Root hypersensitivity is a relatively common problem in periodontal practice.
It may occur spontaneously when the root becomes exposed as a result of gingival recession or pocket formation/ it may occur after scaling &root planing&surgical procedures
DENTINHYPERSENSITIVITY is characterized by short sharp pain arising from exposed dentin in response to stimuli—typically thermal, evaporative, tactile, osmotic or chemical—that cannot be ascribed to any other dental defect or disease. 1 ( Addy M. )
Dentine hypersensitivity is sensation felt when the nerves inside the dentin are exposed to the environment
The sensation can range from irritation all the way to intense, shooting pain.
This sensitivity can be caused by several factors, including wear , decaying teeth or exposed tooth roots.
Images of dentin surface(2000x)
Enamel loss exposing dentin
Gum loss exposing dentin
It is manifested as pain induced by cold or hot temperature by citrus fruits or sweets,or by contact with a toothbrush or a dental instrument.
Root sensitivity occurs more frequently in the cervical area of the root,where the cementum is extremely thin
Scaling &root planing procedures remove this thin cementum inducing the hypersensitivity
Transmission of stimuli from the surface of the dentin to the nerve endings located in the dental pulp or in the pulpal region of the dentin could result from the hydrodynamic mechanism or from the odontoblastic process
An important factor for reducing or eliminating hypersensitivity is adequate plaque control
Dentine contains many thousands of microscopic tubular structures that radiate outwards from the pulp
These dentinal tubules are typically 0.5-2 microns in diameter.
Changes in the flow of the plasma-like biological fluid present in the dentinal tubules can trigger mechanoreceptors present on nerves located at the pulpal aspect thereby eliciting a pain response.
This hydrodynamic flow can be increased by cold, air pressure, drying, sugar, sour (dehydrating chemicals ), or forces acting onto the tooth.
Hot or cold food or drinks , and physical pressure are typical triggers in those individuals with teeth sensitivity
CHARACTERISTIC OF DENTIN HYPERSENSITIVITY
Clinical features .
DENTIN HYPERSENSITIVITY usually is diagnosed after other possible conditions have been eliminated.
Alternative causes of pain include chipped or fractured teeth, cracked cusps, carious lesions, leaky restorations and palatogingival grooves.
The clinical features of DENTINHYPERSENSITIVITY are well-documented.
PREVALENCE: The prevalence of DENTINHYPERSENSITIVITY varies from 4 to 57 percent. 6
These variations are likely due to differences in the populations studied and the methods of investigation (for example, questionnaires or clinical examinations).
The prevalence of DH is between 60 and 98 percent in patients with periodontitis.
A majority of patients, however, do not seek treatment to desensitize their teeth because they do not perceive DH to be a severe oral health problem.
In response to questionnaires, dentists have reported that DH affects between 10 and 25 percent of their patients.
Schuurs and colleagues also reported that dentists believe DH presents a severe problem for only 1 percent of their diagnosed patients
While DH mostly occurs in patients who are between 30 and 40 years old,it may affect patients of any age. It affects women more often than men, though the sex difference rarely is statistically significant.
The condition may affect any tooth, but it most often affects canines and premolars .
The affected teeth tend to vary among studies and populations, and different distribution patterns have been described
Mechanisms of sensitivity
Dentin is naturally sensitive owing to its close structural and functional relationship with the dental pulp.
This inherent sensitivity usually is not a problem because other tissues cover the dentin.
Microscopic examination reveals that patent dentinal tubules are more numerous and wider in HYPERSENSITIVE DENTIN than in Non sensitive dentin
These observations are consistent with the hypothesis that dentinal pain is mediated by a hydrodynamic mechanism.
In the hydrodynamic sequence, a pain-provoking stimulus applied to dentin increases the flow of dentinal tubular fluid.
In turn, this mechanically activates the nerves situated at the inner ends of the tubules or in the outer layers of the pulp .
Cooling, drying, evaporation and hypertonic chemical stimuli that stimulate fluid to flow away from the pulp more effectively activate intradental nerves than do stimuli such as heating or probing that cause fluid to flow toward the pulp.
