Thousands of microorganisms coexist within the human microbiota. However, certain conditions can predispose the organism to the overgrowth of specific pathogens that further lead to opportunistic infections. One of the most common such imbalances in the normal oral flora is the excessive growth of Candida spp., which produces oral candidiasis. In immunocompromised individuals, this fungal infection can reach the systemic level and become life-threatening. Hence, prompt and efficient treatment must be administered. Traditional antifungal agents, such as polyenes, azoles, and echinocandins, may often result in severe adverse effects, regardless of the administration form. Therefore, novel treatments have to be developed and implemented in clinical practice. In this regard, the present paper focuses on the newest therapeutic options against oral Candida infections, reviewing compounds and biomaterials with inherent antifungal properties, improved materials for dental prostheses and denture adhesives, drug delivery systems, and combined approaches towards developing the optimum treatment.

The inner ear is sensitive to various infections of viral, bacterial, or fungal origin, which, if left untreated, may lead to hearing loss or progress through the temporal bone and cause intracranial infectious complications. Due to its isolated location, the inner ear is difficult to treat, imposing an acute need for improving current therapeutic approaches. A solution for enhancing antimicrobial treatment performance is the use of nanoparticles. Different inorganic, lipidic, and polymeric-based such particles have been designed, tested, and proven successful in the controlled delivery of medication, improving drug internalization by the targeted cells while reducing the systemic side effects. This paper makes a general presentation of common inner ear infections and therapeutics administration routes, further focusing on newly developed nanoparticle-mediated treatments.

Background—Children with genetic disorders have multiple anatomical and physiological conditions that predispose them to obstructive sleep apnea syndrome (OSAS). They should have priority access to polysomnography (PSG) before establishing their therapeutic protocol. We analyzed the prevalence and the severity of OSAS in a particular group of children with genetic disorders and strengthened their need for a multidisciplinary diagnosis and adapted management. Methods—The retrospective analysis included children with genetic impairments and sleep disturbances that were referred for polysomnography. We collected respiratory parameters from sleep studies: apnea–hypopnea index (AHI), SatO₂ nadir, end-tidal CO₂, and transcutaneous CO₂. Subsequent management included non-invasive ventilation (NIV) or otorhinolaryngological (ENT) surgery of the upper airway. Results—We identified 108 patients with neuromuscular disorders or multiple congenital anomalies. OSAS was present in 87 patients (80.5%), 3 of whom received CPAP, 32 needed another form of NIV during sleep, and 15 patients were referred for ENT surgery. The post-therapeutic follow-up PSG parameters confirmed the success of the treatment. Conclusions—The upper airway obstruction diagnostics and management for children with complex genetic diseases need a multidisciplinary approach. Early detection and treatment of sleep-disordered breathing in children with genetic disorders is a priority for improving their quality of life.

Autoimmune thyroiditis (AIT) may impair radioiodine (¹³¹I) uptake in papillary thyroid cancer (PTC). Finding the mechanisms that govern immune cells during ¹³¹I therapy of PTC with concomitant AIT (PTC + AIT) could provide a rationale. Our study aimed to evaluate the effects of ¹³¹I on anti-thyroglobulin antibodies (TgAb), matrix metalloproteinase-9 (MMP-9) and its tissue inhibitor TIMP-1 and tumor necrosis factor-α (TNF-α) and its receptors TNFR1 and TNFR2, in PTC and PTC + AIT patients. Peripheral blood was collected from 56 female patients with PTC and 32 with PTC + AIT before and 4 days after ¹³¹I (3.7 GBq). The serum levels of TgAb, MMP-9, TIMP-1, TNF-α, TNFR1 and TNFR2 were measured by ELISA. The mean radioactivity of blood samples collected after ¹³¹I intake was higher in the PTC + AIT group than in PTC (p < 0.001). In the PTC + AIT group, TNF-α/TNFR1 and TNF-α/TNFR2 ratios decreased by 0.38-fold and 0.32-fold after ¹³¹I and were positively correlated with the MMP-9/TIMP-1 ratio (r = 0.48, p = 0.005, and r = 0.46, p = 0.007). In the PTC group, TNF-α/TNFR1 and TNF-α/TNFR2 ratios increased by 3.17-fold and 3.33-fold and were negatively correlated with the MMP-9/TIMP-1 ratio (r = −0.62, p < 0.001 and r = −0.58, p < 0.001). Our results demonstrate that TNF-α may exert different antitumor effects in response to ¹³¹I therapy depending on the patient’s immune profile.

Publications investigating the effect of radioactive iodine (¹³¹I) therapy on the circulating peripheral blood cells in patients with differentiated thyroid cancer (DTC) are limited to blood samples collected more than 92 h after ¹³¹I. Studies conducted on blood samples collected up to 92 h are rare due to the radioactive contamination risk. This research aimed to assess the relationship between the prescribed ¹³¹I activity, human whole blood activity, and peripheral blood cells at many time points (6, 22, 46, 69, and 92 h after ¹³¹I). The study enrolled 50 female patients with DTC who received a ¹³¹I median activity of 90.54 mCi (3.35 GBq). The neutrophil-to-lymphocyte ratio (NLR) was measured as an inflammatory marker. ¹³¹I uptake in the residual thyroid tissue peaked after 46 h. Blood activity decreased in the first 46 h and increased 69 h after the ¹³¹I intake. Blood activity was associated with the absolute lymphocyte count and the NLR at 69 h (r = −0.49 and r = 0.52, p < 0.001). Our results demonstrate that the time interval between 46 and 69 h should be associated with the release of hematological inflammatory mediators, such as neutrophils and lymphocytes, to eradicate tumor cells in response to ¹³¹I therapy.

No clinical studies have investigated the effect of radioiodine (¹³¹I)-targeted therapy on the neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) as inflammatory response markers in patients with differentiated thyroid cancer (DTC) associated with type 2 diabetes mellitus (T2DM) and obesity. This study aimed to assess the relationship between blood radioactivity, body mass index (BMI), and peripheral blood cells three days after ¹³¹I intake in 56 female patients without T2DM (DTC/−T2DM) vs. 24 female patients with T2DM (DTC/+T2DM). Blood radioactivity, measured three days after ¹³¹I intake, was significantly lower in the DTC/+T2DM than in the DTC/−T2DM patients (0.7 mCi vs. 1.5 mCi, p < 0.001). The relationship between blood radioactivity and BMI (r = 0.83, p < 0.001), blood radioactivity and NLR (r = 0.53, p = 0.008), and BMI and NLR (r = 0.58, p = 0.003) indicates a possible connection between the bloodstream ¹³¹I uptake and T2DM-specific chronic inflammation. In patients without T2DM, ¹³¹I therapy has immunosuppressive effects, leading to increased NLR (19.6%, p = 0.009) and PLR (39.1%, p = 0.002). On the contrary, in the chronic inflammation context of T2DM, ¹³¹I therapy amplifies immune metabolism, leading to a drop in NLR (10%, p = 0.032) and PLR (13.4%, p = 0.021). Our results show that, in DTC/+T2DM, the bidirectional crosstalk between neutrophils and obesity may limit ¹³¹I uptake in the bloodstream. Considering the immune response to ¹³¹I therapy, the two groups of patients can be seen as a synchronous portrait of two sides. The explanation could lie in the different radiosensitivity of T and B lymphocytes, with T lymphocytes being predominant in patients with DTC/−T2DM and, most likely, B lymphocytes being predominant in T2DM.