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International Journal of Dental and Health Sciences Review Article Volume 02,Issue 06

DENTINE HYPERSENSITIVITY: A REVIEW Abdul Saheer1*, Shanila Abdul Majeed2, Pallavi SK3 1.Post Graduate student, Department of Public Health ,Vokkaligara Sangh Dental College And ,Bangalore 2.Post graduate student,Department of and Radiology, Dayanada Sagar College of Dental Science,KS layout,Bangalore 3.Reader,Department of Public Health Dentistry,Vokkaligara Sangh Dental College And Hospital,V.V.Puram,Bangalore

ABSTRACT: Dentine hypersensitivity is one of the prevalent disease among aged population which results in compromising quality of life to a lesser extent. Literature explains various theories and explanations about the etiopathogenesis. Prevalence of dentine hypersensitivity varies among country to country and even within the same populations based on the study criteria used and age group of the study population. Keywords: Dentine hypersensitivity,etiopathogenesis,Prevalence

INTRODUCTION:

Dentinal hypersensitivity is a common under-reported and under-managed painful condition of the teeth, problem, despite making some dental associated with the exposure of treatments more stressful than dentine. hypersensitivity, or necessary and having a negative impact more precisely known as dentine on the patient's quality of life. Dentine sensitivity or hypersensitivity. The hypersensitivity can be particularly suitability of the terms dentine uncomfortable and unpleasant for sensitivity and dentine hypersensitivity patients and can dictate types of foods have been questioned since both terms and drinks ingested. Patients may are often used to describe the same describe the condition as dull or sharp, clinical condition. Although it has been vague or specific and intermittent or suggested that true hypersensitivity constant. [2] can develop as a result of pulp Dentine hypersensitivity is defined as inflammation, the symptoms are “sharp short pain arising from exposed thought to be more severe and dentine in response to stimuli typically persistent than the typical short sharp thermal, chemical, tactile or osmotic pain of dentine hypersensitivity. [1] and which cannot be ascribed to any Dentine hypersensitivity is a response other form of dental defect or from a non-noxious stimuli and a pathology. [3] chronic condition with acute episodes Terminologies whereas dentinal pain is a response Dentine hypersensitivity/ Dentine from a noxious stimulus and usually an sensitivity /Dentinal sensitivity-Pain or acute condition. Dentine sensitivity felt at the exposed dentine hypersensitivity remains a worldwide surfaces

*Corresponding Author Address: Dr Abdul saheer Email: [email protected] Saheer A.et al, Int J Dent Health Sci 2015; 2(6):1564-1572 Cervical hypersensitivity/sensitivity- 2. Lesion initiation- In the second phase, Sensation of pain in the cervical region for the exposed to be sensitized, Root hypersensitivity/sensitivity- the tubular plugs and the smear layer Cemental hypersensitivity/sensitivity.- are removed and consequently, Pain in the cemental regions due to the dentinal tubular and pulp are exposed exposed root surfaces.[4] to the external environment.[6] Plug and Phases in the development of dentine smear layer on the surface of exposed hypersentivity dentine are composed of elements of Based on the studies, DH is developed protein and sediments which are in two phases.[1,5] derived from salivary calcium 1. Lesion localization phosphates and seal the dentinal 2. Lesion initiation tubules inconsistently and transiently. The findings of laboratory research 1. Lesion localization- In the first phase, indicate that both mechanical and dentinal tubules, due to loss of chemical factors are effective in enamels, are exposed by , removing the smear layer from the , erosion, and . dentinal tubules. However, the results However, dentinal exposure mostly of clinical investigations, the occurs due to along mechanical factors are not the only key with the loss of on the root factors in removal of the smear layer surface of canines and premolars in the and when they are accompanied with buccal surface. It is worth noticing that acidic foods or drinks they lead to the not all the exposed dentins are removal of smear layer. [15,20]Lesion sensitive. Their calcified smear layer, as initiation requires removal of compared to non sensitive dentin, is cementum or smear layers. This is thin and this leads to an increase in the achieved by abrasive or erosive agents. fluid movement and consequently the The evidence available indicates pain response. [6,7] erosion is the more dominant factor but can be potentiated by abrasion.

