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-plasia
(Ana)plasia - dedifferentiation
(Hyper)plasia - physiological proliferation
(Neo)plasia - abnormal proliferation
(Dys)plasia - maturation abnormality
(Meta)plasia - cell type conversion
(Desmo)plasia - connective tissue growth
Squamous cells.jpg
Dysplastic cells.jpg

Dysplasia (from the Greek δυσπλασία "malformation", δυσ- "mal-" + πλάθω "to create, to form"), is a term used in pathology to refer to an abnormality of development.[1] This generally consists of an expansion of immature cells, with a corresponding decrease in the number and location of mature cells. Dysplasia is often indicative of an early neoplastic process. The term dysplasia is typically used when the cellular abnormality is restricted to the originating tissue, as in the case of an early, in-situ neoplasm.

Dysplasia, in which cell maturation and differentiation are delayed, can be contrasted with metaplasia, in which cells of one mature, differentiated type are replaced by cells of another mature, differentiated type.

The terms hip dysplasia and fibrous dysplasia also refer to abnormal development, but at a more macroscopic level.

Contents

Examples

For example, epithelial dysplasia of the cervix (cervical intraepithelial neoplasia - a disorder commonly detected by an abnormal pap smear) consists of an increased population of immature (basal-like) cells which are restricted to the mucosal surface, and have not invaded through the basement membrane to the deeper soft tissues. Analagous conditions include vaginal intraepithelial neoplasia and vulvar intraepithelial neoplasia.

Myelodysplastic syndromes, or dysplasia of blood-forming cells, show increased numbers of immature cells in the bone marrow, and a decrease in mature, functional cells in the blood.

Microscopic changes

Dysplasia is characterised by four major pathological microscopic changes:

  1. Anisocytosis (cells of unequal size)
  2. Poikilocytosis (abnormally shaped cells)
  3. Hyperchromatism
  4. Presence of mitotic figures (an unusual number of cells which are currently dividing).

Dysplasia vs. carcinoma in situ vs. invasive carcinoma

These terms are related since they represent the three steps in the progression of many malignant neoplasms (cancers) of epithelial tissues. The likelihood of developing carcinoma is related to the degree of dysplasia.[2]

  • Dysplasia is the earliest form of pre-cancerous lesion recognizable in a pap smear or in a biopsy by a pathologist. Dysplasia can be low grade or high grade (see "Carcinoma in situ," below). The risk of low grade dysplasia transforming into high grade dysplasia, and eventually cancer, is low. Treatment is usually straightforward. High grade dysplasia represents a more advanced progression towards malignant transformation.
  • Carcinoma in situ, meaning "cancer in place," represents the transformation of a neoplastic lesion to one in which cells undergo essentially no maturation, and thus may be considered cancer-like. In this state, epithelial cells have lost their tissue identity and have reverted back to a primitive cell form that grows rapidly and without regulation. However, this form of cancer remains localized, and has not invaded past the basement membrane into tissues below the surface.
  • Invasive carcinoma is the final step in this sequence. It is a cancer which has invaded beyond the basement membrane and has potential to metastasize (spread to other parts of the body). Invasive carcinoma can usually be treated, but not always successfully. However, if it is left untreated, it is almost always fatal.

References

  1. ^ dysplasia at Dorland's Medical Dictionary
  2. ^ Ridge JA, Glisson BS, Lango MN, et al. "Head and Neck Tumors" in Pazdur R, Wagman LD, Camphausen KA, Hoskins WJ (Eds) Cancer Management: A Multidisciplinary Approach. 11 ed. 2008.
  • Richard Cote, Saul Suster, Lawrence Weiss, Noel Weidner (Editor). Modern Surgical Pathology (2 Volume Set). London: W B Saunders. ISBN 0-7216-7253-1. 
  • Ramzi S. Cotran, Vinay Kumar, Tucker Collins (Editor) (1999). Robbins Pathologic Basis of Disease, sixth edition. London: W B Saunders. ISBN 0-7216-7335-X. 
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