Regenerative dentistry is an emerging field of medicine involving stem cell technology, tissue engineering and dental science. It exploits biological mechanisms to regenerate damaged oral tissues and restore their functions. Platelet‐rich plasma (PRP) is a biological product that is defined as the portion of plasma fraction of autologous blood with a platelet concentration above that of the original whole blood. A super‐mixture of key cytokines and growth factors is present in platelet granules. Thus, the application of PRP has gained unprecedented attention in regenerative medicine. The rationale underlies the utilization of PRP is that it acts as a biomaterial to deliver critical growth factors and cytokines from platelet granules to the targeted area, thus promoting regeneration in a variety of tissues. Based on enhanced understanding of cell signalling and growth factor biology, researchers have begun to use PRP treatment as a novel method to regenerate damaged tissues, including liver, bone, cartilage, tendon and dental pulp. To enable better understanding of the regenerative effects of PRP in dentistry, this review describes different methods of preparation and application of this biological product, and provides detailed explanations of the controversies and future prospects related to the use of PRP in dental regenerative medicine.

The results suggest that with further improvement in terms of its sensitivity and specificity, it may be feasible to use the automated hearing screening test system to conduct routine school hearing screenings.

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The data demonstrate that VitD is required to maintain the stability of mast cells. The deficiency of VitD results in mast cell activation.

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Epithelial barrier integrity is critical to maintain the homeostasis in the body. The regulatory mechanism of the epithelial barrier function has not been fully understood. This study aims to elucidate the role of the TWIK-related potassium channel-1 (Trek1) in the regulation of the epithelial barrier function of the nasal mucosa. In this study, the levels of Trek1 were assessed by real time RT-PCR and Western blotting. The epithelial barrier function of the rat nasal epithelia was evaluated by the Ussing chamber system. The results showed that Trek1 was detected in the human and rat nasal epithelia, which were significantly lower in patients and rats with allergic rhinitis than that in healthy controls. Exposure to the signature T helper 2 cytokine, interleukin (IL)-4, markedly suppressed the expression of Trek1 in the nasal mucosa via up regulating the expression of the histone deacetylase (HDAC)1. The IL-4-induced rat nasal epithelial barrier dysfunction could be blocked by HDAC1 inhibitor (Trichostatin A), or sodium butyrate, or administration of Clostridium Butyricum. We conclude that Trek1 is critical to maintain the nasal epithelial barrier function.

The therapeutic efficacy of allergen specific immunotherapy (SIT) on allergic diseases is to be improved. Probiotics can regulate immune response. This study aims to promote the effect of SIT on allergic rhinitis (AR) by co-administration with Clostridium butyricum (Cb). In this study, patients with AR sensitized to mite allergens were enrolled to this study, and treated with SIT or/and Cb. The therapeutic efficacy was evaluated by the total nasal symptom scores (NSS), medication scores, serum specific IgE levels and T helper (Th)2 cytokine levels. The improvement of immune regulation in the AR patients was assessed by immunologic approaches. The results showed that treating AR patients with SIT alone markedly reduced NSS and medication scores; but did not alter the serum specific IgE, Th2 cytokines and skin prick test (SPT) index. The clinical symptoms on AR in SIT group relapsed one month after stopping SIT. Co-administration of Cb significantly enhanced the efficacy of SIT on AR as shown by suppression of NSS, medication scores, serum specific IgE, Th2 cytokines and SPT index; the regulatory B cell frequency was also markedly increased. Such an effect on AR was maintained throughout the observation period even after stopping the treatment. Butyrate blocked the activation of histone deacetylase-1, the downstream activities of epsilon chain promoter activation, and the IgE production in the antigen specific B cells. On the other hand, butyrate induced the IL-10 expression in B cells with a premise of the B cell receptor activation by specific antigens. In conclusion, administration with Cb can markedly enhance the efficacy of SIT on AR.