Characterization of Hypoxia in Pulpal Inflammation Misonidazole (MISO) is a bioreductively-activated marker of cellular hypoxia which preferentially binds to cells with decreased oxygen content. Research using MISO experimentally in rats has been divided into three phases. In phase I, tritiated MISO retention in rat dental pulp was determined using liquid scintillation counting. Comparisons were made between normoxia (normal oxygen tension) and induced hypobaric hypoxia. Induced hypoxia significantly increased MISO retention over the normoxic condition. In phase II, the localization of tritiated MISO in normoxic and hypoxic states were determined through use of autoradiography. Increased MISO retention in the induced hypoxic animals was via two meshanisms: (1) an overall increased retention due to a uniform reduction of the oxygen supply to the tissues, and (2) a site-specific increase in hypoxic retention due to either poor oxygen diffusion (in cementoblasts) or to capillary shutdown (pulp horn odontoblasts). Pulpal inflammation was induced in the rat molar via cavity preparation in phase III. Autoradiographic preparation of the histologic slides revealed that hypoxic cores occurred in inflammatory lesions greater than 0.35 mm in diameter (+-0.05 mm SD). As the inflammatory lesion's area increased, the ypoxic core's area also increased (Sperman's coefficient =0.95). Hypoxic mediated binding of 3H-MISO occurs in the pulp as a result of inflammatory stress. 3H-MISO may be useful in examining dynamic changes not just in pulpal blood flow, but in actual cellular oxygen perfusion under circumstances that cause a deviation from the normoxic condition. KEY WORDS: Hypoxia, Dental Pulp, Inflammation
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