Search Results (534)

Polycystic ovary syndrome (PCOS) is a systemic metabolic and endocrine disorder that significantly disrupts reproductive physiology and endometrial function. In this narrative review, we examine the molecular impact of metabolic and hormonal imbalances on the endometrium of women with PCOS. We investigate the specific mechanisms that delineate how hyperinsulinemia and insulin resistance, chronic low-grade inflammation, and estrogen/progesterone/androgen imbalance contribute to altered epigenetic, transcriptomic, metabolomic, and signaling profiles in a wide array of different cell types within endometrial tissues. The synergistic interplay between upregulated inflammatory cytokines (e.g., IL-1,2,6,8,17,18, and TNF-α), along with key changes in critical molecular pathways associated with hyperinsulinemia and insulin resistance (e.g., PI3K/AKT/MAPK, and Wnt/β-catenin), in addition to aberrant sex steroid hormone signaling (e.g., CYP19A1, COX-2, PGE₂, HOXA10, 11βHSD2), promotes deleterious changes within the endometrial microenvironment. These anomalies underpin a spectrum of clinical manifestations observed in women with PCOS at each stage of the life course, including abnormal uterine bleeding in reproductive-age women, impaired decidualization in pregnancy, and altered postmenopausal endometrial physiology. Clinically, these alterations are associated with abnormal uterine bleeding, subfertility, implantation failure, miscarriage, pregnancy complications, and postmenopausal endometrial hyperplasia and cancer. Overall, our review provides novel insights into the molecular mechanisms linking systemic metabolic and endocrine dysfunction with endometrial pathology in PCOS and has broader implications that apply to all women. Full article

Endocrine disruptors contaminate indoor and outdoor air, water, and food. Besides modifications of the androgen/estrogen balance, endocrine disruptors can alter thyroid function, metabolic balance, immune defenses, and brain development during fetal life, childhood, and adolescence. Among the consequences of fetal exposure to endocrine disruptors, neurobehavioral disorders, particularly psychiatric disorders (for example, schizophrenia and bipolar disorder), attention deficit disorders, and mood disorders, occupy a special place. Therefore, endocrine disruptors are also neuroendocrine disruptors. This review article first summarizes the direct and transgenerational effects of endocrine disruptors. Then, data from a French national cohort of patients whose mothers were treated with synthetic hormones (estrogens and/or progestogens) during their pregnancy(ies) are used to describe the psychiatric disorders developed by children exposed in utero and the multigenerational and potentially transgenerational impacts. Full article

Objective: To determine the prevalence of mood and eating disorders, chronotype, and social jetlag in a cohort of women with polycystic ovarian syndrome (PCOS). Methods: A total of 70 patients, 35 with PCOS and 35 healthy controls, aged between 18 and 40 years, were included in the study. PCOS was diagnosed according to the Rotterdam criteria. Five different questionnaires, namely the “Morningness–Eveningness Questionnaire (MEQ)”, “Social Jetlag Status (SJL)”, “Night Eating Questionnaire (NEQ)”, “Beck Depression Inventory (BDI)”, and “Beck Anxiety Inventory (BAI)”, were administered to patients with and without PCOS, and the “total questionnaire scores” of both groups were compared. Results: In addition to BMI (p = 0.004), serum insulin (p < 0.001), HOMAIR (p < 0.001), total testosterone (p = 0.006), DHEAS (p = 0.004), and LH (p < 0.001) levels were significantly higher in women with PCOS than in the controls. BAI (p = 0.006), BDI (p = 0.007), and NEQ (p = 0.013) scores of participants with PCOS were significantly higher than those in the control group, while MEQ scores were significantly lower than those in the control group (p = 0.005). When categorized according to the total test scores, the number of individuals with moderate and severe anxiety was significantly higher in the PCOS group than in the control group (p = 0.030). Morningness was significantly lower in the PCOS group than in the control group, whereas eveningness was higher than that in the control group (p = 0.013). There was no difference between the PCOS and control groups in terms of the number of individuals with SJL ≥ 2 h and night eating disorders. The NEQ score was positively correlated with BAI, BMI, insulin, and HOMA-IR. Both the BDI and BAI scores were positively correlated with BMI, HOMA-IR, and total testosterone levels. Conclusions: PCOS can lead to mood, appetite, and circadian rhythm issues through variations in chronotype. PCOS-related endocrine, metabolic, and adiposity factors influence mood, eating habits, and chronotype disorders. Full article

