Tooth whitening has recently become one of the most popular aesthetic dentistry procedures. Beyond classic hydrogen peroxide-based whitening agents, photo-catalysts and piezo-catalysts have been demonstrated for non-destructive on-demand tooth whitening. However, their usage has been challenged due to the relatively limited physical stimuli of light irradiation and ultrasonic mechanical vibration. To address this challenge, we report here a non-destructive and convenient tooth whitening strategy based on the pyro-catalysis effect, realized via ubiquitous oral motion-induced temperature fluctuations. Degradation of organic dyes via pyro-catalysis is performed under cooling/heating cycling to simulate natural temperature fluctuations associated with intake and speech. Teeth stained by habitual beverages and flavorings can be whitened by the pyroelectric particles-embedded hydrogel under a small surrounding temperature fluctuation. Furthermore, the pyro-catalysis-based tooth whitening procedure exhibits a therapeutic biosafety and sustainability. In view of the exemplary demonstration, the most prevalent oral temperature fluctuation will enable the pyro-catalysis-based tooth whitening strategy to have tremendous potential for practical applications.

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Understanding the bioelectrical properties of bone tissue is key to developing new treatment strategies for bone diseases and injuries, as well as improving the design and fabrication of scaffold implants for bone tissue engineering. The bioelectrical properties of bone tissue can be attributed to the interaction of its various cell lineages (osteocyte, osteoblast and osteoclast) with the surrounding extracellular matrix, in the presence of various biomechanical stimuli arising from routine physical activities; and is best described as a combination and overlap of dielectric, piezoelectric, pyroelectric and ferroelectric properties, together with streaming potential and electro‐osmosis. There is close interdependence and interaction of the various electroactive and electrosensitive components of bone tissue, including cell membrane potential, voltage‐gated ion channels, intracellular signaling pathways, and cell surface receptors, together with various matrix components such as collagen, hydroxyapatite, proteoglycans and glycosaminoglycans. It is the remarkably complex web of interactive cross‐talk between the organic and non‐organic components of bone that define its electrophysiological properties, which in turn exerts a profound influence on its metabolism, homeostasis and regeneration in health and disease. This has spurred increasing interest in application of electroactive scaffolds in bone tissue engineering, to recapitulate the natural electrophysiological microenvironment of healthy bone tissue to facilitate bone defect repair.

The maintenance and incremental growth of the alveolar bone at the tooth extraction site, to achieve the required height and width for implant restoration, remains a major clinical challenge.

process resulting in capillary bed formation. [1,2] However, sprouting angiogenesis can proceed as an overshooting reaction that results in the formation of additional blood vessels, followed by delayed decelerating growth. [3] This decelerating phase occurs simultaneously with the regression of superfluous vessels at a later stage of healing so that vessel beds are pruned back to normal vascular density and vascular homeostasis is maintained; [4] this process is particularly important because uncontrolled vessel growth leads to pathological effects such as proliferative diabetic retinopathy, [5,6] and incorrect vascular patterning causes vessel instability and poor network functionality. [7] Therefore, organized angiogenesis deceleration at the later stage of healing is crucial for vessel normalization and stabilizing the mature vessels, ensuring that tissue regeneration including bone defect healing can be carried out within a controllable range; however, the mechanism behind this remains unclear. Alteration of extrinsic microenvironment, such as hypoxia improvement, is known as a common cause of capillary deceleration, [8,9] yet the decelerating angiogenesis response is usually accompanied by the repairing process of various injured tissue. [10] Therefore, it's reasonable to assume that intrinsic Deceleration of sprouting angiogenesis until its final disappearance after blood vessel reconstruction is crucial for controlled tissue repair; however, its underlying mechanism remains unclear. It is reported that osteogenic differentiated bone marrow stem cells (OD-BMSCs) contribute to sprouting angiogenesis deceleration by releasing intrinsic "OFF" signals. In vitro experiments show that insulin-like growth factor-binding protein 7 (IGFBP7) is the main component of OD-BMSCs paracrine products which could inhibit the tube formation ability of endothelial cells. In addition, cell functional experiments show that IGFBP7 inhibits sprouting angiogenesis by reducing cell migration and tip cell specification. Furthermore, it is found that early IGFBP7 intervention, which accelerates sprouting angiogenesis deceleration during the early stage of healing, impedes bone defect healing. These results demonstrate that OD-BMSCs could offer intrinsic inhibitory signals on sprouting angiogenesis and the appropriate emergence timing of these signals is crucial to maintain vasculature homeostasis during bone repairing. These results provide insight into the complex interaction between osteogenesis-angiogenesis coupling and suggest the potential therapeutic application of IGFBP7 in regulating vascular homeostasis.