Effects Of Female Sex Hormones Research Articles

Sex Differences in Airway Remodeling in a Mouse Model of Chronic Obstructive Pulmonary Disease.

After adjustment for the amount of smoking, women have a 50% increased risk of chronic obstructive pulmonary disease (COPD) compared with men. The anatomic basis and/or mechanism(s) of these sex-related differences in COPD are unknown. To characterize the impact of female sex hormones on chronic cigarette smoke-induced airway remodeling and emphysema in a mouse model of COPD. Airway remodeling and emphysema were determined morphometrically in male, female, and ovariectomized mice exposed to 6 months of cigarette smoke. Antioxidant- and transforming growth factor (TGF)-β-related genes were profiled in airway tissues. The selective estrogen receptor modulator tamoxifen was also administered during smoke exposure in a short-term model. Airway wall thickness of male and female human smokers at risk of or with mild COPD was measured using optical coherence tomography. Small airway wall remodeling was increased in female but not male or ovariectomized mice and was associated with increased distal airway resistance, down-regulation of antioxidant genes, increased oxidative stress, and activation of TGF-β1. These effects were prevented by ovariectomy. Use of tamoxifen as a therapeutic intervention mitigated smoke-induced increase in oxidative stress in female mice. Compared with male human smokers, female human smokers had significantly thicker airway walls. The excess risk of small airway disease in female mice after chronic smoke exposure was associated with increased oxidative stress and TGF-β1 signaling and also was related to the effects of female sex hormones. Estrogen receptor antagonism might be of value in reducing oxidative stress in female smokers.

Abstract 19017: Sex Differences in Severe Pulmonary Arterial Hypertension Produced by SU5416 in a Colony of “Hyper-responsive” Sprague Dawley Rats

Introduction: Our lab has identified a sub-strain of Sprague Dawley (SD) rats from Charles River Labs, obtained from a specific colony housed at a Canadian facility (Sherbrooke, Quebec), which develop severe progressive PAH in response to single injection of SU5416 (SU), a VEGFR2 antagonist, even in absence of chronic hypoxia (CH). This trait appears to due to the presence of unique genetic modifiers found only in this colony. Interestingly, there was a strong sex difference with >70% of males and only <30% of females showing the SU hyper-responsive (HR) phenotype. The purpose of the project was to explore the mechanisms contributing to sex related differences in response to SU alone in a hyper-responsive sub-strain of SD rats. Hypothesis: Sex dependent differences in the HR phenotype are due to the protective effects of female sex hormones, reducing the susceptibility to PAH in response to VEGFR2 inhibition. Methods and Results: Male and female rats were injected with SU (20mg/kg, sc) or vehicle. Right ventricular systolic pressure (RVSP) was measured at four and seven weeks after SU injection. In male SD rats, 72% (13 of 18) of rats exhibited an HR phenotype in response to SU with mean RVSP of 97±18 mmHg in absence of CH; whereas only 27% (7 of 26) of the female rats were responsive to SU alone. We studied the SU responsiveness in the oophorectomized female rats to investigate the role of female sex hormones in the sex-specific HR phenotype. Interestingly, the proportion of HR animals increased drastically in oophorectomized female rats to 71% (10 of 14), compared to non-operated female rats (33%, 4 of 12). Moreover, estradiol replacement completely abrogated the HR phenotype in both male rats and oophorectomized female rats. Conclusion: These data support a role of female sex hormones in modulating the development of severe PAH in response to SU alone in a unique colony of SD rats that exhibit increased sensitivity to VEGFR2 blockade. The HR SD rat colony model exhibits exquisite sensitivity to estrogen and thus provides a unique opportunity to further define the complex interactions between hormonal and genetic modifiers in the development of PAH.

The Association Between Menarche and Myopia: Findings From the Korean National Health and Nutrition Examination, 2008-2012.

