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Year : 2016  |  Volume : 3  |  Issue : 2  |  Page : 49-50

Dental hypersensitivity: A common cold in dentistry

Department of Periodontology, Dr. DY Patil Dental College and Hospital, Dr. DY Patil Vidyapeeth, Pune, Maharashtra, India

Date of Web Publication16-Jun-2016

Correspondence Address:
Rahul Kathariya
Department of Periodontology, Dr. DY Patil Dental College and Hospital, Dr. DY Patil Vidyapeeth, Pune, Maharashtra
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2348-2915.184217

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How to cite this article:
Kathariya R. Dental hypersensitivity: A common cold in dentistry. J Dent Res Rev 2016;3:49-50

How to cite this URL:
Kathariya R. Dental hypersensitivity: A common cold in dentistry. J Dent Res Rev [serial online] 2016 [cited 2023 Mar 27];3:49-50. Available from: https://www.jdrr.org/text.asp?2016/3/2/49/184217

Dental hypersensitivity (DH) is defined as, sharp pain arising from the exposed dentin typically in response to chemical, thermal, evaporate, tactile, or osmotic stimuli that cannot be ascribed to any other form of dental defect or disease.[1] It has been described as, “common disease of dentistry” by some authors [2] and “tooth brush disease” by others.[3] The primary cause that has been claimed is that the condition is dependent on dentin exposure to the oral environment and the patency of dentinal tubules. Greater the number of widened open dentinal tubules, greater is the sensitivity. Physiologically, a person may have a gap joint (5–10%), butt joint (30–35%), and an overlap joint (60–65%) at the cemento-enamel junction. These “butt” and “overlap” joints can easily be disjoined and can be turned into a “gap” joint by enamel loss due to attritions, abrasions, abfraction, parafunctional habits, faulty or overzealous tooth brushing, etc., leading to exposed dentinal surface and DH.[4] DH can also occur as a consequence of periodontitis, and there are iatrogenic causes such as root planing and periodontal surgical procedures.[4],[5]

Various theories have been postulated to decipher the underlying mechanism of DH such as odontoblastic transduction theory,[6] neural theory,[7] gate control theory,[8] modulation theory,[8] and hydrodynamic theory.[9] The hydrodynamic theory, given by Gysi in 1900 and later scientifically explained by Brännström and Aström [9] in 1966, is the most accepted one. It is based on the concept that fluid within the dentinal tubule can flow inward or outward, depending on pressure differences in the surrounding tissue. This fluid flow within the tubules serves as a medium to excite intradental nerves, which is perceived as pain by the patient.[9]

DH can be evaluated by subjective (patient response) or objective (tests) assessment;[10] subjective assessments include verbal rating scale, visual analog scale, McGill pain questionnaire, and verbal descriptor checklist. Tests includes mechanical (tactile), chemical (osmotic), thermal stimuli (using probe, mild-acids, or heated ball burnisher, respectively), cold air blast, cold water testing, thermo-electric devices, and electric stimuli.[10]

Classifying treatments for DH can be challenging because its modes of actions are often unknown and overlapping. It can be simpler to classify treatment modalities according to their mode of delivery. Treatments can be self-administered by the patient at home or can be applied by a dental professional in the dental office. Different ingredients that can be used for DH can also be classified as follows.

  1. Nerve desensitization: Potassium nitrate
  2. Covering or plugging dentinal tubules:

  1. Plugging dentinal tubules:

    1. Ions/salts

      • Aluminum
      • Ammonium hexafluorosilicate
      • Calcium (hydroxide, carbonate, phosphate, and silicate)
      • Dibasic sodium citrate
      • Fluorosilicate
      • Potassium oxalate
      • Silicate
      • Sodium (monofluorophosphate and fluoride)
      • Stannous fluoride
      • Sodium fluoride and stannous fluoride combination
      • Strontium acetate with fluoride
      • Strontium chloride.

    2. Protein precipitants

      • Formaldehyde
      • Gluteraldehyde
      • Silver nitrate
      • Strontium chloride hexahydrate
      • Zinc chloride.

      • Phytocomplexes
      • Rhubarb rhaponicum
      • Spinacia oleracea.

    3. Fluoride iontophoresis.

  2. Dentine sealers

    • Glass ionomer cement
    • Composites
    • Dental adhesives
    • Resionous dentinal desensitizers
    • Varnishes
    • Sealants
    • Methyl methacrylate.

  3. Periodontal soft tissue grafting
  4. Lasers:

    • Low output power: Helium-Neon, Gallium/Aluminum/Arsenide
    • Medium output power: Nd: YAG, CO2

  5. Homeopathic medication

    • Plantago major
    • Propolis.

