Dentine is covered and protected by hard tissues such as enamel or cementum. Dentin itself is a vital tissue, consisting of dentinal tubules, and is naturally sensitive because of extensions of odontoblasts and formation of dentine–pulp complex.[¹⁶] Although dentin and pulp are histologically different, their origin is embryologically from the same precursor, i.e., the ectomesenchyme.[¹⁶] Pulp is integrally connected to dentine, i.e., physiologic and/or pathologic reactions in one of the tissues will also affect the other. Dentin consists of small canal like spaces, dentinal tubules. These tubules occupied by odontoblastic processes.[¹⁶] The odontoblastic processes may extend through the entire thickness of dentin from pulp to dentino-enamel junction. The odontoblastic processes are actually the extensions of odontoblasts, which are the major cells of pulp–dentin complex.[¹⁶] The odontoblastic processes are surrounded by dentinal fluid inside the tubules. The dentinal fluid forms around 22% of total volume of dentin.[¹⁶] It is an ultrafiltrate of blood from the pulp via dentinal tubules and forms a communication medium between the pulp (via the odontoblastic layer) and outer regions of the dentin.

It has been stated in the literature that DH develops in two phases: lesion localization and lesion initiation.[¹⁷] Lesion localization occurs by loss of protective covering over the dentin, thereby exposing it to external environment. It includes loss of enamel via attrition, abrasion, erosion or abfraction. Another cause for lesion localization is gingival recession which can be due to toothbrush abrasion, pocket reduction surgery, tooth preparation for crown, excessive flossing or secondary to periodontal diseases.[¹⁸] As stated earlier, not all exposed dentine is sensitive. For DH to occur, the lesion localization has to be initiated. It occurs after the protective covering of smear layer is removed, leading to exposure and opening of dentinal tubules.

As like any other clinical condition, an accurate diagnosis is important before starting the management of DH. DH has features which are similar to other conditions like caries, fractured or chipped enamel/dentine, pain due to reversible pulpitis, and post dental bleaching sensitivity.[^{15, 24}] Diagnosis of DH starts with a thorough clinical history and examination. The other causes of dental pain should be excluded before a definite diagnosis of DH is made. Some of these techniques include pain response upon the pressure of tapping teeth (to indicate pulpitis/periodontal involvement), pain on biting a stick (suggests fracture), use of transilluminating light or dyes (to diagnose fractures), and pain associated with recent restorations.[²⁵] A simple clinical method of diagnosing DH includes a jet of air or using an exploratory probe on the exposed dentin, in a mesio-distal direction, examining all the teeth in the area in which the patient complains of pain.[²⁶] The severity or degree of pain can be quantified either according to categorical scale (i.e., slight, moderate or severe pain) or using a visual analogue scale.[¹⁷]

An often, neglected phase of clinical management of DH is the identification and treatment of the causative factors of DH. By removing the etiological factors, the condition can be even prevented from occurring or recurring. The etiological factors include faulty tooth brushing, poor oral hygiene [Figure 1], premature contacts, gingival recession because of periodontal therapy or physiological reasons, and exogenous/endogenous non-bacterial acids.[¹⁷]

Faulty tooth brushing includes hard brushes, excessive forces, excessive scrubbing at the cervical areas or even lack of brushing which causes plaque accumulation and gingival recession [Figures 2 and 3].[²⁷] The patient should be taught the correct method of tooth brushing with the help of a model. Highly abrasive tooth powder or pastes should be avoided.[¹⁷] Also, the patients should be instructed to avoid brushing for at least 2 hours after acidic drinks to prevent agonist effect of acidic erosion on tooth brush abrasion.

Erosive agents are also important agents in initiation and progression of DH [Figure 4]. They tend to remove the enamel or open up the dentinal tubules.[^{28, 29}] The erosive agents can be either exogenous dietary acids or endogenous acids. The exogenous dietary acids include carbonated drinks, citrus fruits, wines, yogurt, and professional hazards (workers in battery manufacturing, wine tasters).[^{28, 29}] A detailed dietary history should be taken. The quantity and frequency of the foods containing acids should be reduced. Patient should be advised to take something alkaline (milk) or at least neutral (water) after acidic drinks and to use a straw to sip the drink and avoid swishing it around the teeth. The endogenous acid comes from gastroesophageal reflux or regurgitation. It is also common in patients with eating disorders. The condition is characterized by generalized erosion of the palatal surfaces of maxillary anterior teeth.[³⁰] Such a patient should be referred to the medical practitioner for expert management of the underlying disease. An occlusal splint can be fabricated to cover the affected areas, to prevent their contact with the acids.

