Changes in the Oral Cavity in Menopausal Women—A Narrative Review

Oral health awareness during the menopausal period is essential to minimize the inevitable inconveniences which may occur due to hormonal changes. The decrease in estrogen hormone concentration impacts the oral mucosa in a similar way to the vaginal mucosa due to the presence of estrogen receptors in both of these structures. An estrogen deficiency also affects the maturation process of the oral mucosal epithelium and can lead to its thinning and atrophy, making it more susceptible to local mechanical injuries, causing a change in pain tolerance and problems in the use of removable prosthetic restorations. Mucosal epithelium during the menopausal period is more vulnerable to infections, candidiasis, burning mouth syndrome, oral lichen planus (OLP), or idiopathic neuropathy. Moreover, salivary glands are also hormone-dependent which leads to changes in saliva secretion and its consistency. In consequence, it may affect teeth and periodontal tissues, resulting in an increased risk of caries and periodontal disease in menopausal women. Due to the large variety of complaints and symptoms occurring in the oral cavity, menopausal women constitute a significant group of patients who should receive special preventive and therapeutic care from doctors and dentists in this particular period.

Ginsenoside Rg3 Induces Apoptosis and Inhibits Proliferation By Down-Regulating TIGAR in MNNG-Induced Gastric Precancerous Lesions in Rats

BACKGROUND Ginsenoside Rg3 (GRg3) is one of the main active ingredients in Chinese ginseng extract and has various biological effects, such as immune-enhancing, antitumour, antiangiogenic, immunomodulatory and anti-inflammatory effects. This study aimed to investigate the therapeutic effect of GRg3 on gastric precancerous lesion (GPL) induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and the potential mechanism of action. METHODS The MNNG–ammonia composite modelling method was used to establish a rat model of GPL. Histopathological changes in the rat gastric mucosa were observed by pathological analysis using haematoxylin–eosin staining to assess the success rate of the composite modelling method. Alcian blue–periodic acid Schiff staining was used to observe intestinal metaplasia in the rat gastric mucosa. Apoptosis was detected in rat gastric mucosal cells by terminal deoxynucleotidyl transferase-mediated dUTP nick end labelling staining. The expression level of reactive oxygen species (ROS) was determined by the dihydroethidium fluorescent probe method, and that of TP53-induced glycolysis and apoptosis regulator (TIGAR) protein was determined by immunohistochemical staining and western blotting. The expression levels of nicotinamide adenine dinucleotide phosphate (NADP) and glucose-6-phosphate dehydrogenase (G6PDH) were determined by an enzyme-linked immunosorbent assay, and that of glutathione (GSH) was determined by microanalysis. RESULTS GRg3 significantly alleviated the structural disorganization and cellular heteromorphism in the form of epithelial glands in the gastric mucosa of rats with GPL and retarded the progression of the disease. Overexpression of TIGAR, NADP, GSH and G6PDH occurred in the gastric mucosal epithelium of rats with GPL, which in turn led to an increase in the ROS concentration. After treatment with GRg3, the expression of TIGAR, NADP, GSH and G6PDH decreased, causing a further increase in the concentration of ROS in the gastric mucosal epithelium, which in turn induced apoptosis and played a role in inhibiting the abnormal proliferation and differentiation of gastric mucosal epithelial cells. CONCLUSION Grg3 can induce apoptosis and inhibit cell proliferation in MNNG-induced GPL rats. The mechanism may be related to down regulating the expression levels of TIGAR, GSH, NADP and G6PD, up regulating the concentration of ROS and inducing apoptosis.

Spatial and Functional Organization of Human Papillomavirus Replication Foci in the Productive Stage of Infection

Human papillomaviruses are small DNA viruses that cause chronic infection of cutaneous and mucosal epithelium. In some cases, persistent infection with HPV can result in cancer, and 5% of human cancers are the result of HPV infection.

