Table 1.

Main characteristics of the studies enrolled

Authors and years (reference)	Study design, country, and time of realization	Participants and main inclusion criteria	Samples, timing, and methods	Main outcomes
Cicinelli, 2008	Prospective controlled study, Italy, from January 2005 to April 2006	2190 women undergoing hysteroscopy for different indications. Vaginal and endometrial samples were collected from 438 women with a CE diagnosis at hysteroscopy and 100 women with no signs of CE (controls).	Diagnostic office hysteroscopy in the follicular phase of the menstrual cycle. Women had a vaginal swab taken and an endometrial sampling using a 3-mm Novak’s curette connected to a 20-mL syringe. Cultures for common bacteria, Neisseria gonorrhoeae and Mycoplasma and molecular biology testing for Chlamydia were performed.	More than 70% of CE cases resulted from non-gonococcal and non-chlamydial infections. Common bacteria and Mycoplasma were the most frequent etiologic agents. Vaginal cultures have low concordance with endometrial cultures.
Mishra, 2008	Retrospective case-control study, India, from January 2005 to June 2007	20 granulomatous endometritis, 10 chronic non-specific endometritis, and 30 controls	Endometrial curettings were obtained in the fourth week of the menstrual cycle. Immunohistochemistry for ER, PR, and Ki-67.	Higher ER, PR and Ki-67 expression in endometrial glandular and stromal cells. Endometrial inflammation interferes with local expression of ER, PR, and Ki-67.
Cicinelli, 2009	Prospective controlled study, Italy, from January 2005 to April 2006	181 women in whom diagnostic hysteroscopy had showed the presence of CE.	Mini-hysteroscopy in the follicular phase of the menstrual cycle. Vaginal and cervical swabs were obtained and endometrial sampling took place, using a 3-mm Novak curette connected to a 20-ml syringe. Histological examination, cultures for common bacteria, Neisseria gonorrhoeae and Mycoplasma and molecular biology testing for Chlamydia were performed.	Both vaginal and endocervical cultures have low concordance with endometrial cultures in women with diagnosed CE.
Matteo, 2009	Case-control study, Italy, no dates reported	23 infertile women. 9 with CE diagnosed and 14 without.	Diagnostic office mini-hysteroscopy and endometrial biopsy in the follicular phase of menstrual cycle. All patients, in the late secretory phase (LS) of the subsequent spontaneous menstrual cycle, underwent endometrial biopsies by a 3-mm Novak’s curette connected to a 20 mL syringe. Histological examination, flow cytometry, and antibody labeling.	The secretory endometrium of patients with CE displayed significantly lower percentage of CD56+ CD16- and of CD56bright CD16- cells as compared with group CE-, while the percentage of CD3+ cells was significantly higher.
Kitaya, 2010	Case-control study, Japan, no dates reported	76 infertile women with histological biopsy. 22 of them diagnosed with CE	Endometrial specimens were obtained from patients with unexplained infertility and who had undergone biopsy in search of endometrial pathology on days 6 to 8 after urinary luteinizing hormone-surge detection. Histological Examination and Immunoassay were performed.	B cell density is higher in CE endometrium. CXCL13 expression in CE microvascular endothelial cells is higher.
Carvalho, 2013	Observational cohort study, Brazil, from 2009 to 2010	435 infertile women	Diagnostic hysteroscopy followed by blind endometrial aspiration biopsy using a silicone urethral catheter number 8. All the biopsies were performed after the 10th day of the menstrual cycle until the 5th postovulatory day.	Association between vascular changes, CE, and infertility.
Di Pietro, 2013	Case-control study, Italy, no dates referred	16 women with hysteroscopic and histological diagnosis of CE and 10 healthy women as controls.	Hysteroscopy and endometrial sampling using a Novak’s curette connected to a 20-mL syringe. The procedures were performed in the secretory phase during the implantation window. Histological examination and gene Expression Profiling by Real-Time RT-PCR.	IGFBP1, BCL2, and BAX are upregulated, while IL11, CCL4, IGF1, and CASP8 are downregulated.
