The oral mycobiome plays a critical role in maintaining oral and systemic health, with its composition and function influenced by various physiological and environmental factors. This descriptive review explores the changes in the oral mycobiome among postmenopausal women, examining how aging and associated inflammatory processes contribute to these alterations. These changes are linked to an increased prevalence of xerostomia, oral dysbiosis, and inflammation, which can negatively impact both oral and systemic health. We discuss the impact of hormonal fluctuations and immune senescence on fungal diversity and abundance, highlighting key species implicated in oral and systemic diseases. The review also examines the role of systemic conditions and medications, which are common in postmenopausal women, in further exacerbating oral mycobiome alterations. Lastly, it highlights the need for future research to better understand these interactions and develop targeted therapeutic strategies. The current literature indicates a significant association between menopausal status, age-related mycobiome shifts, and increased inflammatory responses, suggesting potential pathways for intervention.

Background: Oral wound healing in the aging population is a multifaceted issue requiring a comprehensive approach, considering the physiological changes that come with aging and the frequent presence of comorbidities. Methods: This descriptive review summarizes the factors influencing oral wound healing in aging patients, including age-related physiological changes, hormonal modifications, multimorbidities, polypharmacy, oralome alterations, and nutritional status. Results: The aging population encounters numerous challenges in oral wound healing due to intrinsic factors, such as biological aging and hormonal changes, and extrinsic factors, such as medication use and lifestyle. Conclusion: Understanding these factors and their combined impact is essential for effective clinical management and improved outcomes in older adults.

Cervical intraepithelial neoplasia (CIN) is a premalignant cervical condition closely linked to persistent high-risk HPV infection, a major risk factor for cervical cancer. This study aims to investigate the relationship between cervicovaginal infections, HPV infection, and CIN development in 94 Romanian women with cervical lesions. Comprehensive assessments included HPV genotyping, cytology, colposcopy, and histopathology. In 53.20% of cases, vaginal infections were identified, with Candida albicans most frequently associated with HPV. Histopathology revealed 48.94% low-grade CIN, 42.55% high-grade CIN, and 8.51% invasive carcinoma. There was a strong correlation between high-risk HPV types (especially HPV 16 and 18), colposcopic findings, histopathology, and age. This study emphasizes the mutual effect of cervicovaginal infections and HPV infection in increasing the risk of developing CIN and cervical cancer among Romanian women. Persistent infection with high-risk HPV types, particularly HPV 16 and 18, has been confirmed as a primary driver of CIN and cervical cancer progression.

Cleft lip and/or palate are prevalent congenital anomalies. Early and accurate diagnosis allows proper case management. The Objective: This retrospective cohort study aimed to investigate the association between cleft lip and palate and other congenital anomalies. Methods: This study analyzed 17 pregnancies prenatally diagnosed with cleft lip and palate. The investigations consisted of ultrasound examination, fetal karyotyping through amniocentesis, and family tree analysis. In the presence of an abnormal fetal karyotype, the parental karyotype was also indicated. Results: Of the 17 cases identified, 9 (52.94%) were syndromic and 8 (47.06%) were non-syndromic. The genetic syndromes identified in association with cleft lip and palate in this study included translocation syndrome (one case), Patau syndrome, trisomy 13 (seven cases), and Edwards syndrome, mosaic trisomy 18 (one case). Conclusions: A comprehensive approach ensures a thorough assessment and accurate diagnosis. Early detection and a multidisciplinary approach allow appropriate case management.

Background: Endometrial proliferative lesions are common in the menopausal transition and carry a measurable risk of carcinoma. Early risk stratification may guide evaluation and follow-up. Methods: We performed a single-center retrospective study of 315 women aged 45–55 years (May 2021–May 2024) at a private clinic in Bucharest. Lesions were classified per WHO 2014 as hyperplasia without atypia, atypical hyperplasia/endometrial intraepithelial neoplasia (AH/EIN), or adenocarcinoma; “advanced pathology” was defined as AH/EIN or adenocarcinoma. Clinical comorbidities and transvaginal ultrasound endometrial thickness were recorded. Associations were tested with χ²; odds were estimated with multivariable logistic regression (adjusted ORs), with a modified Poisson sensitivity analysis for adjusted relative risk. Thickness differences were compared by one-way ANOVA, and severity correlations by Spearman’s ρ. Internal validation used 1000-bootstrap resampling. Results: Hyperplasia without atypia comprised 74.6% of cases, AH/EIN 20.0%, and adenocarcinoma 5.4% (advanced pathology 25.4%). Diabetes was independently associated with advanced pathology (aOR 2.75; 95% CI 1.14–6.61; p = 0.0237), while a history of non-atypical hyperplasia was inversely associated (aOR 0.31; 95% CI 0.13–0.72; p = 0.0068). Obesity showed a borderline association (aOR 1.79; 95% CI 0.98–3.26; p = 0.058), and long-term oral contraceptive use also approached significance (aOR 0.42; 95% CI 0.18–1.00; p = 0.051). Endometrial thickness increased stepwise with histopathological severity (ANOVA p < 0.0001; η² = 0.44) and correlated with ordered severity (ρ = 0.634). The multivariable model showed moderate discrimination (AUC 0.68; optimism-corrected 0.66) with acceptable calibration (slope 0.92; Hosmer–Lemeshow p = 0.052) and overall accuracy (Brier 0.18). Conclusions: In perimenopausal abnormal bleeding, metabolic comorbidities—especially diabetes—together with increased endometrial thickness identify women at higher risk of AH/EIN or carcinoma. Histopathology remains the diagnostic reference. The model can aid clinical prioritization but requires external validation and should not be used as the sole basis for decisions.

Background: Chromosomal instability (CIN) may underlie a subset of idiopathic infertility, and chronic periodontitis could contribute to genomic fragility. We tested whether periodontal status is associated with cytogenetic instability in adults with idiopathic infertility. Methods: This was a cross-sectional study of 60 adults aged 20–40 years, comprising idiopathic infertility (n = 30) and fertile controls (n = 30), each with 18 women and 12 men. Significant exclusions included systemic inflammatory disease, pregnancy/lactation, recent antibiotics/NSAIDs, and periodontal therapy within 6 months. Periodontal examination recorded probing depth (PD), clinical attachment loss (CAL), and bleeding on probing (BOP). Cytogenetic testing used mitomycin C-induced chromosomal breakage to derive the Breakage Index (BI); CIN was defined as BI ≥ 4.0. Analyses compared infertile with CIN (n = 19), infertile without CIN (n = 11), and controls (n = 30). Results: Infertile participants with CIN had a higher periodontitis burden compared to infertile participants without CIN and to controls (moderate–severe: 89.5% vs. 54.5% vs. 26.7%); mean BI also differed (5.2 ± 0.9 vs. 1.3 ± 0.5 vs. 0.4 ± 0.2). Periodontal measures followed the same gradient, with greater CAL and PD in CIN-positive infertility. Conclusions: In idiopathic infertility, CIN was cross-sectionally associated with more severe periodontitis, and the BI correlated with CAL, PD, and BOP. Causality cannot be inferred and residual confounding cannot be excluded. Periodontal screening is a feasible adjunct that may help identify a modifiable inflammatory burden; prospective and interventional studies are warranted.