Grossman[³¹] listed the requirements for an ideal dentine desensitizing agent as: rapidly acting with long-term effects, non-irritant to pulp, painless and easy to apply, and should not stain the tooth. Traditionally, the therapy for management of DH is primarily aimed at occluding the dentinal tubules or making coagulates inside the tubules.[¹⁷] Patients are often prescribed over-the-counter desensitizing agents. These “at home” desensitizing agents include toothpastes, mouthwashes and chewing gums.[¹⁷] Majority of the toothpastes contain potassium salts (potassium nitrate, potassium chloride or potassium citrate), sodium fluoride, strontium chloride, dibasic sodium citrate, formaldehyde, sodium monofluorphosphate and stannous fluoride. Potassium salts act by diffusion along the dentinal tubules and decreasing the excitability of the intradental nerve fibers by blocking the axonic action.[^{32, 33}] Various clinical studies have shown the efficacy of potassium salts in controlling the DH.[^{34, 35}] It has been shown that toothpastes containing 5% potassium nitrate and 0.454% stannous significantly reduced the DH. Also, toothpastes containing potassium nitrate and fluorides have been shown to reduce post-bleaching sensitivity.[^{36, 37}] The desensitizing toothpastes should be used with the help of a toothbrush with soft bristles. Patients should be advised to use minimal amount of water to prevent the dilution of the active agent. Along with the desensitizing toothpastes, mouthwashes and chewing gums containing potassium nitrate, sodium fluoride or potassium citrate are also recommended.[¹⁷] The results of “at-home” desensitizing therapy should be reviewed after every 3–4 weeks. If there is no relief in DH, “in-office” therapy should be initiated.

Theoretically, the in-office desensitizing therapy should provide an immediate relief from the symptoms of DH. The in-office desensitizing agents can be classified as the materials which undergo a setting reaction (glass ionomer cement, composites) and which do not undergo a setting reaction (varnishes, oxalates).

Traditionally, fluorides have been used as a caries preventive material which can help in remineralization of enamel/dentin.[³⁸] Also, various clinical trials have shown that application of fluoride solution can decrease the DH.[^{39, 40}] Fluorides decrease the dentinal permeability by precipitation of calcium fluoride crystals inside the dentinal tubules.[¹⁷] These crystals are partially insoluble in saliva. SEM revealed granular precipitates in the peritubular dentin after application of fluorides.[⁴¹] Various fluoride formulations are used to treat DH. These include sodium fluoride, stannous fluoride, sodium monofluorophosphate, fluorosilicates and fluoride combined with iontophoresis.[¹⁷] Sodium fluoride has been used in dentifrices or may be professional applied in a concentration of 2%. The precipitates formed by sodium fluoride can be mechanically removed by the action of saliva or mechanical action. Therefore, an addition of acid formulation is recommended. The acidulated sodium fluoride can form precipitates deep inside the tubules. Also, some authors have recommended the use of ionotophoresis along with sodium fluoride.[^{41, 42}] The electric current is supposed to increase the ion diffusion. A clinical study has shown that 0.4% stannous fluoride along with 0.717% of fluoride can provide an immediate affect after a 5 minute professional application.[⁴³] Stannous fluoride acts in a similar fashion as that of sodium fluoride, i.e., formation of calcium fluoride precipitates inside tubules. Also, SEM studies have shown that stannous fluoride itself can form insoluble precipitates over the exposed dentine.[⁴⁴] Fluorosilicates act by formation of precipitates of calcium phosphates from saliva. Ammonium hexafluorosilicate has been used as a desensitizing agent. It can present a continuous effect of dentinal tubule occlusion via precipitation of a mixture of calcium fluoride and fluoridated apatite.[^{45, 46}] If the precipitate is predominantly composed of fluoridated apatite, it can form stable crystals deposited deep inside the dentinal tubules.[^{45, 46}] These crystals are resistant to removal from the action of saliva, brushing or action of dietary substances.