Polycystic ovary syndrome (PCOS) is a prevalent endocrine disorder connected with insulin resistance (IR), low-grade inflammation, dyslipidemia, and altered adipokine secretion. We evaluated serum levels of leptin, adiponectin, visfatin, resistin, IL-6, and TNF-α in 150 women with PCOS, stratified by IR status (IR, n = 76; non-IR, n = 74), and examined their associations with anthropometric, metabolic, hormonal, inflammatory, and atherogenic parameters. Anthropometric data included body weight, height, BMI, waist circumference, and waist-to-height ratio (WHtR), while IR was assessed using HOMA-IR and the Matsuda index. Serum adipokines were measured using ELISA, and lipid parameters and atherogenic indices—including non-HDL cholesterol, AIP, leptin/adiponectin, and adiponectin/resistin ratios—were calculated. Women with IR had higher levels of leptin, visfatin, resistin, and TNF-α, and lower levels of adiponectin. Leptin correlated positively with weight, WHtR, HOMA-IR, and atherogenic indices. Adiponectin showed the strongest and most consistent associations with anthropometric indices, HOMA-IR, and the Matsuda index. Resistin was linked to IR indices and IL-6, and visfatin correlated negatively with HDL-C and insulin sensitivity. In a multivariate general linear model, WHtR, but not HOMA-IR, remained independently associated with higher leptin levels and with atherogenic indices. These findings suggest that in PCOS, central adiposity rather than IR explains a substantial part of the adverse adipokine and inflammatory profile, thereby contributing to elevated cardiometabolic risk and highlighting the need for targeted treatment strategies. Full article

Bone immunity represents a dynamic interface where skeletal homeostasis intersects with systemic immune regulation. We synthesize emerging paradigms by contrasting two functionally distinct microenvironments: the marrow cavity, a hematopoietic and immune cell reservoir, and cancellous bone, a metabolically active hub orchestrating osteoimmune interactions. The marrow cavity not only generates innate and adaptive immune cells but also preserves long-term immune memory through stromal-derived chemokines and survival factors, while cancellous bone regulates bone remodeling via macrophage-osteoclast crosstalk and cytokine gradients. Breakthroughs in lymphatic vasculature identification challenge traditional views, revealing cortical and lymphatic networks in cancellous bone that mediate immune surveillance and pathological processes such as cancer metastasis. Central to bone immunity is the neuro–immune–endocrine axis, where sympathetic and parasympathetic signaling bidirectionally modulate osteoclastogenesis and macrophage polarization. Gut microbiota-derived metabolites, including short-chain fatty acids and polyamines, reshape bone immunity through epigenetic and receptor-mediated pathways, bridging systemic metabolism with local immune responses. In disease contexts, dysregulated immune dynamics drive osteoporosis via RANKL/IL-17 hyperactivity and promote leukemic evasion through microenvironmental immunosuppression. We further propose the “brain–gut–bone axis” as a systemic regulatory framework, wherein vagus nerve-mediated gut signaling enhances osteogenic pathways, while leptin and adipokine circuits link marrow adiposity to inflammatory bone loss. These insights redefine bone as a multidimensional immunometabolic organ, integrating neural, endocrine, and microbial inputs to maintain homeostasis. By elucidating the mechanisms of immune-driven bone pathologies, this work highlights therapeutic opportunities through biomaterial-mediated immunomodulation and microbiota-targeted interventions, paving the way for next-generation treatments in osteoimmune disorders. Full article

