The hydrodynamic theory of dentin sensitivity states that movement of tubule contents or tubule fluid, in either direction, causes dentin sensitivity. A corollary of that theory is that anything that can decrease dentinal fluid movement or dentin permeability should decrease dentin sensitivity. The fact that many postsurgical periodontal patients exhibit spontaneous recovery from a hypersensitive state in a 1-to 2-wk period suggests that their exposed dentin becomes less permeable with time. There are a wide variety of physicochemical mechanisms that can lead to such reductions in the permeability and sensitivity of exposed dentin. These include the growth of intratubular crystals from salivary or dentinal fluid mineral, adsorption of plasma proteins to the inner surfaces of dentinal tubules, or formation of a smear layer on the exposed dentin surface. All of these procedures result in partial tubule occlusion. In the absence of such events, patients may continue to have sensitive dentin surfaces for months to years, which require therapeutic intervention. Recently, several therapeutic approaches to tubule occlusion have been developed which show promise as dentin desensitizing agents. These include application of unfilled resins to sensitive areas or the topical application of oxalate salts. The latter method produces crystals of calcium oxalate which occlude the tubules leading to immediate desensitization. Blind clinical trials should be done to evaluate the efficacy of these therapies.
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