The endometrium is the inner lining of the uterus, playing a fundamental role in reproduction. Its primary function is to prepare a receptive environment each month for the potential implantation of a fertilized egg. This lining is dynamic, changing dramatically in thickness and structure under the influence of ovarian hormones. Measuring this tissue is a common gynecological procedure, used as an indicator of health, hormonal status, and fertility potential. Measurement is typically obtained non-invasively using a transvaginal ultrasound, recorded in millimeters (mm).
Thickness During the Menstrual Cycle
For women of reproductive age, the endometrium undergoes predictable, cyclical changes in thickness, which directly correspond to the phases of the menstrual cycle. The process begins during the menstrual phase, which corresponds to days one through five, when the functional layer of the endometrium is shed. At this stage, the lining is at its thinnest, typically measuring between 2 and 4 mm.
Following menstruation, the proliferative phase begins, lasting until ovulation, approximately days six through fourteen of a typical cycle. During this time, rising estrogen levels stimulate the rapid regrowth of the endometrium. The thickness increases from about 5 to 7 mm in the early proliferative stage, reaching up to 10 or 11 mm by the time of ovulation.
After ovulation, the secretory phase takes over, lasting from roughly day fifteen to day twenty-eight. Progesterone becomes the dominant hormone, causing the endometrium to become lush and highly vascularized in preparation for implantation. The lining reaches its maximum thickness during this phase, commonly ranging from 7 to 16 mm. If pregnancy does not occur, hormone levels drop, signaling the start of the next menstrual phase and the shedding of the lining.
Endometrial Thickness and Fertility Outcomes
In the context of fertility treatment, particularly for assisted reproductive technologies like in vitro fertilization (IVF), a specific endometrial thickness is generally sought for optimal embryo implantation. While successful pregnancies have occurred outside these parameters, clinicians often aim for a thickness in the range of 7 to 14 mm on the day of embryo transfer. A measurement below 6 mm is often considered suboptimal, as it is associated with significantly lower implantation and clinical pregnancy rates.
Beyond just the measurement, the appearance of the endometrium on ultrasound is highly relevant to assessing its readiness. A desirable feature is the “triple-line” pattern, also known as the trilaminar pattern, which is usually seen during the late follicular phase leading up to ovulation.
The Triple-Line Pattern
This pattern consists of three distinct layers: an inner central echogenic line, surrounded by two hypoechoic (darker) layers, and then two outer echogenic (brighter) layers. The presence of this trilaminar pattern suggests that the endometrium has appropriately developed in response to estrogen stimulation, indicating a potentially receptive environment for the embryo.
Once progesterone takes over after ovulation, the triple-line pattern typically disappears, and the lining becomes uniformly echogenic (bright). Both the appropriate thickness and the transformation of the lining’s appearance are considered important predictors of a favorable fertility outcome.
Postmenopausal Thickness Thresholds
After menopause, when menstrual cycles have ceased for at least twelve months, the endometrium naturally becomes thin due to the sustained decline in estrogen levels. The function of measuring thickness in this group shifts from assessing fertility to screening for potential pathology, such as endometrial hyperplasia or cancer. For postmenopausal women who are not experiencing any vaginal bleeding, the thickness is typically less than 5 mm, and often even less than 4 mm.
If a postmenopausal woman experiences uterine bleeding, a transvaginal ultrasound is typically performed to measure the endometrial thickness. A measurement of 4 to 5 mm or less is generally considered reassuring and carries a very low risk of malignancy, often allowing for conservative management. However, a thickness exceeding 5 mm in a woman with postmenopausal bleeding is a signal for further investigation, usually involving an endometrial biopsy or hysteroscopy.
The use of hormone replacement therapy (HRT) or certain medications can alter these thresholds. Women taking estrogen combined with progesterone as HRT may have a slightly thicker but still benign endometrium, often up to 8 mm.
The medication Tamoxifen, used in breast cancer treatment, has an estrogen-like effect on the uterus, frequently causing the endometrium to thicken, often measuring 9 to 13 mm. While the risk of pathology is present with Tamoxifen use, the typical 5 mm cut-off is less reliable, and further investigation is often needed for any thickness above 5.5 mm in symptomatic patients.
Factors Causing Deviations in Endometrial Thickness
The thickness of the endometrium is highly dependent on a balanced hormonal environment, and deviations can result from various factors that disrupt this balance. The most common cause of an abnormally thick endometrium, or endometrial hyperplasia, is the presence of unopposed estrogen stimulation. This hormonal imbalance can occur due to conditions like polycystic ovary syndrome (PCOS), obesity, or the use of estrogen-only hormone therapy without progesterone.
An excessively thick lining can also be caused by structural issues within the uterine cavity, such as benign growths like endometrial polyps or submucosal fibroids. For postmenopausal women, any unexplained thickening is a concern that requires immediate clinical evaluation.
Conversely, an abnormally thin endometrium (atrophy or hypoplasia) can be a sign of low estrogen levels, most commonly seen in postmenopausal women. In younger women, a thin lining may result from long-term use of certain hormonal birth control methods or conditions that cause low estrogen production. A more severe cause of thinning is Asherman’s Syndrome, characterized by scarring within the uterine cavity, often resulting from aggressive dilation and curettage procedures. This scar tissue prevents the functional layer from regrowing properly, leading to a consistently thin lining that is unreceptive to implantation.