The purpose of this study was to analyze the relationship between age at menarche and myopia in Korean adult females. A total of 8398 women of at least 19 years of age, who participated in the Korean National Health and Nutrition Examination Survey from 2008 to 2012, underwent a refractive examination using an autorefractor. The association between age at menarche and the severity of myopia was evaluated using a four-level multinomial logistic regression analysis. The prevalence of myopia was 61.77% (95% confidence interval [CI], 60.46-63.08), including 40.02% with low, 15.46% with moderate, and 6.29% with high myopia. The mean age at menarche was 14.09 ± 0.03 years. Age at menarche was inversely associated with the severity of myopia. In fully adjusted models, older age at menarche decreased the risk of moderate myopia (odds ratio [OR], 0.93; 95% CI, 0.86-0.99; P = 0.0261), and high myopia (OR, 0.85; 95% CI, 0.77-0.95; P = 0.0012). Later age at menarche is associated with a decreased risk of moderate and high myopia. The effects of female sex hormones on ocular structures and growth spurts may mediate this relationship between age at menarche and myopia.

Effects of female sex hormones on expression of the Ang-(1-7)/Mas-R/nNOS pathways in rat brain.

Female sex hormones are considered to reduce the risk of ischemic stroke. As a part of the renin-angiotensin system, angiotensin-(1-7) [Ang-(1-7)] has recently been reported to play a role in protecting neuronal tissues from ischemic stroke. Thus, we examined the effects of female sex hormones on the levels of Ang-(1-7) and its downstream pathways in the brain. Female rats were ovariectomized and 17β-estradiol (17β-EST), progesterone (PGR), or a combination of 17β-EST plus PGR were administered. Our data demonstrated that lack of female sex hormones significantly decreased the levels of Ang-(1-7) in the cerebral cortex and hippocampal CA1 area. Also, we observed a linear relationship between cortex levels of Ang-(1-7) and plasma brain natriuretic peptide levels (as an indicator for risk of ischemic stroke). We further showed that lack of female sex hormones decreased the expression of Ang-(1-7), Mas-receptor (Mas-R), and neuronal nitric oxide synthase (nNOS). Overall, our findings show for the first time that Ang-(1-7) and Mas-R/nNOS in the cortex are influenced by circulating 17β-EST and (or) PGR, whereas Ang-(1-7) and its pathways in the hippocampal CA1 area are primarily altered by 17β-EST. This suggests that female sex hormones play a role in regulating the expression of Ang-(1-7) and its pathways during ischemic brain injuries.

Suppressive effects of androgens on the immune system

Sex-based disparities in immune responses are well known phenomena. The two most important factors accounting for the sex-bias in immunity are genetics and sex hormones. Effects of female sex hormones, estrogen and progesterone are well established, however the role of testosterone is not completely understood. Evidence from unrelated studies points to an immunosuppressive role of testosterone on different components of the immune system, but the underlying molecular mechanisms remains unknown. In this review we evaluate the effect of testosterone on key cellular components of innate and adaptive immunity. Specifically, we highlight the importance of testosterone in down-regulating the systemic immune response by cell type specific effects in the context of immunological disorders. Further studies are required to elucidate the molecular mechanisms of testosterone-induced immunosuppression, leading the way to the identification of novel therapeutic targets for immune disorders.

Effects of 17β-estradiol and progesterone on the production of adipokines in differentiating 3T3-L1 adipocytes: Role of Rho-kinase