The observation that about 75 percent of patients with DH complain of pain on receiving cold stimuli supports this hypothesis
During periodontal therapy, scaling and root planing removed the outer layer of hyper mineralized dentine and thus leaves the surface expose to the effect of hydrodynamic phenomenon .
Surgical periodontal treatment, usually involves complete debridement of root surface.
Post operative recession of soft tissue further exposes the dentinal tubules.
Patient inability to maintain plaque control in the healing phase further complicates the problem,
ACID PRODUCTION DUE TO PLAQUE ACCUMULATION could act as a noxious stimuli and cause dehydration and leads to fluid movement across the dentinal tubule.
Instrumentation of the root creates an outer contiguous smear layer covering the instrumented surface as well as pushing debris into the dentinal tubules for several micrometer.
Thus The smear layer is a natural iatrogenic yet transient treatment for dentin hypersensitivity.
Another quality is that the ideal desensitizer should not interfere with the subsequent regenerative outcome, if such procedures are deemed necessary at the future time.
We can break down the methods of desensitizing dentine into
use of restorative material,
guided tissue regeneration to cover gingival recession .
THEORIES OF PAIN TRANSMISSION THROUGH DENTIN
DIRECT NEURAL STIMULATION
The nerves in the dentinal tubules are not commonly seen &even if they are present they do not extend beyond the inner dentin.
Topical application of local anesthetics do not abolish sensitivity.Hence this theory is not accepted
FLUID/HYDRO DYNAMIC THEORY
Various stimuli as heat,cold,air blast desiccation/mechanical/osmotic pressure affect fluid movement in the dentinal tubules.
This fluid movement,either inward(due to cold stimuli)/outward(due to drying of exposed dentinal surface),stimulates the pain mechanism in the tubules by mechanical disturbance of the nerves closely associated with the odontoblast &its process
Thus these endings may act as mechanoreceptors as they are affected by mechanical displacement of the tubular fluid
Odontoblast process is the primary structure excited by the stimulus &that the impulse transmitted to the nerve endings in the inner dentin.
This is not a popular theory since there are no neurotransmitter vesicles in the odontoblast process to facilitate the synapse
Or synaptic specilization
HISTORY, EXAMINATION& DIAGNOSIS
A diagnosis of DH should be determined only when the practitioner has considered differential diagnoses after conducting a methodical history and examination of the patient.
The other causes of transient tooth pain must be excluded for a diagnosis of DH to be made. Quantifying the initial degree of sensitivity provides a baseline from which to chart subsequent changes in the condition
Although dentin hypersensitivity is a common clinical problem, there is no standard method of diagnosis, and confusion exists about the most effective treatment
The condition should be diagnosed only after excluding other possible causes of pain.
Flowchart for the clinical management of dentin hypersensitivity (DH). (Adapted with permission of George Warman Publications [UK] Ltd., from Addy and Urquhart.) Note 1. Pain evoked by thermal, evaporative (jet of air), probe, osmotic or chemical stimuli. Note 2.
Dental pain can be categorized using different taxonomies.
It may arise from a problem in the tooth or its supporting structures, or it may be due to a problem elsewhere that is misperceived by the patient as originating there (e.g., referred pain).
Dental pain can also be classified by etiology. All occurrences require dental referral.
Pain Originating in the Tooth or Periodontium
This type of pain can be due to trauma, a cracked tooth, pulpitis, or a host of other causes.
Trauma: Dental pain may be caused by a traumatic event, perhaps a recent fall, a blow to the face from sports or fighting, or other facial or dental trauma.
Trauma may have occurred some time ago, and the patient may have endured longstanding pain.
Cracked Tooth Syndrome
The patient may have "cracked tooth syndrome" from trauma, as well as from tooth grinding, accidental insults (e.g., biting down on an unpopped kernel of corn or a concealed olive pit), or bad habits, such as compulsively chewing ice.
