Hormone replacement therapy and periodontitis progression in postmenopausal women: A prospective cohort study.

OBJECTIVE: This study aimed to investigate the responses of periodontal environment to hormone replacement therapy (HRT) in postmenopausal women with or without periodontitis. BACKGROUND: HRT is a common and effective strategy for controlling menopausal symptoms, while the changes of periodontal environment under it, particularly in postmenopausal women with periodontitis, remain unclear. METHODS: As a prospective cohort study, a total of 97 postmenopausal women receiving HRT were screened, including 47 with and 50 without periodontitis. Correspondingly, 97 women did not receiving HRT were screened as controls during the same period. The full-mouth sulcus bleeding index (SBI), bleeding on probing (BOP), probing pocket depth (PPD), and clinical attachment level (CAL) were measured using periodontal probes. The levels of interleukin-6 (IL-6) and tumor necrosis factor α (TNF-α) in the gingival crevicular fluid were measured using enzyme-linked immunosorbent assay. In addition, cone beam computed tomography was performed to measure the alveolar bone height (ABH) and bone mineral density (BMD). RESULTS: In postmenopausal women without periodontitis, no significantly changes on periodontal parameters were observed after HRT. In women with stage II periodontitis, SBI, BOP, IL-6, and TNF-α were significant decreased after one year and two years of HRT. Compared to the controls, women with stage II periodontitis who underwent HRT had significantly lower CAL and ABH and higher BMD in the second year. The incidence of at least one site with CAL increase ≥1 mm between baseline and 2 years was significantly lower in the HRT group than in the control group in women with stage II periodontitis. In addition, HRT was significantly associated with a decrease in SBI, BOP, IL-6, and TNF-α in the first year and with a decrease in CAL, SBI, BOP, IL-6, and ABH and an increase in BMD in the second year. CONCLUSIONS: In postmenopausal women with stage II periodontitis, HRT is associated with the alleviation of inflammation within two years and the remission of alveolar bone loss in the second year. HRT appears to decrease the incidence of CAL increase ≥1 mm within 2 years in women with periodontitis by inhibiting inflammation and alveolar bone loss.

The "double-edged" role of progesterone in periodontitis among perimenopausal women undergoing or not undergoing scaling and root planing.

Objective: Progesterone (PG) is an important sex steroid hormone commonly administered to protect the endometrium in perimenopausal women. The present study aimed to explore differential responses of periodontitis to PG in perimenopausal women who did or did not undergo scaling and root planing (SRP). Methods: A total of 129 perimenopausal women with mild-to-moderate periodontitis were enrolled and underwent treatment as follows: SRP (n = 35); SRP + PG (n = 34); PG (n = 31); and no treatment (s) (n = 29). Pocket probing depth (PPD), clinical attachment level (CAL), sulcus bleeding index (SBI), and bleeding on probing (BOP) were measured using periodontal probes. Three inflammatory markers, including C-reactive protein (CRP), interleukin (IL)-6, and tumor necrosis factor-alpha (TNF-α) in gingival crevicular fluid (GCF) were measured using ELISA techniques. Results: PPD, CAL, SBI, BOP, and levels of inflammatory factors in GCF were all significantly decreased in perimenopausal women with periodontitis after SRP. In patients who did not undergo SRP, 6 months of PG treatment significantly elevated PPD, SBI, BOP, and GCF levels of CRP, IL-6, and TNF-α. In contrast, PG exhibited inhibitory effects on periodontal inflammation in patients who underwent SRP, evidenced by significantly decreased BOP and IL-6, and slightly decreased SBI, CRP, and TNF-α. PG-induced changes dissipated 6 months after withdrawal of PG (at 12 months). Conclusions: Among perimenopausal women with periodontitis, PG enhanced periodontal inflammation in the absence of SRP but inhibited periodontal inflammation in those who underwent SRP.

Exogenous progesterone short-termly affects the periodontal environment in perimenopausal women.