Effect of female sex hormones on the production/release of adipocyte-derived cytokines has been debatable. Furthermore, whether the cellular signaling triggered by these hormones involve Rho-kinase has not been investigated yet. Therefore, in this study, effects of 17β-estradiol and progesterone as well as the Rho-kinase inhibitor, Y-27632 on the level of adipokines such as resistin, adiponectin, leptin, TNF-α and IL-6 were investigated in 3T3-L1-derived adipocytes. Differentiation was induced in the post-confluent preadipocytes by the standard differentiation medium (Dulbecco’s modified Eagle’s medium with 10% fetal bovine serum together with the mixture of isobutylmethylxanthine, dexamethasone and insulin) in the presence of 17β-estradiol (10−8–10−7M), progesterone (10−6–10−5M), the Rho-kinase inhibitor, Y-27632 (10−5M) and their combination for 8days. Measurements of the adipokines were performed in the culturing medium by ELISA kits using specific monoclonal antibodies. 17β-estradiol elevated resistin but decreased adiponectin and IL-6 levels; however, it did not alter the concentration of leptin and TNF-α. Y-27632 pretreatment inhibited the rise of resistin and the fall of adiponectin by 17β-estradiol without any effects by its own. Progesterone did not change resistin, leptin and TNF-α level; however, it elevated adiponectin and decreased IL-6 production. Neither 17β-estradiol nor Y-27632 was able to antagonize the increase of adiponectin and the reduction of IL-6 levels by progesterone. While Y-27632 alone lowered IL-6 level, it increased leptin and TNF-α concentration without altering resistin and adiponectin. In conclusion, 17β-estradiol could modify adipokine production in 3T3-L1 adipocytes with the actions some of which involve Rho-kinase mediation.

Review of the Multiscale Effects of Female Sex Hormones on Matrix Metalloproteinase-Mediated Collagen Degradation.

Collagenases and gelatinases regulate many physiological processes and are involved in the pathogenesis and progression of various disease states, such as osteoarthritis, renal fibrosis, and atherosclerosis. These enzymes belong to the matrix metalloproteinase (MMP) family and are regulated by a number of factors, including sex hormones. Estrogen, relaxin, and progesterone can alter the balance between tissue degradation and repair by modulating MMPs, leading to gender disparities in many MMP-related disease states. In these diseases, MMPs initiate collagen degradation at the nanoscale when they cleave and denature collagen molecules. However, the net effect on tissue is generally observed at the macroscale. To understand how nanoscale events lead to macroscale changes, we must examine the intermediate scales. In this article, we review the literature that examines the effects of estrogen, relaxin, and progesterone on MMP production and activity, connecting the nanoscale, microscale, and macroscale details to relevant disease states.

Endogenous female sex hormones delay the development of renal dysfunction in apolipoprotein E-deficient mice.

BackgroundHypercholesterolemia is a well-established risk factor for the development of kidney injury. Considering that female sex hormones may play a preventative role in both cardiovascular and renal diseases, the aim of the present study was to evaluate the effects of female sex hormones on hypercholesterolemia-induced renal dysfunction.MethodsApolipoprotein E-deficient (ApoE) and C57 control female mice underwent an ovariectomy (OVX) or sham surgery and after 2 months, creatinine clearance, uremia and proteinuria were determined. Renal oxidative stress and lipid deposition were also quantified. Values are presented as mean ± SEM. Statistical analyses were performed using Two-way ANOVA followed by Tukey’s post hoc test.ResultsCreatinine clearance (μL/min) was similar between C57 (171 ± 17) and ApoE (140 ± 26) mice underwent sham surgery. OVX resulted in a reduced glomerular filtration rate in both C57 (112 ± 8, ~ − 35%, p < 0.05) and ApoE (61 ± 10, ~ − 56%, p < 0.05) animals. Plasma levels of urea (mg/dL) were higher in both ApoE groups (Sham: 73 ± 7; OVX: 73 ± 8, p < 0.05) when compared to C57 animals (Sham: 49 ± 3; OVX: 60 ± 4), with no changes among ovariectomized groups. Proteinuria levels (mg/24 h) were similar between C57 (Sham: 25.1 ± 5.7; OVX: 33.7 ± 4.7) and ApoE sham animals (26.4 ± 3.5), however, 24-h urine protein excretion was augmented in ApoE OVX animals (49.6 ± 5.8, p < 0.05). Histological kidney analysis demonstrated that the absence of female sex hormones resulted in increased oxidative stress, which was more severe in ApoE mice (C57 Sham: 9.2 ± 0.4; C57 OVX: 22.9 ± 1.0; ApoE Sham: 13.9 ± 0.7; ApoE OVX: 34.0 ± 1.4 au x 103, p < 0.05). As expected, ApoE mice presented higher lipid deposition, which was not affected by OVX (C57 Sham: 0 ± 0; C57 OVX: 0 ± 0; ApoE Sham: 6.8 ± 1.6; ApoE OVX: 5.2 ± 0.8% x 10−2, p < 0.05). Ovariectomy resulted in a similar reduction in ER-α protein expression in the renal cortex (C57: 0.78 ± 0.04; ApoE: 0.81 ± 0.04 au, p < 0.05) when compared to sham animals (C57:1.00 ± 0.04; ApoE: 1.03 ± 0.03 au).ConclusionTaken together these data indicate that female sex hormones may delay hypercholesterolemia-induced renal dysfunction and emphasizes the importance of plasma cholesterol control in post-menopausal women.