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Saheer A.et al, Int J Dent Health Sci 2015; 2(6):1564-1572 Structural differences between processes. If the true synapse were sensitive and non-sensitive dentine present between these two elements There are the differences in the to facilitate the transmission of structure of sensitive versus non dentinal sensation, then a neural sensitive dentine. Sensitive dentine transmitting substance such as appears to have more dentinal tubules acetylcholine would be expected in this per unit area than non-sensitive area of the odontoblastic process and dentine (eight times as many tubules at the predentine. There is no direct the root surface compared with non- evidence for the presence of sensitive teeth) and the channels are acetylcholine activity in the neural wider, with the average diameter of transmission in the pulp.[25] Direct tubules in sensitive teeth being two mechanical stimulation of these nerves times greater than that of tubules in will initiate an action potential. There non-sensitive teeth (0.83 _m versus 0.4 are many shortcomings of this theory. _m, respectively).[8] It has also been There is lack of evidence that outer shown that smear layers in sensitive dentin, which is usually the most dentine are thinner and under calcified sensitive part, is innervated. compared with those on non-sensitive Developmental studies have shown dentine. [9] The greater number of open that the plexus of Rashkow and and wider tubules leads to increased intratubular nerves do not establish fluid permeability through dentine and themselves until the tooth has erupted; therefore increased stimulus yet, newly erupted tooth is sensitive. transmission and, eventually, the pain Moreover, pain inducers such as response. bradykinin fail to induce pain when applied to dentine, and bathing dentine THEORIES OF DENTINE with local anesthetic solutions does not HYPERSENSITIVITY prevent pain, which does so when 1.Transduction /direct innervations applied to skin.[10] theory: According to this theory, the 2. Modulation theory: has a special sensory According to Turkar, the nerve function and the functional complex impulses in the pulp are modulated with the nerve ending in or near the through the liberation of polypetides odontoblastic layer acts as an from the , when injured. excitatory synapse. The odontoblast These substances may selectively alter and its process have been perceived as the permeability of the odontoblastic a transducer mechanism. This theory of cell membrane through dentinal sensation takes into hyperpolarization, so that pulp neurons consideration the “synaptic” like are more prone to discharge upon relationship between the odontoblastic receipt of subsequent stimuli. When an

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Saheer A.et al, Int J Dent Health Sci 2015; 2(6):1564-1572 irritating stimulus comes to contact outer dentin surface, there is a with the dentine, the odontoblast may displacement of the contents of the become injured and subsequently dentinal tubules that gives rise to a release a variety of neuro transmitting mechanical stimulation of the pain at agents as well as vasoactive and pain the pulpodentinal border. This theory is producing amines and proteins. These the most widely accepted until now substances may modulate associated and consider that the stimulation of nerve fiber action potentials by the nerve endings next to the increasing neuronal cyclic AMP levels odontoblastic layer is provoked by the through cell membrane adenylate variation of the intrapulpal pressure cyclase receptors .[10] toward the pulp or in the opposite direction, depending on the stimulus 3. Gate control theory: Ronald Melzack nature. The nerve fibers stimulation and Patrick Wall, 1960 occurs because of the deformation of When the dentine is irritated (for these fibers, caused by the fluid example-by cavity preparation) the movement, leading to a widening of pulpal nerves become activated from the nerve membrane ionic canals, vibrations. The larger myelinated fibers allowing the entrance of Na++ in the may accommodate to the sensations. cell, depolarizing the fibers and The smaller c fibers may tend to be provoking pain. The presence of lesions maintained and not adjust to the involving enamel and/or cementum stimulus. Thus as the low intensity loss in the cervical area and the “pain gates” from the larger fibers are consequent opening of dentinal closed, the high intensity “pain gates” tubules to the oral environment, under from the smaller fibers are enhanced. certain stimuli, allows the movement of “pain gates” may be opened by some dentinal fluid inside the tubules, stimuli, such as anxiety, and may be indirectly stimulating the extremities of closed by distracting stimuli such as the pulp nerves, causing the pain “audio analgesia” or ‘gingival sensation. stimulation’. However the gate control The hydrodynamic theory is the most theory does little to explain how pain widely demonstrated and accepted responses from the dentine are physiopathological theory of DS. transmitted and perceived by the nerve According to this theory, most pain- endings of the pulp. [10] inducing stimuli increase centrifugal fluid flow within the dentinal tubules, 4. Hydrodynamic theory: Proposed by giving rise to a pressure change Brännström and Astron in 1964 . throughout the entire dentine. This in According to Brännström’s turn activates the Aδ intradentinal hydrodynamic theory, when an nerves (of medium conduction velocity) appropriate stimulus is applied to the at the pulp-dentinal interface, or within

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Saheer A.et al, Int J Dent Health Sci 2015; 2(6):1564-1572 the dentinal tubules - thereby proportion are actually diagnosed as generating pain. Two phases must having cervical dentine hypersensitivity coincide in order to produce DS. In on the basis of defined clinical effect, dentinal exposure (location of diagnostic criteria. In general, it the lesion) must occur, and the appears that the incidence of dentinal tubular system must open or hypersensitivity in most populations become permeable towards the pulp ranges between 10 to 30 per cent of compartment (start of the lesion). the general population.[11]The Dentinal exposure may be secondary to incidence of DH can vary considerably loss of enamel or periodontal tissue depending on the cohort being studied (gingival recession). Enamel loss or with periodontal patients, patients with dental wear is due to attrition, abrasion gingival recession and smokers with and erosion, and although dental periodontitis showing the highest erosion is the most important single incidence of diagnosed dentinal factor to be taken into account, hypersensitivity. increased dentine wear and tubular aperture occurs when it acts in synergy Most studies describe a preferential with abrasion. order of pain location according to the type of teeth involved. The canines EPIDEMIOLOGY and first premolars are the most Prevalence affected teeth, followed by the incisors Dentinal hypersensitivity appears to be and second premolars. The molars are a common problem with various the teeth least affected by DS. As reports globally indicating an incidence regards the anatomical location of DS, between 1 to 98 per cent of the most cases are circumscribed to the population. One reason for this large bucco-cervical region of permanent discrepancy relates to the variations in teeth. [12] the methods of data collection. The Most affected patients are in the 20-50 diversity of reports may be in part years of age interval, with a peak caused by different methods used to between 30-40 years of age. As regards diagnose the condition and it is to the sex distribution, DS affects generally considered that surveys women more often than men. [13] It has which rely on patient questionnaires been suggested that with the lifespan alone greatly exaggerate the of the general population increasing, prevalence figures and thereby yield and more people keeping their teeth misleading data. longer, hypersensitivity will increase in Several studies indicate that even prevalence. This seems to make sense though high percentages of a on the basis that gingival recession and population may report to have loss of enamel and cementum is more sensitive teeth, a much smaller prevalent in older individuals. The