Background: Polycystic ovarian syndrome (PCOS) is one of the most prevalent reproductive, endocrine, and metabolic disorders inflicting women of childbearing age. Dietary interventions have gained interest as non-pharmacological approach to control obesity and metabolic disturbances. However, the effects of intermittent fasting (IF) on metabolic and hormonal profiles of PCOS patients is debatable. Objectives: We performed this systematic review and meta-analysis to explore IF’s effect on PCOS women’s metabolic and hormonal profile (PROSPERO: CRD42024511520). Eligible studies included IF interventions in women with PCOS, with metabolic and hormonal profiles being reported. Methods: A systematic literature search using three databases, including PubMed, SCOPUS, and Web of Science, was conducted. The systematic review was performed following PRISMA guidelines. Results: A total of four studies were included (N = 4). IF is not associated with significant change in BMI (MD = −0.200, 95% CI [−0.807, 0.407], p = 0.518). The analysis revealed that IF had no statistically significant impact on FBG (MD = −0.569, 95% CI [−9.955, 8.818], p = 0.906), HOMA-IR (MD = −0.862, 95% CI [−1.737, 0.014], p = 0.054), and FINS (MD = −2.749, 95% CI [−6.441, 0.943], p = 0.145). No significant change in TG (MD = −3.120, 95% CI [−9.624, 3.385], p = 0.347), total cholesterol (MD = −0.918, 95% CI [−2.960, 1.124], p = 0.378), and LDL levels (MD = −0.433, 95% CI [−1.224, 0.359], p = 0.284) between IF and pre-fasting or non-intervention diet groups. However, the explanation is limited by the small number of studies, duration of fasting regimes, and/or variations in fasting strategies. Sex hormone data were collected but were insufficient for a pooled analysis. Conclusions: Overall, our study suggests that IF is not an effective intervention to enhance BMI, glycaemic control, and lipid metabolism in PCOS patients. Nevertheless, the current conclusion is inconclusive and preliminary, as additional well-designed studies are required to support this conclusion. Full article

Hypothyroidism is a multifactorial endocrine disorder where genetic predisposition plays a significant role. The MTHFR, MTRR, and MTR genes influence thyroid hormone regulation via homocysteine remethylation and DNA methylation. This study examined associations between hypothyroidism and polymorphisms in MTHFR (C677T–rs1801133, A1298C–rs1801131), MTRR (A66G–rs1801394), and MTR (A2756G–rs1805087) genes. Eighty-six patients with hypothyroidism and 87 healthy controls were included. Genotyping was performed using PCR-RFLP. Post hoc analysis confirmed adequate statistical power (95% for MTRR A66G, 84.6% for MTR A2756G). The study adhered to STROBE guidelines. MTHFR polymorphisms showed no significant association when considered individually. However, the MTRR A66G AA genotype was significantly more frequent in patients and conferred a markedly increased disease risk (OR: 4.373; 95% CI: 2.174–8.797; p < 0.001), while the MTR A2756G AG genotype was also more prevalent among patients and associated with higher susceptibility (OR: 2.178; 95% CI: 1.156–4.104; p = 0.008). Genotype combination analysis revealed that CT–AA (OR = 6.898; 95% CI: 1.941–24.516; p = 0.001) and AG–AA (OR = 6.892; 95% CI: 1.494–31.797; p = 0.007) conferred high risk. Certain genotypes correlated with clinical features, including hypercholesterolemia, diabetes, and cardiovascular disease. MTRR A66G and MTR A2756G polymorphisms are associated with hypothyroidism and metabolic comorbidities, both individually and in genotype combinations. These findings underscore the value of multilocus genetic models for understanding thyroid disorders and support the potential role of genetic biomarkers in personalized risk assessment and early diagnosis. GRS analysis demonstrated that each additional risk allele increased hypothyroidism risk (OR = 1.58; 95% CI: 1.18–2.10; p = 0.0018), and the total score showed moderate predictive power (AUC = 0.665; p < 0.001). Full article

Obesity is a chronic, multifactorial disease characterized by excess body fat and is a major risk factor for various metabolic disorders. Bioactive compounds from the diet have been recognized for their role in preventing chronic non-communicable diseases and as adjuvants in managing endocrine–metabolic dysfunctions. Hibiscus sabdariffa L. (HSL) is rich in bioactive compounds with antioxidant, antihypertensive, and antihyperlipidemic properties. This study evaluated the effects of HSL flower extract supplementation on body composition, lipid profile, and biochemical parameters in both eutrophic and high-fat diet-induced obese rats. Thirty-two Wistar rats were assigned to four groups: control, control plus HSL extract, high-fat diet, and high-fat diet plus HSL extract. The extract was administered orally at 150 mg kg⁻¹ for thirty days. Dual-energy X-ray absorptiometry revealed that HSL supplementation significantly attenuated fat mass gain (from 98 g to 75 g) and adiposity indices (10.23 to 8.86) in obese rats without altering total body mass. Moreover, the HSL extract improved lipid profiles by reducing LDL cholesterol from 23 to 13 mg dL⁻¹ and exhibited potential hepatoprotective effects linked with decreased ALT (40 to 26.7 U L⁻¹) and total bilirubin (0.12 to 0.07 mg dL⁻¹) levels. Although glucose metabolism parameters had no significant differences, a trend toward improved insulin sensitivity was observed. These results suggest that the aqueous HSL extract may exert cardioprotective, hepatoprotective, and anti-obesity effects, supporting its potential as a complementary therapeutic agent in obesity and related metabolic disorders. Full article

