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 Dentistry,Vokkaligara Sangh Dental College And Hospital,Bangalore 2.Post graduate student,Department of Oral Medicine 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. Tooth 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 dentin 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 attrition, removing the smear layer from the abrasion, erosion, and abfraction. dentinal tubules. However, the results However, dentinal exposure mostly of clinical investigations, the occurs due to gingival recession along mechanical factors are not the only key with the loss of cementum 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. 1565 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: odontoblast 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 odontoblasts, 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 1566 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.