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Saheer A.et al, Int J Dent Health Sci 2015; 2(6):1564-1572 above assumptions are somewhat dentine hypersensitivity in studies confounded by reports in the literature based on patients’ perception of this which indicate that most sufferers of problem. [14] Furthermore, studies dentine hypersensitivity range in age carried out at or from 20 to 40 years with the peak practices tend to report higher incidence occurring at the end of the prevalence values. The prevalence was third decade and decreases during the observed to be greater in patients fourth and fifth decades of life. [14] This referred to specialist may be explained by the decrease in clinics and hospital clinics than in permeability of dentine and neural general practice patient populations, sensitivity with ageing. Such responses presumably because of the greater risk may arise from the natural of root exposure as a result of desensitization of sclerosis and periodontal attachment loss and secondary dentine formation. In gingival recession following periodontal addition, long-term use of fluoride treatment. dentifrices can add to the of Even though numerous studies have open dentine tubules resulting in a been conducted on this topic, a bulk of decrease in sensitivity. them has focused on a specifically Reasons for the variability of targeted group of general practices, prevalence values recorded in the which in turn, might have biased the literature, including: the different study findings. Accordingly, there is a clear designs used to assess the condition, need to explore the nature of dentine variation in patients’ hypersensitivity in a randomly selected habits,consumption of erosive foods sample of general practices. Such an and drinks, and the type of setting investigation would no doubt enhance where the study was carried out. It was the understanding of this problem claimed that questionnaire studies amongst the dental practitioners and tend to overestimate the prevalence as consequently benefit patients to mentioned previously. Virtually 50% or maintain better oral health more of adults have complained of

Summary of Various prevalence studies Study Country No Study type Setting Prevalence Peak of M: F ratio Commonly % with GRa (%) age affected 1 teeth Bamise et Nigeria 2165 Q2+ CE3 University 1.34% 4th decade 1.4:1 Molars 12.8% al. 16(1991) Rees and UK 5477 Q + CE GDP6 2.8% 4th decade 1:1.5 Max71st 93% Addy 17 molars (2003) Rees et Hong Kong 226 Q + CE PSC8 67.7% 5th decade 1:1.5 Mand9inciso 76.8% al.18( 2004) rs

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Saheer A.et al, Int J Dent Health Sci 2015; 2(6):1564-1572 Clayton et UK 250 Q GDP 50% 3rd decade 1:1 Mand right NA 10 al.19(2008) sextant

Tanni and Saudi 259 Q + CE GDP + PSC GDP 42.4% 4th decade GDP 1:4 Max molars 5% Awartani 20 Arabia PSC 60.3% PSC 1:2 and mand (1987) anteriors

Gillam et UK and 557 Q GDP 52- 55.4% 3rd and NA NA NA al. Korea 4th 13(1966) decades Fischer et Brazil 635 Q + CE Marine 17% M: 6th, F: 1:1 Incisors and NA al. dental 3rd decade premolars 11(1991) clinic

Flynn et al. UK 369 Q + CE University 8.7% 4th decade 1:1 Premolars NA 21(1987) Gillam et UK 277 Q GDP 6 52% 3rd decade 1:1.4 NA NA al.22 ( 1999) Chabanski UK 51 Q + CE PSC 72.5-98% 5th decade 1:1 Molars NA et al.23 ( 2008) Liu et al. Taiwan 780 Q + CE University 32% NA 1:1 Premolars 23% 24(2006) & molars Vijaya et India 655 Q+CE University 55% 3rd decade 1:0.8 Molars NA al25 (2013) Rane P et India 960 Q Hospital 42.5% 4th decade 1:0.9 Lower NA 26al(2013) anteriors Dhaliwal JS India 650 Q+CE Rural 25% 6th decade 1:1.3 Lower NA et population anteriors al27(2012)

1gingival recession, 2questionnaire, 3clinical examination, 4sensitivity to air blast, 5periodontal disease assessment, 6general dental practice, 7maxillary, 8periodontal specialty clinic, 9mandibular, 10not applicable, 11cold water mouth rinse

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