ETIOLOGY AND CLINICAL IMPLICATION OF DENTINE HYPERSENSITIVITY Introduction : • Relatively common cause of pain associated with teeth. • “An enigma”, frequently encountered but ill understood : • • Suitability of term questionable. In most cases pain is initiated and persists only during the application of a suitable stimulus to the exposed dentin surface, associated with many conditions including dental caries. • There is no evidence to indicate that “Hypersensitive” dentin differs in anyway from normal dentin or that specific pulpal changes occur. Term “Dentine sensitivity” may be more appropriate. Definition : Dentin hypersensitivity may be defined as pain arising from exposed dentine, typically in response to chemical, thermal, tactile or osmotic stimuli that cannot be explained as arising from any other form of dental defect or pathology. It is perhaps a symptom complex rather than a true disease and results from stimulus transmission across exposed dentine. Other conditions which may produce some symptoms include: • Chipped teeth • Fractured restorations • Restorative treatments • Dental caries • Undisplaced cracked cusps. • Palatogingival grooves / other enamel invaginations. History :
1
Tooth / dentin hypersensitivity is one of the oldest recorded complaints of discomfort to people. Inspite of a considerable amount of research over the last 50 years clinical management of dentin hypersensitivity still remains largely empirical because the physiologic mechanism remains ill defined and to some extent poorly understood. Mid 19th Century : Dr. John Neill of Philadelphia, postulated that “Dentin consists of hallow tubules filled with a fluid secreted by the pulp, and pressure applied without, by compressing the enamel and fluid of the tubules, affects the nervous pulp within, by subjecting the letter to a species of hydrostatic pressure, the amount of which can be measured. Whatever reduces the thickness of the enamel or uncovers any portion of the dentin, increases the painful impression caused by external pressure”. 100 years later Kramer proposed the “Hydrodynamic theory” as “The dentinal tubules contain fluid or semifluid materials and their walls are relatively rigid. Peripheral stimuli are transmitted to the pulp surface by movements of this column of semifluid material within the tubules. Work by Braunstrom resulted in widespread and current acceptance of the hydrodynamic theory. The early years from BC to 20th century : Pain in the teeth “Ya-Tong” treated by Chinese some 2000 years ago by application of “Xiao –Shi” believed to be Niter or potassium nitrate. Egyptian papyous Ebers, (3700 BC to 1550 BC), described gingivitis, the pain associated with tooth erosion and tooth ache. Rhages an Arabian physician 875 AD, first recognized the pain associated with gum recession, which occurred mostly in older people, and observed that it may be a difficult ailment in some and simple in others. Suggested treatment with astringent salts. 2
Leeuwenhock, shortly, after his invention of microscope described “tooth canals in dentin”. In 1678, he reported “It is asserted that the tooth is formed from very narrow, transparent tubes six or seven hundred of these pipes put together exceed not the thickness of one hair of a man’s beard”. Mid 1860’s Francis presented view of fluid movement impinging on pulpal nerves and causing pain and supported the practice of using cavity liners to promote the development of secondary dentin for “Better self protection”. For serious sensitivity problems, he recommended a paste of arsenous acid, tannin and creosote. Late 1880’s use of carbolized potash (Robinson’s Remedy) (trituation of equal proportion of carbolic acid and potassium hydroxide) came into widespread use for treating sensitivity of dentin. (No one had yet ascribed the effect to potassium ions until quite recently i.e. In 1900 issue of British Journal of Dental Sciences, a published report appeared by Alfred Gysi, stated that “dental conaliculi are devoid of nervous substances”, but that at inner boundary of dentine around the odontoblasts there is an “abundant network of finest nerve fibers. He proposed that movement of fluid in dental canuliculi in either direction results in a sensation of pain in the nerves interwoven with the odontoblasts. “Drawing” or movement of fluid away from pulp can be induced by “salt, sugar, alcohol etc.” He also stated that “when however the externalportion of the contents of the tubuli is caused to coagulate albumen, such as by carbolic acid or formed of sublimate and thereby loses its mobility, then also the great sensibility disappears”. Although Gysi was not the first to describe fluid movement in dentinal tubules, he was among the first to suggest relieving dentin sensitivity by coagulating its protein content.
3
1st edition of a textbook of dental pathology and therapeutics including pharmacology by Henry H. Burchard in 1898 provides a categorization of 3 approaches for controlling pain of hypersensitivity of dentin. 1. Administration of agents to lower the pain perceptive centers of the brain (anesthetic and analgesic agents) 2. Use of agents to destroy or coagulate the dentinal protoplasm (zinc chloride, silver nitrate, carbolic acid, mineral acids, concentrated alkalies and others). 3. Use of local anesthetic agents on the dentin (essential oils, sedative alkaloids, morphine, atrophine, cocaine etc.) Suggestion was made for the use of an electric current to deliver medicaments more effectively. First half of twentieth century : Textbook dental pathology and therapeutics, Henry Burchard states “The exposure of dentine to external agencies is so commonly followed by an increase in sensitivity that the condition requires description in itself. It is a general condition attendant upon abrasion, erosion and caries, and has a therapeutics of its own”. The nitrate of silver powerfully coagulates fibrillar protoplasm, forming albuminate of silver, which turns black upon exposure to light. Subsequent use of sodium chloride reduces staining. “Potassium carbonate in glycerin may be given to the patient for self treatment at home”. Mid 1930’s, 2 important publications appeared that include Charles F Bodecker and Edward Applebaum’s and second by Louis I. Grossman. First was regarding active metabolism in the dentin. Their conclusions were that there is an active exchange between the fluids of the dental pulp and the structure of the teeth. In young teeth, fluid flows readily 4
from the pulp and provides the necessary calcium phosphorus and carbonate to carry on mineralization process. The odontoblasts that line the pulp chamber and pulp canal are probably secretory cells. Residual fluid, depleted of salts, passes back through Neumann’s sheath into the circumtubular space. When caries threatens the tooth structure, a defensive mechanism occurs to put down a layer of secondary dentin to help protect the pulp. In young teeth, this process is not yet well developed, and the carious process proceeds rapidly to involve the pulp. 2nd publication by Louis I. Grossman 1935 gave a comprehensive summary of causes of hypersensitive dentin and the methods used to treat it. According to him, hypersensitiveness in dentin describes an uncommonly sensitive or painful response of the exposed dentin to an irritation. This includes dentin exposed by caries, attrition, abrasion or erosion, by failure of the enamel to meet the cementum and by marked atrophy of the alveolar process, exposing both dentin and cementum. Chemical stimuli that affect hypersensitive dentine include citrus fruits, berries, acid food stuffs such as tomatoes or rhubarb, vinegar, candy, sugar, salt and other condiments and many raw and cooked foods. Physical stimuli include temperature below 100C or above 400C or tactile pressure. He pointed to Gysi’s explanation that because fluid in tubules is incompressible, a stimulus induces a wave like motion transmitted to the pulp. Grossman listed the requirements for an ideal therapy : 1. It should not usually irritate or in any way endanger the integrity of the pulp. 2. It should be relatively painless on application or shortly afterward. 3. It should be easily applied. 5
4. It should be rapid in its action 5. It should be permanently effective 6. It should not discolor tooth structure. 1936, Dr. Hartmann proposed application of a balanced micture of ether chloroform and thymol based on the theory that lipoids present in dentin play an important role in transmission of sensation. “Semitex” a commercial densitizing agent in solution form was a chloride of metals : sodium, magnesium, zinc, potassium, aluminium, calcium, aluminium oxide, and triple distilled water. In 1941, Lukomsky advocated sodium fluoride as a desensitizing obtundent. Hoyt & Bobby (1943) reported an effectiveness of a paste made of equal parts of sodium fluoride, white clay and glycerin. Since this report, it has probably been the most extensively used dental office therapy to treat hypersensitivity. 2nd half of 20th century : Emoform toothpaste was introduced in Switzerland by Dr. Wild in late 1940’s. It contained : - Formaldehyde 1.4%] - Calcium carbonate 14% - Magnesium carbonate 15% - “Mineralizing salt” mixture of Sodium bicarbonate 3.4% Sodium chloride 1.45% Potassium sulfate 0.0075% Sodium sulfate 0.0075% Introduced in U.S. as Thermodent. Pawlowska 1956 published a report stating that strontium chloride “combined with biocolloids of teeth” exerted a favourable effect on
6
hypersensitivity, based on this report sensodyne toothpaste was developed with strontium chloride hexohydrate. A possible explanation for mechanism of strontium ion was advanced by Gutentag. He proposed that since calcium has been shown to stabilize excitable neural membranes by modifying their permeability to sodium and potassium, the effect is more pronounced and longer lasting with strontium. In 1962, Bromstrom summarized the “Hydrodynamic theory of dentinal pain excitation. Everett and colleagues summarized in 1966 therapies popular for treatment. 1. A paste containing 2% formaldehyde in a vehicle of calcium carbonate, magnesium carbonate, sodium bicarbonate and soap powder. 2. A formaldehyde containing mouthwash. 3. Fluorides in various forms and their vehicles, applied either alone or by a sequential treatment with calcium hydroxide. 4. Strontium chloride 5. 28% Ammoniacal silver nitrate. 6. Zinc chloride – potassium ferrocyanide impregnation (Gottlieb’s solution) in which the active ingredients are applied sequentially. 7. Corticosteroids 8. Sontophoresis with fluoride In 1974, Hodosh proposed a “superior” densensities, potassium nitrate. Presumably, the mechanism depends on the ability of K + to permeate through the dental tubules to nerve endings at the dentin-pulpal junction and there to modify the usual exchange of sodium and potassium in nerves (Na + K+ Pump)
7
Berman proposed the term “dentinalgia” to differentiate sensitivity from “Pulpalgia”. The “gate control therapy” and the hydrodynamic theory were proposed as most probable mechanisms. Orchardson and coworker published reports on some characteristics of tooth hypersensitivity. In one report, 109 patients in Scotland were examined for hypersensitive dentin 80% were sensitive to cold alone or to cold and some other stimuli. Lower 1st molars and upper canines were most frequently affected, and 68% of hypersensitive teeth had significant recession but only 25 percent had evidence of abrasion, attrition or erosion. Use of iontophoresis with sodium fluoride has been reevaluated in recent years. Carla Ciancio and Seyrek reported that over 90% of patients thus treated had a significant reduction in sensitivity. Kleinberg (1986) summarized the different approaches that have been used to treat hypersensitive dentin. 1) Remineralization by saliva deposits of calcium phosphate complex within dentinal tubules. 2) Formation of secondary dentin, which may occur naturally or can be stimulated by daily burnishing. 3) Calcium hydroxide facilitates calcium phosphate deposition from dentinal fluid and saliva. 4) Potassium oxalate forms calcium oxalate within dentinal tubules. 5) Sodium fluoride promotes the deposition of less soluble fluoropatite 6) Sliver nitrate precipitates proteins within dentinal tubules 7) Strontium chloride forms strontium hydroxyapatite and strontium phosphate within dentinal tubules. 8) Resins seal the outer ends of dentinal tubules. 9) Potassium nitrate appears to be effective.
