The human oral microbiome has emerged as a focal point of research due to its profound implications for human health. The involvement of short-chain fatty acids in oral microbiome composition, oral health, and chronic inflammation is gaining increasing attention. In this narrative review, the results of early in vitro, in vivo, and pilot clinical studies and research projects are presented in order to define the boundaries of this new complicated issue. According to the results, the current research data are disputable and ambiguous. When investigating the role of SCFAs in human health and disease, it is crucial to distinguish between their local GI effects and the systemic influences. Locally, SCFAs are a part of normal oral microbiota metabolism, but the increased formation of SCFAs usually attribute to dysbiosis; excess SCFAs participate in the development of local oral diseases and in oral biota gut colonization and dysbiosis. On the other hand, a number of studies have established the positive impact of SCFAs on human health as a whole, including the reduction of chronic systemic inflammation, improvement of metabolic processes, and decrease of some types of cancer incidence. Thus, a complex and sophisticated approach with consideration of origin and localization for SCFA function assessment is demanded. Therefore, more research, especially clinical research, is needed to investigate the complicated relationship of SCFAs with health and disease and their potential role in prevention and treatment.

Transplantation of various types of stem cells as a possible therapy for stroke has been tested for years, and the results are promising. Recent investigations have shown that the administration of the conditioned media obtained after stem cell cultivation can also be effective in the therapy of the central nervous system pathology (hypothesis of their paracrine action). The aim of this study was to evaluate the therapeutic effects of the conditioned medium of hiPSC-derived glial and neuronal progenitor cells in the rat middle cerebral artery occlusion model of the ischemic stroke. Secretory activity of the cultured neuronal and glial progenitor cells was evaluated by proteomic and immunosorbent-based approaches. Therapeutic effects were assessed by overall survival, neurologic deficit and infarct volume dynamics, as well as by the end-point values of the apoptosis- and inflammation-related gene expression levels, the extent of microglia/macrophage infiltration and the numbers of formed blood vessels in the affected area of the brain. As a result, 31% of the protein species discovered in glial progenitor cells-conditioned medium and 45% in neuronal progenitor cells-conditioned medium were cell type specific. The glial progenitor cell-conditioned media showed a higher content of neurotrophins (BDNF, GDNF, CNTF and NGF). We showed that intra-arterial administration of glial progenitor cells-conditioned medium promoted a faster decrease in neurological deficit compared to the control group, reduced microglia/macrophage infiltration, reduced expression of pro-apoptotic gene Bax and pro-inflammatory cytokine gene Tnf, increased expression of anti-inflammatory cytokine genes (Il4, Il10, Il13) and promoted the formation of blood vessels within the damaged area. None of these effects were exerted by the neuronal progenitor cell-conditioned media. The results indicate pronounced cytoprotective, anti-inflammatory and angiogenic properties of soluble factors secreted by glial progenitor cells.

Stroke represents a significant global health burden, with a substantial impact on mortality, morbidity, and long-term disability. The examination of stroke biomarkers, particularly the oral microbiome, offers a promising avenue for advancing our understanding of the factors that contribute to stroke risk and for developing strategies to mitigate that risk. This review highlights the significant correlations between oral diseases, such as periodontitis and caries, and the onset of stroke. Periodontal pathogens within the oral microbiome have been identified as a contributing factor in the exacerbation of risk factors for stroke, including obesity, dyslipidemia, atherosclerosis, hypertension, and endothelial dysfunction. The alteration of the oral microbiome may contribute to these conditions, emphasizing the vital role of oral health in the prevention of cardiovascular disease. The integration of dental and medical health practices represents a promising avenue for enhancing stroke prevention efforts and improving patient outcomes.

Regenerative medicine is a rapidly evolving field of contemporary biomedical research that offers new therapeutic strategies for conditions previously considered untreatable. Cell therapy shows particular potential in this domain. However, rigorous biosafety measures are required in its development and clinical application. This review proposes a practice-oriented biosafety framework for cell therapy, translating key risks into operational principles: toxicity, oncogenicity/tumorigenicity/teratogenicity, immunogenicity, biodistribution; and cell product quality. For each principle, preclinical approaches and regulatory expectations are summarized. Criteria for immunological safety are addressed, including activation of innate immunity (complement, T- and NK-cell responses) and the need for HLA typing. Biodistribution assessment involves the use of quantitative PCR and imaging techniques (PET, MRI) to monitor cell fate over time. The risks of oncogenicity, tumorigenicity, and teratogenicity can be analyzed using a combination of in vitro methods and in vivo models in immunocompromised animals. Product quality assessment includes sterility, identity, potency, viability, and genetic stability, with alignment of procedures to regulatory requirements and an emphasis on quality-by-design principles to ensure safe and reproducible clinical use. Integrating toxicity and safety pharmacology data supports a balanced risk–benefit assessment and clinical trial planning.

Articular cartilage damage still remains a major problem in orthopedical surgery. The development of tissue engineering techniques such as autologous chondrocyte implantation is a promising way to improve clinical outcomes. On the other hand, the clinical application of autologous chondrocytes has considerable limitations. Mesenchymal stromal cells (MSCs) from various tissues have been shown to possess chondrogenic differentiation potential, although to different degrees. In the present study, we assessed the alterations in chondrogenesis-related gene transcription rates and extracellular matrix deposition levels before and after the chondrogenic differentiation of MSCs in a 3D spheroid culture. MSCs were obtained from three different tissues: umbilical cord Wharton’s jelly (WJMSC—Wharton’s jelly mesenchymal stromal cells), adipose tissue (ATMSC—adipose tissue mesenchymal stromal cells), and the dental pulp of deciduous teeth (SHEDs—stem cells from human exfoliated deciduous teeth). Monolayer MSC cultures served as baseline controls. Newly formed 3D spheroids composed of MSCs previously grown in 2D cultures were precultured for 2 days in growth medium, and then, chondrogenic differentiation was induced by maintaining them in the TGF-β1-containing medium for 21 days. Among the MSC types studied, WJMSCs showed the most similarities with primary chondrocytes in terms of the upregulation of cartilage-specific gene expression. Interestingly, such upregulation occurred to some extent in all 3D spheroids, even prior to the addition of TGF-β1. These results confirm that the potential of Wharton’s jelly is on par with adipose tissue as a valuable cell source for cartilage engineering applications as well as for the treatment of osteoarthritis. The 3D spheroid environment on its own acts as a trigger for the chondrogenic differentiation of MSCs.

Obesity, along with metabolic disorders such as dyslipidemia and insulin resistance, increases the risk of cardiovascular disease, diabetes, various cancers, and other non-communicable diseases, thereby contributing to higher mortality rates. The intestinal microbiome plays a crucial role in maintaining homeostasis and influencing human metabolism. This study enrolled 82 young obese individuals, who were stratified into groups with or without metabolic disturbances. No significant differences in the alpha or beta diversity of the microbiota were observed among the groups. Insulin resistance was characterized by an increase in the number of Adlercreutzia and Dialister as well as a decrease in Collinsella, Coprococcus and Clostridiales. The dyslipidemia and dyslipidemia+insulin resistance groups had no significant differences in the gut microbiota. Dietary patterns also influenced microbial composition, with high protein intake increasing Leuconostoc and Akkermansia, and high fiber intake boosting Lactobacillus and Streptococcus. The genus Erwinia was associated with increases in visceral fat and serum glucose as well as a decrease in high-density lipoprotein cholesterol. Our findings highlight a significant association between gut microbiota composition and metabolic disturbances in young obese individuals, and they suggest that dietary modifications may promote a healthy microbiome and reduce the risk of developing metabolic disorders.