Diagnosis and treatment of dentinal hypersensitivity pdf
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- Dentin Hypersensitivity: Etiology, Prevalence and Treatment Modalities
- Dentine hypersensitivity: aetiology, differential diagnosis and management
- Dentine hypersensitivity: aetiology, differential diagnosis and management
- Dentin Hypersensitivity: Etiology, Diagnosis and Treatment; A Literature Review
Dentin Hypersensitivity: Etiology, Prevalence and Treatment Modalities
The objective of this review is to inform practitioners about dentin hypersensitivity DH ; to provide a brief overview of the diagnosis, etiology and clinical management of dentin hypersensitivity and to discuss technical approaches to relieve sensitivity. This clinical information is described in the context of the underlying biology.
Abstracts and also full text articles to identify studies describing etiology, prevalence, clinical features, controlled clinical trials of treatments and relevant laboratory research on mechanisms of action were used.
Many dentists have some problems in determining the etiology, diagnosing and treating dental hypersensitivity and some limitations have been observed in this regard. Some of the introducing titles relating to determination, diagnosis, prevalence, etiology and treatment of dental hypersensitivity are listed as follows:. Different terms have been used to describe dentin hypersensitivity a list of which has been shown in table 1 [ 1 ].
These terms are used based on the place of occurrence of hypersensitivity and include: cervical, root, dentine, cemental, and the terms sensitivity, and hypersensitivity [ 2 - 3 ]. All of these terms convey the same clinical conception and can be used interchangeably Table 1. However, the term dentin hypersensitivity DH has been used in this article. Although DH is a prevalent disorder and one of the most annoying diseases, the treatments which have been suggested for it are not sufficient and very successful [ 5 ].
This can lead to both physical and psychological problems for the patient. The prevalence distribution and appearance of the disease have been reported differently in different studies. These differences are due to the differences in populations, habits, dietaries, and methods of investigation [ 3 ].
The disease is prevalent in the patient with the age range of years. However, it is more prevalent in the patient with the age range of and more prevalent in female individuals that would probably be related to their dental hygiene and dietary [ 2 - 3 , 5 - 6 , 9 ].
There are two common methods to determine the intensity of DH. One of them is through asking some questions from the patient and the other is through clinical examination. The prevalence distribution of DH in the first method is usually estimated higher than that of the second method [ 10 ]. Furthermore, the occurrence of DH in canines and premolars is more than other teeth [ 2 , 5 - 6 , 8 - 9 , 11 ].
The buccal surface of the teeth has been reported to be more involved with the disease than other places. In some of the studies, it has been reported that DH can occur at any age [ 13 ]. It has been observed that some people with DH do not pursue treatment of the disease. However, they may report it in a clinical visit to the dentist. This is perhaps due to the fact that they do not consider DH as a specific disease [ 14 ].
Dentin is considered as a vital tissue and has the capacity to respond to physiologic and pathologic stimuli [ 15 ]. As it is known, dentin is covered by enamel in the crown surface and by a thin layer of cementum in the root surface of the tooth. Dentin is sensitive to stimuli due to the lesion extension of odontoblastic process and formation of dentin-pulp complex [ 1 , 3 , 6 ].
Dentin and pulp are histologically different. However, they have the same embryonic origin; ectomesenchymal origin. The formation of dentin-pulp causes dentin to be affected by pulp and vice versa. Dentin has very minute tubules which are filled with odontoblastic process. The fluid is completely filtrated and originates from the blood vessels of the pulp [ 13 ]. The results of scanning electron microscope SEM indicate that the number of tubules in sensitive dentin is eight times more than the number of tubules in non sensitive dentin.
Furthermore, tubules of sensitive dentin are thicker than those in non sensitive dentin [ 1 , 3 , 9 , 13 ]. Based on the studies, DH is developed in two phases [ 16 - 17 ]:. In the first phase, dentinal tubules, due to loss of enamels, are exposed by attrition, abrasion, erosion, and abfraction.
However, dentinal exposure mostly occurs due to gingival recession along with the loss of cementum on the root surface of canines and premolars in the buccal surface. It is worth noticing that not all the exposed dentins are sensitive. However, their calcified smear layer, as compared to non sensitive dentin, is thin and this leads to an increase in the fluid movement and consequently the pain response [ 9 , 13 , 18 ].
In the second phase, for the exposed dentin to be sensitized, the tubular plugs and the smear layer are removed and consequently, dentinal tubular and pulp are exposed to the external environment [ 17 ].
Plug and smear layer on the surface of exposed dentine are composed of elements of protein and sediments which are derived from salivary calcium phosphates and seal the dentinal tubules inconsistently and transiently. The findings of laboratory research indicate that both mechanical and chemical factors are effective in removing the smear layer from the dentinal tubules.
However, the results of clinical investigations, the mechanical factors are not the only key factors in removal of the smear layer and when they are accompanied with acidic foods or drinks they lead to the removal of smear layer [ 3 , 19 ]. It seems that Microbial plaque is not a significant factor in triggering DH [ 1 ].