8
10) Dentrifices may provide one of the active ingredients above or function by occluding tubular orifices. Krawer pointed out that severe cases of sensitivity can be so problematic as to cause an emotional change among sufferers that can alter lifestyle. SUMMARY : For well over a century, there has been cognizance that sensitivity is a serious problem, that is arises when the dentin and cementum are exposed, that fluid movement within the dentinal tubules acts as a provocative stimulus, that tubules can be sealed off (apparently in most instances) without damage to the tooth or the dental pulp, and that the problem can also be at least partially resolved by suppressing nerve firing within the pulp. Sealing off the dentinal tubules or dampening neural impulses, although admittedly none meet all of the hypothetic requirements proposed by Grossman over 50 years ago. Fluorides, strontium chloride, potassium nitrate, potassium oxalate, sodium citrate, surface sealing agents (varnishes, resins, cyanoacrylate), calcium hydroxide, and others. Tooth hypersensitivity in the spectrum of pain : As an exaggerated response to a non-noxious sensory stimulus. The sensory stimuli usually considered are thermal by the application of a burst of air to the tooth and tactile by running a metal instrument across the hypersensitive region of the tooth. Tooth hypersensitivity is viewed as originating from the underlying exposed dentin. Merskey for the international association for the study of pain (IASP). Pain is described as an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage. Tooth hypersensitivity is not associated with actual tissue damage in the acute
9
sense but can involve potential tissue damage with constant erosion of the enamel or cementum along with the concomitant Pulpal response. Allodynia pain resulting from a non- noxious stimulus to normal skin. “Allodontia” to describe appropriately tooth hypersensitivity is a chronic condition with acute exacerbations. Chronicity ends when the enamel or cementum defect is restored; however, differs from dentinal and Pulpal pain in that the patient’s ability to locate the source of pain is very good. Aside from that characteristic Tooth hypersensitivity is similar in its description to dentinal pain – i.e., in terms of its differential diagnosis. The character of the pain does not outlast the stimulus, the pain in intensified by thermal change, and sweet and sour. Pain intensity is usually mild to moderate; both can be associated with caries, defective restorations, and exposed dentin. The pain can be duplicated by hot or cold application or by scratching the dentin, and both tooth hypersensitivity and dentinal pain usually show a normal radiographic architecture of the peripheral region. Dentinal hypersensitivity is a response from a non-noxious stimulus and a chronic condition with acute episodes; whereas dentinal pain is a response from a noxious stimulus and usually an acute condition. A clear understanding of tooth sensory conduction still needs further elucidation to aid the clinical investigator in choosing the most appropriate clinical model. The fact that local anesthetics applied topically to dentin are not affective and that one can still elicit a pain response from a root-canaled tooth (from exteroceptors from the periodontal ligament) present challenging in vitro and in vivo hurdles to overcome in the future by dental scientists in deciphering the mechanism of action. DENTAL HYPERSENSITIVITY : Pulpal considerations : The tooth pulp and dentin are now known to be innervated by A-delta and C-fibers that form an interlacing network, the subodontoblastic plexus. 10
From this plexus, nerve fibers extend to the odontoblastic layer, predentin, and dentin and terminate as free nerve endings. The sensory receptors respond to chemical, thermal and mechanical stimuli and are thus termed polymodal. It has been proposed that A-delta fibers are responsible for dentinal pain, and C-fiber nociceptors (receptors preferentially sensitive to a noxious or potentially noxious stimulus account for the pain from external irritants that reach the pulp. Morphologically, nerve fibers may penetrate into the dentin as far as 150 to 200 Âľm only. Except possibly for serotonin, many vasoactive substances implicated in pain (such as substance P, bradykinin, and histamine) appear to have no direct effect on A-delta Pulpal afferent but may activate C-fiber Pulpal afferents. Sympathetic nerve simulation and changes in blood flow can alter Pulpal afferent activity, and it now seems likely that these substances may have indirect effects by altering blood flow. The neural theory attributes activation to an initial excitation of those nerves ending within the dentinal tubules. These nerve signals are then conducted along the parent primary afferent nerve fibers in the pulp into the dental nerve branches and then into the brain. The hydrodynamic theory proposes that the stimuli cause a displacement of the fluid that exists within the dentinal tubules. This mechanical disturbance activates the nerve endings in the dentin or pulp. The odontoblastic transduction theory proposes that the stimuli initially excite the process or body of the odontoblast, the membrane of which may come into close apposition with that of nerve endings in the pulp or in the dentinal tubule, and that the odontoblast transmits the excitation to these associated nerve endings. Technically, enamel and cementum erosion of a tooth would satisfy the definition of inflammation (i.e., a localized protective response elicited by injury or destruction of tissue), which serves to destroy, dilute, or wall off both the injurious agent and the injured tissue. The tooth can mask the 11
classical signs of acute inflammation including heat, redness, and swelling to some extent, but not pain and loss of function (sensitivity to chewing, percussion and air). It is interesting to speculate the role, if nay that the process of inflammation plays in the chronic conditions of dentinal hypersensitivity. The biochemical cascade involved would allow a wide range of clinical and Pharmacologic approaches for its treatment. Currently the treatment of choice for the chronic management of dentinal hypersensitivity. The active agent that has the widest data base of in vivo as well as in vitro studies is strontium. 1) cariostatic effects, especially in the pre-eruptive phase of tooth formation, 2) strontium can be taken up at extra-vascular site and the retention is by surface adsorption; 3) strontium can be sued to differentiate two different forms of acetylcholine (ACh) secretion and is effective in supporting asynchronous, neurally evoked ACh release asynchronous ACh secretion is the delayed, residual increase in miniature end-plate potential frequency evoked by repetitive nerve impulses that can be analogous to dentinal hypersensitivity; 4) in many secretory processes, strontium can substitute for calcium in activating the secretory mechanism, and can possibly affect or modulate the Pulpal cholinergic
and
adrenergic
mechanisms
involved
in
dentinal
hypersensitivity; and 5) strontium can increase the time of the rat trial-flick response suggesting analgesia and may possess central analgesic potency similar to narcotic drugs by possibly altering the calcium disposition including binding or transport. Strontium chloride dentifrices have been suggested to work by occluding dentinal tubules by binding to the tubules matrix and / or stimulating reparative dentin formation. The simplest conclusion to be drawn is that in vitro models do not provide a good model to extrapolate data to explain human dentinal sensitivity. In humans stimuli are applied to outer dentin, whereas in animal models the stimuli are applied to deep cavities, where the length and width 12
of the tubules would facilitate a direct action on nerves in the inner dentin or pulp. Additionally, dentin electrodes can record from only a limited sample of the total intradentinal nerve population, not taking into account neural convergence or summation. More than twenty peptides have been identified in the nervous system; some (such as bradykinin, serotonin, and substance P) have been identified or associated with sensitization of the tooth. Sensitization of tooth neciceptors after repeated exposure to noxious stimuli can lower the nociceptor threshold, allowing for increased sensitivity to what was normal and is now a suprathreshold stimuli (hypersensitivity) and if persistent to spontaneous activity (odontalagia). Subjective considerations : To evaluate the subjective responses of pain, many pain-word questionnaires, visual analog scales, and lists of worlds are currently available and have been used to assess various pain syndromes with controversy as to which are the most appropriate. To assess a patient completely an evaluation of the physical determinants of pain should be supplemented by an assessment of at least two other components – one observable, the other more subjective. Gracely has listed five properties for an ideal pain measure to both optimize the information gained on the subjective component, and to relate the clinical and experimental assessment of pain. They are 1) sensitive measurement free of biases inherent in different assessment methods; 2) provision of immediate information about the accuracy and reliability of the subject’s performance in the task; 3) separation of the sensory – discriminative aspects of the pain experience from its hedonic qualities; 4) usefulness for clinical as well a experimental pain measurement, allowing reliable comparisons between these fundamentally different types of pain; 5) absolute measures that increase the validity of pain comparisons between and the within groups over time. 13
Chronic pain is a learned behavior, and the chronic pain patient is a person who acts like a chronic pain patient. It is immaterial whether the pain is somatogenic, neurogenic, or psychogenic (or for that matter, whether there “really” is any subjectively experienced pain). Chronic dentinal hypersensitivity patients acquire learned behavior characteristics such as avoiding cold drinks and certain foods, not opening their mouths, on cold days, and avoiding tooth brushing in sensitive areas – possibly making them susceptible to gingival and periodontal problems. Recently, Woolf described a distinction that should be made between two forms of organic pain: physiologic and pathologic. The distinction between the two depends on the premise that physiologic pain is a “normal” sensation, whereas pathologic pain is the consequence of an “abnormal” state. Dynamic sensations perceived as a result of stimuli “of sufficient intensity to threaten to damage tissue or produced small localized areas of injury, but which neither provoke an extensive inflammatory response nor damage the nervous system” as physiologic pain. It can be manifested in response to mechanical, thermal, or chemical stimulation. It is characterized by quantifiable stimulus-response relationships, yet it is particularly susceptible to interference from psychologic factors. This definition aptly describes dentinal hypersensitivity, takes into account the polymodal nature of the nerve fibers, and considers the psychological component. SUMMARY : It is estimated that the frequency of dentinal hypersensitivity affects one of six people, and one or more teeth can be affected. The incidence of dentinal hypersensitivity appears to peak around the third decade of life and may appear as root sensitivity in the fifth decade of life as root sensitivity particularly in patients undergoing periodontal surgery. The neurophysiology of the teeth :
14
It is well known that even the most peripheral part of dentin can be sensitive. Recent neuroanatomic studies have shown that only the inner 100 to 200 µm of dentin is innervated, odontoblasts would act as receptor cells and mediate the effects of external stimuli to the nerve ending located in the pulp – dentin border. However, there are few experimental data supporting this theory. Moreover, combined electrophysiolgic and histologic studies have shown that dentin can be sensitive despite irritation – induced odontoblasts aspiration and other tissue injury in the pulp-dentin border area. Also, the nerve endings in dentin were found to be injured in these studies. Human dentin can be sensitive despite considerable tissue trauma in the pulp-dentin border. INNERVATION OF THE PULP AND DENTIN : As already mentioned, the dental pulp is enormously richly innervated. The mean number of axons entering one human premolar tooth is 926. a great majority of the axons are unmyleinated. To Byers, one axon may innervate more than a hundred dentinal tubules. The density of the innervation in the pulp-dentin border is enormous. However, most of the recent studies indicate that only the inner 100 to 200 µm, of dentin is innervated. This has been confirmed with electron microscopic techniques as well as with light microscopic studies employing autordiographic and immunohistochemical nerve labeling methods. The density of the innervated tubules is highest in the area of pulp horns. Although close contacts have been shown to exist between the nerve fibers and the odontoblasts synapses or other junctions that would allow nerve impulse transduction between the cells do not seem to exist. Although the results of many histologic studies are conflicting, the most recent results indicate that the odontoblast process is restricted to the inner third of the dentinal tubule. Accordingly, it seems probable that the 15
outer part of the dentinal tubules does not contain any cellular elements but is only filled with dentinal fluid.