Background: This multicenter cross-sectional study aimed to assess the prevalence of vascular, hepatic, cardiac, endocrine, and bone complications and to identify factors associated with their occurrence in adult patients with neo-transfusion-dependent thalassemia (neo-TDT). Methods: A total of 140 adult neo-TDT patients (defined as receiving >4 transfusions/year; mean age 44.3 ± 12.1 years; 56.4% female) were retrospectively enrolled from the Extension–Myocardial Iron Overload in Thalassemia (E-MIOT) network. Iron overload (IO) was assessed by magnetic resonance imaging and complications were classified according to established clinical criteria. Logistic regression analyses were performed to investigate associations of complications with age, sex, splenectomy status, chelation therapy, hemoglobin < 9 g/dL, ferritin ≥ 1000 ng/mL, and hepatic, pancreatic, and cardiac IO. Results: Complications affecting fewer than 5% of patients—including leg ulcers, cirrhosis, thrombosis, heart failure, and hypoparathyroidism—were excluded from statistical analysis. Bone metabolism disorders were the most prevalent complications (68.6%), followed by impaired glucose metabolism (15.7%). The prevalence of other complications was: extramedullary hematopoiesis (EMH) 19.3%, pulmonary hypertension (PH) 7.1%, arrhythmias 12.1%, hypogonadism 11.4%, and hypothyroidism 15.0%. Male sex was independently associated with EMH (odds-ratio [OR] = 2.67; p = 0.027). Hepatic IO was the only significant predictor of PH (OR = 4.12; p = 0.047). Arrhythmias were strongly associated with older age (OR = 22.67; p < 0.0001), while both older age (OR = 4.42; p = 0.004) and pancreatic IO (OR = 7.40; p = 0.012) were independently associated with impaired glucose metabolism. No significant associations were identified for hypogonadism, hypothyroidism, or bone metabolism disorders. Conclusion: This study offers updated insights into the burden of complications in neo-TDT patients and highlights specific risk factors that may inform comprehensive, multidisciplinary surveillance strategies. Full article

Background/Objectives: Autism Spectrum Disorder (ASD) is a neurodevelopmental condition often accompanied by gastrointestinal (GI) symptoms and gut microbiota imbalances. The microbiota–gut–brain (MGB) axis is a bidirectional communication network linking gut microbes, the GI system, and the central nervous system (CNS). This narrative review explores the role of the MGB axis in ASD pathophysiology, focusing on communication pathways, neurodevelopmental implications, gut microbiota alteration, GI dysfunction, and emerging therapeutics. Methods: A narrative review methodology was employed. We searched major scientific databases including PubMed, Scopus, and Google Scholar for research on MGB axis mechanisms, gut microbiota composition in ASD, dysbiosis, leaky gut, immune activation, GI disorders, and intervention (probiotics, prebiotics, fecal microbiota transplantation (FMT), antibiotics and diet). Key findings from recent human, animal and in vitro studies were synthesized thematically, emphasizing mechanistic insights and therapeutic outcomes. Original references from the initial manuscript draft were retained and supplemented for comprehensiveness and accuracy. Results: The MGB axis involves neuroanatomical, neuroendocrine, immunological, and metabolic pathways that enable microbes to influence brain development and function. Individuals with ASD commonly exhibit gut dysbiosis characterized by reduced microbial diversity (notably lower Bifidobacterium and Firmicutes) and overpresentation of potentially pathogenic taxa (e.g., Clostridia, Desulfovibrio, Enterobacteriaceae). Dysbiosis is associated with increased intestinal permeability (“leaky gut”) and newly activated and altered microbial metabolite profiles, such as short-chain fatty acids (SCFAs) and lipopolysaccharides (LPSs). Functional gastrointestinal disorders (FGIDs) are prevalent in ASD, linking gut–brain axis dysfunction to behavioral severity. Therapeutically, probiotics and prebiotics can restore eubiosis, fortify the gut barrier, and reduce neuroinflammation, showing modest improvements in GI and behavioral symptoms. FMT and Microbiota Transfer Therapy (MTT) have yielded promising results in open label trials, improving GI function and some ASD behaviors. Antibiotic interventions (e.g., vancomycin) have been found to temporarily alleviate ASD symptoms associated with Clostridiales overgrowth, while nutritional strategies (high-fiber, gluten-free, or ketogenic diets) may modulate the microbiome and influence outcomes. Conclusions: Accumulating evidence implicates the MGB axis in ASD pathogenesis. Gut microbiota dysbiosis and the related GI pathology may exacerbate neurodevelopmental and behavioral symptoms via immune, endocrine and neural routes. Interventions targeting the gut ecosystem, through diet modification, probiotics, symbiotics, or microbiota transplants, offer therapeutic promise. However, heterogeneity in findings underscores the need for rigorous, large-scale studies to clarify causal relationships and evaluate long-term efficacy and safety. Understanding MGB axis mechanisms in ASD could pave the way for novel adjunctive treatments to improve the quality of life for individuals with ASD. Full article