Oxalates can reduce dentinal permeability and occlude dentinal tubules. Thirty percent potassium oxalate had shown a 98% reduction in dentinal permeability.[⁴⁷] Also, topical application of 3% potassium oxalate reduced DH after periodontal therapy.[⁴⁷] The oxalate reacts with the calcium ions of dentine and forms calcium oxalate crystals inside the dentinal tubules as well as on the dentinal surface. This results in a better sealing as compared with an intact smear layer.[¹⁷] It has been shown that the effect of oxalates on DH diminishes over a period of time. This can be attributed to the removal of the calcium oxalate crystals by brushing or dietary acids. The condition can be improved by acid etching of the dentinal surface, thus increasing the penetration of calcium oxalate crystals deep into the dentinal tubules.[⁴⁸] Many vegetables like rhubarb, spinach and mint contain oxalates. It has been shown that phytocomplexes obtained from these natural products can reduce the dentinal permeability. This can also be followed by covering the exposed surface with a dental adhesive.[⁴⁹] Potassium oxalate can lead to gastric irritation. Therefore, it should not be used with a tray with prolonged placement.

Varnishes are commonly used useful in-office measures to treat DH. Copal varnish can be applied to cover the exposed dentinal surface. But its effect is for short term and is not recommended for long term management of DH.[⁵⁰] To improve its efficacy, removal of smear layer is advocated. Also, the varnishes can act as a vehicle for fluoride. The fluoride varnishes can be acidulated to increase the penetration of ions.[⁵⁰]

Resin-based dental adhesive systems can provide a more durable and long lasting dentine desensitizing effect. The adhesive resins can seal the dentinal tubules effectively by forming a hybrid layer.[¹⁷] Various clinical studies have demonstrated the effectiveness of adhesives in management of DH.[⁵¹–⁵³] Traditionally, resin composites or dentin bonding agents are used as desensitizing agents. The conventional dentin bonding agents (DBA) removes the smear layer, etches the dentinal surface and forms deep dentinal resin tags inside the dentinal tubules. The combined dentin–resin layer (consisting of penetrating resinous tags) has been termed as hybrid layer. It effectively seals the dentinal tubules and prevents DH.[⁵¹–⁵³] Newer bonding agents modify the smear layer and incorporate it in into the hybrid layer.[⁵⁴] Recently, some dentin bonding agents have been introduced in the market with the sole purpose of treating DH. Gluma Desensitizer (Heraeus Kulzer, Hanau, Germany) contains hydroxyethyl methacrylate (HEMA), benzalkonium chloride, gluteraldehyde and fluoride. Gluteraldehyde causes coagulation of the proteins inside the dentinal tubules.[⁵⁴] It reacts with the serum albumin in the dentinal fluid, causing its precipitation. HEMA forms deep resinous tags and occludes the dentinal tubules.[⁵⁴] Gluma has shown promising results in the clinical trials.[^{54, 55}]

Bioglass was developed to stimulate the formation of new bone.[⁵⁶] It is used in orthopedics to cover the implants to promote union between implant and bone.[^{56, 57}] It has been used in dentistry to fill up the osseous defects during periodontal surgery.[⁵⁸] It has been reported that a formulation of bioglass can promote infiltration and remineralization of dentinal tubules.[⁵⁹] The basic component is silica, which acts as a nucleation site for precipitation of calcium and phosphate. SEM analysis has shown that bioglass application forms an apatite layer, which occludes the dentinal tubules.[⁵⁹] The use of bioglass in management of DH has been shown by some products such as NovaMin (NovaMin Technology Inc., FL, USA).

Some authors have shown that calcium silicate cement derived from Portland cement can help in the management of DH.[¹⁷] It helps to occlude the dentinal tubules by remineralization.

Laser is an acronym for light amplification by stimulated emission of radiations. It has been shown in various studies that lasers can be used in the effective management of DH.[⁶⁰–⁶³] The mechanism of action of lasers in treating DH is not very clear. Some authors have shown that Nd–YAG laser application occluded the dentinal tubules.[^{61, 62}] GaAlA laser is thought to act by affecting the neural transmission in the dentinal tubules.[⁶³] It has also been proposed that lasers coagulate the proteins inside the dentinal tubules and block the movement of fluid.[⁶¹]

Recently, milk protein casein has been used to develop a remineralizing agent (GC Tooth Mousse). The casein phosphopeptide (CPP) contains phosphoseryl sequences which get attached and stabilized with amorphous calcium phosphate (ACP).[⁶⁴] The stabilized CPP–ACP prevents the dissolution of calcium and phosphate ions and maintains a supersaturated solution of bioavailable calcium and phosphates.[⁶⁴] Various studies have shown that CPP–ACP can effectively remineralize the enamel subsurface lesions.[^{65, 66}] By virtue of its remineralizing capacity, it has also been proposed by the manufacturers that it can also help in prevention and treatment of DH.