THE FUNCTION OF INTRADENTAL NERVES : Much of the information concerning the function of intradental nerves, especially that of C-fibers, originates from single unit recordings performed on experimental animals. The recent electrophysiologic recordings indicate that intradental nerves in cats, dogs, and monkeys function in the same way as those in human teeth. Also the structure of intradental innervation is similar in all these species. As already mentioned, the dental pulp is innervated by both myelinated and unmyelinated axons. Correspondingly, according to conduction velocities (c.v.), the nerve units can be classified into A- (c.v >2 m/s) and C-groups (c.v. ≤2 m/s). Most of the A-fibers have their conduction velocities – velocities within the Aδ range (<30 m/s). This functional organization of intradental innervation is significant because in other parts of the body the first, sharp, better localized pain is mediated by Aδ-fibers, whereas C-fiber activation seems to be connected with the second, dull, radiation pain sensations. Some intradental nerve axons have conduction velocities higher than 30 m pre second and thus they can be classified as Aβ-fibers. They have bee suggested to mediate non-painful sensations induced by low-intensity electrical stimulation of human teeth. However, their responses to other stimuli applied to the tooth indicate that they belong to the same functional group as the intradental Aδ-fibers. There is little evidence that stimuli other
16
than electrical can induce non-painful sensation when applied to human teeth. Intradental A-fibers respond to drilling of dentin. They also respond to probing and air drying of dentin and hyperosomotic solutions applied to the exposed dentin surface as well as to direct mechanical irritations of the pulp. The C-fibers of the pulp do not respond to the same type of dentinal stimulation. A fibers also respond to rapid heating of the tooth. The nerve firing starts within a few seconds few the beginning of stimulation. In this stage, no considerable change in the temperature of the pulp-dentin border has occurred. Accordingly, the nerve responses cannot be due to a direct effect of heat on nerve terminals. If heating of the tooth crown is slow, Afibers do not respond, even if the pulp temperature is elevated up to 50 to 600C. Temperature changes are able to induced fluid flow in dentinal tubules. With intense heating, the fluid flow is strong enough to induce activation of intradental A-fibers (see Pashleyâ&#x20AC;&#x2122;s article, Mechanisms of Dentin Sensitivity). A common effect of the stimuli activating A-fibers is that they can induce fluid flow in dentinal tubules, as studied in vitro. The C-fibers of the pulp are polymodal and respond to several different stimuli when they reach the pulp proper. In heat stimulation their mean threshold temperature is 43.8 Âą 3.40C. Considering the function of both intradental nerve fiber groups, rapid heating induces A-fiber activation within a few seconds followed by a delayed C-fibers firing. Sharp pain is induced within a few seconds, and if stimulation is continued, a dull, aching, and radiating pain sensation is evoked. Intradental C-fibers also respond to direct mechanical irritation of the pulp tissue and to such chemicals as bradykinin and histamine. A-fibers are not activated by these chemicals. From this point to view, it is interesting that bradykinin applied on the exposed human pulp induces dull pain. 17
In general, unmyelinated axons are more resistant to the effects of pressure and hypoxia than myelinated fibers. Both pressure elevation and hypoxia may occur in the pulp during inflammation. Accordingly, the function of intradental A-fibers may be locked. On the other hand, such inflammatory mediators as histamine and bradykinin are released and are able to activate intradental C-fibers. Explain why the pain connected with advanced pulpitis is dull, aching, and poorly localized. THE MECHANISMS OF DENTIN SENSITIVITY : Myelinated A-fibers seem to be responsible for dentin sensitivity. The sensitivity of the nerve units is very dependent on the condition of the dentin surface, with either open or blocked dentinal tubules. Acid etching of the drilled dentin surface removes the smear layer and pen the dentinal tubules, and the sensitivity of the nerve fibers to dentinal stimulation is increased to a great extent. Blocking of the tubules with resin impregnation or potassium oxalate treatment prevents the nerve activation. Because pain in general is evoked by intense stimuli that induce tissue damage (noxious stimuli), a clinically relevant problem is whether stimulation of dentin, for example with air blasts, is noxious to the pulp. On the other hand, if tissue damage is induced in connection with dentinal stimulation and pulp nerve activation, it would be important to know how the nerve function might be affected by the injury. Air drying of human dentin induces odontoblast aspiration into dentinal tubules. Moreover, chronic dentin exposure may result in considerable tissue damage and inflammation in the pulp-dentin border area. It seems that thee morphologic change do not affect dentin sensitivity that much. In dog teeth, dentinal stimulation causes tissue damage in the pulp dentin border area, and the dentinal innervation is injured. The responsiveness of the units seems to be more dependent on the openness of the dentinal tubules than the tissue injury in the pulp â&#x20AC;&#x201C; dentin border. These 18
results from human and animal experiments support the view that the activation of intradental nerves by dentinal stimulation must be induced by an indirect effect. These result also indicate that sensitive dentin does not necessarily mean that the dental pulp is healthy. Neither does insensitive dentin mean that the pulp is dead. Sometimes patients may have wide areas exposed dentin without feeling any discomfort or pain. In these the dentinal tubules may be blocked by dentinal sclerosis or irritation dentin formation in the pulp 窶電entin border area. Certain inflammatory mediators, such as prostaglandins, histamine, serotonin (5-HT), and neuropeptides, such of the nerve endings. Accordingly, their thresholds to external irritation may change. For example, after local application of serotonin on dentin close to the pulp, the responses, of the intradental nerve fibers to dentinal stimulation are much enhanced. MECHANISMS OF DENTIN SENSITIVITY : HISTORIC CONSIDERATIONS : Clinician knew that freshly exposed dentin was extremely sensitive and concluded (erroneously) that nerve fibers in teeth must extend to the DEJ to be responsible for such pain. When histologists began looking for nerve fibers in peripheral dentin using light microscopy and special heavymetal stains, they found that branches of Pulpal nerves did not extend more than 100 ﾂｵm into peripheral dentin. Rapp and his colleagues, proposed that odontoblasts could serve as receptors. Stimulation of odontoblast processes in peripheral dentin was proposed to cause change in the membrane potential of odontoblasts via synaptic junctions with nerves, thereby causing pain. However, careful electron microscopy failed to demonstrate any synaptic complexes between Pulpal nerves and odontoblasts. Perhaps the most damaging blow to that
19
hypothesis was the observation that odontoblast processes may not extend peripherally beyond one third to one half of the length of dentinal tubules. Anderson and colleagues and Brannstrom, working independently, found that peripheral dentin, although very sensitive to a variety of physical stimuli (tactile, thermal, evaporative) was uncreative to KCI and local anesthetics,
which
normally
modified
nerve
activity.
