JIAOMR 10.5005/jp-journals-10011-1108 REVIEW ARTICLE Dentin Hypersensitivity: Recent Concepts in Management Dentin Hypersensitivity: Recent Concepts in Management

1Vijay Mantri, 2Rahul Maria, 3Neeraj Alladwar, 4Savita Ghom 1Reader, Department of Conservative and Endodontics, Modern Dental College and Research Center Indore, Madhya Pradesh, India 2Professor, Department of Conservative Dentistry and Endodontics, Modern Dental College and Research Center Indore, Madhya Pradesh, India 3Professor, Department of Orthodontics, Swargiya Dadasaheb Kalmegh Smruti Dental College and Hospital Nagpur, Maharashtra, India 4Postgraduate Student, Department of Oral Medicine and Radiology, Chhattisgarh Dental College and Research Institute Rajnandgaon, Chhattisgarh, India

Correspondence: Vijay Mantri, Reader, Department of Conservative Dentistry and Endodontics, Modern Dental College and Research Center, B-307, Staff Quarters, Airport Road, Gandhi Nagar, Indore, Madhya Pradesh, India e-mail: [email protected]

ABSTRACT

Tooth sensitivity is a very common clinical presentation which can cause considerable concern for patients. Dentin hypersensitivity (DH) is characterized by short sharp pain arising from exposed dentin in response to stimuli. The most widely accepted theory of how the pain occurs is Brannstrom’s hydrodynamic theory, fluid movement within the dentinal tubules. The condition generally involves the facial surfaces of teeth near the cervical aspect and is very common in premolars and canines. This condition is frequently encountered by dentists, periodontists, hygienists and dental therapists. Some dental professionals lack confidence in treating DH. The management of this condition requires a good understanding of the complexity of the problem, as well as the variety of treatments available. This review considers the etiopathogenesis, incidence, diagnosis, prevention and management of dentinal hypersensitivity. DH is diagnosed after elimination of other possible causes of the pain. Any treatment plan for DH should include identifying and eliminating predisposing etiologic factors. Professionals should appreciate the role causative factors play in localizing and initiating hypersensitive lesions. It is important to identify these factors so that prevention can be included in the treatment plan. Treatments can be self-administered by the patient at home or be applied by a dental professional in the dental office. At-home methods tend to be simple and inexpensive and can treat simultaneously generalized DH affecting many teeth. Desensitizing treatment should be delivered systematically, beginning with prevention and at-home treatments. The latter may be supplemented with in-office modalities. Keywords: Dentinal hypersensitivity, Prevention, In-office desensitizing agents, Oxalates, Dentin bonding agents.

INTRODUCTION permutations to describe the apparently same condition 1 Dentin hypersensitivity (DH) is a relatively common, painful (Table 1). dental condition. Typically, the pain is short and sharp, and Despite the existence of these various terms, several authors occurs in response to certain stimuli applied to exposed dentin.1 prefer the term DH, commonly used and accepted for many It is clinically described as an exaggerated response decades, to describe a specific painful condition of teeth, which application of a stimulus to exposed dentin, regardless of its is distinct from others types of dentinal pain having different location.2,3 etiologies. Dentinal hypersensitivity is characterized by short sharp pain PREVALENCE AND EPIDEMIOLOGY arising from exposed dentin in response to stimuli typically thermal, evaporative, tactile, osmotic or chemical and which DH is a painful clinical condition that affects 8 to 57% of the cannot be ascribed to any other form of dental defect or pathology.4 adult population and is associated with the dentin exposure to 2,6 A modification of this definition was suggested by the the oral environment. The variations in the reports may be Canadian Advisory Board on Dentin Hypersensitivity5 in 2003, because of difference in populations and different methods of which suggested that ‘disease’ should be substituted for Table 1: Expressions in frequent usage for DH ‘pathology’. The definition provides a clinical description of the condition and identifies DH as a distinct clinical entity. • Dentin sensitivity • Dentin hypersensitivity Others terms to describe DH have been created by substituting • Dentinal hypersensitivity the word dentinal, adding site descriptors, such as cervical or • Cervical hypersensitivity/sensitivity root, and combining this with either hypersensitivity or • Root hypersensitivity/sensitivity • Cemental hypersensitivity/sensitivity sensitivity. This practice resulted in a significant number of