Sex Differences in the Pharmacokinetics of Antidepressants: Influence of Female Sex Hormones and Oral Contraceptives

Women are twice as likely to develop depression as men. Moreover, the symptoms they experience also show sex differences: women tend to develop depression at an earlier age and show more severe symptoms than men. Likewise, the response to antidepressant pharmacotherapy appears to have sex differences. These differences can partially be explained by differences in pharmacokinetic properties (i.e., absorption, distribution, metabolism, and excretion) of drugs in males and females. More recent research has shown that sex hormones may influence all these previously named pharmacokinetic processes. As concentrations of sex hormones vary throughout the female lifespan, these hormonal variations can have effects on therapeutic responses to antidepressants as well as the occurrence of adverse events. The purpose of this paper is therefore to review the literature reporting on the effects of female sex hormones on the pharmacokinetics of antidepressants and to discuss and evaluate the implications of changes in levels of sex hormones throughout life for the treatment of depression.

The role of pregnancy-associated hormones in the development and function of regulatory B cells.

During mammalian pregnancy, highly specialized mechanisms of immune tolerance are triggered in order to allow the semi-allogeneic fetus to grow within the maternal uterus in harmony with the maternal immune system. Among other mechanisms, changes in the endocrine status have been proposed to be at least part of the machinery responsible for the induction of immune tolerance during pregnancy. Indeed, pregnancy-associated hormones, estradiol, progesterone, and human chorionic gonadotropin are known to confer immune suppressive capacity to innate as well as adaptive immune cells. Regulatory B cells, a subpopulation of B lymphocytes with strong immunosuppressive functions, were shown to expand during pregnancy. Furthermore, it is well-known that some women suffering from multiple sclerosis, significantly improve their symptoms during pregnancy and this was attributed to the effect of female sex hormones. Accordingly, estradiol protects mice from developing experimental autoimmune encephalomyelitis by triggering the expansion and activation of regulatory B cells. In this review, we discuss different mechanisms associated with the development, activation, and function of regulatory B cells with a special focus on those involving pregnancy-associated hormones.

Cardiovascular disease in transsexual persons treated with cross-sex hormones: reversal of the traditional sex difference in cardiovascular disease pattern

The incidence of heart disease increases with age, but is lower in women than in men up to 75 years. A protective effect of female sex hormones or, alternatively, acceleration in male heart disease by testosterone at younger ages, could explain this sex difference. In contrast with the above, male-to-female transsexual subjects (MtoF) treated with estrogens (+anti-androgens) show more cardiovascular pathology than female-to-male transsexual subjects (FtoM) receiving testosterone. Why MtoF suffer more frequently from cardiovascular disease than females is as yet unclear. The mode of cross-sex hormone treatment may be a factor, and, if so, it may need adaptations. Studies in transsexual people on the effects of cross-sex hormone treatment on surrogate cardiovascular risks and on clinical endpoints were reviewed. With regard to MtoF, a parallel was sought with men with prostate cancer, undergoing androgen deprivation and estrogen administration. Exposure of FtoM to testosterone was not associated with a strong increase in cardiovascular events. Aging and pre-existing cardiovascular pathology contributed to the risk of cardiovascular disease in MtoF. Use of the synthetic biopotent compound ethinyl estradiol in a dose two to four times of oral contraceptives increased cardiovascular risk substantially. The route of administration of estrogens (oral vs transdermal) may have impacted on the risks. MtoF should not be treated with oral ethinyl estradiol. Transdermal estrogens are probably safer than oral estrogens. Pre-existing cardiovascular risks should be taken into consideration when prescribing and choosing the type of estrogens in cross-sex hormone administration (oral vs transdermal). In addition, risk factors, as they emerge with aging, should be addressed.