Brannstrom
reintroduced Gysi’s concept that sensitivity may be due to the movement of tubule contents, the so called hydrodynamtic theory of sensitivity. Unlike Gysi, Brannstrom accumulated a great deal of laboratory and clinical evidence to support the concept that, although the peripheral one half of dentin is devoid of nerve or odontoblastic processes, movement of fluid within dentin transduces surface stimuli by deformation of Pulpal mechanoreceptors, which in turn, cause pain. This hypothesis, which is currently the most popular theory. PULPAL INNERVATION : Nerve type : The dental pulp is richly innervated with a variety of nerve fibers. Only a few of the 1000 to 2000 nerves found in each tooth reach the dentin. Of these nerves, approximately 75 per cent are nonmyelinated and 25 per cent are myelnated. The myelinated nerves are classified as A-α, β, or -δ fibers, depending upon their axon diameter and their conduction velocity. Most of the myelinated nerve fibers in teeth are A-δ nerves, which are thought to be responsible for the brief, sharp, well-localized pain associated with dentin sensitivity. These fibers have a relatively low stimulation threshold. As they are relatively large, their depolarization causes much more current flow than smaller nerves, and their activity can be recorded extracellular from cavities cut into dentin. When investigators measure intradental nerve activity, the implication is that it is A-δ nerve activity. The unmyelinated nerve of the pulp are composed of small c-fibers and 20
sympathetic nerves. The c-fibers contain peptides that may contribute to both pain sensation and local inflammation. The poorly localized, dull, burning ache of Pulpal pain is thought to be due to c-fiber. They are too their fibers from the mandibular nerve as “single units,” which are then placed on recording electrodes. The stimulation threshold of c-fibers is relatively high. The proportion of sympathetic nerves in the total number of unmyelinated nerves has been reported to vary from 10 pre cent to a majority of the fibers. Normal electric pulp testing stimulates the lowest threshold nerves first which are A-δ fibers. Higher currents are required to activate c-fibers. Few electric pulp testers used in clinical practice can stimulate c-fibers, although the development of such devices may be useful in future clinical research. Nerve Reactions : Vasoactive peptides such as substance P, calcitonin gene – related peptide (CGRP), and neurokinins A and B (NKA, NKB) are found in cfibers often in close association with blood vessels. They can be released by tissue destruction (pulp exposure, elevated cutting temperature, antigenantibody reactions, complement activation) or by antidromic stimulation of the inferior alveolar nerve. These peptides all promote vasodilation and plasma extravasation. These
agents
contribute
to
the
phenomenon
called
“neurogenic
inflammation and they have been demonstrated in the dental pulp. The utility of neurogenic inflammation was developed in Lewis’s nocifensor system, which consisted of a peripheral neurogenic defense mechanism by which exogenous or endogenous toxic material was removed by local increases in tissue blood flow, interstitial fluid production, and lymph drainage. The dental pulp contains for more unmyelinted than myelinated neurons. These nerves proliferated in response to bacterial challenge. In the 21
low-compliance environment of the pulp, neurogenic inflammation may, under some conditions, promote and sustain dentin sensitivity rather than leading to its resolution. The wave of depolarization traveling along the nerve which depolarize back toward the periphery. Recent modifications to the original concept suggest that the nerve can act as both receptors and effectors. In this way, painful impulses may perpetuate Pulpal inflammation and perhaps aggravate it. Nerves that contain these neurogenic peptides are capsaicin-sensitive. The most interesting effect of capsaicin is its ability to desensitize tissues to the effects of SP, CGRP, and NKA. Capsaicin itself can cause pain when applied to dentin, presumably by causing the release of substance P. A-δ fibers can be stimulated repeatedly for hours with no apparent change in their sensitivity. They are polymodal (sensitive to changes in temperature, osmotic pressure, or tactile stimuli) fibers that are not sensitive to bradykinin or histamine. They mediate the sharp, transient pain that is typical of dentinal sensitivity. In contrast, c-fibers are activated by chemical mediators of inflammation. They produce a dull, aching pain when bradykinin or histamine is placed in deep cavities cut into human teeth. A brief application of hot gutta-percha on crown enamel can produce a transient burst of A-δ nerve active. If a tooth is heated continuously but very slowly, no nerve activity is produced until tissue damage results, causing cfibers to fire. Based on indirect evidence, Kim has suggested that vasodilating agents may actually decrease Pulpal blood flow following a transient increase in blood flow. As the pulp is a low-compliance environment, any increase in its volume, whether due to dilation of vessels or filtration of fluid across capillaries following dilation, would increase tissue pressure, which would compress local venules, thereby increasing postcapillary resistance and decreasing blood flow. 22
DENTIN CONSIDERATIONS : When the Pulpal terminations of the tubules are sealed by reparative dentin, the dentin is generally insensitive for two reasons. First, reparative dentin generally has fewer tubules than primary dentin. Second, reparative dentin generally has few nerves innervating the dentin. There are two mechanisms responsible for the permeation of substances across dentin: diffusion and convection. Diffusion is the process by which substances are transported from an area of high concentration to an area of low concentration. In pure diffusion, there is no bulk fluid movement but only molecular translocation. In convective transport or filtration, bulk fluid movement occurs from an areas of high hydrostatic pressure to an area of low hydrostatic pressure. This type of fluid movement can be quantitated by measuring the hydraulic conductance of dentin. Hydraulic conductance is the reciprocal of resistance. That, is dentin with a high conductance has a low resistance. The important variables regulating hydraulic conductance of dentin are the length of the tubules (that is, dentin thickness), the number of tubules per unit surface area, the applied pressure, the viscosity of the fluid, and the radius of the tubules raised to the fourth power. These are expressed in the Poiseuille-Hagen equation. Q=
II∆Pr4N 8nL
Where: Q = Fluid flow ∆P = applied pressure (hydrostatic or osmotic) r4 = radius of tubules (that is, ± smear layer) N = tubules density (depth – dependent) n = viscosity of fluid (temperature –dependent) L = length of tubule (remaining dentin thickness)
23
The amount of fluid that can shift across a full preparation is much larger than the amount that can shift across a buccal pit preparation. The most important variable is the radius of the tubule because it is raised to the fourth power. The creation or dissolution of smear layers and smear plugs from dentinal tubules can have a profound influence on the hydraulic conductance of that dentin and hence its sensitivity. However, the hydraulic conductance of dentin is not uniform but is highest over pulp horns, high on axial walls, and relatively low on root surfaces. This is due in part to regional differences in tubules density and diameter and in part or regional differences in the amount of intratubular material. The surface resistance of dentin is variable owing to the presence or absence of the smear layer or the growth calculus or other surface deposits. Patients with sensitive dentin generally lack smear layers and have open tubules orifices. Several therapies bases on tubule occlusion have been proposed that were designed to decrease fluid flow by decreasing the hydraulic conductance of dentin. Exposed dentin free of a smear layer should have a high hydraulic conductance. If these tubules are open all the way to the pulp, Pulpal fluid should slowly filter down its hydrostatic pressure gradient to the surface. This has actually been demonstrated by Linden and Brannstrom and by Pashely and associates in vivo. Apparently, the spontaneous rate of fluid filtration across open, sensitive dentin is too slow to activate the mechanoreceptors. When an additional stimulus is superimposed on it, however, then the receptors are activated. Steadily applied pressures do not cause as much pain as when the pressure is suddenly applied or released. MECHANISTIC EVALUATION OF ADEQUATE STIMULI : Tactile : All clinicians use a dental explorer to identify regions of sensitive dentin. It is simple yet effective. Although the use of a gently force of 5 to 10 mg on the explorer (measured by performing such maneuvers on an 24
analytical balance) seems as though it would be a trivial stimulus, that force is localized on the tip of the explorer, which is only about 500 Âľm2 (Pashley, unpublished observation). If 5 gm of force is applied over 500 Âľm2, the resulting pressure is gm/5 X 10-6 cm2 = 1000 kg/ cm2 = 102 Mpa. This is sufficient to overcome the elastic limit of dentin, leading not only to compression of dentin and smear layer creation under the explorer tip but also to permanent (yet incroscopic) deformation of dentin, (scratch development). This compression of dentin can presumably cause displacement of fluid inwardly at a rapid rate, which activates mechanoreceptors. Tactile stimuli can be made quantitative by incorporating a calibrated strain gauge in the explorer or by using a Yeaple probe. A Yeaple probe is a compact handpiece that contains an explorer tine in an adjustable electromagnetic fluid. The probe is calibrated such that one can apply forces sequentially to sensitive dentin in a graded manner. The force should be applied to the same area at 90 0 to the surface in a static inwardly directly manner. The patient is asked to respond whether there is either pain or no pain at each test. The instrument is adjusted in 5 to 10-gm increments from 10 to 70 gm. Each increasing force compresses more and more dentin. This is a variable stimulus / constant response type of test. If different laboratories wish to compare testing data, they should all use the same type of explorer tine (that, is identical surface area, sharpness and so on). Osmotic stimuli : The use of osmotic stimuli for evaluation of dentin sensitivity was popularized by Anderson and his colleagues. At the time they developed this methodology, the smear layer had not yet been discovered and the hydraulic conductance of the dentin that they studied was probably very low. This required them to use very large osmotic stimuli (very concentrated solutions of various solutes) in order to induced enough fluid movement to cause, pain. The same concentrations of different solutes amounts of fluid 25
movement. This was due to differences in the reflection coefficients of these solutes for dentin. Reflection coefficients are values that correct the theoretical osmotic pressure of a solution for the relative permeabilities of the solute versus the solvent. Andersonâ&#x20AC;&#x2122;s group found that repeated applications of the same hypertonic solutions to cavity preparations in the teeth of unanesthetized subjects evoked fewer and fewer reports of pain. They also demonstrated that repeated applications of these solutions induced successively smaller amounts of fluid movement across dentin in vitro. This was due to the diffusion of the solute into the dentinal fluid, which â&#x20AC;&#x153;loadedâ&#x20AC;? them so that subsequent applications of the solution produced smaller and smaller osmotic gradients. Osmotic stimuli are effective because the chemical activity of water in these solutions is les than that of the chemical activity of water in dentinal fluid. Water flows from the area of higher activity to the area of lower activity, which is, by definition, osmosis. Horiuchi and Matthews reported that than were osmotic pressure. However, osmotic stimulation continues to be a convenient, popular method of evoking pain in neurophysiologic studies in cat teeth, where it is technically difficult to produce hydrostatic stimulation. Calcium chloride, has multiple effects. when applied to superficial dentin, it excites intradental nerve owing to osmotic movement of fluid. In deep dentin, it may depress nerve activity owing to the direct effect of calcium at stabilizing excitable membranes. Solutions of sodium chloride tend to excite nerves owing to indirect osmotic effects on superficial dentin and direct effects on intradental nerves in deep dentin. Thus, for a variety of reasons, osmotic stimuli are not generally used clinically to quantitate dentin sensitivity although some have tried. For a review of this topic see pashely. Saturated solutions of calcium chloride may be useful for exploring the integrity of margins of drowns or other restorations. A cotton pellet saturated with the solution is place on a suspect 26