Journal of Indian Academy of Oral Medicine and Radiology, April-June 2011;23(2):115-119 115 Vijay Mantri et al investigations. A slightly higher incidence of DH is reported Brannstrom (1964) has proposed that dentinal pain is due in females than in males. While DH can affect the patient of to hydrodynamic mechanism, i.e. fluid force.19 Scanning any age, most affected patients are in the age group of 20 to electron microscopic (SEM) analysis of hypersensitive dentin 50 years, with a peak between 30 and 40 years of age.7 Regarding shows the presence of widely open dentinal tubules.20 The the type of teeth involved, canines and premolars of both the presence of wide tubules in hypersensitive dentin is consistent arches are the most affected teeth. Buccal aspect of cervical with the hydrodynamic theory. This theory is based on the area is the commonly affected site.8 presence and movement of fluid inside the dentinal tubules. DH is a relatively common dental clinical condition in This centrifugal fluid movement, in turn, activates the nerve permanent teeth caused by dentin exposure to the oral endings at the end of dentinal tubules or at the pulp-dentin environment as a consequence of loss of enamel and/or complex.18 As stated before, the hypersensitive dentin has more . It is manifested in a manner that is physically and widely open tubules and thin/under calcified smear layer as psychologically uncomfortable for the patient and it may be compared with non-sensitive dentin. The wider tubules increase defined as acute pain of short duration caused by the presence the fluid movement and thus the pain response.20,21 of open dentinal tubules on an exposed dentinal surface.9 The stimulus that triggers the onset of pain can be of thermal, CLINICAL MANAGEMENT OF DH chemical or mechanical origin. The most common complaint is Diagnosis caused by cold stimuli. Pain may also occur by chemical stimuli, such as acidic foods (mainly fruit), sweets and rarely with salty Like any other clinical condition, an accurate diagnosis is foods. Mechanical stimulus frequently occurs when the patient important before starting the management of DH. DH has rubs the sensitive area with a finger nail or bristles features which are similar to other conditions like caries, during brushing setting off pain. The atmospheric air during fractured or chipped enamel/dentin, pain due to reversible 8,22 mouth breathing, particularly in winter, which is associated with pulpitis, and post dental bleaching sensitivity. Diagnosis of cold, or the air of a triple syringe by dehydration also causes DH starts with a thorough clinical history and examination. The pain.10-12 other causes of dental pain should be excluded before a definite diagnosis of DH is made. Some of these techniques include PATHOGENESIS pain response upon the pressure of tapping teeth (to indicate It has been stated in the literature that DH develops in two pulpitis/periodontal involvement), pain on biting a stick phases: lesion localization and lesion initiation.13 Lesion (suggests fracture), use of transilluminating light or dyes (to localization occurs by loss of protective covering over the diagnose fractures), and pain associated with recent 4 dentin, thereby exposing it to external environment. It includes restorations. A simple clinical method of diagnosing DH loss of enamel via attrition, abrasion, erosion or abfraction. includes a jet of air or using an exploratory probe on the exposed Another cause for lesion localization is which dentin, in a mesiodistal direction, examining all the teeth in the 23 can be due to toothbrush abrasion, pocket reduction surgery, area in which the patient complains of pain. The severity or tooth preparation for crown, excessive flossing or secondary to degree of pain can be quantified either according to categorical periodontal diseases.14 As stated earlier, not all exposed dentin scale (i.e. slight, moderate or severe pain) or using a visual 13 is sensitive. For DH to occur, the lesion localization has to be analog scale. initiated. It occurs after the protective covering of smear layer Prevention of DH/Removal of Etiological Factors is removed, leading to exposure and opening of dentinal tubules. An often neglected phase of clinical management of DH is the MECHANISM identification and treatment of the causative factors of DH. By Three major mechanisms of dentinal sensitivity have been removing the etiological factors, the condition can be even proposed in the literature: prevented from occurring or recurring. The etiological factors • Direct innervation theory include faulty tooth brushing, poor , premature • Odontoblast receptor contacts, gingival recession because of periodontal therapy or • Fluid movement/hydrodynamic theory. physiological reasons, and exogenous/endogenous nonbacterial According to direct innervation theory, nerve endings acids.13 penetrate dentin and extend to the dentinoenamel junction.15 Faulty tooth brushing includes hard brushes, excessive Direct mechanical stimulation of these nerves will initiate an forces, excessive scrubbing at the cervical areas or even lack of action potential. There are many shortcomings of this theory.16 brushing which causes plaque accumulation and gingival Odontoblast receptor theory states that odontoblasts act as recession.24 The patient should be taught the correct method of receptors by themselves and relay the signal to a nerve tooth brushing with the help of a model. Highly abrasive tooth terminal.17 But majority of studies have shown that odontoblasts powder or pastes should be avoided.13 Also, the patients should are matrix forming cells and hence they are not considered to be instructed to avoid brushing for at least 2 hours after acidic be excitable cells, and no synapses have been demonstrated drinks to prevent agonist effect of acidic erosion on toothbrush between odontoblasts and nerve terminals.18 abrasion.