Brain stem auditory evoked response during different phases of menstrual cycle

Background: Due to the existing controversy on the effect of female sex hormones on the cerebral electrophysiology and the absence of conclusive study in south India about the sex hormonal influence on brain stem auditory evoked responses during different phases of menstrual cycle, this study was chosen. Aims & Objective: The aim of the study was to evaluate the correlation of auditory brain stem response (ABR) with different phases of menstrual cycle in young healthy women in our area. Materials and Methods: ABR recording was done in 35 healthy regular menstruating females of 20-40 years of age with normal BMI during 4 different phases of menstrual cycle. Peak latencies of waves I-V and inter peak latencies of I-III, I-V, III-V for four phases of menstrual cycle were compared. Results: Data showed statistically significant increase in peak latencies in wave IV in phase 2 compared to all other phases. Other waves showed a trend of increase in peak latencies in the phase 2 when compared to all other phases. Inter peak latencies did not show any significant variations between different phases of menstrual cycle. Conclusion: The results favour that female sex hormones do affect the central auditory pathway in menstrual cycle.

Reproductive and Exogenous Hormone Factors in Relation to Risk of Meningioma in Women: A Meta-Analysis

Background and ObjectiveA number of studies have focused on the association between oral contraceptive (OC), hormonal replacement therapy (HRT) and reproductive factors and meningioma risk, but the results were inconsistent. Thus, a meta-analysis was performed to obtain more precise estimates of risk.MethodsWe conducted a literature search using PubMed and EMBASE databases to July2013, without any limitations. Random effects models were used to summarize results.ResultsTwelve case-control and six cohort studies were included in this meta-analysis. We found that an increased risk of meningioma was associated with HRT use(RR = 1.19, 95% CI = 1.01–1.40), postmenopausal women(RR = 1.32, 95% CI = 1.07–1.64) and parity(RR = 1.18, 95% CI = 1.00–1.40).No significant associations were observed for OC use (RR = 0.93, 95% CI = 0.83–1.03), age at menarche(RR = 1.06, 95% CI = 0.92–1.21), age at menopause(RR = 1.03, 95% CI = 0.81–1.30), or age at first birth(RR = 0.94, 95% CI = 0.80–1.10).ConclusionIn conclusion, the results of our study support the hypothesis that longer exposure to effect of female sex hormones may increase the risk of meningioma in women, yet additional studies are warranted to confirm our findings and identify the underlying biological mechanisms.

Progesterone Activates Multiple Innate Immune Pathways in Chlamydia trachomatis‐Infected Endocervical Cells

