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Nanoscale replication of the hierarchical organization of minerals in biogenic mineralized tissues is believed to contribute to the better mechanical properties of biomimetic collagen scaffolds. Here, an intrafibrillar nanocarbonated apatite assembly is reported, which has a bone-like hierarchy, and which improves the mechanical and biological properties of the collagen matrix derived from fibril-apatite aggregates. A modified biomimetic approach is used, which based on the combination of poly(acrylic acid) as sequestration and sodium tripolyphosphate as templating matrix-protein analogs. With this modified dual-analog-based biomimetic approach, the hierarchical association between collagen and the mineral phase is discerned at the molecular and nanoscale levels during the process of intrafibrillar collagen mineralization. It is demonstrated by nanomechanical testing, that intrafibrillarly mineralized collagen features a significantly increased Young's modulus of 13.7 ± 2.6 GPa, compared with pure collagen (2.2 ± 1.7 GPa) and extrafibrillarly-mineralized collagen (7.1 ± 1.9 GPa). Furthermore, the hierarchy of the nanocarbonated apatite assembly within the collagen fibril is critical to the collagen matrix's ability to confer key biological properties, specifically cell proliferation, differentiation, focal adhesion, and cytoskeletal arrangement. The availability of the mineralized collagen matrix with improved nanomechanics and cytocompatibility may eventually result in novel biomaterials for bone grafting and tissue-engineering applications. [ABSTRACT FROM AUTHOR]

Temporomandibular disorders (TMDs) predominantly affect reproductive female patients, with pain the most frequent complaint. Although estrogens are believed to play important roles in TMD pain, the mechanism underlying modulation of TMD pain by estrogens remains largely unknown. Accumulating evidence implies that the hippocampus is involved in sexual dimorphism of pain sensitivity. In this study, we investigated the hippocampal TRPV1 (transient receptor potential vanilloid 1) expression in ovariectomized rats that received 17-beta-estradiol substitution and found that 17-beta-estradiol enhanced the mechanical allodynia of inflamed temporomandibular joint (TMJ) induced by complete Freund's adjuvant. Real-time PCR and immunoblotting demonstrated that TMJ inflammation significantly induced hippocampal TRPV1 expression compared with the control group but failed to induce it in the ovariectomized rats that received no estradiol replacement. In addition, estradiol potentiated TMJ inflammation-induced hippocampal TRPV1 expression in a dose-dependent manner in the ovariectomized rats. In contrast, TRPV1 transcription in amygdala, prefrontal cortex, and thalamus was not affected by TMJ inflammation and estradiol. Immunostaining showed TRPV1 localized in the processes and cytoplasm of pyramidal neurons in CA1-CA3 regions of the hippocampus. Moreover, intrahippocampal injection of TRPV1 antagonists capsazepine and 5'-iodo-resiniferatoxin into the CA1 region of the hippocampus significantly attenuated allodynia of inflamed TMJ in both nonovariectomized and ovariectomized rats that received estradiol replacement. Our results suggested that hippocampal TRPV1 can modulate central pain processing and estradiol may contribute to the sexual dimorphism of TMD pain sensitivity through upregulation of TRPV1 expression in the hippocampus.