The epidemiology of endometrial polyps is reported to be between 7.8 and 50% of women. The range remains quite broad and inconsistent due to confounding study factors such as the method of research, population studied, histological type and anatomical location of polyps. The development of polyps is influenced by a multitude of genetic and epigenetic factors. Chromosomes 6,7 and 12 are incriminated in this process. A fraction of these polyps may undergo malignant transformation, most commonly in  postmenopausal patients. 3D ultrasound (US) and hysterosalpingo-contrast-sonography (HyCoSy) provide an accurate diagnosis and location of endometrial polyps (EPs). Expectant management is recommended when the polyp is up to 10mm in length, in asymptomatic young patients. When indicated, hysteroscopic removal of polyps can be performed as an outpatient without requiring a general anaesthetic. The use of a small tip diameter hysteroscope and 5Fr instruments offers safe, efficient and low-cost treatment. The hysteroscopic morcellator and shaver are the best surgical option for bigger polyps since it is a quick and time-effective method with the technique easily learned by surgeons.

Endometrial polyps (EPs) present hyperplastic growths of stroma and endometrial glands [1]. The loss of apoptotic regulation and the overexpression of estrogen and progesterone receptors are seen in both premenopausal and postmenopausal women [2].  These are generally asymptomatic, incidental findings discovered during ultrasound scanning; symptoms include bleeding or abnormal vaginal discharge. Approximately 25% of postmenopausal women with EPs will have abnormal uterine bleeding (AUB). Women on cyclical HRT might have irregular or heavy ‘menstrual' bleeding. In premenopausal patients’ EPs can cause infertility [3]. Polyp occurrence appears to depend on many genetic alterations, in conjunction with metabolic, drug induced, and environmental factors. The involvement of various factors has been reported including:  enzymes, diabetes mellitus, obesity, hypertension, age, menopause status and steroid hormone receptors [2,4]. Rearrangements in the 6p21-22, in the 12q13-15, and in the 7q22 region [5] and the involvement of bcl-2 and bax apoptosis related genes have been shown to play a role in the evolvement EPs. Analysis of EPs showed an increased bcl-2/bax ratio that could ultimately be responsible for a mechanism that promotes their growth [6].

The histological structure of EPs contains an amalgamation of large thickened blood vessels, variably formed glandular spaces and fibrous stroma. They can develop into cancer (infrequently), become atrophied or remain benign [1]. Classification by tissue type is another way to categorise polyps:  adenomatous (most common), cystic, fibrous, vascular, inflammatory, and fibromyomatous. Di Spiezio Sardo et al. [7] contrastingly labelled the possible types as: hyperplastic, atrophic, functional, adenomyomatous and pseudopolyps.

Effects of Polyps in the Endometrial Cavity

Hysteroscopic features such as endometrial erosion, vascular dilatation [6] and chronic endometrial inflammation have been identified in women with EPs [2]. The locations of resected polyps are usually the anterior and posterior walls with the fundus being the third most common location [8]. The locality of a polyp is of considerable importance when addressing fertility issues. For instance, the removal of tubocornual polyps ameliorates the pregnancy rate to a higher degree when compared to those removed polyps from the lower 1/3 of the uterine corpus [2,9].

The higher miscarriage rate in women with EPs may be attributed to an increased production of glycodelin that can inhibit the action of natural killer cells and additionally reduce blood flow to endometrial lining. Other factors may result in abnormal uterine bleeding such as vascular fragility, surface erosion, ischemic necrosis, and disruption of sub-surface capillaries [10,11].

Epidemiology

EPs are the most frequently diagnosed type of polyp of the female genital tract. The older the patient, the higher the incidence, to some extent. Numbers reach their peak incidence during the 6th decade and decline thereafter, following menopause. Their prevalence ranges from 7.8-34.9% in varying populations [7,12]. EPs incidence in patients with abnormal uterine bleeding is 7.8%, [13] however it is estimated to be 10% in women with no abnormal bleeding [14]. Risk factors for the development of EPs include age, diabetes, hypertension, obesity, and tamoxifen use [15,16]. The prevalence of post-menopausal polyps reaches to up to 6

Due to differences in selection criteria in available literature, the frequency of EPs in infertility cases as compared to gynecological cases is inconsistent. Nevertheless, the presence of multiple EPs is more common in fertility cases, 35.4% as compared to gynecological cases, 12-20%. Diagnosis of EPs and their exact localization and size are well defined with recent technological advances made in imaging, such as 3D US. In infertility cases, the average size in length of EPs has been reported to be 19 ± 14 mm. It may be inferred that the identification of smaller endometrial polyps is subsequently increasing the number of patients that will ultimately require treatment. The most frequent polyp location is the posterior wall for both EPs in gynecological 39% and infertility cases 32%. The risk of cancer when an EP is present appears to be 10-fold higher in menopausal women versus women of fertile age. There are no set standards detailing the timing of polyp excision in young, asymptomatic women. In symptomatic polyps, physicians utilise different treatment modalities. Hysteroscopic resection has been coined as the “gold standard” treatment, yet it is not the method of choice for some physicians due to lack of resources and training. Recurrence rates are higher in blind removal techniques. More PRCTs on polyps are needed to further standardize the management of EPs