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Home , Attrition (dental), Chlorhexidine, Dentin hypersensitivity, Gums

Received : 08‑04‑15 Review completed : 14‑05‑15 Review Article Accepted : 23‑05‑15

DENTIN HYPERSENSITIVITY AND ITS MANAGEMENT: A REVIEW

Tusharluthra, * Sandeep Gupta, ** Sudhanshu Bharadwaj, *** Ashish Choubey, † Hitendra Yadav, †† Harimran Singh †††

* Assistant Professor, Department of Orthodontics, Rama Dental College, Kanpur, Uttar Pradesh, India ** Reader, Department of Conservative , Maharana Pratap College of Dentistry, Gwalior, Madhya Pradesh, India *** Post Graduate Student, Department of Conservative Dentistry, Maharana Pratap College of Dentistry, Gwalior, Madhya Pradesh, India † Post Graduate Student, Department of Conservative Dentistry, Maharana Pratap College of Dentistry, Gwalior, Madhya Pradesh, India †† Post Graduate Student, Department of Pedodontics & Preventive Dentistry, Maharana Pratap College of Dentistry, Gwalior, Madhya Pradesh, India ††† Post Graduate Student, Department of Oral and Maxillofacial , Vyas Dental College and Hospital, Jodhpur, Rajasthan, India ______ABSTRACT It has been stated in the literature that Dentinal Dentinal hypersensitivity is a very common hypersensitivity develops in two phases: clinical condition of the teeth, which is  Lesion localization characterized by short sharp pain arising from  Lesion initiation exposed in response to stimuli, there Lesion localization are number of theories of which Brannstrom It occurs by loss of protective covering over the hydrodynamic theory is most widely accepted. dentin which leads to exposing it to external The condition generally involves the facial enviornment. It include loss of enamel via- surfaces of the teeth near the cervical aspect & , , erosion. Another cause of is very common in & canines. lesion localization is which can KEYWORDS: Dentinal hypersensitivity; be due to brush abrasion, pocket reduction etiology; desensitizing agent; management surgery, tooth preparation for , excessive flossing or secondary to periodontal diseases.[4] INTRODUCTION Lesion initiation Dentinal hypersensitivity is defined as an It occurs after the protective covering of smear exaggerated response to a stimulus that usually layer is removed leading to exposure & opening [4] causes no response in a healthy tooth & also an of dentinal tubule. exaggerated response to a non harmful stimulus. Mechanism The non harmful stimuli are the thermal, tactile or The intradentinal nerve are confined to the pre osmotic stimuli that when applied on the exposed dentin & the most pulpal part of dentin. This dentin, evoke pain without causing pathologic support the likelihood of an indirect stimulatory alteration to the dentin-pulpo complex. A mechanism evoking pain several theories have modification of this definition is suggested by the been put forward to explain the mechanism of [5,6] Canadian advisory board on Dentinal dentinal hypersensitivity. They are- hypersensitivity in 2003 which suggested that 1. Transduction theory: It states that disease should be substituted for pathology. The act as a receptors by themselves & rely signal definition provides the clinical description of the to a nerve terminal, but majority of studies condition & identifies Dentinal hypersensitivity have concluded that odontoblsts are matrix as a distinct clinical identity.[1,2,3] forming cells & hence they are not considered Epidemiology to be excitable cells. About 8 to 30% of the population present 2. Modulation theory: According to this theory Dentinal hypersensitivity & the most affected age the nerve impulses in the are modulated is 20-40 yrs. The first are the most through the liberation of polypeptide from the affected teeth reaching more than half of the teeth odontoblast when injured. These substance ay & the most affected region is the cervical area of selectively alter the permeability of the buccal surface.[2] odontoblastic cell membrane through Pathogenesis hyperpolarization. So that pulp neurons are