Susceptibility to Chlamydia trachomatis infection is increased by oral contraceptives and modulated by sex hormones. We therefore sought to determine the effects of female sex hormones on the innate immune response to C. trachomatis infection. ECC-1 endometrial cells, pre-treated with oestradiol or progesterone, were infected with C. trachomatis and the host transcriptome analysed by Illumina Sentrix HumanRef-8 microarray. Primary endocervical epithelial cells, prepared at either the proliferative or secretory phase of the menstrual cycle, were infected with C. trachomatis and cytokine gene expression determined by quantitative RT-PCR analysis. Chlamydia trachomatis yield from progesterone-primed ECC-1 cells was significantly reduced compared with oestradiol-treated cells. Genes upregulated in progesterone-treated and Chlamydia-infected cells only included multiple CC and CXC chemokines, IL-17C, IL-29, IL-32, TNF-α, DEFB4B, LCN2, S100A7-9, ITGAM, NOD2, JAK1, IL-6ST, type I and II interferon receptors, numerous interferon-stimulated genes and STAT6. CXCL10, CXCL11, CX3 CL1 and IL-17C, which were also upregulated in infected secretory-stage primary cells, and there was a trend towards higher levels of immune mediators in infected secretory-phase compared with proliferative-phase cells. Progesterone treatment primes multiple innate immune pathways in hormone-responsive epithelial cells that could potentially increase resistance to chlamydial infection.

The Role of Sex Hormones in the Development of Affective Disorders in Women with Epilepsy

The objective of this study was the comprehensive assessment of the association between the level of hormones, reproductive disorders, symptoms of epilepsy and psychopathological symptoms in female patients with epilepsy and affective disorders. We studied 101 women using clinical and psychopathological examination, hormone measurement and statistical analysis. The data analysis showed correlations between scores on the scales measuring the mental health status and the level of hormones in the blood of patients. It has been concluded that the effect of female sex hormones on affective symptoms depends on characteristics of depressive affect.

Influence of acute tryptophan depletion on verbal declarative episodic memory in young adult females

Diminished synthesis of the neurotransmitter serotonin (5-HT) in the brain has been linked to disturbed memory processes. The present study investigated the effects of diminished central nervous 5-HT synthesis as achieved by an acute dietary tryptophan depletion (ATD) on verbal declarative episodic memory in young women while controlling for the effects of female sex hormones. Eighteen healthy females (aged 20-31 years) participated in a within-subject repeated measures study, with two separate days of assessment spaced at least one individual menstrual cycle apart. On one day, participants were subjected to ATD, thus lowering central nervous 5-HT synthesis. The other day participants received a tryptophan-balanced amino acid load (BAL = control condition). The study was randomized, counterbalanced and double blind in terms of ATD/BAL administration. Measurements took place in the early follicular phase of the participants' menstrual cycle. Estrogen, FSH and LH levels were assessed at baseline. Verbal declarative episodic memory was assessed using a structured word-learning task. Short-term memory, as indexed by immediate recall, was reduced after ATD intake, whereas delayed recall and recognition after a 25-min delay did not show any differences after intake of ATD or BAL. In young women, verbal short-term memory function was more vulnerable to ATD than consolidation processes. In light of the possible interplay between female sex hormones and 5-HT, further studies comparing different menstrual cycle phases are needed.

Measurements of 17β-estradiol levels in mice for migraine research

Since migraine prevalence is 2-3 times higher in women than in men, especially during the reproductive years, fluctuations in female sex hormone levels seem to be one of the key factors involved in the pathogenesis of migraine. During the last decade, lots of animal research in migraine has been performed on mice, since this species is well suited to create transgenic animal models1. To investigate the effect of female sex hormones in a murine model, it is important to analyse the hormone levels and/or to determine the hormone cycle in mice. Although no reliable assay has been available to measure murine plasma estrogen, recently 17β-estradiol assays have been suggested to be able to quantify these hormone levels.

Unexpected clinical sequelae of Gitelman syndrome: hypertension in adulthood is common and females have higher potassium requirements