First, as mentioned previously, the canines and first premolars have the greatest recession and sensitivity. The same teeth also reveal the lowest buccal plaque scores. Secondly, teeth with DH are cleaned extremely by patients suffering from the condition.
This would suggest that plaque does not produce dentin hypersensitivity itself nor does it act as a stimulus for pain [ 20 ]. However, the effect of plaque on DH is a controversial issue [ 17 ]. Three main mechanisms of dentin sensitivity are proposed [ 3 ]: Figure 1. However, there is little evidence to prove this theory; firstly because there is little evidence that can support the existence of nerve in the superficial dentin; where dentin has the most sensitivity; and secondly because the plexus of Rashkov do not become mature until complete tooth eruption.
However, the newly developed teeth can be sensitive too [ 6 ]. In the OR theory, odontoblasts act as receptors of pain and transmit signals to the pulpal nerves. But this theory has also been rejected since the cellular matrix of odontoblasts is not capable of exciting and producing neural impulses. Furthermore, no synopsis has been found between odontoblasts and pulpal nerves [ 3 ].
Hydrodynamic Theory for sensitive dentine was first proposed by Brannstorm [ 21 ]. This theory is the most widely accepted theory for DH. The theory has been proposed based on the movement of the fluid inside the dentinal tubules.
The theory claims that tubules are open between dentine surface which is exposed to the environment and pulp [ 21 - 22 ]. It is believed that DH is made as the result of movement of the fluid inside the dentinal tubules, which is further due to the thermal and physical changes, or as the result of formation of osmotic stimuli near the exposed dentine.
The movement of fluid stimulates a baroreceptor and leads to neural discharge. The process is called the hydrodynamic theory of pain [ 3 , 14 ]. This process is similar to activating the neural fibers around the hair by touching or pressing the hair.
The movement of fluid can be toward the inside of the pulp or the outside of dentin. Cooling, drying, evaporation, and hypertonic chemical stimuli cause the dentinal fluid to flow away from the dentin-pulp complex and lead to an increase in pain [ 15 ].
Heating causes the fluid to flow toward the pulp. As it was stated above, the number of tubules in sensitive dentin is eight times more than the number of tubules in non sensitive dentin.
Furthermore, tubules of sensitive dentin are wider than those in non sensitive dentin. As it is true about other diseases, the accurate diagnosis of dentin hypersensitivity before receiving treatment is critical for successful treatment. DH is similar to other conditions such as dentinal caries, fractured or chipped enamel, pain as a result of irreversible pulpitis, and post dental bleaching sensitivity in some of its features [ 1 , 3 , 23 ].
The diagnosis of the disease starts through investigating the medical history of the patient and examination. In investigating the medical history some questions are asked about the time of the start of DH, the intensity of the pain, the stability of the pain and the factors that reduce or increase the intensification of the disease.
In examination, some techniques such as pure air, pure water, and sounds are used in order to reconstruct the stimulating factors and to determine the degree of pain of the patient. Some other diagnostic tests are as follows: palpitation for diagnosing pulpitis or periodontal involvement, pushing a wood stick or transillumination for diagnosing a fracture or cracked tooth [ 24 ].
All of the teeth with pain should be examined and the degree of pain should be described through qualitative parameters such as slight, medium, and severe pain or through using quantitative parameters such as visual analogue scale [ 1 , 3 ].
Before considering any treatment strategy for the management of DHS, it is important to note from the published literature that there are a number of individuals who may be at risk for dentin hypersensitivity [ 24 ] such as:.
The often forgotten or neglected phase in the treatment of DH is the diagnosis and eliminating or treating the main routs of DH. The etiologic factors can be improper tooth brushing, premature occlusal contacts, gingival recession, and the existence of a large amount of exogenous and endogenous acids in diets.
Improper tooth brushing; which includes using hard- or thick-bristle tooth brushes, brushing teeth with excessive pressure, excessive scrubbing at cervical areas or even missing to brush cervical areas [ 25 ]. To avoid the DH due to improper tooth brushing: The patient should be taught the correct method of tooth brushing [ 3 ]. The patient should avoid the use of abrasive tooth pastes [ 1 ].
The patient should avoid brushing at least for one hour after consuming acid drinks or foods due to agonist effect of acidic erosion on tooth brush abrasion [ 1 , 3 ]. Premature contacts; sometimes through correction of occlusion or the use of an occlusal splint, the problem can be easily resolved [ 24 ].
Gingival recession; the patient should see a periodontist for consultation. Moreover, treatments such as graft or positioning flap might be adopted. It has been proved that erosive agents have a role in the initiation and progression of DH. Erosive agents with exogenous acids include carbonated drinks, citrus fruits, alcoholic drinks, yogurt, dairy products, and occupational hazard such as workers in battery manufacturing plants [ 3 , 26 ].
Erosive agents with endogenous acids enter the mouth through reflux or gastro-esophageal regurgitation [ 27 ]. These agents can be mostly found in patients with eating disorders. The patients are recommended to refer their doctors for the underlying diseases [ 3 ].
