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OBJECTIVE: At present, platelet-rich fibrin is widely used in site retention after tooth extraction, but the effect of platelet-rich fibrin in alveolar ridge preservation is not very clear compared with other materials. This study evaluated the effect of applied platelet-rich fibrin in the preservation of alveolar ridge after tooth extraction to provide theoretical basis for clinical application of platelet-rich fibrin to reduce alveolar bone resorption. METHODS: Up to June 2020, all clinical randomized controlled studies on platelet-rich fibrin for alveolar ridge preservation, including platelet-rich fibrin alone and platelet-rich fibrin combined with heterogeneous bone, were collected by using The Cochrane Library, PubMed, Web of science core set, EMbase, CNKI, and Wanfang databases. Two researchers extracted data from the retrieved documents and used Cochrane bias risk assessment tools to evaluate the bias risk included in the study. RevMan 5.3 software was used for meta-analysis. RESULTS: (1) Totally 159 articles were retrieved, and 11 randomized controlled trials were finally included, involving 531 patients and 575 implants. (2) The results of meta-analysis showed that the difference in the height absorption of tooth alveolar bone was not statistically significant when platelet-rich fibrin was applied alone (SMD=-0.38, 95%CI:-0.83 to -0.06, P > 0.05). There were significant differences between platelet-rich fibrin composite heterogeneous bone and simple xenogeneic bone in alveolar bone resorption height (3 months: SMD=-1.40, 95%CI:-1.79 to -1.01, P < 0.05; 6 months: SMD=-1.37, 95%CI:-1.68 to -1.06, P < 0.05), alveolar bone resorption width at 3 and 6 months after tooth extraction (SMD=-0.18, 95%CI:-0.25 to -0.11, P < 0.05), and mouth mucosa healing rate at 2 weeks after tooth extraction (SMD=9.90, 95%CI:8.61-11.19, P < 0.05). CONCLUSION: Applying platelet-rich fibrin composite heterogeneous bone after tooth extraction can remarkably reduce the resorption of alveolar bone both in height and width and accelerate soft tissue healing. Because of the small sample size included in the study, clinical studies with a large sample size are needed to verify the above conclusions. [ABSTRACT FROM AUTHOR]

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To observe the dynamic change and significance of apoptosis levels in the alveolar macrophages (AM) of the bleomycin-induced pulmonary fibrosis model mice. Methods A total of 100 mice were randomly divided into control group (n=50) and model group (n=50). The model group was received with bleomycin at 2.5 mg/kg via oropharyngeal instillation to molding. The control group was conducted with same volume of normal saline. Ten mice randomly selected were executed on the day 1, 3, 7, 14, and 21 after modeling in the two groups. Hematoxylin and eosin (HE) staining was used to observe the pathological changes of lung tissue and calculate the inflammation score and pulmonary coefficients in five mice of two groups. Alkali hydrolysis method was used to detect the content of hydroxyproline, and the bronchoalveolar lavage fluid (BALF) was collected to assess the cell counts and apoptotic levels of AM in another five mice. Results Mice of model group showed inflammatory cell infiltration and alveolar wall widening on day 3, along with an aggravate inflammation and increased inflammation score on day 7. The fibroplasia and collagen sediment were increased on day 14 and day 21. The inflammation score was decreased significantly in day 21 compared with those in day 7 and day 14. The hydroxyproline contents were increased significantly on day 21 than those on day 1, day 3 and day 7 in model group, but no significant difference when compared with those of day 14. The cell count and apoptotic rates of AM, and pulmonary coefficients showed changes of increasing first and then decreasing in model group, which reached the peak at day 7. Conclusion The cell counts and apoptotic levels increase in the preliminary stage of inflammatory and decrease in pulmonary fibrosis phase in bleomycin-induced pulmonary fibrosis model mice. These changes may play different roles in the progression of pulmonary fibrosis. [ABSTRACT FROM AUTHOR]