Dentinal Hypersensitivity
by Dinh X. Bui, D.D.S., M.S.

Dentinal Hypersensitivity
Hypersensitivity implies that the dentin of the tooth involved is exposed. The prevalence of dentin sensitivity ranged from 8 to 30%. The prevalence increase with age, peaking at 25 to 30 years of age, then declining due to formatio of sclerosis dentin and/or reparative dentin. Dentin sensitivity can wax and wane over time in the same individual. Patient diet and personal habit may play a major role. Acidic food may attribute to the occurence of dentinal hypersensitivity. Most importantly, the presence of plaque may exacerbate the problem due to high amount of bacteria and bacterial product, coupled with acid production and further causing irritation. Dentin sensitivity usually observed on the buccal cervical areas of canines and premolars, commonly occured after oral prophylaxis or root planing due to exposed dentinal tubules. Finally, dentinal hypersensitivity may occur due to systemic problem such as in patient with bulimic problem or stomach regurgitation, which in turn lead to loss of enamel and expose coronal dentin. Exposed coronal dentin is much more difficult to treat than cervical dentin because of its higher permeability and innervation density.
To fully understand all the mechanism behind dentinal hypersensitivity, we must understand the dentin formation and its structure. Dentin is composed of inorganic and organic parts. Inorganic compounds composed mainly of hydroxyappatite, whereas the organic counterpart are mainly collagen. Dentinal tubule is formed as the odontoblast layed down the predentin, the odontoblast recede and leave behind the odontoblastic process trapped within the tubule. The diameter of dentinal tubules after demineralization and /or air drying has been quantified using light microscopy and scanning electron microscopy by J. Arens et al. in 1995. The tubule diameter was measured in wet state, after 10 min and 12 hour air drying as well as after critical point drying (CO2) by SEM. The results show that the drying effects on tubule diameter are small in sound tissue, but are sizeable in demineralized dentine. Comparing the light microscopic and SEM observations show that the difference in tubule diameter are small for sound but substantial for demineralied dentine. The dentine tubules in wet states are 2.5 micron, decrease in diameter as we increase demineralization by drying. The decrease tubule diameter with increasing demineralization occured may be important for permeability and transport phenomena in dentine caries and presumably hypersensitivity. As caries attack the tooth, the acid produced by dnetal plaque demineralized the mineralized tissue. The mineral crystallites in and on collagenous structure prevent collagen expansion. If the mineral is gradually removed by the acid system, the collagenous structure expand. J. Aren showed in his investigation that demineralization increase tubule size initially, but increasing mineral losses decrease the tubule size, and water loss caused by drying, increase tubule size in demineralized dentine, and finally the tubule diameter in sound dentine is not strongly influenced by air drying.
It has been demonstrated that the intradental A type (A beta and A delta) nerve fibers are responsible for the sensitivity of dentin and that the endings of the responding fibers are located in the pulp-dentine area of the tooth. The nerve fiber entering the teeth have been identified histologically as myelineated A fibers and unmyelinated C-fibers. These fibers are grouped in bundles, enter through the apical foramina of the teeth, passing through the radicular to coronal pulp where they fan out and diverge into smaller bundle. The A fiber within small bundles lose there myelin sheath and divide repeatedly before finally ramifying into a plexus of single axon known as the subodontoblastic plexus or plexus of Raschkow. From this plexus, nerve fibers are distributed toward the pulp dentin border with terminals showing a characteristic bead like structure. The fibers are grouped into four types: the marginal fiber which extend from suboddontoblastic nerve plexus to the odontoblast layer but do not reach predentin, the simple predentinal fiber which extend to the odontoblast/predentin border or enter the predentin, the complex predentinal fibers which reach predentin and undergo terminal ramification with multiple branches and multiple ending like enlargement on each branch, and the dentinal fibers which pass through the predentin and enter the dentin throught he dentinal tubule (its penetration is limited to approximately 100 microns). Ten Cate and coworker reported that odontoblast cell process extended only to the amelodentinal junction. Avery and Llja demonstrated approximately 25-27% of dentinal tubules has associated nerve fiber. More recently, sensory nerve fibers were identified in dentinal tubules by autoradiography technique. The A delta fibers are most responsible for the sensitivity of dentin. The A beta fiber respond to the non painful sensation induced by the low intensity electrical stimulation of human teeth. The exact mode of transmission of stimuli (thermal, chemical, mechanical) is investigated by D.G. Gilam in 1995. Three hypothesis suggested the mechanism of dentinal sensitivity transmission: a)nerve ending or nociceptor that respond directly when the dentin is stimulated, located throughout the dentin, b) the odontoblast, being chemically or electrically related to the nerves, function when depolarized as receptors generating nerve impulses; and c) stimuli applied to dentin producing a displacement of dentinal tubule contents which could excite mechanosensitive nerve endings near the pulpal end of the tubules (hydrodynamic mechanism). The mode of transmission to be explained here are direct nerve stimulation, dentinal receptor (transducer/modulation), hydrodynamic, and direct ionic diffusion hypothesis. Firstly, dentinal sensitivity may be caused by direct stimulation of nerve fibers. This theory was disproved in explanation of dentin hypersensitivity since algogenic (pain inducing) substance applied to the exposed dentin did not elicit a response. Similarly, topical anaesthetic solution when applied to the exposed sensitive dentin did not decrease sensitivity. Possible explanation for these phenomena included there is no nerve element in dentin or there are receptor mechanism in dentin that could be stimulated indirectly, but cannot be reached by direct stimulation from chemical agents becauses of some barrier to diffusion in the tubules. Secondly, the proponent of dentinal receptor mechanism hypothesis have suggested that the odontoblast has a special sensory function and that a functional complex with the terminal sensory nerve endings in close proximity to the odontoblast layer acts as an excitatory synapse. Several investigation however have failed to establish the presence of any synaptic junction or special form of connection between odontoblast process and nerve endings. It was unlikely that the odontoblast could perform the function of a special sensory receptor cell, which at the same time functioning as the specialized formation cell of dentin. Thirdly, the hydrodynamic theory is suggest to explain the dentinal hypersensitivity phenomena. The tubule contains fluid and the displacement of tubule contents, if rapid enough, could deform nerve fibers in pulp or predentin, or damage odontoblast cells; both effects capable of producing pain. Minute fluid shifts, either dentinal fluid or tubule contents, across dentin in either direction, in response to tactile, thermal, osmotic (chemical) stimuli, can stimulate mechanoreceptors in or near the pulp, which in turn, excite sensory nerves (A beta and A delta classes) to cause pain. According to Pashley, the hydrodynamic theory of dentin sensitivity as proposed by Brannstrom is based on the premise that sensitive dentin is permeable throughout the length of the tubule. Brannstrom and other investigator demonstrated in a series of experiment that fluid shifts occurred through the dentinal tubules when pressure and dehydration, as well as thermal stimuli, were applied to dentin. Following a decrease in pressure, there appeared an intense evaporation from the dentinal surface, producing a rapid fluid shifts which activate nerves located at some distance form the tubules corresponding to the exposed dentin. Dehydration (may occur due to hypertonic solution such as sugar and calcium chloride) causes the removal of dentinal fluid from the exposed dentin surface and by capillary action elicit an outward flow of tubule contents form the pulp, stimulating the odontoblast structure and causing pain. When cold or thermal change applied to the dentin, it was observed to cause a contraction of tubule contents, which in turn resulted in a rapid outward movement of fluid away from the pulp. Heat usually produced a dull response and took longer to develop, in contrast to the immediate sharp pain elicited from the cold stimulus. This delay in response may occurred due to a specific threshold of pulp temperature must be reached before pain can be experienced. Finally, several investigators suggested that application of various chemical solution to dentin resulted in raising the intratubular K+ content which in turn rendered the intradental nerves less excitable to further stimuli by depolarizing the nerve fibers membrane. Kim and Markowiz proposed the alternative mechanism (modified hydrodynamic theory), namely desensitization of dentin by blocking nerve activity.