margin. There is usually a delay of 5 to 30 seconds as the osmotic stimulus diffuses into any defects. The lack of a painful response in an unanesthetized patient indicates either that the margin is tight or that the dentin in insensitive. Margins should be tested individually to limit identification to a specific leaky margin. Thermal stimuli : Thermal stimuli have been used ever since endodontists began using hot gutta percha to elicit Pulpal nerve responses. Thermoelectric devices are useful for delivering cold or warm stimuli in a controlled quantitative manner. Because patients are generally more sensitive to cold than to hot stimuli, the use of cold water (10,15,20,25, 30 0C) as a simple, quantitative stimulus is gaining in popularity. In using cold water, each tooth tested is isolated with a rubber dam and water at a known temperature is slowly flowed on the exposed dentin surface for a maximum of 3 seconds from a disposable plastic syringe. The patient is forced to decide if that temperature causes pain or not and then the next lower temperature is tried until the patient responds unequivocally. Thermal stimuli are effective hydrodynamic stimuli because of the differences in thermal conductivity and coefficients of expansion or contraction of pula/dentinal fluids and their containers, enamel and dentin. This is, application of cold causes a more rapid volumetric contraction of dentinal fluid than occurs in dentin. This mismatch of volumetric changes produces negative Intrapulpal (and presumably intradental) pressures that displace mechanoreceptors and cause pain. Because many thermal stimuli require that the tooth be touched with a device, they are actually both tactile and thermal. Application of a water stream is almost purely thermal, as there is no pressure application. The use of a thermally â&#x20AC;&#x201C; adjusted air stream provides a â&#x20AC;&#x153;no-touchâ&#x20AC;? thermal
27
stimulation. Unfortunately, it provides both thermal and evaporative stimuli simultaneously. Thermal stimuli to vital dentin cause sharp, well-localized pain (that is, activation of A-δ fibers) before there is a change in dentin temperature near the pulp where the nerves are located. Many seconds later, the thermal wave or pulse arrives at the pulp and may activate other nerves. however. The thermal stimuli that the used in testing dentin sensitivity should be regarded as hydrodynamic stimuli rather than thermal stimuli pr se. That is, they induce fluid movement or pressure changes indirectly rather than directly stimulating temperature â&#x20AC;&#x201C;sensitive receptors. Thus, the term thermal stimuli actually a misnomer. Prolonged application of hot or cold stimuli to dentin eventually cause changes in the temperature of Pulpal nerves. Although this is useful in endodontics it is not used in testing dentin sensitivity. Clinically, cold stimuli are more useful than hot stimuli for testing dentinal sensitivity. Patients tolerate cold stimuli better than hot stimuli, and there is less danger of causing Pulpal damage. Evaporative Stimuli : The use of an air blast as a noxious stimulus in testing for dentin sensitivity has been widely used since Brannstrom, Londen, and Astrom first demonstrated that air blasts to cut dentin caused evaporative fluid movement across dentin. There are two mechanisms operating to cause pain under these conditions. The first is the evaporation of fluid from the dentin by relatively dry 250C air directed at a 320C toot. This occurs very quickly (within 1 second). If longer blasts of air are used, one begins to cool the tooth, and the stimulus becomes complex owing to the addition of a thermal stimulus with an evaporative stimulus. A thermal testing device has been developed that blows air of progressively lower temperature on sensitive teeth. Although it is regarded as primarily a thermal stimulus, it includes an evaporative component. 28
Air blasts are useful stimuli during patient screening. They quickly identify individual sensitive teeth but they are not useful at identifying sensitive tooth surfaces. That is, an air syringe does not identify exactly where, on a tooth, the sensitive dentin is located. The exact location of dentin sensitivity often dictates the type of therapy that might be employed. Whenever permeable dentin is exposed to an environment in which the relative humidity is less than 100 percent, water in dentinal fluid will change from the liquid state to the gaseous state, which, by definition, is evaporation. The important variables in evaporation are the tooth or dentin temperature, the ambient relative humidity, and the presence or absence of convective air movement. Spontaneous evaporation of water from exposed dentin is the same regardless of the presence or absence of a smear layer. However, the accelerated evaporative water loss seen during an air blast is much higher in the absence of a smear layer (Goodis, Tao, Pashley). The direction of the air blast should be 900 to the dentin surface to obtain maximal rates of water evaporation. There is no standard air blast, although perhaps there should be clinicians direct air at teeth at varying distances for varying periods of time. It would be desirable to standardize to a 1-second air blast, 1 cm from the tooth, directed at 900 using room temperature air. Orchardson and Collins - an air syringe that uses a prolonged air blast. The patient holds a cut-off switch that they activate when pain is perceived. A timer begins when the clinician activates the air syringe. The time in milliseconds between the onset of the stimulus and the patients cancellation of the stimulus was found to be proportional to dentin sensitivity. One criticism of the use of prolonged evaporative stimuli is that sufficient water can evaporate from the dentin to cause partial tubule occlusion by the salts and proteins left behind. Prolonged air blasts also tend 29
to decrease dentin sensitivity until the dentin becomes rehydrated. Finally prolonged air blasts cause temperature changes on and in the dentin that can be avoided by using 1-second air blasts. If prolonged air blasts are directed at exposed dentin, the rate of evaporative water loss may occur faster than dentinal fluid can flow into the dentin, causing negative intradental pressures. This may be responsible for the displacement of nerves and odontoblasts nuclei from the cell body into the cytoplasmic processes inside dentinal tubules. Although this phenomenon has been called ‘aspiration’ of odontoblasts, the preferred term is ‘displacement’. These cells die and are generally replaced by underlying mesenchymal cells. Filtration of fluid : The most physiologic stimulus for evoking dentin sensitivity should be the graded, quantitative movement fluid across dentin. Ahlquist and colleagues, by preparing circular cavities on the facial surface of incisors and cementing conical plastic chambers into the preparation with cyanoacrylate. The chamber was connected to a fluid reservoir with polyethylene tubing. Uanesthetized subjects reported the quality and magnitude of their sensation of pain by means of an intermodal matching technique, finger-span potentiometer, and verbal descriptors. In the presence of the smear layer, no pain could be evoked. After using 0.5M EDTA (pH 7.4) for 2 minutes, fluid flow in either direction elicited sensations of sharp pain. Rapid changes evoked higher pain intensities than slow changes in flow. When the dentin was treated topicaly with 3 percent oxalic acid (2 minutes) to occlude the tubules with calcium oxalate crystals, the same stimuli were prevented from producing sufficient fluid flow to evoke pain. This effect could be reversed by EDTA treatment, which restored both dentin permeability and its sensitivity. These results tend to support the hydrodynamic theory of dentin sensitivity. 30
There is a linear relationship between applied pressure and the flow of fluid through dentinal tubules. The hydraulic conductance of dentin is the slope of the linear relationship between fluid flow and the applied hydrostatic pressure gradient. The presence or absence of smear layers has a profound influence on the magnitude of the hydraulic conductance, which also varies inversely with dentin thickness. The histologic appearance of the odontoblast process in dentinal tubules would suggest that it should have an enormous effect on the hydraulic conductance of dentin. However, if one removes the smear layer of dog dentin in vivo and measures the hydraulic conductance of the dentin before and after filtration of water (which should osmotically swell odontoblast processes in tubules) across dentin, there are no statistically significant changes. Similarly hypertonic (3M) NaCl across dentin (which should osmotically shrink the odontoblast process), one sees no change. A prolonged (10 minute) air blast to dentin to cause displacement of odontoblast nuclei up into the tubules, there is not change in Lp even though subsequent histologic examination revealed that more than 50 percent of the tubules contained displaced nuclei. Presence of irregularities in the walls of the tubules, the presence of organic partitions, mineralized and unmineralized collagen fibers, and so on. Their summed effects are apparently much more important in modifying fluid movement across dentin than is the presence of the odontoblast process. Electrical stimuli : Criticized on several grounds as being nonphysiologic, rather than testing the pulpodentin complex via hydrodynamic stimuli, it has been argued that electrical stimulation of teeth directly stimulates pulpal nerves and hence is of little value in evaluation of dentin sensitivity. That is, it only evaluates the presence or absence of nerve vitality rather than the degree of 31
sensitivity. Further, most clinical devices that are used to test pulp vitality pass different currents through teeth because of the different resistances offered by varying enamel and dentin thicknesses. Constant-current stimulators are used in neurophysiology to deliver an exact current flow regardless of the resistance of the tooth. Because current flow is the critical variable in stimulating nerves, constant current stimulators, as they are called, are absolutely necessary in studies of nerve thresholds and sensitivity. There are regional differences in nerve distribution within teeth. One might expect to obtain differences in nerve responses if the electrode was placed on the incisal versus the middle third of coronal enamel. Bender and associates demonstrated that the incisal third of the crown was more sensitive to electric pulp testers than the cervical third. Karlsson and Penney study, the root surfaces became more sensitive after
periodontal
treatment,
whereas
coronal
sensitivity
remained
unchanged. It is theoretically possible for electrical stimuli to induce hydrodynamic fluid movements through open dentinal tubules via a phenomenon called electro-osmosis. Electro-osmosis is the bulk movement of an electrolyte solution through a porous substance in response to the impression of an electrical potential. Until we know much more about electro-osmosis in dentin, we cannot dismiss electrical stimulation of teeth as being unphysiologic. Bacterial contributions to dentin sensitivity : Periodontists have long thought that patients who keep their root surfaces free of plaque will exhibit less dentin sensitivity. Overzealous tooth brushing by some patient may abrade radicular dentin and remove surface salivary mineral deposits, thereby creating dentin sensitivity rather than preventing it. Indeed, Addy and colleagues reported a higher amount of 32
gingival recession and dentin sensitivity on the left side of right-handed individuals than on the teeth on the right side of their mouth. They found an inverse correlation between plaque scores and dentin sensitivity. That is, low plaque scores were associated with high levels of sensitivity. Adrians and coworkers found far more microorganisms in the dentin adjacent to periodontal pockets than in normal radicular dentin. Further, more bacteria were found in superficial root dentin than in middle dentin. However, they found a significant number of bacteria in the pulps of periodontally involved teeth even though these teeth were asymptomatic. A relatively common histologic observation of bacterial penetration into dentin is that it is extremely localized. A few tubules may be filled with bacteria while most of the adjacent tubules remain bacteria free. Bergenholtz clearly demonstrated that bacterial products placed on dentin can induce pulpal inflammation. Some bacterial substances can activate complement, whereas others are strongly chemotactic for PMNs. Still others may activate macrophages to release tumor necrosis factor. bacterial products may have direct vasoactive properties on pulpal vascular smooth muscle. Alternatively, they may have indirect effects on the vasculature through their direct effects on the release of neuropeptides from pulpal nerves. Bacterial products may have cytotoxic effects on pulpal fibroblasts that may modify areas of the pulp during inflammation. They may damage or kill the odontoblast and their mesenchymal stem cells. If there had been multiple episodes of acute pulpal inflammation immediately beneath open sensitive entinaltubules followed by healing, one result might be a local accumulation of fibrous tissue (that is, scarring) and a reduction in capillary density. Such relatively avascular regions would not clear bacterial products diffusing into the pulp from open tubules, thereby permitting their local concentrations to rise to levels that were cytotoxic. The relative lack of 33
capillaries would tend to interfere with or retard the transport of fibrinogen and globulins that might reduce the rate of entry of bacterial products through dentin to the pulp.