BackgroundGitelman syndrome (GS) is a rare inherited disorder caused by mutations in SLC12A3, encoding the thiazide-sensitive transporter NCCT (sodium chloride co-transporter) in the distal tubule. It is characterized by renal potassium (K) and magnesium (Mg) wasting, relative hypotension and hypocalciuria. However, there is phenotypic variability and long-term studies are scarce.MethodsWe retrospectively assessed clinical and genetic characteristics, and electrolyte requirements, in a cohort of 36 patients with genetically proven GS.ResultsThe 21 males and 15 females were of median age 39.5 years, range 17–66 years. Six were diagnosed in childhood. Among the 72 mutant alleles, 41 different sequence alterations were identified, of which 13 were previously unreported. Surprisingly, 44% (n = 16) of the cohort has developed hypertension (13 males, 3 females, P = 0.019; median age 53 versus 57 years, P = 0.95). One was already hypertensive by age 23 years. Currently normotensive patients were significantly younger: median 37 versus 55 years (P = 0.005). Hypertensive patients were more likely to harbour mutations in the C-terminal half of the NCCT protein (P = 0.016). Females required more K (median 128 versus 72 mmol/day; P = 0.01) but not Mg. Those with exon 26 and/or at least one destructive mutation had higher K requirements than those with neither: 108 versus 72 mmol (P = 0.016) and a tendency towards higher Mg needs: 30 versus 7.4 mmol (P = 0.07).ConclusionsOur findings suggest that the development of secondary hypertension may be an expected feature of the ageing GS population despite the obligate salt wasting that characterizes the disorder. We hypothesize that this may be related to chronic secondary hyperaldosteronism. The apparently more severe phenotype in women may be related to the effects of female sex hormones on expression or function of NCCT.

A study to evaluate mobility of teeth during menstrual cycle using Periotest

Background and Objective:Over a century, an increased prevalence of gingival disease associated with increasing plasma sex steroid hormone levels has been reported. These situations present unique challenges to the oral health care professional. It is believed that hormonal fluctuations such as those associated with pregnancy, menstruation, and use of hormonal contraceptives lead to an increase in tooth mobility. However, this effect of female sex hormones on periodontal ligament and tooth supporting alveolar bone has rarely been investigated. So this study was undertaken to understand the effect on tooth mobility because of hormonal changes during the menstrual cycle.Materials and Methods:The mobility of index teeth 16, 13, 21, 23, 24, 36, 33, 41, 43, and 44 was measured with Periotest in 50 females at menstruation, ovulation, and premenstruation time points. Simplified oral hygiene index, plaque index, gingival index, and probing depth were also evaluated during the different phases of menstrual cycle for each subject participating in the study.Statistical Analysis:The results of the study were subjected to statistical analysis. Data analysis was done by applying Z test for comparing difference between two sample means.Result:The stages of menstrual cycle had no significant influence on the Periotest value. Despite no significant change in plaque levels, GI was significantly higher during ovulation and premenstruation time points.Conclusion:No change in tooth mobility was seen during the phases of the menstrual cycle. However, an exaggerated gingival response was seen during ovulation and premenstruation time when the entire menstrual cycle was observed.

Effect of female sex hormones on central auditory conductivity in young rural females in Bathinda district of Punjab.

Background: The auditory, olfactory and taste thresholds get modified by changes in gonadal function. Auditory brainstem responses vary with age and sex of the individual. Auditory acquity also varies with the phase of menstrual cycle. Aims & Objective: To study the effects of cyclical changes of endogenous sex hormones in different phases of menstrual cycle on Brainstem Auditory Evoked Responses. Materials and Methods: The brainstem auditory conduction (BAEPs) recording was done in normal 40 healthy regular menstruating females in age group 19-23 years during three phases of same menstrual cycle. Phase 1:1-3 days with lowest level of oestrogen and progesterone, Phase 2:11-14 days with peak level of β-oestradiol and Phase 3:17-23 days with peak level of progesterone. Absolute latencies of I, III & V waves and interpeak latencies (IPL) of waves I-III, I-V and III-V were recorded in three phases of menstrual cycle and compared statistically. Results: The comparison showed a statistically significant increase in absolute latencies of I, III & V waves in phase 2 compared to phase 1 and a statistical significant decrease in their values in Phase 3 compared to Phase 2. However, the variation in interpeak latencies I-III, I-V and III-V showed insignificant variation. Conclusion: The study showed that variation of hormones during menstrual cycle affect the central auditory conductivity in young rural females.