013). Robbins Basic Pathology. Philadelphia, US: Elsevier. p. 4. ISBN 978-0-8089-2432-6.
  16. ^ Hong WK, Hait WN (2010). Holland Frei Cancer Medicine Eight. PMPH-USA. ISBN 978-1-60795-014-1.
  17. ^ Kemp WL, Burns DK, Brown TG. "Pathology: The Big Picture". AccessMedicine. McGraw Hill Medical. Retrieved 2021-12-06.
  18. ^ "Cushing disease". MedlinePlus Medical Encyclopedia. National Library of Medicine, U.S. Department of Health and Human Services National Institutes of Health. Retrieved 2015-05-30.
  19. ^ "Congenital adrenal hyperplasia". MedlinePlus Medical Encyclopedia. National Library of Medicine, U.S. Department of Health and Human Services National Institutes of Health. Retrieved 2015-05-30.
  20. ^ "Endometrial Hyperplasia". American College of Obstetricians and Gynecologists (ACOG). Retrieved 2015-05-30.
  21. ^ "Hemihyperplasia - Glossary Entry". Genetics Home Reference. National Library of Medicine, U.S. Department of Health and Human Services. Retrieved 2015-05-30.
  22. ^ Subbotin VM (October 2007). "Analysis of arterial intimal hyperplasia: review and hypothesis". Theoretical Biology & Medical Modelling. 4: 41. doi:10.1186/1742-4682-4-41. PMC 2169223. PMID 17974015.
  23. ^ Purkait SK (2011). Essentials of Oral Pathology. JP Medical Ltd. ISBN 9789350252147.
  24. ^ Swatland, Howard (January 1974). "Developmental disorders of skeletal muscle in cattle, pigs and sheep". The Veterinary Bulletin. 44 (4): 187–189 – via ResearchGate.
  25. ^ Evans CC, High WA (October 2011). Skin Diseases in the Elderly: A Color Handbook. CRC Press. ISBN 978-1-84076-615-8.
  26. ^ Kumar V, Abbas AK, Aster JC (September 2014). Robbins & Cotran Pathologic Basis of Disease. Elsevier Health Sciences. ISBN 978-0-323-29635-9.

Further reading

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