Ovarian cysts

Causes of ovarian cysts range from normal physiological processes to genetic mutations involving tumour suppression and growth. Functional varieties, such as corpus luteum cysts, follicular cysts, and theca lutein cysts, arise in response to normal or increased hormonal action.[6]Dolan MS, Hill C, Valea FA. Benign gynecologic lesions. In: Lobo RA, Gershenson DM, Lentz GM, et al (eds). Comprehensive gynecology. 7th ed. Philadelphia, PA: Elsevier; 2016 Thus, extrinsic gonadotrophin and progesterone administration can influence cyst development and persistence. Benign ovarian neoplasms evolve from pluripotent stem cells that lack normal growth regulation but do not possess the ability to invade other tissues.[7]Kurjak A, Kupesic S, Jacobs I. Preoperative diagnosis of the primary fallopian tube carcinoma by three-dimensional static and power Doppler sonography. Ultrasound Obstet Gynecol. 2000 Mar;15(3):246-51. https://obgyn.onlinelibrary.wiley.com/doi/full/10.1046/j.1469-0705.2000.00080.x http://www.ncbi.nlm.nih.gov/pubmed/10846782?tool=bestpractice.com No risk factors have been identified for these benign tumours.

Many genetic mutations have been proposed as potential causes of ovarian cancer.[8]Kurman RJ, Visvanathan K, Roden R, et al. Early detection and treatment of ovarian cancer: shifting from early stage to minimal volume of disease based on a new model of carcinogenesis. Am J Obstet Gynecol. 2008 Apr;198(4):351-6. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2532696 http://www.ncbi.nlm.nih.gov/pubmed/18395030?tool=bestpractice.com Three genetic aetiologies of particular significance are BRCA-1 mutation, BRCA-2 mutation, and Lynch II syndrome. Mutations of the BRCA-1, BRCA-2, or MSH-2 genes (Lynch II syndrome) may alter DNA repair mechanisms, predisposing cells to genetic instability and a disregard for the normal growth cascade.[8]Kurman RJ, Visvanathan K, Roden R, et al. Early detection and treatment of ovarian cancer: shifting from early stage to minimal volume of disease based on a new model of carcinogenesis. Am J Obstet Gynecol. 2008 Apr;198(4):351-6. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2532696 http://www.ncbi.nlm.nih.gov/pubmed/18395030?tool=bestpractice.com [9]Chen MJ, Yang JH, Yang YS, et al. Increased occurrence of tubo-ovarian abscesses in women with stage III and IV endometriosis. Fertil Steril. 2004 Aug;82(2):498-9. http://www.ncbi.nlm.nih.gov/pubmed/15302314?tool=bestpractice.com In this regard, family history may predispose an individual to a higher risk of cancer development.

Follicular cysts develop in response to gonadotrophic stimulation and as a variation of the normal physiological process of follicle growth and atresia. It is unclear whether a dominant follicle fails to rupture or an immature follicle fails to undergo atresia.[10]Hall GH, Turnbull LW, Richmond I, et al. Localisation of somatostatin and somatostatin receptors in benign and malignant ovarian tumours. Br J Cancer. 2002 Jul 1;87(1):86-90. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2364287 http://www.ncbi.nlm.nih.gov/pubmed/12085262?tool=bestpractice.com The lining granulosa cells undergo luteinisation, and hyalinised connective tissue envelopes the growing cyst.[6]Dolan MS, Hill C, Valea FA. Benign gynecologic lesions. In: Lobo RA, Gershenson DM, Lentz GM, et al (eds). Comprehensive gynecology. 7th ed. Philadelphia, PA: Elsevier; 2016

Corpus luteum cysts evolve from mature Graafian follicles approximately 2 to 4 days after ovulation occurs. Vascularisation takes place and a spontaneous capillary bleed fills the cystic cavity, creating pressure.[6]Dolan MS, Hill C, Valea FA. Benign gynecologic lesions. In: Lobo RA, Gershenson DM, Lentz GM, et al (eds). Comprehensive gynecology. 7th ed. Philadelphia, PA: Elsevier; 2016 Rupture is possible at this point. Eventually, the blood is replaced by clear serous fluid.

Theca lutein cysts arise from ovarian theca lutein cells and luteinised granulosa cells responding to stimulation by gonadotrophins or beta-human chorionic gonadotrophin. Fibromas represent neoplastic growth of undifferentiated fibrous stroma.[11]Shwayder JM. Pelvic pain, adnexal masses, and ultrasound. Semin Reprod Med. 2008 May;26(3):252-65. http://www.ncbi.nlm.nih.gov/pubmed/18504700?tool=bestpractice.com Transitional cell (Brenner) tumours arise from metaplasia of coelomic epithelium into uroepithelium, which may result in an inclusion-type cyst. Benign and malignant ovarian tumours stain immunohistochemically for somatostatin.[10]Hall GH, Turnbull LW, Richmond I, et al. Localisation of somatostatin and somatostatin receptors in benign and malignant ovarian tumours. Br J Cancer. 2002 Jul 1;87(1):86-90. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2364287 http://www.ncbi.nlm.nih.gov/pubmed/12085262?tool=bestpractice.com

Aetiological classification

Several classification systems exist; however, ovarian cysts are commonly categorised according to cause:

• Physiological: cyst development as an exaggerated response to normal physiological processes; includes follicular, endometriotic, corpus luteum, and theca lutein cysts

• Infectious: an abscess or cystic collection of cellular debris

• Benign neoplastic: excessive growth of normal ovarian tissue types without dysplasia; includes serous cystadenoma, mucinous cystadenoma, adenofibroma, fibroma, thecoma, mature cystic teratoma (dermoid cyst), and Brenner's tumour

• Malignant neoplastic: includes serous cystadenocarcinoma, mucinous cystadenocarcinoma, endometrioid carcinoma, and immature teratoma

• Metastatic: invasion and growth of neoplastic tissue from another malignant source, most commonly endometrial, colonic, or gastric cancers.