The potential of cassava leaves extract in gingival fibroblasts of periodontitis of rats with ovarian dysfunction

Introduction: The prevalence of periodontitis has reached 42.8% in Indonesia. One contributing factor is Porphyromonas gingivalis. The ovarian dysfunction caused by ovariectomy procedures may also cause periodontitis. Post ovariectomy conditions resemble menopause, lowering the production of estrogen and progesterone hormones, leaving patients vulnerable to periodontitis. To prevent the side effects of the treatment, herbal ingredients are commonly used. The extract of cassava leaves is known to have pharmacological effects as an antioxidant and, thus, can be applied as a medicine for periodontitis. Methods: A total of 21 rats were divided into three groups, (1) control: healthy rats; (2) Group P.1: P. gingivalis-induced rats; (3) Group P.2: ovariectomized rats. Groups P.1 and P.2 were further divided into three subgroups that were administered cassava leaves extract at a dosage of 179.2 mg/ kg BW, aquades and vitamin C. Rats were euthanized at day eight after the initial treatment to collect left mandibular first molar. The mandibular sections were immunohistochemically stained to quantify SOD expression using light microscope while the Image J software was used. Fibroblast cells expressing SOD are characterized by brown coloration in the cytoplasm and darker nucleus. Results: In periodontitis conditions, either due to P.gingivalis induction or ovarian dysfunction, fibroblast cells in rats given cassava leaves extract expressed higher SOD than rats given aquades, but still lower than rats given vitamin C. The result of the one way ANOVA test showed p value of 0,00, which means that there is a significant difference in all groups. Conclusion: Cassava leaves extract demonstrated the potential to increase the antioxidant expression in P. gingivalis-induced and ovarian dysfunction rats.

Diet and Stress Impair Ovarian Function in Mid-life, Increasing Risk of Chronic Diseases of Aging in Primates

Ovarian dysfunction increases risk for chronic diseases of aging including cardiovascular disease, depression, cognitive impairment, and bone and muscle loss which promote frailty. Psychosocial stress disrupts ovarian function and recent observations suggest that Western diet may also. Determination of causal relationships among diet, psychosocial stress, and ovarian physiology is difficult in humans. Nonhuman primates provide relevant opportunities to investigate diet and psychosocial effects on ovarian physiology and aging because, like humans, they have monthly menstrual cycles and recapitulate many aging-related processes similar to humans. We examined ovarian function in 38 socially housed, middle-aged females fed either a Western or Mediterranean diet for 26 months (~ an 8-year period for humans). During the last 12 months, we examined cycle length, peak progesterone per cycle, and frequency of anovulatory cycles using blood sampling (3/week) and vaginal swabbing (6/week). Repeated measures analysis revealed that like middle-aged women, cycle length increased, and progesterone levels fell over time, suggesting that ovarian dysfunction generally increased in our sample with time. In addition, both Western diet and the stress of low social status reduced progesterone levels, disrupting ovarian function, and increasing risk of chronic diseases of aging. This study demonstrates the additive negative effects of poor diet and psychosocial stress on ovarian physiology in mid-life and lays the groundwork for future investigations to uncover associated metabolic signatures of accelerated aging. The results also suggest that a Mediterranean diet may exert a protective influence against ovarian dysfunction and its pathologic sequelae.

MAMLD1 and Differences/Disorders of Sex Development: An Update

<i>MAMLD1</i> (alias <i>CXorf6</i>) was first documented in 2006 as a causative gene of 46,XY differences/disorders of sex development (DSD). <i>MAMLD1</i>/<i>Mamld1</i> is expressed in the fetal testis and is predicted to enhance the expression of several Leydig cell-specific genes. To date, hemizygous <i>MAMLD1</i> variants have been identified in multiple 46,XY individuals with hypomasculinized external genitalia. Pathogenic <i>MAMLD1</i> variants are likely to cause genital abnormalities at birth and are possibly associated with age-dependent deterioration of testicular function. In addition, some <i>MAMLD1</i> variants have been identified in 46,XX individuals with ovarian dysfunction. However, recent studies have raised the possibility that <i>MAMLD1</i> variants cause 46,XY DSD and ovarian dysfunction as oligogenic disorders. Unsolved issues regarding MAMLD1 include the association between <i>MAMLD1</i> variants and 46,XX testicular DSD, gene-gene interactions in the development of <i>MAMLD1</i>-mediated DSD, and intracellular functions of MAMLD1.

Causes of Ovarian Dysfunction and its Sonographic Findings With Respect to Infertility: A Systematic Review

Background: Ovarian dysfunction is a condition in which ovaries stop working and menstrual periods stops before age 40. This can cause fertility problems. There are several causes of ovarian dysfunction causing infertility such as endometriosis, ovarian torsion etc. Aim: To revise the current literature about causes of ovarian dysfunction and its sonographic findings in infertile women. Methods: Electronic data base search was performed (PubMed, Science direct, Google Scholar) with data range from 2000 to 2019. All the data is available online in English. Results: Seventeen articles were found regarding different causes of ovarian dysfunction and their sonographic appearance. Also our results show that ultrasound can be used as a reliable tool for detection of ovarian pathologies. Conclusion: This study supports a temporal association between various causes of ovarian dysfunction and infertility risk. Gray-scale in addition to color Doppler ultrasound serves an important role in detection of different causes of ovarian dysfunction and their sonographic appearances. Keywords: Ultrasound exam, ovarian dysfunction, ovarian volume, ovarian masses

Development of A Recombinant Murine Luteinizing Hormone Binding Protein As A Selective Hormone Inhibitor

Physiological levels of luteinizing hormone (LH), in concert with follicle stimulating hormone (FSH), promote ovarian follicular development and ovulation. However, high LH levels associated with ovarian dysfunction have been shown to inhibit these processes. Thus, developing a selective LH inhibitor could be potentially useful for treating ovarian dysfunction. Here, we developed a mouse LH-binding protein (mLBP) composed of the extracellular domain of LH receptors as a selective inhibitor of mouse LH. After transient introduction of mLBP expressing vectors into Expi293F cells, mLBP was obtained as a soluble protein via a cleavage reaction with thrombin. The binding ability of mLBP for mouse LH was confirmed using sera containing high LH and FSH collected from ovariectomized (OVX) mice. The bioactivity of mLBP was demonstrated by inhibition of cAMP and testosterone productions induced by OVXmouse serum in mouse Leydig MLTC-1 cells expressing LH receptors. In contrast, mLBP did not bind mouse FSH and inhibit cAMP production induced by OVX-mouse serum in 293 cells expressing mouse FSH receptors. The mLBP also showed binding affinity to human LH (hLH), and inhibited hLH-induced cAMP production in MLTC-1 cells. Thus, the mLBP selectively suppresses the action of LH and is a potential therapeutic agent for ovarian dysfunction.