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more prone to discharge upon receipt of  subsequent stimuli.  Silicate 3. Hydrodynamic theory: According to  Sodium Monofluorophosphate Brannstrom hydrodynamic theory when an  appropriate stimulus is applied to the outer  Sodium fluoride/stannous fluoride dentin surface there is displacement of the combination fluid of dentinal tubule that give rise to the  stannous fluoride mechanical stimulation of the pain at the  strontium acetate with fluoride pulpodentinal border.  strontium chloride Diagnosis  Protein precipitants Diagnosis of dentinal hypersensitivity starts with  formaldehyde a thorough clinical history & examination. A  simple clinical method of diagnosing dentinal  silvernitrate hypersensitivity includes the jet of air or using an  strontium chloride hexahydrate exploratory probe on the exposed dentin, in a  chloride mesiodistal direction,by examining all the teeth.  Phytocomplexes The severity or degree of pain can be quantified  Rhubarb Rhaponicum either according to categorical scale or using a  Spinacia oleracea [7-11] visual analog scale.  Fluoride iontophoresis Principles of Management strategy (B) DentinSealers Some of the strategy which could be helpful for  Glass ionomer cements the management of dentinal hypersensitivity are  Composites as follows:  Dentinal adhesives  Removal of etiological & pre-disposing  Resinous dentinal desensitizers factors  Varnishes  Patient with mild to moderate hypersensitivity  Sealants should be adviced at home desensitizing  Methyl Methacrylate therapy (C)Periodontal soft tissue grafting  Patient with severe hypersensitivity treatment (D) Lasers should be initiated in office (E) Hoemeopathic medications  Prevention measure should be given  Plantago major importance & patient should be followed up  Proplis regularly At home Desensitizing Agent Classification of desensitizing agent [9,10,12,13] The advantage of this mode is that it is simple and 1. Mode of administration can be used in number of teeth. The disadvantage  At home desensitizing agents is that about 2-4 week of tie symptom may  In office treatment reoccur. Some of the desensitizing agents that can 2. On the bases of mechanism of action be used at hoe are tooth paste, wash,  Nerve desensitization e.g., potassium ,containing potassium nitrate, nitrate sodium fluoride or can be  Cover or plugging dentinal tubule recommended.[1,5,7,9,14]  /salts In office treatment  Aluminium  Theoretically, the in office desensitizing  Ammonium hexafluorosilicate therapy should provide in immediate relief.  Calcium hydroxide The agent used for office treatment can be  Calcium phosphate classified as:  Calcium carbonate a) The material that don’t undergo a setting  Calcium silicate reaction eg- oxalate, varnishes  Sodium citrate dibasic b) The material that undergo a setting  Fluorosilicate reaction eg . composite

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c) Lasers can also be used to manage Formaldehyde or glutaraldehyde dentinal hypersenstivty. These precipitate the salivary proteins in dentinal Potassium nitrate tubules & can be useful in the management of It has been reported that the potassium salts move dentinal hypersensitivity. These agents should be along the dentinal tubules & decrease the used with extreme caution,as they are strong excitability of the tooth by blocking the axonic tissue fixatives. action of the intra-dental nerve fibers. The agents Adhesive material reduce the excitability of nerves that transmit The adhesive resins can seal the dentinal tubules pain. which contain 5% potassium effectively by forming the hybrid layer. Various nitrate along with other ingredient have been studies have demonstrated the effectiveness of reported to be effective in reducing dentine resin in management of dentinal hypersensitivity. hypersensitivity. Newer bonding agent modify smear layer and Calcium hydroxide incorporate it into hybrid layer, recently some Calcium hydroxide is effective in managing bonding agent have been introduced in the market dentinal hypersensitivity. It acts by of with the sole purpose of treating dentinal dentinal tubules through the binding of loose hypersensitivity. Like gluma desensitizer.[3,5,8,11] protein radicals by calcium ions & additionally Varnishes increases the mineralization of the exposed They help other materials to increase their dentine. therapeutic effect. Fluoride varnishes combine Fluorides with acid to increase its effectiveness. Slow & The desensitizing effects of fluoride are probably continuous release of fluoride occurs with related to precipitated fluoride compounds which . Calcium fluoride gets deposited mechanically block the dentinal tubules or on the tooth surface, resulting in the formation of fluoride within the tubules which mechanically fluorapatite. Copal is used to cover exposed block the tansmission of stimuli. The dentine. -containing varnish forms a improvement with fluoride appears to be due to mechanical barrier after drying. This reduces an increase in the resistance of dentine to acid sensitivity, & provides an antibacterial & decalcification as well as due to precipitations in antiplaque action.[6,9] the exposed dentinal tubules. Restorative materials Composite resins & glass ionomer restorations Oxalate produce desensitizing by deposition of are commonly used restorative materials. The calcium oxalate crystals on the surface of dentine restorations can seal the open dentinal tubules as .It reacts with calcium of dentine & leads to well as restore the tooth to full contour.[2,7,10] deposition of calcium oxalate crystals on the Bioglass surface of dentine & / or inside its tubules. The It has been reported that the formulation of surface of the tooth can be etched to increase the bioglass can promote infiltration and effectiveness of oxalate. remineralization of dentinal tubules. The basic Strontium-containing dentifrices component is silica, which act as a nucleation site The strontium salts like acetate or chloride, for precipitation of calcium and phosphate. Some penetrate the tubules & occlude them. This products have been reported such as reduces the sensitivity by preventing the fluid novamin.[3,5,9] movement. Portland cement Calcium sodium phosphosilicate Some authors have shown that calcium derived Laboratory studies have shown amorphous from Portland cement can help in the sodium calcium sodium phosphosilicate, to management of dentinal hypersensitivity. It helps occlude dentin tubules through the deposition of to occlude the dentinal tubules by particles which react to form a protective layer, remineralization.[5,7,10] on the dentin surface. Calcium sodium phosphosilicate containing Several soft tissue grafting procedures like lateral toothpastes have been shown to significantly sliding grafts ,free gingival grafts, connective reduce dentin hypersensitivity. tissue grafts & coronally repositioned flaps can be

