Nitric oxide and dental pulp

Young-Kyung Kim; Sung-Kyo Kim

doi:10.5395/JKACD.2002.27.5.543

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Original Article Nitric oxide and dental pulp: Young-Kyung Kim, Sung-Kyo Kim; Journal of Korean Academy of Conservative Dentistry 2002;27(5):543-551.
DOI: https://doi.org/10.5395/JKACD.2002.27.5.543
Published online: September 30, 2002

Department of Conservative Dentistry, School of Dentistry, Kyungpook National University, Korea.

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Abstract
REFERENCES

Abstract

Nitric oxide (NO) is a small molecule (mol. wt. 30 Da) and oxidative free radical. It is uncharged and can therefore diffuse freely within and between cells across membrane. Such characteristics make it a biologically important messenger in physiologic processes such as neurotransmission and the control of vascular tone. NO is also highly toxic and is known to acts as a mediator of cytotoxicity during host defense.

NO is synthesized by nitric oxide synthase (NOS) through L-arginine/nitric oxide pathway which is a dioxygenation process. NO synthesis involves several participants, three co-substrates, five electrons, five co-factors and two prosthetic groups.

Under normal condition, low levels of NO are synthesized by type I and III NOS for a short period of time and mediates many physiologic processes. Under condition of oxidant stress, high levels of NO are synthesized by type II NOS and inhibits a variety of metabolic processes and can also cause direct damage to DNA. Such interaction result in cytostasis, energy depletion and ultimately cell death. NO has the potential to interact with a variety of intercellular targets producing diverse array of metabolic effects.

It is known that NO is involved in hemodynamic regulation, neurogenic inflammation, re-innervation, management of dentin hypersensitivity on teeth. Under basal condition of pulpal blood flow, NO provides constant vasodilator tone acting against sympathetic vasoconstriction. Substance P, a well known vasodilator, was reported to be mediated partly by NO, while calcitonin-gene related peptide has provided no evidence of its relation with NO.

This review describes the roles of NO in dental pulp in addition to the known general roles of it.
Keywords: nitric oxide; hemodynamic regulation; constant vasodilator tone; dental pulp

REFERENCES

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Fig. 1

Schematic representation of the biosynthesis of NO from L-Arginine by the NO synthase system.

Fig. 2

Synthesis of NO by three isoforms of NOS. (Adapted from Knowles and Moncada, Biochem. J., 1994, 298:249-258.)

Fig. 3

Amino acid arrangement of type I, II, III NOS and CPR. (Adapted from Dawson and Snyder, Journal of Neuroscience, 1994, 14:5147-59)

Fig. 4

Structural formula of L-arginine and analogue that inhibit NO formation.

Fig. 5

Roles of NO: physiological messengers and cytotoxic agent.

Fig. 6

Diagram illustrating proposed intracellular mechanism for SP in the vascular relaxation.

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Nitric oxide and dental pulp

J Korean Acad Conserv Dent. 2002;27(5):543-551. Published online September 30, 2002

DOI: https://doi.org/10.5395/JKACD.2002.27.5.543

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Figure

Nitric oxide and dental pulp

Fig. 1 Schematic representation of the biosynthesis of NO from L-Arginine by the NO synthase system.

Fig. 2 Synthesis of NO by three isoforms of NOS. (Adapted from Knowles and Moncada, Biochem. J., 1994, 298:249-258.)

Fig. 3 Amino acid arrangement of type I, II, III NOS and CPR. (Adapted from Dawson and Snyder, Journal of Neuroscience, 1994, 14:5147-59)

Fig. 4 Structural formula of L-arginine and analogue that inhibit NO formation.

Fig. 5 Roles of NO: physiological messengers and cytotoxic agent.

Fig. 6 Diagram illustrating proposed intracellular mechanism for SP in the vascular relaxation.