In all of these cases, a living tooth can suffer a partial fracture that extends into the dental pulp (connective tissue lying beneath enamel and dentin in the central portion of the tooth housing the nerve).
This problem is more common in older patients, whose water may not have been fluoridated when they were young.
As a result, many have extensive dental restorations (i.e., fillings).
As those restorations age, they are prone to damage.
Patients with cracked tooth syndrome feel pain when biting down to chew; the pain usually remits when chewing ceases.
Thus, patients often stop chewing on the troublesome side for a period of time.
Some tooth problems are too extensive to repair.
Perhaps the tooth has developed a large cavity in a previously unfilled area or there is extensive erosion beneath an older amalgam.
If the cause is addressed properly, it may cease.
If the patient is unable or unwilling to see a dentist, the tooth may progress to irreversible pulpitis.
In these cases, if the damage reaches an area proximal to the pulp, repair cannot be done.
Advanced periodontal disease that leads to bone loss may also be the cause.
The tooth affected with irreversible pulpitis causes moderate to severe pain and is also painful after cold, heat, or other stimuli, but in this case, the pain lasts for minutes to hours.
The pain can be severe and disrupt sleep.
Investigators hypothesize that tiny air bubbles trapped under a root filling or adjacent to dentin expand or contract.
Patients experience a sensation of sharp or squeezing tooth pain.
In the worst case, alveolar mucosa may rupture.
If the patient describes a pressure-related problem, treatment may be restoration of damaged teeth.
This term refers to inflammation of the dental pulp that can be reversed with a professional appointment.
Patients complain of discomfort lasting less than five seconds when the tooth is contacted by cold, an air blast, or ingestion of sweet foods.
The cause can be minor (e.g., dentinal hypersensitivity, a new filling, recent dental cleaning) or due to such problems as gingival recession, caries, or a defective restoration.
Nonsteroidal nonprescription products can be recommended as an emergency measure until patients see the dentist.
However, ibuprofen or naproxen does not affect the underlying pathology and the problem will continue to worsen until a professional intervenes.
Referred dental pain
Dental pain may occur as a result of extradental causes.
For instance, several types of headache can cause pain in the teeth and jaw.
A cluster headache can result in toothache.
Migraine and paroxysmal hemicrania can produce pain in the maxillary molars.
Barodontalgia: Barodontalgia is tooth pain resulting from extremes of pressure.
Pilots in unpressurized cabins (e.g., high-performance aircraft) experience barodontalgia from low pressures at about 3,000 feet, and scuba divers experience the same problem at the elevated atmospheric pressures encountered 10 meters below the surface and deeper .
Hemicrania continua is a headache that can produce toothache in the maxillary premolars.
In each case, the dentist may discover that the pain does not originate in the teeth or periodontium.
A physician may use diagnostic criteria to identify the type of headache that caused the tooth pain.
Jaw/tooth pain can be caused by trigeminal neuralgia, characterized by pain on one side of the head, in most cases the right side
The pain occurs in the areas innervated by the trigeminal nerve's mandibular and/or maxillary branches.
Some patients insist that the pain started without any provoking factor, while others recall that it began after trivial stimulation of the mucosa around the teeth, tongue, or skin (e.g., chewing, yawning).
Attacks come in waves of electric-like pain, lasting from a few seconds to several minutes.
Temporomandibular disorders, involving the temporomandibular joints, chewing structures, and other associated areas, may produce dental pain.
Appropriate treatment for this condition may encompass such interventions as intraoral appliances, prescription drugs, moist heat, ice, ethyl chloride spray, exercise, physiotherapy, electrotherapy, and iontophoresis.
Methods used to measure tooth hypersensitivity
The simplest tactile method used is to lightly pass a sharp dental explorer over the sensitive area of the tooth (usually the cemento – enamel junction) and to grade the response of the patient on a severity scale from 0 to 3.
If no pain is felt – 0,
slight pain or discomfort – 1,
severe pain – 2,
severe pain that lasts –3
Other sophisticated tactile methods used were a device by Smith and Ash, force sensitive electronic probe devised by Yeaple, pressure probe device used by McFall and Hamrick and a hand held scratch device.