OBJECTIVE: This study aimed to evaluate the effects of exogenous progesterone in the periodontal environment of perimenopausal women. METHODS: Either with or without periodontitis, 100 perimenopausal women received 3 months of progesterone treatment, as well as age-matched 100 perimenopausal and 100 postmenopausal women without treatments were enrolled (N = 50). The gingival index (GI), probing depth (PD), clinical attachment level (CAL), and tooth mobility (TM), as well the gingival crevicular fluid (GCF) levels of IL-6 and TNF-α were analyzed. RESULTS: Periodontitis showed higher GI, PD, and CAL than non-periodontitis at perimenopausal and postmenopausal periods. In women without periodontitis, the GI and PD, and the GCF levels of IL-6 and TNF-α were increased by 3 months of progesterone treatment, but recovered from the 6th month in the absence of progesterone. In women with periodontitis, only the PD was short-termly increased by progesterone treatment. For those without progesterone treatment, the GI, PD, and TM were not significantly different between perimenopausal and postmenopausal women either with periodontitis or not. CONCLUSIONS: Exogenous progesterone short-termly exacerbated the inflammation and PD in perimenopausal women without periodontitis, and the PD in those with periodontitis.

Mitochondrial protein LETM1 and its-mediated CTMP are potential therapeutic targets for endometrial cancer.

Leucine zipper/EF hand-containing transmembrane-1 (LETM1) is an important mitochondrial protein, while its function in endometrial cancer remains unknown. This study aimed to explore the function of LETM1 in endometrial cancer and reveal the underlying mechanisms involving carboxy-terminal modulator protein (CTMP). Immunohistochemistry was performed to detect the expression of LETM1 and CTMP in normal, atypical hyperplastic and endometrial cancer endometrial tissues. LETM1 and CTMP were silenced in two endometrial cancer cell lines (ISK and KLE), which were verified by western blot. Cell viability, colony number, migration and invasion were detected by cell counting kit-8, colony formation, wound healing and trans-well assays, respectively. A xenograft mouse model was established to determine the antitumor potential of LETM1/CTMP silencing in vivo . In addition, CTMP was overexpressed to evaluate its regulatory relationship with LETM1 in endometrial cancer cells. The expression of LETM1 and CTMP proteins were higher in endometrial cancer tissues than atypical hyperplastic tissues and were higher in atypical hyperplastic tissues than normal tissues. LETM1 and CTMP were also upregulated in ISK and KLE cells. Silencing of LETM1 or CTMP could decrease the viability, colony number, migration and invasion of endometrial cancer cells and the weight and volume of tumor xenografts. In addition, CTMP was downregulated by LETM1 silencing in KLE cells, and its overexpression enhanced the malignant characteristics of si-LETM1-transfected KLE cells. Silencing of LETM1 inhibits the malignant progression of endometrial cancer through downregulating CTMP.

MMP-9 and miR-181a-5p in serum and placenta are associated with adverse outcomes of patients with severe preeclampsia and their infants.

This study explored the correlation of MMP-9 with miR-181a-5p in severe preeclampsia (SPE). Placental tissues and serum were collected from 30 pregnant SPE patients (aged 29.42 ± 3.75) and 30 normal pregnant women (aged 27.72 ± 2.21), followed by detecting MMP-9 and miR-181a-5p fold changes using RT-qPCR, and grouped as follows: high expression groups (≥median value): H-MMP-9 and H-miR-181a-5p vs. low expression groups (

The miRNA mir-582-3p suppresses ovarian cancer progression by targeting AKT/MTOR signaling via lncRNA TUG1.

Ovarian cancer (OC) is one of the most common malignancies of the female reproductive system. The miRNA miR-582-3p is associated with a variety of tumors, and the aim of this study was to investigate the role and mechanisms of miR-582-3p specifically in ovarian carcinogenesis and progression. Low expression of miR-582-3p was noted in OC tissue and cell lines, and lower expression of miR-582-3p correlated with lower overall survival in OC patients. Knockdown of miR-582-3p promoted the proliferation and migration of OC cells, while overexpression inhibited them. TUG1, a long non-coding RNA, was found to bind to miR-582-3p, and inhibition of lncRNA TUG1 decreased viability and migration and weakened the effect of miR-582-3p knockdown in OC cells. Implantation of OC cells with reduced miR-582-3p caused increased tumor growth, while lncRNA TUG1 knockdown suppressed tumor growth and relieved the impact of reduced miR-582-3p in vivo. Phosphorylation of AKT and mTOR were significantly enhanced with decreased miR-582-3p expression, but lncRNA TUG1 knockdown attenuated this trend in vitro and in vivo. The novel miR-582-3p represses the malignant properties of OC via the AKT/mTOR signaling pathway by targeting lncRNA TUG1. This axis may represent valuable prognostic biomarkers and therapeutic targets for OC.