Dentin hypersensitivity : Some authors use the term hypersensitivity dentin or dentin hypersensitivity, whereas others simply refer to it as dentin sensitivity. Can dentin become hypersensitivity and if so, how ? The hydrodynamic theory of dentin sensitivity implicates both dentin and nerves as important elements. it follows, then, that one could have “dentin hypersensitivity” or nerve hypersensitivity or both. As dentin becomes thinner (from multiple root planings or tooth abrasion), its hydraulic conductance increases. The most important variable is the condition of the tubule apertures. Tubule orifices plugged with smear plugs have a much lower hydraulic conductance than those same tubules devoid of smear plugs and smear layers. As dentin loses its smear layer, it becomes hyperconductive and hence “hypersensitivity” relative to what it was when it was covered with a smear layer, especially from the patient’s perspective. Alternatively, changes may occur in nerve sensitivity. The ionic concentration of sodium and potassium of predentin fluid, in nonexposed dentin determined by micropuncture technique, has been reported to be 48.0 and 9.0 mEq per L, respectively. The concentrations of the same ions in exposed dentin have been reported to be 150 and 3 mEq per L, respectively. Because resting membrane potentials of nerves are more sensitivity to changes in extracellular potassium than sodium, one would expect the membrane potential of intradental nerves to be more negative (and less excitable) in open, exposed dentinal tubules (owing to the lower, more 34
plasma like potassium concentration) than the same nerves in nonexposed dentin. Hypersensitive states may also develop during inflammation via several mechanisms. The small unmyelinated c-fibers that are normally thought of as nociceptors may release small but important quantities of neuropeptides without firing. They increase local blood flow and increase capillary permeability. Extravasation of plasma tends to cause local elevations in pulpal tissue pressure that may lower the excitatory threshold of mechanoreceptor nerves, thereby contributing to a true hypersensitivity of that dentin. The supporting of nerves may increase the innervation density of dentin or the subodontoblastic regions, further increasing dentin sensitivity. Clinical considerations : Generally, patients who have had extensive root planning will have lost all of the cementum on the cervical third of the root as well as variable amounts of root dentin. These patients seldom complain of dentin sensitivity until their periodontal packs are removed. Although the subsequent events vary considerably among individuals, many patients complain of increases in dentin sensitivity of the planed teeth over the next 7to 10 days. This is generally followed by a gradual decline in sensitivity over the following 7 to 10 days. As saliva is saturated in calcium and phosphate with respect to most forms of insoluble calcium phosphate at normal salivary flow rates and pH, there are numerous physiochemical mechanisms tending to occlude dentinal tubules with a wide variety of crystal types. This may lower the hydraulic conductance of the exposed dentin below levels that permit activation of mechanoreceptors hydrodynamically. The transudation of plasma and the macromolecules that it contains may tend to fill tissue spaces and perhaps even the pulpal ends of the tubules with fibrin, thereby decreasing the size 35
of diffusion channels, decreasing dentin permeability. The pulp may then have an opportunity to heal and the thresholds and distribution of sensory fibers should return to normal leaving the patient relatively comfortable.
DENTINAL PERMEABILITY IN ASSESSING THERAPEUTIC AGENTS Isotonic potassium chloride does not elicit pain when applied to dentin but does when in direct contact with the pulp ; and acetic acid buffer (pH 5.7), reported to induce pain in subcutaneous injections, had no effect on the dentin or the pulp. Brannstrom observed that dentin exposed by drilling was less sensitive than dentin exposed by fracture, which he attributed to the blockage of tubule openings caused by the debris produced during drillings. These observations together with the observations that pain could be produced from air blasts, application of sugar solution, and dry absorbent paper led to the conclusion that a central vital part of the tooth pulp acts as a mechanoreceptor, and any stimulating agent causing mechanical disruption or movement of fluid flow through the tubules is a potential cause of pain. Furthermore, Brannstrom reasoned that the geometry, that is, the conical shape, of the dentinal tubules combined with capillary action could make instaneous minute amounts of fluid flow possible, and could explain the acute pain reported in the clinical operatory. Citing three natural defense mechanisms for reducing dentin permeability as formation of irregular atubular dentin at the pulpal wall, obturation of dentinal tubules by sclerosis, and mineralization of a superficial layer of pellicle or plaque, Brannstrom proposed a clinical technique for sealing dentin using a resin material. 36
Brannstrom later suggested the application of cavity lining and varnishes under restorations, the retention of smear plugs in restorative procedures, and use of calcium hydroxide and non-abrasive fluoride gels for treatment of exposed sensitive dentin. Following Brannstrom, the greatest protagonist of the hydrodynamic theory and the role of dentin permeability has been D.H. Pashley who has presented numerous reports in the field of evaluating agents for the treatment of hypersensitivity. 1) Hydraulic conductance (Lp) measures the ease with which fluid movement occurs across a membrane in a hydraulic gradient. 2) Permeability coefficients (P) are a property of solutes for a particular membrane. In the absence of bulk fluid movement, P is a measure of the ability of solute to diffuse across a membrane because of a concentration gradient. In an analysis of factors influencing P, molecular size, configuration, polarity, Van der Waals forces, London forces, and interaction potentials need be considered. 3) Reflection coefficient (Ď&#x192;) is a factor that reports the relative ability of a solute and a solvent to diffuse through a membrane. By definition, Ď&#x192; = 1 when the membrane is impermeable to the solute but completely permeable to the solvent, and when Ď&#x192; = 0 the membrane cannot distinguish between the solvent and solute. In 1974, Pashley published the first experimental work utilizing a laboratory
method
to
measure
dentin
permeability
by
hydraulic
conductance. In this work, a split chamber device was described wherein thin slices (0.99mm) of coronal dentin from extracted human third molars were placed between fixed surface area plexiglass reservoirs, one end of which could be connected to a source of hydrostatic pressure or treatment solution and the other end to a means of measuring flow rate or to collect 37
diffused fluid. Movement through a micropipette was found to be an accurate flow meter. Fluid movement through dentin was nil with no hydrostatic pressure, flow was a linear function of hydrostatic pressure, acid-etched discs had flow rates nearly 32 times greater than unetched discs, permeability was inversely proportional to dentin thickness, and permeability was directly proportional to surface area. 86 percent of the resistance to dentinal fluid flow was due to the surface characteristics of dentin, strongly suggesting that the alteration of permeability by surface agents could be a useful clinical treatment modality. Flow was greater in the direction from the enamel to the pulp. In 1983, Pashley measured the effect of temperature on the flow rate of saline solutions, through etched and unetched dentin. Generally, permeability increased with temperature, however, the increases were greater with etched dentin. In 1982, Pashley measured the influence of saliva, bacterial suspensions, and plasma proteins on fluid movement across dentin. Pashley speculated that after injury, a natural defense mechanism originating from the pulp could be the formation or release of plasma proteins, leaked into the dentinal fluid in an attempt to occlude tubular passageways and reduce hydrodynamic transmission to the mechanoreceptors in the pulp. Using a modification of the split chamber deice wherein the enamel side was acid etched and then brushed with slurries of a series of dentifrices, Pashley determined fluid flow through dentin in the direction pulp to enamel, and interpreted the reduction in flow as a measure of the dentifrices ability to occlude dentin. In the series of products tested, no significant differences were reported among Sensodyne, Crest, Denquel, Promise, and Thermodent, but an experimental oxalate dentifrice developed by Pashley was significantly more able to reduce hydraulic conductance (Lp). 38
Pashley also applied iontophoretic currents in the range 0 to 1.0 mA to dentin discs in a further modification of the split chamber device. Using Na I and C lidocaine as test materials, iontophoresis was reported to significantly increase the permeability of dentin, and it was concluded that iontophoresis may be useful for enhancing dentin permeability to deliver therapeutic agents to the pulp. Pashely and colleagues in 1985 evaluated a series of commercial cavity varnishes and bases for their ability to reduce dentin permeability. The split chamber device was employed in two ways. 1) to measure permeability by a radiotracer applied to the top reservoir of a split chamber device, collecting the perfusion in the bottom portion with a fraction collector and 2) to measure hydraulic conductance by fluid filtration through dentin as driven by 30 cm of hydrostatic pressure. the products tested were Copalite, Tubulitec, Dropsin, Universal Cavity Varnish, Durelon, Dycal, ZnPO4 cement, and ZnO/ eugenol cement. All cavity varnishes decreased dentin permeability by 20 to 50 percent. In the filtration method, only Tubulitec produced a statistical reduction in Lp. Furthermore, the effect of varnishes was found proportional to their solid content, but cavity bases and liners produced larger reductions in dentin permeability. Burnishing dentin with orangewood and a paste composed of sodium fluoride, kaolin and glycerin. Act of burnishing with orangewood alone was the most effective part of the therapy, reducing permeability by 80 percent. NaF had no appreciable positive contribution, and kaolin and glycerin slightly diminished the reduction in flow rates. Oxalic acid reduced flow by 95 percent. Smear layers produced by burnishing were found to be more resistant to acid than those produced by a bur. Burnishing may force more debris deeper into the tubule openings than bur cutting could.