Electrical measurements differ from others in that a pain response can be obtained from non–sensitive as well as from sensitive teeth and with either an enamel–covered crown or a cementum–covered root site of stimulation.
Improvements in pulp testers led to better quantification of the electric stimulus and discovery that a condition of “pre-pain” consisting of a tingling or warm sensation is observed before real pain and discomfort are felt by the subject as the magnitude of a stimulus is increased.
A stark device and a commercial digital pulp tester have also been tried.
An osmotic method consisting of the subjective pain response to a sweet stimulus was used to measure the effect of several test dentifrices on dentinal sensitivity.
A simple thermal method for testing for tooth sensitivity is directing a burst of room temperature air from a dental syringe onto the test tooth.
Blowing air on a tooth involves drying and pain can be easily detected by this method if the teeth are sensitive.
Air stimulation has been standardized as a one – second blast from the air syringe of a dental unit, where its temperature is set generally between 65 – 70 degrees fahrenheit and at a pressure of 60 psi.
An air thermal device has been devised.
Instruments that involve electric cooling or heating of direct contact metal probes have also been used in some studies.
DENTIN DISK MODEL
Small dentin disks prepared from extracted teeth can be used to measure the permeability of dentin.
Permeability is derived from the hydraulic conductance or ease of fluid flow through the dentin.
Some desensitizing agents such as oxalates reduce dentin permeability, while others such as potassium nitrate do not.
Treated dentin disks can be examined using a scanning electron microscope to visualize surface deposits and tubule occlusion.
By incorporating the dentin disk specimens in intraoral appliances, experiments can be conducted in situ under natural conditions in the mouth.
It is possible to replicate the outward flow of dentinal fluid, which can oppose pulpward diffusion of desensitizing agents .
An in vitro study of hydraulic conductance in dentin disks confirmed the findings of these clinical trials.
The product containing 5 percent potassium nitrate and 0.454 percent stannous fluoride in a silica base, which caused significantly greater reduction in DH, also demonstrated the lowest hydraulic conductance (permeability) and greatest inward potassium ion flux in dentin disks.
RECORDING CONDUCTION IN ISOLATED NERVE FIBERS
. This model identifies agents (e.g., potassium salts) or procedures (e.g., use of lasers) that may block nerve conduction.
Although these in vitro methods allow for rapid screening of potential desensitizing agents, they generally do not mimic natural conditions or indicate how the agent will behave when exposed to saliva and masticatory forces.
The ultimate test of any treatment is how well it works in the clinic.
A randomized, blinded and controlled trial is the gold standard for determining efficacy.
In such a clinical trial, the product is compared with the same formulation minus the active ingredient, which can be called "minus active," "negative control" or "placebo.“
A product also can be tested "head-to-head" against existing products to determine its effective equivalency or superiority with its comparators
Classifying treatments for DH can be challenging because its modes of action often are unknown.
It can be simpler to classify treatments according to their mode of delivery.
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.
In-office treatments are more complex and generally target DH localized to one or a few teeth.
These various treatment options can be graded by their complexity
PREVENTION OF DENTIN HYPERSENSITIVITY
Prevention of dentin hypersensitivity should include identifying and eliminating predisposing etiologic factors such as endogenous or exogenous acids and toothbrush trauma.
The role erosive agents play in the development of DH is well-established.
Exogenous dietary sources like fruits, fruit juices and wine contain acids that can remove smear layers and open dentinal tubules.
Endogenous acids arising from gastric acid reflux or regurgitation also can produce DH, which characteristically affects palatal surfaces.
Toothbrushing with an abrasive toothpaste can abrade the dentin surface and may open up dentinal tubules if combined with erosive agents.
Patients should avoid toothbrushing for at least two to three hours after consuming acidic foods or drinks to reduce the deleterious co effects of acids and abrasion.
Most patients are unable to remember details of their food and drink consumption.