Autophagy is required during high MUC2 mucin biosynthesis in colonic goblet cells to contend metabolic stress

Goblet cells are specialized for the production and secretion of MUC2 glycoproteins that forms a thick layer covering the mucosal epithelium as a protective barrier against noxious substances and invading microbes. High MUC2 mucin biosynthesis induces endoplasmic reticulum (ER) stress and apoptosis in goblet cells during inflammatory and infectious diseases. Autophagy is an intracellular degradation process required for maintenance of intestinal homeostasis. In this study, we hypothesized that autophagy was triggered during high MUC2 mucin biosynthesis from colonic goblet cells to cope with metabolic stress. To interrogate this, we analyzed the autophagy process in high MUC2-producing human HT29-H and a clone HT29-L silenced for MUC2 expression by lentivirus-mediated shRNA, and WT and CRISPR/Cas9 MUC2 KO LS174T cells. Autophagy was constitutively increased in high MUC2 producing cells characterized by elevated pULK1S555 expression and increased numbers of autophagosomes as compared to MUC2 silenced or gene edited cells. Similarly, colonoids from Muc2+/+ but not Muc2-/- littermates differentiated into goblet cells showed increased autophagy. IL-22 treatment corrected misfolded MUC2 protein and alleviated the autophagy process in LS174T cells. This study highlights that autophagy plays an essential role in goblet cells to survive during high mucin biosynthesis by regulating cellular homeostasis.

The Protective Effects of Indole-3-carbinol on Stomach Injury in Rats

The objective of this research was to analyze the protective effect of indole-3-carbinol against the stomach injury induced by acetylsalicylic acid. Male rats were randomly divided into eight groups of six animals in each group. Control group, OMP group, I3C group, OMP+I3C group, AA group, AA+OMP group, AA+I3C group, and AA+OMP+I3C group. The control rats were received distilled water and the experimental rats were received AA at a dose of 500 mg/kg body weight, OMP at a dose of 20 mg/kg body weight, and I3C at a dose of 50 mg/kg body weight either alone or in combination with each other, orally for seven consecutive days. Results of the present study showed ulcer protection in indole-3-cabinol treated rats was confirmed by histoarchitecture, which was comprised of the reduced size of ulcer crater and restoration of mucosal epithelium. Thus, reduced neutrophil infiltration, antiapoptotic and antioxidant action have a pivotal role in the gastroprotective effect of indole-3-carbinol. Keywords: Histopathological; Stomach; Acetylsalicylic acid; Indole-3-carbinol; Rats

Role of Elastin Expression in Thickening the Postpartum Vaginal Wall in Virgin and Postpartum Rat Models

Childbirth induces a number of alterations, including ligament weakening and increased vaginal distensibility. The occurrence of vaginal laxity or distensibility is associated with the vaginal wall and introitus overstretching during vaginal parturition while the pathophysiology is due to increased levator dimension and trauma to the levator ani muscle through avulsion (macrotrauma) or overdistension (microtrauma). Elastin is an extracellular matrix protein that confers elastic properties to organs and tissues, particularly those requiring elasticity. Elastin plays a vital role in the functioning of numerous tissues, such as the lungs, blood vessels, heart valves, ligaments, tendons, and skin. It is also a component of the vaginal mucosa. The aim of the present was to evaluate the role of elastin in the thickening of the postpartum vaginal wall composed of epithelial mucosa, and to understand the mechanism underlying vaginal laxity or distensibility within parous and nulliparous animal models. A total of 32 female white rats (Rattus norvegicus) were used in the present study. They were divided into two groups, each group consisting of 16 rats. The control group (C0) consisted of virgin nulliparous rats, which were sacrificed on the second day after vaginal parturition. Pregnant rats (group C1) were sacrificed on the second day after vaginal parturition. The median elastin expression in group C1 was higher (3 ± 0.56) than group C0 (2.85 ± 0.75). The mean thickness of the vaginal mucosal epithelium in group C0 (56,8 931µm) was greater than group C1 (44,98 349µm). The comparison of vaginal mucosal epithelium thickness between the two groups indicated a significant difference between groups C0 and C1. Elastin levels were significantly correlated with epithelial thickness. The expression of elastin significantly affects the vaginal wall thickness, which further affects vaginal laxity or vaginal distensibility.

Barrett’s Esophagus and Intestinal Metaplasia

Intestinal metaplasia refers to the replacement of the differentiated and mature normal mucosal epithelium outside the intestinal tract by the intestinal epithelium. This paper briefly describes the etiology and clinical significance of intestinal metaplasia in Barrett’s esophagus. This article summarizes the impact of intestinal metaplasia on the diagnosis, monitoring, and treatment of Barrett’s esophagus according to different guidelines. We also briefly explore the basis for the endoscopic diagnosis of intestinal metaplasia in Barrett’s esophagus. The identification techniques of goblet cells in Barrett’s esophagus are also elucidated by some scholars. Additionally, we further elaborate on the current treatment methods related to Barrett’s esophagus.