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anestesia intrapulpar
intrapulpal anesthesia
Son Güncelleme: 2014-12-09
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anestesia intrapulpar (procedimiento)
intrapulpal anesthesia (procedure)
Son Güncelleme: 2014-12-09
Kullanım Sıklığı: 1
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Uyarı: Bu hizalama yanlış olabilir..
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es notable que la pulpa dental pueda manejar las agresiones microbianas debido a su extenso sistema linfático intrapulpar.
it is notable that the dental pulp is capable of managing the microbial insults because of its extensive intrapulpal lymphatic system.
el exceso de activación de calor aumenta la temperatura intrapulpar, dañando odontoblastos y causando cambios inflamatorios en las porciones orgánicas del diente, que a menudo lleva a daño pulpar irreversible.
excess heat activation increases the intrapulpal temperature, damaging odontoblasts, and causing inflammatory changes to the organic portions of the tooth that often lead to irreversible pulpal damage.
lps y lta se unen a los receptores tipo toll (tlr), presentes en la superficie de algunas células inmunes en la pulpa e inducen la liberación de mediadores inflamatorios como prostaglandinas, citocinas y quimiocinas.64 en particular, está bien descrito el papel en la pulpitis del factor de necrosis tumoral alfa (tnf-α), la interleucina-1 (il-1), il-8, il-12, y las quimiocinas ccl2 y cxcl2.52 se sabe que il-1 es liberado de macrófagos tras la estimulación con lps y es responsable de la reabsorción ósea que lleva a la periodontitis peri-radicular.59 durante la pulpitis aguda, los mediadores inflamatorios activan la vasodilatación, el aumento transitorio del flujo sanguíneo pulpar (pbf), la infiltración de células inflamatorias, el aumento de la presión intrapulpar y por último la necrosis pulpar isquémica (suplemento a figura 51 1).
lps and lta bind toll-like receptors (tlrs), present on the surface of some immune cells in the pulp, and induce the release of inflammatory mediators such as prostaglandins, cytokines, and chemokines.64 in particular, tumor necrosis factor alpha (tnf-α), interleukin-1 (il-1), il-8, il-12, and chemokines ccl2 and cxcl2 are well described for their role in pulpitis.52 il-1 is known to be released from macrophages after stimulation with lps and responsible for bone resorption leading to periradicular periodontitis.59 during acute pulpitis, the inflammatory mediators trigger vasodilation, transient increase of pulpal blood flow (pbf), inflammatory cell infiltration, increased intrapulpal pressure, and finally ischemic necrosis of the pulp (supplement a figure 51-1).