They should be asked to keep a daily diet diary in which they record their food and drink consumption over a period of consecutive days spanning a week and weekend.
The diary may reveal changes in the patient’s diet that may contribute to DH.
The diary also could present an opportunity for practitioners to review their patients’ oral hygiene practices.
B)ANTI INFLAMMATORY AGENT
C) COVER /PLUGGING DENTINAL TUBULES
PLUGGING/SCLEROSING DENTINAL TUBULES
SODIUM MONOFLUORO PHOSPHATE
SODIUM FLUORIDE/STANNOUS FLUORIDE COMBINATION
GLASS IONOMER CEMENT
III)PERIODONTAL SOFT TISSUE GRAFTING
IV) CROWN PLACEMENT/RESTORATIVE MATERIAL
NERVE DESENSITIZATION BY DESENSITIZING AGENTS
Desensitizing agents do not produce immediate relief &must be used for several days or even weeks to produce results
Desensitizing agents can be applied by the patient at home or by the dentist or hygienist in the dental office
The most likely mechanism of action is the reduction in the diameter of the dentinal tubules so as to limit the displacement of fluid in them
Tooth-pastes are the most widely used dentifrices for delivering over-the-counter desensitizing agents.
The first desensitizing toothpastes to appear on the market claimed either to occlude dentinal tubules (those that contained strontium salts and fluorides) or destroy vital elements within the tubules (those that contained formaldehyde).
Now, most desensitizing toothpastes contain a potassium salt such as potassium nitrate, potassium chloride or potassium citrate,
Though one study reported that a remineralizing toothpaste containing sodium fluoride and calcium phosphates reduced DH.
Grossman in 1931 suggested that the ideal desensitizer should be:
NOT UNDULY IRRITATING TO THE PULP
PAINLESS WHEN APPLIED
EASY TO APPLY
NOT CAUSING TOOTH DISCOLORATION
Toothpastes containing potassium nitrate have been used since 1980.
Since then, pastes containing potassium chloride or potassium citrate have been made available.
Potassium ions are thought to diffuse along dentinal tubules and decrease the excitability of intra dental nerves by altering their membrane potential.
The efficacy of potassium nitrate to reduce DH, however, is not supported strongly by the literature, according to Poulsen and colleagues.
Two studies support the desensitizing effectiveness of pastes containing potassium citrate.
Many toothpastes contain other ingredients such as fluorides (for example, sodium monofluoro-phosphate, sodium fluoride, stannous fluoride) and antiplaque agents in conjunction with desensitizing and abrasive agents.
Further studies are needed to determine that these various ingredients do not interfere with each other.
Practitioners should educate patients on how to use dentifrices and monitor their toothbrushing techniques.
Dentifrices should be applied by toothbrushing .
There is no evidence to suggest that finger application of the paste increases effectiveness.
Many patients habitually rinse their mouths with water after toothbrushing.
Rinsing with water may cause the active agent to be diluted and cleared from the mouth and, thus, reduce the efficacy of the caries-reducing effect of fluoride toothpastes.
Mouthwashes and chewing gums
Studies have found that mouthwashes containing potassium nitrate and sodium fluoride, potassium citrate or sodium fluori deor a mixture of fluorides can reduce DH.
In only one of these studies, however, was the effect of the active mouthwash significantly greater than that of the control product.
Another study concluded that a chewing gum containing potassium chloride significantly reduced DH, but the study did not include a control group.
DH severity should be reassessed two to four weeks after commencement of treatment to determine the effectiveness of the first level of desensitizing treatment .
If at-home care fails to reduce DH compared with baseline levels, the next level of treatment, an in-office method should be started.
Desensitizing agents intended for at-home use by patients generally are simple to administer.
Dental professionals can deliver a wider range of more complex and more potent desensitizing treatment.
Treatment of exposed root surfaces with fluoride toothpaste and concentrated fluoride solutions has been found to be very efficient in managing dentinal hypersensitivity.
The improvement appears to be due to an increase in the resistance of dentine to acid decalcification as well as precipitated fluoride compounds mechanically blocking exposed dentinal tubules or fluoride within the tubules blocking transmission of stimuli.