Currently, the most accepted mechanism of intradental nerve activation associated with dentin sensitivity appears to be hydrodynamic in nature, although alternative mechanism of transmission cannot be ruled out. Recent investigation in the animal study (cat) has provided evidence substantiating the hydrodynamic hypothesis.

Rimondini and Carrassi in 1994 determined the relationship between the dentine ultrastructure and the clinical symptoms in patients with cervical dentine exposures. Total of 28 teeth with cervical noncariouus lesions and dentine exposures were obtained before and after acid etching. 120 areas were randomly selected from the 28 dentine surfaces were analyzed. The presence and morphology of smear layers and the density and diameter of dentine tubules were recorded. In the unetched specimens, the nonsensitive dentin surface were frequently coated by the amorphous smear layer (88%) and occasionally by a crystalline smear layer (2.7%). Only a few and narrow tubules were observed on the nonsensitive dentine (9.3%). On the other hand, the unetched hypersensitive specimen exhibited less frequently (33.3%) an amorphous smear layer, many and wider patent tubules, and grooves between tubules due to loss of intertubular dentine. In hypersensitive dentine, acid etching always removed the smear layer whereas removal in nonsensitive dentine was partial or absence. The hypersensitiv dentine smear layer was different in structure and undercalcified. These findings are supportive of the theory of increased hydrodynamic permeability of hypersensitive dentine.

During periodontal therapy, scaling and root planing removed the outer layer of hypermineralized dentine and thus leaved the surface expose to the effect of hydrodynamic phenomena. Surgical periodontal treatment, similarly, usually involved complete debridement of root surface. Post operative recession of soft tissue further exposed the dentinal tubules. Patient inability to maintain plaque control in the healing phase further complicated the problem, as plaque and acid production due to plaque accumulation could act as a noxious stimuli and cause dehydration and lead 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 dentin tubules for several micrometer. The smear layer thus is a natural iatrogenic yet transient treatment to dentin hypersensitivity. Removal of the outer smear layer and smear plugs with acids permits an increased in outward fluid flow and thus increase the patient postoperative dentine hypersensitivity.
Grossman in 1931 suggested that the ideal desensitizer should be: not unduly irritating to the pulp, painless when applied, easy to apply, consistently effective, permanently effective, quick acting, and not causing tooth discoloration. Another quality that we might add is that the ideal densensitizer 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 topical methods, iontophoresis, use of restorative material, electrosurgery, lasers, and guided tissue regeneration to cover gingival recession.

Firstly, the topical methods included the topical applications of caustics obtundants, fluorides, varnishes, oxalates, and potassium nitrates. The caustics chemical are usualyy silver nitrate, zinc chloride, phenol, formaldehyde, concentrated alcohol, strong acid and alkalis. They are used in attempt to precippitate 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 precippitating 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. 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. 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.

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 same 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. 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 recommend 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 (lasting over 1 year). 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.

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 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. Hygienist can perform iontophoresis, whereas dentist must perform all restorative technique.

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.

The Nd: YAG laser have been investigated in its use as an ideal desensitizing agent, except for the long term effects, which were not measured. 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.

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 retreatment. His or her oral hygiene must be emphasized to reduce the plaque accumulation in the area. The dentist also required to evaluate his or her 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.

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References

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