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Erosive agents are also important agents in initiation and – Phytocomplexes progression of DH. They tend to remove the enamel or open up - Rhubarb rhaponicum the dentinal tubules.25,26 The erosive agents can be either - Spinacia oleracea exogenous dietary acids or endogenous acids. The exogenous - Fluoride iontophoresis dietary acids include carbonated drinks, citrus fruits, wines, b. Dentin sealers yogurt and professional hazards (workers in battery – Glass ionomer cements manufacturing, wine tasters).25,26 A detailed dietary history – Composites should be taken. The quantity and frequency of the foods – Dentinal adhesives containing acids should be reduced. Patient should be advised – Resinous dentinal desensitizers to take something alkaline (milk) or at least neutral (water) after – Varnishes acidic drinks and to use a straw to sip the drink and avoid – Sealants swishing it around the teeth. The endogenous acid comes from – Methyl methacrylate gastroesophageal reflux or regurgitation. It is also common in c. Periodontal soft tissue grafting patients with eating disorders. The condition is characterized d. Lasers by generalized erosion of the palatal surfaces of maxillary e. Homeopathic medications anterior teeth.27 Such a patient should be referred to the medical – Plantago major practitioner for expert management of the underlying disease. – Propolis. An occlusal splint can be fabricated to cover the affected areas, At Home Desensitizing Therapy to prevent their contact with the acids. Traditionally, the therapy for management of DH is primarily CLASSIFICATION OF DESENSITIZING AGENTS28 aimed at occluding the dentinal tubules or making coagulates inside the tubules.13 Patients are often prescribed over-the- I. Mode of administration counter desensitizing agents. These “at home” desensitizing • At home desensitizing agents agents include toothpastes, and chewing .13 • In-office treatment Majority of the toothpastes contain potassium salts (potassium II. On the basis of mechanism of action nitrate, potassium chloride or potassium citrate), sodium • Nerve desensitization fluoride, strontium chloride, dibasic sodium citrate, a. Potassium nitrate formaldehyde, sodium monofluorophosphate and stannous • Cover or plugging dentinal tubules fluoride. Potassium salts act by diffusion along the dentinal a. Plugging dentinal tubules tubules and decreasing the excitability of the intradental nerve – Ions/salts fibers by blocking the axonic action.29,30 Along with the - Aluminium desensitizing toothpastes, mouthwashes and chewing gums - Ammonium hexafluorosilicate containing potassium nitrate, sodium fluoride or potassium - Calcium hydroxide citrate are also recommended.13 The results of “at-home” - Calcium carbonate desensitizing therapy should be reviewed after every 3 to - Calcium phosphate 4 weeks. If there is no relief in DH, “in-office” therapy should - Calcium silicate be initiated. - Sodium citrate dibasic - Fluorosilicate In-office Desensitizing Agents - Potassium oxalate Theoretically, the in-office desensitizing therapy should provide - Silicate an immediate relief from the symptoms of DH. The in-office - Sodium monofluorophosphate desensitizing agents can be classified as the materials which - Sodium fluoride undergo a setting reaction (glass ionomer cement, composites) - Sodium fluoride/Stannous fluoride and which do not undergo a setting reaction (varnishes, combination oxalates). - Stannous fluoride - Strontium acetate with fluoride Fluorides - Strontium chloride Various clinical trials have shown that application of fluoride – Protein precipitants solution can decrease the DH.31,32 Fluorides decrease the - Formaldehyde dentinal permeability by precipitation of calcium fluoride - Glutaraldehyde crystals inside the dentinal tubules.13 These crystals are partially - Silver nitrate insoluble in saliva. SEM revealed granular precipitates in the - Strontium chloride hexahydrate peritubular dentin after application of fluorides.33 Various - Zinc chloride fluoride formulations are used to treat DH. These include sodium