39
Multistep dentin bonding procedure containing ferric oxalate, NTGGMA (N-tolyl glycine-glycidlymethacrylate), and PMDM (pyromellitic dianhydride + 2-hydroxyehtylmethacrylate) developed by Bowen and associates. Ferric oxalate â&#x20AC;&#x201C; reducing dentin permeability by 65 percent. Ferric oxalate at pH 0.9 may dissolve the smear layer and then re-precipitate as calcium oxalate and ferric phosphate salts, occluding the patent and exposed tubules. Takahashi - the lactate, tartarate, citrate, maleate, and chlorides of Al, Zn, Ca, Sn and Mg were evaluated, with Saforide (diamine silver fluoride), silver nitrate, calcium hydroxide, Hyperband Kimura (paraformaldehyde), and Gottliebâ&#x20AC;&#x2122;s recipe (zinc chloride and potassium ferrocyanate solutions) serving as positive controls. 2.18 percent aluminum lactate (pH 17) emerged as the agent of choice for further clinical investigation. Addy and his coworkers - the sensitive teeth were found to have an average number of 59.9 open tubules per unit area versus 7.47 for the nonsensitive examples. The average tubule diameter was estimated as 0.83 microns for the sensitive teeth and 0.43 microns for the non-sensitive exposed dentin areas. Addy and associates also reported the effects of acids and acidic dietary substances on root-planed and bur-cut dentin. Using SEM, the authors observed that the strong mineral acids such as nitric, sulfuric, citric and lactic removed the smear layer, as did red wines, citrus fruit juices, apple juice and yogurt. Finally, the recent work by Absi and colleagues, which involved the development of a replica technique to study sensitive and non-sensitive cervical dentin, is a rather novel approach. Silicone impressions were taken of extracted human teeth that had been root planed to expose dentin and then acid etched to expose dentinal tubules. These replica SEMs were 40
compared with SEMs of the original dentin surfaces. Excellent correlation between the original and replica SEMs in terms of tubule cunts was reported as well as excellent resolution of surface details such as tubule diameters as low as 1 micron, illustrating patent tubules. Kim used a refined electrophysiologic method on the vital teeth of cats, dogs, and humans to measure baseline pulpal sensory nerve activity (SNA) or electric potential and the effects of therapeutic agents on their activity. Kim reported for the first time that potassium ion is the active portion of potassium nitrate and any other potassium compound. When potassium ions reached the pulpal sensory nerve, after passage through dentinal tubules in Kimâ&#x20AC;&#x2122;s deep-cut cavities, the external part of the nerve membranes became regions of greatly increased potassium concentration. This localized increase in potassium caused rapid firing of the sensory nerve that ceased quickly because the extracellular potassium ions subsequently inhibited hyperpolarization of the pulpal sensory nerve, that is, they raised the nerve action potential and produced a desensitizing effect. HYPERSENSITIVE TEETH : Experimental studies of dentinal desensitizing agents : Not all teeth with exposed dentine are sensitive. Teeth with toothbrush or other forms of abrasion and erosion may have extensive loss of tooth structure without sensitivity. 1) The dentinal smear layer consists of small amorphous particles of dentin, minerals, and organic matrix, which cover the cut surface of dentine, obstructing the orifices of the tubules. 2) Salivary proteins adhere to the outer dentine surface and, in addition, plasma proteins can adhere to the inner dentine surface, blocking the tubules.
41
3) Reparative dentine forms in response to chronic irritation. This type of dentine is less permeable than primary dentine and serves to insulate the pulp from irritating stimuli. Anatomic study of pulpal nerves shows that in the coronal area of the tooth there is extensive peripheral branching of axons and many axons entering the dentine. This is in sharp contrast to the cervical and radicular areas, where most of the axons are found in central bundles and very little branching occurs. How then can the roots becomes so sensitive ? One possible explanation is provided by Byers and coworkers. Following grinding of the roots f rat molars they found sprouting of new axons branches in the area of injury. Thus, the dentine in the area of injury may be more richly innervated than intact sites. 1) It can reduce fluid flow through the dentine by clogging the tubules. 2) It can decrease the activity of the dentinal sensory nerves, preventing the pain signal from being transmitted to the central nervous system. Toothpastes containing SrCl2 and KNO3 have gained wide popularity. Both agents have been hypothesized to cause blockage of dentinal tubules. Historically, KNO3 was preceded by silver nitrate, and this substance was reported to be effective but permeability stained teeth black and was never popular in our cosmetically conscious society. Method for measuring sensory nerve activity : In order to study the effects of desensitizing agents, the multi-unit intradental recording method developed by Scott and modified by others was used. In the canine teeth of anesthetized cats and dogs, two dentinal cavities were prepared, one deep cavity over the incisal pulp horn and a second less deep cavity near the gingival margin. The incisal cavity an active low impedance platinum or silver / silver chloride electrode was placed. The incisal cavity was also used to apply various stimulating and 42
desensitizing solutions. The gingival cavity held a reference electrode and was always filled with saline. The electrodes were connected to standard pre-amplifier and recording equipment. Using this method, many intradental nerve units can be recorded simultaneously. In order to study the effect of desensitizing agents, some means of stimulating neuronal firing had to be used. First the excitatory solution 3M NaCl was applied to the cavity for 2 minutes. The nerve activity during this time constitutes the control sensory nerve activity. Then, following a 2-minute saline rinse, the test desensitizing agent was placed in the cavity for 2 minutes. Immediately following removal of the test desensitizing agent, the 3M NaCl was reapplied. KNO3, the active ingredient in Sensodyne F and Denquel, significantly reduced the sensory nerve activity. Strontium chloride, which is the active ingredients in Sensodyne toothpaste, was shown to be effective only at the higher concentration. 1) The NO3â&#x20AC;&#x201C; anion is not effective as a desensitizing agent. 2) K+ is an effective desensitizing agent regardless of the anion with which it is combined. 3) Divalent cation solutions were effective in reducing sensory nerve activity but less effective then K+. Both K+ and divalent cation solutions had a reversible effect, that is, they did not appear to damage the dentinal sensory apparatus. Mode of action of effective agents : The extracellular potassium ion concentration is the principal determinant of the nerve resting electrical potential. The normal resting potential for nerve fibers is approximately â&#x20AC;&#x201C; 90 mv measured from the inside of the cell. When the concentration of K+ is increased above the normal physiologic level the cell depolarizes, that is, the inside becomes less negative. Once a certain critical (threshold) potential level is reached, 43
action potentials begin to occur. Owing to the properties of the membrane gates that mediate the action potential, the burst of spikes in response to increase K+ does not last long. After 15 to 20 seconds of prolonged depolarization, the action potentials cease as a result of the closing of the action potential membrane gates. Divalent cations such as Ca++, Mg++, and Sr++ can act to stabilize the nerve membrane by raising the membrane threshold without actually changing the resting potential. Recent evidence also suggests that divalent cations may block the membrane channel that mediates the action potential. Patients who brush with KNO3â&#x20AC;&#x201C; containing toothpastes do not complain of pain when applying these agents. Also, in our experiments, desensitization occurs immediately and is of short duration in contrast to the clinical situation, in which all desensitizing agents require time and repeated application of the agent of order to have maximal benefit. Future directions : Pain and inflammation are interconnected phenomena. The presence of inflammation in hypersensitive teeth has yet to demonstration. Inflammation is marked by an increase in blood flow. The laser Dopper flowmeter â&#x20AC;&#x201C; allows continuous monitoring of pulpal blood flow. When the effect of agents that stimulate sensory nerve activity such as hypertonic NaCl and KCl solutions are tested, these solutions cause an increase in pulpal blood flow. When lidocaine is applied to block nerve activity, the blood flow changes evoked by KCl are greatly attenuated. ETIOLOGY AND CLINICAL IMPLICATIONS OF DENTINE HYPERSENSITIVITY : Dentine hypersensitivity may be defined as : pain arising from exposed dentine, typeically in response to chemical. A number of other dental conditions are associated with dentine exposure and therefore may produce the same symptoms. Such conditions include chipped teeth, 44
fractured restorations, restorative treatments, dental caries, undisplaced cracked cusps (the cracked tooth syndrome), and palato-gingival grooves or other enamel invaginations. Thus, a careful history, together with a thorough clinical and radiographic examination, is necessary before arriving at a definitive diagnosis of dentine hypersensitivity. However, the problem may be made difficult when two or more conditions co-exist. There can be few other conditions or diseases in man besides dentine hypersensitivity that are treated apparently successfully by so many compounds. Some authors have commented that â&#x20AC;&#x153;because of their subjective nature many of the earlier reports on desensitization have little scientific basis and belong in the realms of testimonials. The lesion : Direct evidence has been gathered of tubule patency associated with dentine hypersensitivity. Thus, teeth diagnosed as exhibiting dentine hypersensitivity, when extracted and studied by scanning electron microscopy, exhibited in excess of seven times the mean surface tubule count at buccal cervical dentine sites compared with teeth classified as nonsensitive. Incidence and distribution : Cross-sectional prevalence studies for dentine hypersensitivity have been limited in number and there are no longitudinal incidence figures for the condition. The available prevalence data vary considerably, and dentine hypersensitivity has been stated to range from 8 to 30 per cent of adult dentate populations. Most sufferers range in age from 20 to 40 years a peak occurrence is found at the end of the third decade. The reduced incidence of dentine hypersensitivity in older individuals despite increasing dentine exposure with age, particularly through gingival recession, presumably reflects age changes in dentine and the dental pulp. Sclerosis of dentine, the laying down of secondary dentine, and fibrosis of the pulp would all 45