Brown adipose tissue (BAT) has shifted from being considered a transient thermogenic organ of infancy to a metabolically dynamic and multifunctional tissue throughout life. Histologically and developmentally distinct from white and beige adipocytes, BAT originates from a myogenic lineage and is characterised by a high mitochondrial density, multilocular lipid droplets, and abundant sympathetic innervation. Its defining function, non-shivering thermogenesis, is mediated by uncoupling protein 1 (UCP1) and complemented by alternative mechanisms such as futile creatine and calcium cycling. Beyond heat production, thermogenic fat is crucial in regulating whole-body metabolism. It contributes to glucose, lipid, and branched-chain amino acid homeostasis, and engages in endocrine and paracrine signalling through a rich secretome of batokines, lipid mediators, and extracellular vesicle-bound microRNAs. These signals orchestrate crosstalk with the liver, skeletal muscle, pancreas, and immune system, enhancing insulin sensitivity, vascularisation, and anti-inflammatory responses. Brown/Beige fat also exhibits notable anti-fibrotic properties and supports adipose tissue remodelling, maintaining structural and functional plasticity under metabolic stress. This review offers a comprehensive synthesis of thermogenic adipose tissue biology, integrating its structural, developmental, and molecular features with its expanding physiological functions, highlighting its pivotal role in energy balance as well as its emerging therapeutic potential in obesity, type 2 diabetes, and related metabolic disorders. Full article

Objective: Obesity induces hypothyroidism with unknown mechanisms. This study investigates the role of (Receptor for Hyaluronan-Mediated Motility (RHAMM) in obesity-associated thyroid dysfunction, focusing on hepatic oxidative stress. Methods: Global RHAMM-deficient mice and their wildtype littermate controls were fed a normal chow diet or high-fat diet (HFD) for 16 weeks. Thyroid function was evaluated by measuring plasma thyroid-stimulating hormone (TSH) levels. The hepatic oxidative response was assessed by measuring signaling pathways associated with nuclear factor erythroid 2-related factor 2 (Nrf2) activity. Results: HFD feeding increased plasma TSH levels in male mice but not in female mice. RHAMM deletion in male mice mitigated HFD-induced TSH elevation, which was associated with enhanced hepatic antioxidant defenses and reduced inflammation. This was evidenced by elevated expression of the Nrf2 target gene NAD(P)H: quinone oxidoreductase 1 (Nqo1), reduced protein carbonylation and nitration levels, and reduced expression of the pro-inflammatory cytokines IL-1β and TNF-α in livers of male RHAMM-deficient mice. Mechanistically, RHAMM deletion decreased AKT/ERK signaling, increased GSK3 signaling, increased CD44 protein expression, and increased Nqo1 levels in the liver. Conclusions: RHAMM promotes obesity-induced thyroid dysfunction by regulating oxidative stress and inflammation in male mice. Targeting RHAMM may provide a novel therapeutic strategy for mitigating obesity-related endocrine and metabolic disorders. Full article

