Effects of inorganic ions,organic particles,blood cells,and cyclic loading on in vitro corrosion of Mg–Al alloys

Recently,magnesium(Mg)alloys have attracted extensive attention as biodegradable implant materials.However,cyclic loading and the corrosive environment of the body are significant challenges for the practical use of alloys,and there are few studies on this topic.In this study,we conducted a four-point bending fatigue test for 86,400 cycles(12 h)in simulated body fluid(SBF),plasma,and whole blood with an AZ series alloy Mg-9Al-0.5Zn-0.27Mn-0.12Ag,to examine the effects of inorganic ions,organic particles,blood cells,and cyclic loading on Mg alloy corrosion.The Mg^(2+)concentration and solution pH were measured before and after experimentation,and the sample surfaces were characterized by 3D digital microscopy,scanning electron microscopy(SEM),energy-dispersive X-ray spectroscopy(EDS),Fourier-transform infrared(FTIR)spectroscopy,Raman spectroscopy,and X-ray photoelectron spectroscopy(XPS).Our results showed that in the non-loading condition,a porous and weak inorganic product layer(mainly Mg/Ca phosphate and carbonate)formed on the surface of the Mg alloy sample immersed in SBF,which hardly had a protective effect on Mg alloy corrosion.For the samples immersed in plasma,the organic particles promoted the formation of an organic and more compact product layer,which protected the Mg alloy from severe corrosion.For the sample immersed in whole blood,the blood cells affected organic particle deposition on the product layer and thus interfered with the formation of an organic compact product layer,which slightly accelerated the corrosion process.Furthermore,cyclic loading damaged the layer integrity and significantly increased the corrosion rates of all the studied materials compared to the samples not subjected to cyclic loading.Nonetheless,under cyclic loading,blood cells adsorbed on the Mg alloy surfaces,and formed films,which protected the Mg alloy substrate and delayed Mg alloy corrosion.

Oral administration of Bifidobacterium breve improves anti-angiogenic drugs-derived oral mucosal wound healing impairment via upregulation of interleukin-10

Recent studies have suggested that long-term application of anti-angiogenic drugs may impair oral mucosal wound healing.This study investigated the effect of sunitinib on oral mucosal healing impairment in mice and the therapeutic potential of Bifidobacterium breve(B.breve).A mouse hard palate mucosal defect model was used to investigate the influence of sunitinib and/or zoledronate on wound healing.The volume and density of the bone under the mucosal defect were assessed by micro-computed tomography(micro-CT).Inflammatory factors were detected by protein microarray analysis and enzyme-linked immunosorbent assay(ELISA).The senescence and biological functions were tested in oral mucosal stem cells(OMSCs)treated with sunitinib.Ligated loop experiments were used to investigate the effect of oral B.breve.Neutralizing antibody for interleukin-10(IL-10)was used to prove the critical role of IL-10 in the pro-healing process derived from B.breve.Results showed that sunitinib caused oral mucosal wound healing impairment in mice.In vitro,sunitinib induced cellular senescence in OMSCs and affected biological functions such as proliferation,migration,and differentiation.Oral administration of B.breve reduced oral mucosal inflammation and promoted wound healing via intestinal dendritic cells(DCs)-derived IL-10.IL-10 reversed cellular senescence caused by sunitinib in OMSCs,and IL-10 neutralizing antibody blocked the ameliorative effect of B.breve on oral mucosal wound healing under sunitinib treatment conditions.In conclusion,sunitinib induces cellular senescence in OMSCs and causes oral mucosal wound healing impairment and oral administration of B.breve could improve wound healing impairment via intestinal DCs-derived IL-10.

BMP-IHH-mediated interplay between mesenchymal stem cells and osteoclasts supports calvarial bone homeostasis and repair

Calvarial bones are connected by fibrous sutures. These sutures provide a niche environment that includes mesenchymal stem cells(MSCs), osteoblasts, and osteoclasts, which help maintain calvarial bone homeostasis and repair. Abnormal function of osteogenic cells or diminished MSCs within the cranial suture can lead to skull defects, such as craniosynostosis. Despite the important function of each of these cell types within the cranial suture, we have limited knowledge about the role that crosstalk between them may play in regulating calvarial bone homeostasis and injury repair. Here we show that suture MSCs give rise to osteoprogenitors that show active bone morphogenetic protein(BMP) signalling and depend on BMP-mediated Indian hedgehog(IHH) signalling to balance osteogenesis and osteoclastogenesis activity. IHH signalling and receptor activator of nuclear factor kappa-Β ligand(RANKL) may function synergistically to promote the differentiation and resorption activity of osteoclasts. Loss of Bmpr1a in MSCs leads to downregulation of hedgehog(Hh) signalling and diminished cranial sutures. Significantly, activation of Hh signalling partially restores suture morphology in Bmpr1a mutant mice, suggesting the functional importance of BMP-mediated Hh signalling in regulating suture tissue homeostasis. Furthermore, there is an increased number of CD200+ cells in Bmpr1a mutant mice, which may also contribute to the inhibited osteoclast activity in the sutures of mutant mice. Finally, suture MSCs require BMPmediated Hh signalling during the repair of calvarial bone defects after injury. Collectively, our studies reveal the molecular and cellular mechanisms governing cell–cell interactions within the cranial suture that regulate calvarial bone homeostasis and repair.

Diagnosis and treatment of thyroglossal duct carcinoma:Report of three cases with review of literatures

Thyroglossal duct carcinoma,which is usually diagnosed postoperatively,is a rare malignant tumor arising in the thyroglossal duct cyst.The definitive diagnosis can be made only after microscopic examination.We retrospectively reviewed three cases of thyroglossal duct carcinoma diagnosed in Peking University School and Hospital of Stomatology from January 1986 to August 2006.Clinical and pathological features were investigated and the optimal treatment protocol was proposed.The constituent ratio of thyroglossal duct carcinoma among surgically excised thyroglossal duct lesions was 2.9%.The clinical presentation of thyroglossal duct carcinoma was very similar to that of its benign counterpart.Two cases were diagnosed as thyroglossal duct cyst prior to the operation,the remaining one as dermoid cyst.All three cases were diagnosed as papillary carcinoma of thyroid origin after microscopic examination.Primary thyroglossal duct carcinoma should conform to the following criteria:localization of the carcinoma to a clearly demonstrable thyroglossal duct cyst or tract;clinically or histologically confirmed absence of carcinoma of the thyroid gland.Papillary carcinoma is the most common histological type,which usually develops slowly with an excellent prognosis.The histological characteristics including:formation of papillary structure;nuclear morphological variations such as ground glass nuclei,pseudoinclusions,intranuclear grooves and filaments;concentrically calcified structures termed psammoma bodies which is regarded as a strong indication of papillary carcinoma;and positivity in immunohistological staining for thyroglobin.Sistrunk procedure of excision is the choice for treatment.A close follow-up is needed.In the presence of thyroid gland masses or cervical lymphadenopathy,thyroidectomy or neck dissection should be recommended.The effect of thyroid suppression therapy and radioactive iodine therapy is not conclusive.