Kitaya, 2014	Case-control study, Japan, From January 2011 to December 2012	179 infertile women with repeated implantation failure (RIF). 59 were diagnosed with CE.	Fluid hysteroscopy was performed on days 6–12 of the menstrual cycle. Histological biopsy was performed using a 3-mm-wide curette. Histological Examination and Immunoassay were performed.	The density of IgM+, IgA1+, IgA2+, IgG1+, and IgG2+ stromal cells were significantly higher in the RIF-CE group than that in the RIF-non-CE and control group.
Pinto, 2015	Case-control study, Italy, from March 2012 to December 2013	45 women referred for hysteroscopy with diagnosis of CE. 45 age-matched women as controls with no evidence of CE at hysteroscopy and biopsy.	Hysteroscopy, histology examination, and TVS evaluation of the EW pattern during the periovulatory (days 11–14) and midluteal (days 19–22) phases of the same cycle.	CE could influence uterine contractility. CE induces a reduction of retrograde motility in the periovulatory phase and an increase of anterograde and retrograde motility in the midluteal phase.
Kushnir, 2016	Retrospective cohort study, USA, from January 2014 to August 2015	55 patients with recurrent pregnancy loss (RPL) and/or implantation failure (RIF).	Hysteroscopic and histological examination. Serum examination.	No findings in the periphery serum that support the hypothesis that CE may, at least in some cases, have an autoimmune component. Dysregulation of local inflammatory pathways may play a role in the pathophysiology of RPL as well as RIF.
Wu, 2017	Case-control study, Japan, no dates reported.	17 patients, 9 CE (5 endometriosis), 8 non-CE (4endometriosis)	Hysteroscopy and curettage performed at 7 or 8 days after predicted ovulation. Endometrial Cultures, Immunoassay, Gene Expression Profiling by Real-Time RT-PCR, Immunohistochemistry	Increased cell numbers and reduced secretion of PRL and IGFBP-1. Increased expressions of ERα, ERβ, PRA, and PRB.
Moreno, 2018	Case-control study, Italy, no dates reported	113 women with CE diagnosed using endometrial histology, hysteroscopy, and/or microbial culture.	Hysteroscopy performed in the follicular phase (cycle day 7–12) and endometrial sampling using a 3-mm Novak curette connected to a 20-mL syringe. Microbiological culture and molecular microbiology diagnosis by RT-PCR.	RT-PCR effectively detects and quantifies bacterial DNA from chronic endometritis-causing pathogens in endometrial samples providing a feasible, faster, and cheaper method for the diagnosis of chronic endometritis.
Di Pietro, 2018	Case-control study, Italy, from October 2016 to March 2017	15 women with hysteroscopic and histological diagnosis of CE and 15 healthy women.	Hysteroscopy was performed in follicular phase. Endometrial biopsies were taken with Pipelle de Cornier. Histological Examination and Serum Examination, Gene Expression Profiling by Real-Time RT-PCR.	Upregulation of miR-27a-3p and miR-124-3p in the endometrium and serum from women with CE and an anti-correlation relationship between miR-27a-3p and IGF1 in endometrium.
Liu, 2019	Case-control observational study, China	130 infertile women. 12 with CE diagnosed.	Endometrial fluid and scratch collection 7 days after LH surge. Endometrial scratch was performed with a Pipelle (Prodimed). Genomic DNA Extraction and PCR amplification using primers targeting the 16S rRNA gene.	Defining endometrial microbiota of women with or without CE.
Wang, 2019.	Case-control study, China, from February 2015 to July 2018	75 CE women with recurrent implantation failure and 75 women with male factor infertility.	Office hysteroscopy was scheduled during the follicular phase (between cycle day 8 to 12) of the menstrual cycle. All women with clinical CE by hysteroscope underwent endometrial biopsy using a curette for histological confirmation. Subsequently, gene expression profiling by real-time RT-PCR, immunohistochemistry, and immunoassay.	Decreased endometrial TGF-β and IL-10 expression and increased IL-17 expression. Increased autophagy (LC3-II) and mTORC1 downregulation.