Pesticides are used in agriculture to protect crops from disease. Among these, the herbicide glyphosate, the insecticide deltamethrin, and the fungicides propamocarb and tebuconazole are approved for use in Europe. These pesticides, along with their metabolites, have been detected in the environment including in food and water sources. Human biomonitoring studies have confirmed the presence of these compounds in biological samples, indicating persistent exposure even among the general population, unrelated to agricultural occupations. Consequently, numerous studies have investigated the health effects of these four pesticides and their metabolites. This review focuses on their impacts on gut health primarily the gut microbiota, inflammation, metabolism, cancer and gut–brain axis. Epidemiological studies were included to assess health risks among various groups including adults, children and pregnant women. Animal and in vitro models have been employed to explore in a more controlled and targeted way the physiological and biochemical effects observed in epidemiological studies. Despite some controversy, pesticides and their metabolites have been linked to gut dysbiosis, inflammatory bowel disease (IBD), metabolic disorders, cancer and neurodevelopmental disorders. Mechanistically, these pesticides influence gut microbiome composition, sugar and lipid metabolism, oxidative stress, inflammatory pathways, cell death, oncogenic signalling pathways, endocrine disruption, and epigenetics. However, further studies are needed to confirm these risks and health impacts, particularly concerning low-dose, long-term exposure as experienced by the general population. A comprehensive investigation of these effects is essential, incorporating dietary factors, age, sex, health status, and the cumulative impact of multiple pesticides, to develop a thorough risk assessment. Full article

Background and Objectives: Polycystic ovary syndrome (PCOS) is a heterogeneous endocrine disorder often associated with metabolic disturbances such as insulin resistance and metabolic syndrome (MetS). Visceral adiposity index (VAI) is a validated marker that reflects visceral fat distribution and cardiometabolic risk. This study aimed to compare VAI levels among different PCOS phenotypes to evaluate cardiometabolic risk across these phenotypes. Materials and Methods: This prospective case–control study included 180 PCOS patients and 51 healthy controls without any metabolic or reproductive issues. Patients were divided into the following subtypes based on the Rotterdam criteria: Phenotype A (n = 96), clinical and/or biochemical hyperandrogenism (HA) + oligo-anovulation (OA) + polycystic ovarian morphology (PCOM); Phenotype B (n = 19), HA + OA; Phenotype C (n = 35), HA + PCOM; and Phenotype D (n = 30), OA + PCOM. VAI was calculated for women using anthropometric and biochemical parameters. Results: In the total PCOS group, VAI levels were significantly higher than in controls (p < 0.001). Phenotypes A and B had higher VAI values than controls and also higher in Phenotype A than in Phenotypes C and D (p = 0.003 and p = 0.001, respectively). While present in 38 patients (21.10%) in the PCOS group, there was no metabolic syndrome (MetS) in controls (p < 0.001). In Phenotypes A, B, and D, while more patients had MetS than controls (p < 0.001, 0.004, and 0.021, respectively), more patients had MetS in Phenotype A compared to Phenotypes C and D (p = 0.003 and p = 0.021, respectively). Given ROC analysis, the VAI cut-off value in predicting MetS in the PCOS group was 1.66 (sensitivity = 94.74% and specificity = 83.10%). Conclusions: PCOS phenotypes characterized by HA and OA, particularly Phenotypes A and B, are associated with higher VAI values and an increased frequency of MetS risk. Early identification of these phenotypes may facilitate the implementation of targeted metabolic risk reduction and early intervention strategies, thereby contributing to the reduction of cardiovascular risk. Full article

Background: Polycystic ovary syndrome (PCOS) is an endocrine disorder characterized by hyperandrogenism, irregular ovulation, and polycystic ovarian morphology. The severity of periodontal inflammation in PCOS may be linked to elevated levels of inflammatory mediators, like interleukins (IL-6, IL-17), and matrix metalloproteinase-8 (MMP-8), found in both serum and saliva samples. This systematic review aims to assess the presence, nature, and variations in salivary inflammatory biomarkers in individuals with PCOS and their potential connection to periodontal disease (PD). Materials and Methods: Selected databases were PubMed, Scopus, Google Scholar, and Web of Science. The search strategy included the following terms: “oral inflammatory biomarkers”, “Salivary mediators,” “metabolic indicators,” “periodontal diseases,” “periodontitis,” “polycystic ovary syndrome,” “PCOS,” and “ovulatory dysfunction.” Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines were used. Results: Several salivary inflammatory biomarkers are present in women with PCOS, including cytokines, C-reactive protein (CRP), reactive oxygen species (ROS), MMPs, and microbial diversity alterations. Additionally, the reviewed studies suggest a correlation between PCOS and PD, as patients with PCOS exhibit greater periodontal alterations compared to healthy women. The heightened periodontal response in PCOS appears to be associated with a systemic inflammatory state, probably increasing the susceptibility to PD. Conclusions: Salivary inflammatory biomarkers in PCOS patients are a useful diagnostic tool for evaluating the heightened risk of periodontal disease. Further research with stricter protocols is necessary to better define the diagnostic potential of these biomarkers for PCOS patients and determine their role in the early detection of periodontal disease. Full article