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Journal of Oral Science & Rehabilitation No. 2, 2017

O z o n e t r e a t m e n t f o r d e n t i n a l h y p e r s e n s i t i v i t y Introduction Dentinal hypersensitivity is defined as a “sensa- tion of pain that appears in response to chemical, thermal, tactile or osmotic stimuli in contact with exposed dentin, which cannot be related with other alterations or dental pathologies.”1 Although dentinal hypersensitivity is a widespread condi- tion, therapeutic strategies available today are not always effective or satisfactory.2 Today, there are three prevailing theories regarding the etiopathogenesis of dentinal hypersensitivity: 1. The direct innervation theory assumes that a direct stimulation of the nerve endings occurs in response to external events that excite the processes of the odontoblastic body.3 This theory is not sufficiently supported: Few tests support the existence of nerve endings in the dentin surface, precisely where the dentin is more sensitive; moreover, the plexus of Raschkow does not become mature until com- plete eruption of the tooth. 2. The odontoblast receptor theory supposes, consequent to painful stresses, the release of neurotransmitter substances by odontoblasts is responsible for a reaction of the nerve end- ings present in the dentin that stimulates the pulp response. This theory assumes the ability of the odontoblasts to behave as nerve recep- tors and transmit signals to the nerves of the pulp. This theory has been discredited because the cellular matrix of the odontoblasts cannot be stimulated and produce nerve impulses; moreover, there are no synapses between the odontoblasts and nerves of the pulp.4 3. The hydrodynamic theory, proposed by Martin Brännström, is the most widely recognized and accredited for the pathophysiology of dentinal hypersensitivity.5 This theory claims that den- tinal hypersensitivity is the result of fluid move- ment within the tubules caused by thermal and physical changes or the presence of osmotic stimuli at the level of the exposed dentin. The fluid movement stimulates the baroreceptors and causes the nervous discharge. From a clinical point of view, dentinal hypersen- sitivity is caused by: – gingival recession; – abrasion; – erosion; – abfraction; – hypoplasia or abnormalities of enamel devel- opment. Moreover, dentinal hypersensitivity may also have an iatrogenic origin: in conservative treat- ments, when dentin is exposed to an etching acid for too long or as a result of periodontal surgery (mucogingival, resective or regenerative).1 T h e r a p y a n d c l a s s i f i c a t i o n o f d e s e n s i t i z i n g a g e n t s The desensitizing agents currently on the market essentially have two modes of action: 1. occlusion of the dentinal tubules, with conse- quent permeability reduction; 2. reduction of the dentinal nerve fiber activity and therefore of the transmission of the pain stimulus to nerve centers. Professional treatments include application of paints, varnishes, resins and bonding agents to occlude the dentinal tubules. The materials most frequently used are fluoride, potassium nitrate, potassium oxalate and calcium phosphate, and these generate endodontic crystallizations with consequent reduction of the movement of fluid in the tubules.6 We report a complete list of all compounds, which could be used for desensitization: 1. Composite resins, glass ionomer cements, glass ionomer modified-resins and com- pomers: applied on the dentin-exposed sur- face, these ensure the occlusion of the tu- bules.3 2. Resin-based products with hydrophilic char- acteristics that contain hydroxyethyl meth- acrylate (HEMA), ammonium chloride, fluo- ride and glutaraldehyde: the last, used in different desensitizers, causes coagulation of the plasma and closing proteins in tubules, thus inhibiting the movement of dentinal fluid outward. The HEMA penetrates into the tu- bules and, after polymerization, occludes them, reducing permeability. 3. Portland cements based on silicate calcium, tricalcium silicate, tricalcium aluminate and tetra-calcium aluminoferrite: these have shown efficacy in reducing dentin permeabil- ity owing to the ability to produce hydroxy- apatite in contact with body fluids containing phosphate. 4. Sealants: They contain microfillers, which occlude the tubules and create a barrier effect in the tooth. 5. Paints: These are generally based on synthet- ic resins, contain calcium fluoride and sodium fluoride, and exert a remineralizing, protective Journal of Oral Science & Rehabilitation Volume 3 | Issue 2/2017 17

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