In India, in 2013, the overall oral-care product markets were estimated at a whopping 900 million USD,[11] and it is estimated to expand at an average annual pace of 9–10% for the next 3 years and will be worth about 1.4 billion USD by 2016.[12] The DH market is pegged at nearly 100 million USD annually.[11] The nascent market for these niche products is worth about 300 million USD,[11] and it is growing at a pace of about 25% annually,[12] with every two in five Indians suffering from DH.[11] The sensitivity segment has quadrupled in the past 2 years,[11] thanks to the aggressive marketing efforts both by GSK and Colgate, which have captured more than 50% market share.

Calling it the “common cold in dentistry” is apt as occurs easily, is caused by various etiological factors (explained above), and subsides within a few days. Multiple treatment modalities are available and appear as viable options, as are most over-the-counter (OTC) medications. The long-term effectiveness of these treatment options is a relatively unexplored territory as most of them provide clinical success in managing dentin hypersensitivity temporarily. Few systematic reviews and meta-analyses have tried to decipher the superiority of one treatment over another. Most of these conclude with short-term definitive benefits over placebo.[13],[14],[15],[16] Systematic reviews on the effectiveness of lasers are conflicting and remain unclear.[17],[18],[19]

There is no evidence of a single gold standard treatment. The entire body of clinical data is far from being unequivocal in pronouncing a single superior treatment strategy. Market sales and superiority of these products is a play of aggressive branding and promotion of their products, not because they are the best. Long-term clinical data are warranted on the efficacy of these hundreds of treatment options to claim one as being superior to another. Considering the number of options available, it is unlikely to simultaneously compare all of them.

It is advisable for the patients to start using any available and affordable topical OTC medication, before going for extensive treatment modalities such as restorative procedures or iontophoresis, periodontal surgeries, or lasers.

  References Top

von Troil B, Needleman I, Sanz M. A systematic review of the prevalence of root sensitivity following periodontal therapy. J Clin Periodontol 2002;29 Suppl 3:173-7.  Back to cited text no. 1
Strassler HE, Drisko CL, Alexander DC. Dentin hypersensitivity: Its inter-relationship to gingival recession and acid erosion. Compend Contin Educ Dent 2008;29:1-9.  Back to cited text no. 2
Bamise CT, Olusile AO, Oginni AO. An analysis of the etiological and predisposing factors related to dentin hypersensitivity. J Contemp Dent Pract 2008;9:52-9.  Back to cited text no. 3
Dababneh RH, Khouri AT, Addy M. Dentine hypersensitivity – An enigma? A review of terminology, mechanisms, aetiology and management. Br Dent J 1999;187:606-11.  Back to cited text no. 4
Miglani S, Aggarwal V, Ahuja B. Dentin hypersensitivity: Recent trends in management. J Conserv Dent 2010;13:218-24.  Back to cited text no. 5
[PUBMED]  Medknow Journal  
Bernick S. Innervations of the human tooth. Anat Res 1948;101:293-7.  Back to cited text no. 6
Bartold PM. Dentinal hypersensitivity: A review. Aust Dent J 2006;51:212-8.  Back to cited text no. 7
Selitzer S, Bender IB. The nerve supply of the pulp and pain perception. The dental pulp. Philadelphia: JB Lippincott Co.; 1975. p. 131-51.  Back to cited text no. 8
Brännström M, Aström A. The hydrodynamics of the dentine; its possible relationship to dentinal pain. Int Dent J 1972;22:219-27.  Back to cited text no. 9
Gillam DG, Newman HN. Assessment of pain in cervical dentinal sensitivity studies. A review. J Clin Periodontol 1993;20:383-94.  Back to cited text no. 10
Lin PY, Cheng YW, Chu CY, Chien KL, Lin CP, Tu YK. In-office treatment for dentin hypersensitivity: A systematic review and network meta-analysis. J Clin Periodontol 2013;40:53-64.  Back to cited text no. 13
da Rosa WL, Lund RG, Piva E, da Silva AF. The effectiveness of current dentin desensitizing agents used to treat dental hypersensitivity: A systematic review. Quintessence Int 2013;44:535-46.  Back to cited text no. 14
Shiau HJ. Dentin hypersensitivity. J Evid Based Dent Pract 2012;12 3 Suppl: 220-8.  Back to cited text no. 15
Orchardson R, Gillam DG. Managing dentin hypersensitivity. J Am Dent Assoc 2006;137:990-8.  Back to cited text no. 16
Jokstad A. The effectiveness of lasers to reduce dentinal hypersensitivity remains unclear. J Evid Based Dent Pract 2012;12 3 Suppl: 231-2.  Back to cited text no. 17
Blatz MB. Laser therapy may be better than topical desensitizing agents for treating dentin hypersensitivity. J Evid Based Dent Pract 2012;12 3 Suppl: 229-30.  Back to cited text no. 18
Sgolastra F, Petrucci A, Gatto R, Monaco A. Effectiveness of laser in dentinal hypersensitivity treatment: A systematic review. J Endod 2011;37:297-303.  Back to cited text no. 19

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