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  • Title: The role of selected cations in the desensitization of intradental nerves.
    Author: Markowitz K, Kim S.
    Journal: Proc Finn Dent Soc; 1992; 88 Suppl 1():39-54. PubMed ID: 1508896.
    Abstract:
    Dentinal sensitivity is a common complaint of patients. Removal of cementum or enamel leaves the dentin exposed allowing various stimuli to produce fluid movement through the dentinal tubules. These fluid movements are believed to activate pulpal sensory nerves leading to pain. Various therapeutic approaches have been investigated to treat this problem. Resins, fluoride compounds and oxalate solutions have been used to block the dentinal tubules. KNO3 and SrCl2 are active ingredients in desensitizing tooth pastes but neither compound reduces the permeability of dentine. The ability of various solutions to decrease hypertonic (3M NaCl) evoked nerve activity was tested in the canine teeth of anesthetized cats. Excitatory and desensitizing solutions were placed into a deep dentinal cavity prepared over the incisal pulp horn. An electrode used to record nerve activity was also placed into this deep cavity. KNO3 and other K+ ion containing solutions elicit a biphasic effect on nerve activity. Immediately following application of these solutions into the deep dentinal cavity there is a brief burst of high frequency spike activity. Following this brief period of excitation, the intradental nerves are silent and respond weakly to hypertonic NaCl. CaCl2 and other divalent cation solutions also inhibit hypertonic NaCl induced nerve activity, but have a weaker effect than that exerted by K+. These observations can be explained based on the effects of various ions on nerve excitability. Increasing the K+ ion concentration in the vicinity of the dentinal nerve terminal depolarize and activates the nerve fibers. Following a prolonged period of depolarization the action potential mechanism is inactivated. Divalent cation solutions stabilize the nerve membrane without changing the membrane potential. Desensitizing solutions do not decrease nerve activity by an effect on pulpal blood flow. This experimental model does not entirely explain the clinical action of these desensitizing agents. The role of inflammation in hypersensitivity and dental pain is currently being investigated.
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