Umbilical cord mesenchymal stem cell therapy (Sclnow Biotechnology)

Osteoporosis in the jawbone can compromise the success of dental implant treatment. Human umbilical cord mesenchymal stem cells (hUCMSCs) have demonstrated osteogenic differentiation potential. This study aimed to evaluate the effect of hUCMSC induction on implant osseointegration in an osteoporotic animal model.

Twenty-eight osteoporotic female Wistar rats were divided into control and hUCMSC-induced groups and observed at 2 and 4 weeks. The treatment group received hUCMSC injections into the implant area of the femur osteoporotic model. Specimens were stained using immunohistochemical and haematoxylin and eosin techniques to assess osteogenic marker expression. Data were analysed using Kruskal-Wallis and Mann-Whitney U test.

Bone-implant volume (BIV) was significantly greater in the hUCMSC-induced groups compared to controls. The expression of osterix, RUNX family transcription factor 2 (RUNX2), tumor necrosis factor (TNF)-α, nuclear factor of activated T cells 1 (NFATc1), collagen type 1, and osteocalcin decreased in osteoblasts from week 2 to week 4. Significant differences (P < 0.05) were observed between control and hUCMSC groups at both time points. These findings suggest that bone formation was completed by week 4, entering the bone maturation phase, supported by the increased BIV in the hUCMSC group.

Induction with hUCMSCs promotes both early and late osseointegration in osteoporotic animal models. These results highlight the efficacy of hUCMSCs in enhancing bone healing after implant placement under osteoporotic conditions.

This study aimed to investigate the impact of human umbilical cord–derived mesenchymal stromal cells (hUC-MSCs) on food allergy (FA) mice induced by ovalbumin. The percentage of regulatory T cells (Tregs) was assessed by administering hUC-MSCs intravenously to FA mouse models with oral challenges, allergic responses and levels of related allergic cytokines. The phenotypes of hUC-MSCs were analysed using flow cytometric analysis. Immunohistochemistry was used for histology observation. Real-time polymerase chain reaction (PCR) was used for gene expression. Jejunum tissue was analysed by transcriptome sequencing. Our results demonstrated that in the current FA model, hUC-MSC therapy significantly alleviated allergic responses and diarrhoea. Levels of immunoglobulin E (IgE), as well as cytokines, such as interleukin (IL)-6 and tumour necrosis factor-α associated with T helper 2 cells, were reduced. Conversely, transforming growth factor (TGF)-β levels increased with hUC-MSC therapy. In addition, enhanced TGF-β expression along with IL-10 messenger ribonucleic acid levels and an increased percentage of CD4 + Foxp3 + Tregs were observed. In long-term FA mice models, hUC-MSC therapy exhibited sustained effects in mitigating rectal temperature decrease and mortality rates while reducing the levels of IgE, IL-6 and proportion of IgE+ cells; it also elevated TGF-β levels. Furthermore, hUC-MSC therapy attenuated pathological injury in both current and long-term FA mouse models. Transcriptome sequencing showed that upregulated differentially expressed genes were mainly concentrated in neural activation–ligand interaction, the cyclic guanosine monophosphate–protein kinase G signalling pathway and the TGF-β signalling pathway. The hUC-MSC therapy holds promise for alleviating both immediate and persistent FA conditions; targeting TGF-β and IL-10 secreted by hUC-MSCs may be a potential approach for treating FA.