Journal of Indian Academy of Oral Medicine and Radiology, April-June 2011;23(2):115-119 117 Vijay Mantri et al fluoride, stannous fluoride, sodium monofluorophosphate, that lasers coagulate the proteins inside the dentinal tubules fluorosilicates and fluoride combined with iontophoresis.13 and block the movement of fluid.42 Sodium fluoride has been used in dentifrices or may be professionally applied in a concentration of 2%. Casein Phosphopeptide—Amorphous Calcium Phosphate Oxalates Recently, milk protein casein has been used to develop a Oxalates can reduce dentinal permeability and occlude dentinal remineralizing agent (GC Tooth Mousse). The casein tubules. About 30% potassium oxalate had shown a 98% phosphopeptide (CPP) contains phosphoseryl sequences which reduction in dentinal permeability.34 Also, topical application get attached and stabilized with amorphous calcium phosphate 45 of 3% potassium oxalate reduced DH after periodontal (ACP). The stabilized CPP-ACP prevents the dissolution of therapy.34 The oxalate reacts with the calcium ions of dentin calcium and phosphate ions and maintains a supersaturated 45 and forms calcium oxalate crystals inside the dentinal tubules solution of bioavailable calcium and phosphates. as well as on the dentinal surface. This results in a better sealing Management Strategy as compared with an intact smear layer.13 • Take a detailed clinical and dietary history Adhesive Materials • Differentially diagnose the condition from other dental pain conditions The adhesive resins can seal the dentinal tubules effectively by • Identify and manage etiological and predisposing factors forming a hybrid layer.13 Various clinical studies have • In case of mild-to-moderate sensitivity, advice at-home demonstrated the effectiveness of adhesives in management of desensitizing therapy DH.35-37 • If there is no relief or in case of severe sensitivity, initiate Newer bonding agents modify the smear layer and in-office treatment incorporate it into the hybrid layer.38 Recently, some dentin • In extreme cases, if patient does not respond to the therapy bonding agents have been introduced in the market with the and there are individual teeth exhibiting the symptoms, then sole purpose of treating DH. Gluma desensitizer (Heraeus endodontic therapy can be initiated Kulzer, Hanau, Germany) contains hydroxyethyl methacrylate • A regular review should be made with an emphasis on (HEMA), benzalkonium chloride, gluteraldehyde and fluoride. prevention of the condition. Gluteraldehyde causes coagulation of the proteins inside the 38 dentinal tubules. It reacts with the serum albumin in the REFERENCES dentinal fluid, causing its precipitation. HEMA forms deep resinous tags and occludes the dentinal tubules.38 Gluma has 1. Addy M. Dentin hypersensitivity: New perspectives on an old 38,39 problem. Int Dent J 2002;52:367-75. shown promising results in the clinical trials. 2. Addy M. Dentin hypersensitivity: Definition, prevalence distribution and aetiology. In: Addy M, Embery G, Edgar WM, Bioglass Orchardson R (Eds). Tooth wear and sensitivity: Clinical advances in restorative dentistry. 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