ABSTRACT
Objective To synthesis and characterization nano-composite biomaterials-polyamidoamine dendrimers/nano-hydroxyapatite (PAMAM/n-HAP),which has the properties of both organic and inorganic materials,and then evaluate its role in dentin tubule occlusion. Methods PAMAM/n-HAP was characterized and validated by Fourier transform infrared spectrometry and transmission electron microscopy after its preparation via the Pramanik aqueous-based chemical method. Scanning electron microscope was used to evaluate its role in dentin tublule occlusion. Results The peak absorption bands were found at 1244 cmand 1650 cmin Fourier transform infrared spectroscopy. A relatively low-density coating (about 10 nm) appeared on the n-HAP. The results of Fourier transform infrared spectrometry and transmission electron microscopy confirmed the successful synthesis of PAMAM/n-HAP. The scanning electron microscope showed that PAMAM/n-HAP could effectively reduce the diameter of the dentin tubule and close dentin tubule. Conclusion PAMAM/n-HAP,as a newly synthesized biomaterial,has a good binding capacity with collagen fibers with the help of superficial carboxyl. It can induce effective dentinal tubule occlusion,indicating that PAMAM/n-HAP have great potential in clinical practice for dentin hypersensitivity.
ABSTRACT
Objective:To study the effects of deoxyadenosine(dAdo) on methotrexate (MTX) induced suppression of inflammatory bone destruction.Methods:The culture system of whole bone marrow cells (WBMCs) was utilized to evaluate osteoclastogenesis.TRAP staining and μCT analysis were utilized to evaluate osteoclastogenesis and bone destruction in adjuvant arthritis rats.Results:In the bone marrow culture system,MTX-induced suppression of osteoclastogenesis was abrogated by the addition of dAdo.dAdo canceled MTX-induced suppression of osteoclastogenesis in the rats with arthritis,and significantly abolished the therapeutic effects of MTX on inflammatory bone destruction in the rats.Conclusion:The accumulation of dAdo may be one cause of the losing effectiveness of MTX in bone destruction.