Poor oral hygiene contributes to periodontal diseases leading to root exposure. It has been also reported that periodontal treatment that exposes more root surface could increase incidence of DH [ 28 ].
Classification of desensitizing agents which are used in treatment of DH is a challenging task. It is due to the fact that these agents are frequent. Furthermore, the mode of their action has not been determined yet.
They can be easily classified into two groups based on the mode of their administration:. At home: this mode is simple and reasonable and can be used in treatment of many teeth. In office: This is a complicated and expensive mode which can be used in treatment of a limited number of teeth.
Furthermore, the agents can be classified into two groups based on mechanism of action:.
Dentine hypersensitivity: aetiology, differential diagnosis and management
Understanding the etiology of dentinal hypersensitivity can help practitioners implement patient-specific preventive and therapeutic measures. How many patients do you treat for dentinal hypersensitivity? These are silent sufferers. These patients will avoid activities, shun ice cream, and skip brushing areas that elicit pain. Of course, not brushing sensitive areas will only lead to more disease and more pain. The truth is, dentinal hypersensitivity is easy to treat once it is diagnosed. This article will help you diagnose hypersensitivity and provide immediate and effective treatment.
Dentine hypersensitivity: aetiology, differential diagnosis and management
With careful consideration of myriad factors—from self-report to clinical exam—oral health professionals can effectively diagnosis and treat this common condition. How many patients do you treat for dentinal hypersensitivity? These are silent sufferers.
Dentin hypersensitivity DH is a frequent condition in adults and difficult to treat. Significant reduction in pain perception from DH surfaces was demonstrated from ozone treated test teeth as well as in placebo treated control teeth. We found a moderate
The objective of this review is to inform practitioners about dentin hypersensitivity DH ; to provide a brief overview of the diagnosis, etiology and clinical management of dentin hypersensitivity and to discuss technical approaches to relieve sensitivity. This clinical information is described in the context of the underlying biology. Abstracts and also full text articles to identify studies describing etiology, prevalence, clinical features, controlled clinical trials of treatments and relevant laboratory research on mechanisms of action were used. Many dentists have some problems in determining the etiology, diagnosing and treating dental hypersensitivity and some limitations have been observed in this regard. Some of the introducing titles relating to determination, diagnosis, prevalence, etiology and treatment of dental hypersensitivity are listed as follows:.
Interface Oral Health Science pp Cite as. Dentin hypersensitivity is a very common clinical symptom, which consists of sharp pain arising from exposed dentin in response to various types of stimuli and thus can cause considerable concern for patients. This condition is frequently encountered by periodontists, dentists and hygienists.
Dentin Hypersensitivity: Etiology, Diagnosis and Treatment; A Literature Review
Metrics details. Though dentin hypersensitivity DHS is one of the most common complaints from patients in dental clinics, there are no universally accepted guidelines for differential diagnosis as well as selection of reliable treatment modalities for this condition. The neurosensory mechanisms underlying DHS remain unclear, but fluid movements within exposed dentinal tubules, i. As several dental conditions have symptoms that mimic DHS at different stages of their progression, diagnosis and treatment of DHS are often confusing, especially for inexperienced dental practitioners. In this paper we provide an up-to-date review on risk factors that play a role in the development and chronicity of DHS and summarize the current principles and strategies for differential diagnosis and management of DHS in dental practices. We will outline the etiology, predisposing factors and the underlying putative mechanisms of DHS, and provide principles and indications for its diagnosis and management.
Затем он его уничтожит, и Цифровая крепость навсегда исчезнет из Интернета. - Действуй своим маячком очень осторожно, - сказал Стратмор. - Если Северная Дакота заподозрит, что мы его ищем, он начнет паниковать и исчезнет вместе с паролем, так что никакая штурмовая группа до него не доберется. - Все произойдет, как булавочный укол, - заверила его Сьюзан. - В тот момент, когда обнаружится его счет, маяк самоуничтожится. Танкадо даже не узнает, что мы побывали у него в гостях.
Продвигаясь по служебной лестнице, Тревор Стратмор прославился умением сжато и одновременно глубоко анализировать сложнейшие ситуации. Он обладал почти сверхъестественной способностью преодолевать моральные затруднения, с которыми нередко бывают связаны сложные решения агентства, и действовать без угрызений совести в интересах всеобщего блага. Ни у кого не вызывало сомнений, что Стратмор любит свою страну. Он был известен среди сотрудников, он пользовался репутацией патриота и идеалиста… честного человека в мире, сотканном из лжи. За годы, прошедшие после появления в АНБ Сьюзан, Стратмор поднялся с поста начальника Отдела развития криптографии до второй по важности позиции во всем агентстве. Теперь только один человек в АНБ был по должности выше коммандера Стратмора - директор Лиланд Фонтейн, мифический правитель Дворца головоломок, которого никто никогда не видел, лишь изредка слышал, но перед которым все дрожали от страха.
PDF | The objective of this review is to inform practitioners about dentin hypersensitivity (DH); to provide a brief overview of the diagnosis.