As alternatives with more accessible cost and simpler techniques of hypersensitivity treatment which aim at producing an occlusive effect on the dentin tubules, blocking the hydrodynamic flux,there are the application of fluoridated varnish, restorative or adhesive systems, e. g
silver nitrate ,
zinc chloride ,
calcium hydroxide ,
potassium oxalate (PEREIRA22, 1995),
propolis (MAHMOUD et al.17, 1999)
potassium nitrate (TOUYZ & STERN25, 1999).
Potassium nitrate in bioadhesive gels at 5% and 10% have been shown to be highly effective in reducing hypersensitivity.
Potassium ions are the active component, and potassium nitrate can reduce dentinal sensory nerve activity due to the depolarizing activity of the K+ ion.
It has been effectively and widely used to reduce hypersensitivity.
It has been suggested that strontium deposits are produced by an exchange with calcium in the dentin resulting in recrystallisation in the form of a strontium apatite complex.
Restorative resins&composite resins
The use of restorative material also have been proposed to treat dentine hypersensitivity.
Treating hypersensitivity with resins was pioneered by Brannstrom and his colleagues.
Second generation composite (Scotch bond) can be laid down successfully over lesions treated with fluoride iontophoresis.
Application of cyanoacrylate has been done with good desensitizing effect.
However, the complication of the first and second generation composites was that the incidence of sensitivity actually increased during use for aesthetic restoration.
The third and fourth generation bonding agents such as Gluma, Scotchbond II, All Bond, and C&B metabond allow better bonding to dentine, require less bulk for strength, penetrate the tubules better.
The use of materials like composite resins and glass ionomer restorations can be used in situations where there has been significant prior loss of cervical tooth structure or as a last resort for a tooth which does not respond to other less invasive desensitizing protocols
The use of restorative material to treat dentine sensitivity is technique sensitive and expensive but offer the hope of longer lasting and more predictable results than topical agents.
The choice of technique between iontophoresis and restorative material may depend on availability of the materials and the office personnel involved.
Firstly, the topical methods included the topical applications of caustics ,obtundants, fluorides, varnishes, oxalates, and potassium nitrates .
The caustics chemical are silver nitrate, zinc chloride, phenol, formaldehyde, concentrated alcohol, strong acid and alkalis.
They are used in attempt to precipitate proteins; however, they are harmful to the pulp and should be avoided.
Fluorides, on the other hand, have been proven to be effective for several days to several weeks (Hoyt and Bibby, 1943) when applied topically to the area of dentinal exposure.
Its mechanism of action involved a formation of barrier by precipitating the CaF2 at the tooth interface.
However, this precipitate is slowly soluble in saliva and thus the effect is temporary and needed to be reapplied.
The common commercial preparation of fluoride is 4% stannous fluoride in glycerine vehicle; however, the glycerine vehicle can activate the hydrodynamic mechanism and cause pain upon application.
Neutral sodium fluoride should be used when patient had esthetic porcelain restoration or implant in their mouth, since the acidity of stannous fluoride may etch the restoration.
Finally, 5-30% potassium nitrate, as proposed by Markowitz and Kim, can act directly on pulp nerves.
However, it would have to be applied frequently and reach a sufficient concentration at the site of neural transduction
Another topical method is the copal varnish but its action only last several hours and thus is used as the vehicle for fluoride.
Oxalates consisting of 3% KH2PO4 followed by 30% K2HPO4.
Commercial product including potassium oxalate and ferric oxalate are effective in bloking the tubules.
However, they have the same draw back as in the case of topical fluoride: eventually the saliva dissolves the surface precipitate that forms the barrier.
Toothpastes containing this agent have been shown to be effective in reducing hypersensitivity
This agent either in aqueous solution or in glycerine has been found effective.
The mode of action appears to be through the induction of a high mineral content which creates a calcific barrier blocking the tubular openings on the dentine surface.
Alternatively, it may precipitate on the dentine surface leading to occlusion of the exposed dentinal tubules.
