Objectives The aim of this study was to evaluate the influence of different bleaching gels on the masking and caries-arresting effects of infiltrated and non-infiltrated stained artificial enamel caries lesions. Materials and methods Bovine enamel specimens (n = 240) with each two sound areas (SI and SC) and each two lesions (DI and DC) were infiltrated (DI and SI), stained (1:1 red wine-coffee mixture,70 days), and randomly distributed in six groups to be bleached with the following materials: 6%HP (HP-6), 16%CP (CP-16), 35%HP (HP-35), 40%HP (HP-40), and no bleaching (NBl,NBl-NBr). Subsequently, specimens were pH-cycled (28 days, 6 × 60 min demineralization/day) and all groups except NBl-NBr were brushed with toothpaste slurry (1.100 ppm, 2×/day, 10 s). Differences in colorimetric values (ΔL, ΔE) and integrated mineral loss (ΔΔZ) between baseline, infiltration, staining, bleaching, and pH cycling were calculated using photographic and transversal microradiographic images. Results At baseline, significant visible color differences between DI and SC were observed (ΔEbaseline = 12.2; p < 0.001; ANCOVA). After infiltration, these differences decreased significantly (ΔEinfiltration = 3.8; p < 0.001). Staining decreased and bleaching increased ΔL values significantly (p ≤ 0.001). No significant difference in ΔΔE was observed between before staining and after bleaching (ΔEbleaching = 4.3; p = 0.308) and between the bleaching agents (p = 1.000; ANCOVA). pH-cycling did not affect colorimetric values (ΔEpH-cycling = 4.0; p = 1.000). For DI, no significant change in ΔZ during in vitro period was observed (p ≥ 0.063; paired t test). Conclusions Under the conditions chosen, the tested materials could satisfactorily bleach infiltrated and non-infiltrated stained enamel. Furthermore, bleaching did not affect the caries-arresting effect of the infiltration. Clinical relevance The present study indicates that bleaching is a viable way to satisfactorily recover the appearance of discolored sound enamel and infiltrated lesions.
Platelets have important functions in hemostasis. Best investigated is the aggregation of platelets for primary hemostasis and their role as the surface for coagulation leading to fibrin- and clot-formation. Importantly, the function of platelets does not end with clot formation. Instead, platelets are responsible for clot retraction through the concerted action of the activated αIIbβ3 receptors on the surface of filopodia and the platelet’s contractile apparatus binding and pulling at the fibrin strands. Meanwhile, the signal transduction events leading to clot retraction have been investigated thoroughly, and several targets to inhibit clot retraction have been demonstrated. Clot retraction is a physiologically important mechanism allowing: (1) the close contact of platelets in primary hemostasis, easing platelet aggregation and intercellular communication, (2) the reduction of wound size, (3) the compaction of red blood cells to a polyhedrocyte infection-barrier, and (4) reperfusion in case of thrombosis. Several methods have been developed to measure clot retraction that have been based on either the measurement of clot volume or platelet forces. Concerning the importance of clot retraction in inborn diseases, the failure of clot retraction in Glanzmann thrombasthenia is characterized by a bleeding phenotype. Concerning acquired diseases, altered clot retraction has been demonstrated in patients with coronary heart disease, stroke, bronchial asthma, uremia, lupus erythematodes, and other diseases. However, more studies on the diagnostic and prognostic value of clot retraction with methods that have to be standardized are necessary.
Besides their function in primary hemostasis, platelets are critically involved in the physiological steps leading to wound healing and tissue repair. For this purpose, platelets have a complex set of receptors allowing the recognition, binding, and manipulation of extracellular structures and the detection of pathogens and tissue damage. Intracellular vesicles contain a huge set of mediators that can be released to the extracellular space to coordinate the action of platelets as other cell types for tissue repair. Therapeutically, the most frequent use of platelets is the intravenous application of platelet concentrates in case of thrombocytopenia or thrombocytopathy. However, there is increasing evidence that the local application of platelet-rich concentrates and platelet-rich fibrin can improve wound healing and tissue repair in various settings in medicine and dentistry. For the therapeutic use of platelets in wound healing, several preparations are available in clinical practice. In the present study we discuss the physiology and the cellular mechanisms of platelets in hemostasis and wound repair, the methods used for the preparation of platelet-rich concentrates and platelet-rich fibrin, and highlight some examples of the therapeutic use in medicine and dentistry.
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