IJOCR July - Sep 2015; Volume 3 Issue 3 61 Dentin hypersensitivity & management Tusharluthra, Gupta S, Bharadwaj S, Choubey A, Yadav H, Singh H carried out to cover exposed root surfaces. These dentistry. London: Martin Dunitz 2000:239- procedures may cover exposed dentinal tubules, 48. but are not very predictable in terms of efficacy to 3. Addy M. Etiology and clinical implications cover root surface.[10,12] of dentin hypersensitivity. Dent Clin North Laser Amer 1990;34:503-14. It has been shown in various studies that lasers 4. Dowell P, Addy M. Dentin Hypersensitivity: can be used in the effective management of A review: Aetiology, symptoms and theories dentinal hypersensitivity some authors have of pain production. J Clin Periodontol shown that Nd-YAG laser application occluded 1983;10:341-50. the dentinal tubules. GaA1A laser is thought to 5. Canadian Advisory Board on Dentin act by affecting the neural transmission in the Hypersensitivity. Consensus-based dentinal tubules. It has also been proposed that recommendations for the diagnosis and laser coagulate the protein inside the dentinal management of dentin hypersensitivity. J tubules and block the movement of fluid.[12,13] Can Dent Assoc 2003;69:221-26. Casein phosphopeptide –amrphous calcium 6. Markowitz K, Pashley DH. Personal phosphate reflections on a sensitive subject. Journal of Recently milk protein casein has been used to Dent Res 2007;86(4):292-95. develop a remineralizing agent (gc tooth 7. Flynn J, Galloway R, Orchardson R. The mousse).the casein phosphopeptide contains incidence of hypersensitive teeth in the west phosphoseryl sequences which get attached and of Scotland. J Dent 1985;13:230-36. stabilized with amorphous calcium 8. Addy M, Mostafa P, Newcombe RG. Dentin phosphate.[14,15] hypersensitivity: The distribution of CONCLUSION recession, sensitivity and plaque. J Dent Dentinal hypersensitivity is a relatively common 1987;15:242-48. and significant dental problem which can be 9. Rees JS, Jin U, Lam S, Kudanowska I, successfully managed by a very wide variety of Vowles R. The prevalence of dentin procedures, agents and formulations applied hypersensitivity in a hospital clinic locally either “in office” or“at home”. It is clear population in Hong Kong. J that some products appear to be more effective Dent 2003;31:453-61. than others. For those products developed for self 10. Gillam DG, Seo HS, Newman HN, Bulman application at home, potassium nitrate, stannous JS. Comparison of dentin hypersensitivity in fluoride, sodium fluoride, sodium selected occidental and oriental populations. monofluorophosphate and strontium chloride J Oral Rehabil 2001;28:20-5. have all been extensively studied and shown to be 11. Clayton DR, McCarthy D, Gillam DG. A not only safe to use but of benefit to individuals study of the prevalence and distribution of suffering fro dentinal hypersensitivity. dentin sensitivity in a population of 17 to CONFLICT OF INTEREST & SOURCE OF 58-year-old serving on an RAF base in the FUNDING Midlands. J Oral Rehabil 2002;29:14-23. The author declares that there is no source of 12. Chidchuangchai W, Vongsavan N, funding and there is no conflict of interest among Matthews B. Sensory transduction all authors. mechanisms responsible for pain caused by BIBLIOGRAPHY cold stimulation of dentin in man. Arch Oral 1. Addy M. Dentin hypersensitivity: New Biol 2007;52:154-60. perspectives on an old problem. Int Dent J 13. Orchardson R, Gilliam D. Managing dentin 2002;52:367-75. hypersensitivity. J Am Dent Assoc 2. Addy M. Dentin hypersensitivity: 2006;137:990-98. Definition, prevalence distribution and 14. Dababneh R, Khouri A, Addy M. Dentin aetiology. In: Addy M, Embery G, Edgar hypersensitivity: An enigma. A review of WM, Orchardson R (Eds). and terminology, epidemiology, mechanisms, sensitivity: Clinical advances in restorative aetiology and management. Br Dent J 1999;187:606-11.

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15. Irvine JH. Root surface sensitivity: A review of aetiology and management. JNZ Soc Periodontol 1988;66:15-18.

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