Since their initial development as a desensitizing agent, the oxalates have gained rapid popularity.
Potassium oxalate and ferric oxalate solutions make available oxalate ions that can react with calcium ions in the dentinal fluid to form insoluble calcium oxalate crystals that are deposited in the apertures of the dentinal tubules.
Resins and adhesives
Sealing of dentinal tubules with resins and adhesives have been advocated for managing this condition with encouraging results however problems arise when they break away resulting in exposure of the tubules.
It is usually reserved for cases of specific and localized areas of hypersensitivity rather than generalized dentinal pain.
A combination of 5% potassium nitrate:fluoride dentifrice has been found to be safe and effective in providing patients relief from sensitivity and protection against dental caries.
DENTAL IONTOPHORESIS is used most often in conjunction with fluoride pastes or solutions and reportedly reduces DH.
LASERS . The effectiveness of lasers for treating DH varies from 5 to 100 percent, depending on the type of laser and the treatment parameters.
Studies have reported that the neodymium:yttrium-aluminum-garnet (YAG) laser, the erbium:YAG laser and galium-aluminium-arsenide low level laser all reduce DH.
Low level laser therapy for dentin hypersensitivity
Dentine hypersensitivity is a disease that affects both man and women, and it is an overreaction for a stimulus that normally would not cause pain in a healthy tooth.
The etiology is multifactorial , and the pain appears specially when the cervical region dentine is exposed to the oral environment.
The laser therapy has been proposed for the treatment of cervical hypersensitivity because it is painless for the patient.
The GaAlAs laser has been used for the treatment of dentin hypersensitivity.
It increases the production of mitochondrial ATP, increasing the threshold of the free nerve endings, providing an analgesic effect due to the increase of b-endorphine in the cephalorrhachidian liquid (BENEDICENT 1982).
The reduction of pain occurs because of the inhibition of the cyclooxygenase enzyme , which suspends the conversion of the arachidonic acid into prostaglandin
The laser also increases the formation of a secondary dentin by the odontoblasts .
The GaAlAs laser is easy to apply and presents good results as described in the literature (MEZAWA et al. 1988; FURUOKA et al., 1988, YAMAGUCHI et al.1990; GROTH )
BDP 660 class IIIb Laser – MMOPTICS
The laser therapy is a painless, safe, fast, conservative treatment, and it is well accepted by the patients (MARSÍLIO, 1999).
However, the lasers,especially high-level ones, are very expensive and the professional has to be qualified to its use.
The low-level ones, on the other hand, are more accessible to most professionals
Long-term studies are necessary to confirm the durability of the therapeutic effect of the treatment with low-level lasers compared to conventional forms of treatment, bearing in mind that the search for the cause of the problem is extremely important,
diet regularization ,
strength control and hygiene habits
CO2 laser irradiation and stannous fluoride gel has also been shown to be effective for inducing tubule occlusion for upto 6 months after treatment.
The pulpal effect of laser requires more investigation prior to its acceptance to be used with the hard tissue.
Currently, hard tissue application using laser has not been approved.
Iontophoresis is a technique using a small electric charge to deliver a medicine or other chemical through the skin.
Basically an injection without the needle.
The technical description of this process is a non-invasive method of propelling high concentrations of a charged substance, normally medication or bioactive agents, transdermally by repulsive electromotive force using a small electrical charge applied to an iontophoretic chamber containing a similarly charged active agent and its vehicle.
To clarify, one or two chambers are filled with a solution containing an active ingredient and its solvent, termed the vehicle.
The positively charged chamber, termed the anode will attract a negatively charged chemical, while the negatively charged chamber, termed the cathode , will attract a positively charged chemical into the skin.
Iontophoresis is well classified for use in transdermal drug delivery. Unlike transdermal patches, this method relies on active transportation within an electric field.
In the presence of an electric field electro migration and electro osmosis are the dominant forces in mass transport
These movements are measured in units of chemical flux, commonly µmol/cm 2 h
Fick's laws of diffusion
describe diffusion and can be used to solve for the diffusion coefficient,
They were derived by Adolf Fickin the year 1855
Fick's first law relates the diffusive flux to the concentration field, by postulating that the flux goes from regions of high concentration to regions of low concentration, with a magnitude that is proportional to the concentration gradient (spatial derivative). In one (spatial) dimension,
Fick's second law predicts how diffusion causes the concentration field to change with time
Iontophoresis is the process of introducing ionic drugs into the body surfaces for therapeutic purpose.
Iontophoresis requires that a charged drug (fluoride usually) be delivered at the electrode of the opposite polarity, the condition or disease under treatment be at or near surface, and a modern sophisticated source of direct current, with appropriate means of application be used
MECHANISM OF ACTION OF IONOTOPHORESIS
The mechanism of action of iontophoresis have been proposed as: a) rapid formation (7-28 days) of reparative dentine following application of current,
b) the alteration of the sensory nerve condution by the electrical currents , and c) fluoride ion, when introduced into dentinal tubule via iontophoresis , can reduce dentine permeability.
The third mechanism has been supported the most by literatures. Iontophoretic fluoride desensitization occurred by two mechanism: the intratubular microprecipitation of CaF2 affecting dentine permeability and an effect of fluoride on the neural transduction mechanism.
Murthy et al. in 1973 reported the effectiveness of fluoride iontophoresis.
They concluded that the desensitization occurred immediately after iontophoresis in most patients, whereas the placebo was ineffective.
The 1% fluoride iontophoresis provided a statistically more effective treatment than placebo or topical applications.
Also the burnishing of 33% topical fluoride paste was only modestly effective .
Gangarosa recommended that fluoride iontophoresis is permanent in its effect when the dentist applies it correctly to exposed dentine
however, highly sensitive teeth require two or rarely three treatments about 1 week apart before the effect can be considered permanent .
Iontophoretic fluoride desensitization occurred by two mechanism:
the intratubular microprecipitation of CaF2 affecting dentine permeability
an effect of fluoride on the neural transduction mechanism.
Treatment of hypersensitivity by electrosurgery has been advocated by Oringer in 1975.
However, the postoperative complications included irritation and pain due to pulpal injury by excessive heat generation are the major draw back.
Finally, the use of gingival graft on recession defect has been documented successfully.
Regenerative procedures using resorbable membrane, free gingival graft for root coverage, connective tissue graft have provided successful result in terms of both functional and esthetics.
The major draw back is the selection criterias for each procedures, the technique sensitive, and the cost of treatment.
Nevertheless, when can be done, periodontal plastic surgery is the best and ideal treatment in providing a long lasting result and esthetically pleasing.
The clinical goal to treat hypersensitive dentin is to provide a permanent seal of dentin tubules.
The seal can be established by any of the above methods and if done correctly, will provide the therapeutic effects .
Patient must recognized in some situation the condition may recur and require several application or re treatment.
Patient oral hygiene must be emphasized to reduce the plaque accumulation in the area.
The dentist also required to evaluate Patient systemic condition, nutritional diet, and be able to communicate with the patient on issues regarding his or her periodontal health and its correlation to the dentinal hypersensitivity.
. A large number of reports support alternative approaches for tooth desensitization.
Although these reports are not truly evidence-based, they may apply to some clinical situations.
For example, periodontal surgery involving coronally positioned flaps reportedly eliminates DH in extensively exposed root dentin.
If the DH is associated with an ABFRACTION LESION , OCCLUSAL ADJUSTMENT may be effective.
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.
Active management of DH usually will involve a combination of at-home and in-office therapies.
Root dentin hypersensitivity frequently develops as an uncomfortable& sometimes difficult ailment to treat,subsequent to scaling&root planing procedures in periodontal therapy.(jan lindhe 4 th edition)
Canadian Advisory Board on Dentin Hypersensitivity. Consensus-based recommendations for the diagnosis and management of dentin hypersensitivity. J Can Dent Assoc 2003;69:221–6.
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