interfere with the hydrodynamic transmission of stimuli through exposed dentine and the response of pulpal nerves. A slightly higher incidence of dentine hypersensitivity is reported in females than in males, however, the differences are not usually statistically significant. Most surveys do not conform to standard epidemiologic methods, and therefore a gender difference may or may not exist. Dentine hypersensitivity is most commonly reported from the buccal cervical zones of permanent teeth. Dentine exposure may occur occlusally and at lingual cervical sites, but in many populations this is less frequently found and sensitivity only rarely reported. Canines and premolars in either jaw are the most frequently involved. Additionally, in a group of patients characterized as moderate to severe sufferers, the dominant factor influencing the distribution of recession and dentine hypersensitivity was the side of the mouth. Etiology and predisposing factors : Dentine may become exposed by two processes either loss of enamel or loss of covering periodontal structures, usually termed â&#x20AC;&#x153;gingival recessionâ&#x20AC;?. Loss of enamel occurs by attrition associated with occlusal function and may be exaggerated by habits or Parafunctional activity such as bruxism; by abrasion from dietary components or habits such as toothbrushing; or by erosion associated with environmental or dietary components, particularly acids. Probably rarely, if ever, is enamel loss due to a single agent. Exposure of root dentine by gingival recession similarly is multifactorial, but acute and chronic periodontal diseases, toothbrushing, or chronic trauma from other habits and some forms of periodontal surgery are important causal factors. Indirect and direct evidence indicates that for dentine to be sensitive, not only must it be exposed to the oral environment but dentinal tubules have to be patent at the surface. Clearly not all factors that expose dentine 46
necessarily open dentinal tubules. Indeed, most mechanical influences applied to dentine, including abrasion and attrition, cause this plastic tissue to flow, producing the so-called smear layer. This very thin layer thus will cover the dentine surface and obturate the tubules. The buccal cervical site predilection for dentine exposure and sensitivity is consistent with toothbrushing practices, with lingual sites receiving little attention during the brushing cycle of most individuals. The particular involvement of canines and premolars is therefore not surprising, because epidemiologic evidence and data from dentine hypersensitivity sufferers indicate these are the most well cleaned teeth. Interestingly, the finding that females are more commonly affected by dentine hypersensitivity than males, if actually correct, would also relate in part to oral hygiene practices. Females have increased grooming behavior compared with males, and this is associated with better oral hygiene. In vitro studies suggest that brushing with water will remove the dentine smear layer to expose tubules only after protracted periods of continuous brushing. Brushing with a toothpaste may produce occlusion of tubules both by a smearing effect on the dentine and by the deposition of toothpaste ingredients on the dentine and into the tubule orifices. Some artificial silicas readily adhere to dentine, occlude open dentinal tubules, and are resistant to removal by washing or dietary acids. Workers exposed to fumes of hydrochloric, sulfuric, nitric, picric and tartaric acids exhibit extensive tooth decalcification as do individuals with a high dietary acid intake or suffering gastric regurgitation. Organic hydroxy acids, in particular citric acid, appear more erosive than inorganic acids, and clearly activity is not directly pH dependent. The rate of erosion is rapid, and buffering by saliva is probably too slow to prevent the initial decalcification. Loss of enamel or dentine due to toothbrushing is very markedly increased with prior exposure to dietary acids. 47
The role of plaque as an etiologic factor in dentine hypersensitivity would appear to be an area of controversy. Through, even over-enthusiastic, toothbrushing has long been associated with gingival recession and sensitivity, yet other authors have suggested that plaque causes dentine hypersensitivity. Marginal leakage around restorations leading to bacterial activity may be responsible for pulpal pathology and sensitivity beneath restorations. The possible role of saliva and bacterial contamination of exposed dentine in dentine hypersensitivity has been proposed but not proved. Bacteria do penetrate into tubules of dentine left open to the oral environment and therefore toxins may diffuse to the pulp. This diffusion would have to occur over relatively large distances and against the outward flow of dentinal fluid. Additionally, the concentration gradient would be just as great if not greater in an outward direction. Plaque-induced dentine sensitivity is considered in the differential diagnosis, in which the emphasis of management would be quite different from that of dentine hypersensitivity. Clinical implications : The possible consequence of dentine hypersensitivity could be reduced oral hygiene. Thus, the scenario has been proposed of pain on toothbrushing leading to a vicious circle of reduced plaque control, more gingival disease, more recession, and more sensitivity. The dental surgeon will have to choose the treatment to provide from an extensive range of possibilities. Indeed, different treatments may be chosen for different teeth in the same mouth. Whatever is decided, all treatments are designed either to block the dentine sensitivity mechanisms or to interrupt nerve transmission. These treatment modalities encompass extremes, from the use of toothpaste and applications of restorative materials to dentine, to endodontia or even exodontias. There is a need for greater public awareness, through education, of the effects of exposure to 48
acids on the teeth, particularly dietary acids. Accepting the nutritional and health value of many acidic foods and beverages, as with any item in the diet, excessive quantities or frequency of intake rarely produce proportional increase in benefits and may have deleterious effects on certain systems, including the teeth. The need to determine etiologic factors in dentine hypersensitivity is essential if management is to be successful, and this should include the taking of a diet history or evaluating the less common possibilities of exogenous erosive elements in an individualâ&#x20AC;&#x2122;s living or occupational environment. In the light of the aggravating effect of toothbrushing, advice on method and frequency would appear sensible. Excessive force should be avoided, as should the use of very abrasive toothpastes. Little benefit to periodontal health is obtained with frequencies of toothbrushing in excess of twice a day. Indeed, advice to brush before meals should be provided, and because there are clear benefits from such a regimen derived not only from mechanical cleaning but also from the properties of toothpaste, before-meal brushing should be the norm for all individuals. Summary : Management requires the determination of etiologic factors and predisposing influences, and where possible, their control or modification. METHODS OF MEASURING TOOTH HYPERSENSITIVITY : Electrical stimulation differs from the other stimuli in that the stimulus is not transmitted by the movement of the dentinal fluid. Rather, it is transmitted by the passage of electrical charge via the moisture associated with the organic material in enamel, cementum, and dentine as well as that in dentinal tubules, especially if they are open. Factors affecting measurement of hypersensitivity : Using a silicone rubber impression method to obtain replicas of root dentine surfaces in vivo, Absi, Addy and Adams showed that non-sensitive 49
teeth have closed dentinal tubules, whereas tubules of sensitive teeth are open. Because enamel is thicker than cementum, it generally provides greater protection of the underlying coronal dentinal tubules except perhaps near the cemento-enamel junction where the enamel is thin. Enamel, because of its thickness, also provides greater electrical resistance. A greater electrical stimulus is required to produce a sensation in molars because of their thicker enamel coverings than in premolars and cuspids and in turn, incisors. Loss of the thin protective cementum easily occurs with use of a hard toothbrush and/or an abrasive toothpaste, or by root scaling and planning during oral hygiene and periodontal therapy. Another factor that may affect hypersensitivity values is the state of the pulp. Inflamed pulpal tissue could result in a reading of greater sensitivity than normal, whereas necrotic pulp tissue generally results in readings of lower sensitivity or non-sensitivity. Still another factor is the fact that stimuli for some sensitivity measurements persist. This means that more time is required for the tooth and pulp tissues to return to baseline values before another or a repeat stimulus can be applied. A placebo effect occurs remarkably frequently in clinical studies on tooth hypersensitivity. McFall and Hamrick and Addy and his coworkers suggest that toothpaste components may also contribute to this frequently observed placebo effect. Methods used to measure tooth hypersensitivity : Tactile : The simplest tactile method used to test fro hypersensitivity is to lightly pass a sharp dental explorer over the sensitive area of a tooth (usually along the cemento-enamel junction) and to grade the response of the patient on a severity scale, generally 0 to 3. a score of 0 is assigned if no pain is 50
felt, 1 if there is slight pain or discomfort, 2 if there is severe pain, and 3 if there is severe pain that lasts. Smith and Ash a device with a 15mm (0.26 gauge) stainless steel wire with a tip ground to a fine point and moveable across the highest arc of curvature of the facial surface of the sensitive tooth under test. The scratching force could be increased with a small screw that moves the tip closer to or away from the totoh surface. As the wire is passed across the surface of the test tooth it bends, and the amount of bending of the wire and therefore the force applied can be measured from a scale on the device. To start the measurement, the screw for adjustment of the wire tip is set so that the tip just barely touches the root surface being tested. Then the wire is moved laterally in an arc across the area of sensitivity. This procedure is repeated after the pressure is increased with the adjustment screw. This is continued, usually in steps of 1/4 or 1/3 of a millimeter, until the subject is able to feel a pain sensation. At that point, the scratching force, expressed in millimeters, is taken as the threshold value. To permit accurate repositioning for a subsequent re-examination, a matrix of dental compound is fitted over the lingual and occlusal surfaces of two or three teeth near the tooth being measured. While the compound material is still soft, the frame of the device is impressed in the compound material. Another tactile device that has been used is the force-sensitive electronic probe devised by Yeaple for measurement of the depth of periodontal pockets at fixed pressures. Such a pressure sensitive probe has been modified to accept the tine of a dental explorer tip. The operator can vary the force applied to the tip of this device by regulating the amount of current to an electromagnet controlling the tip position. The probing force is set, and when reached, the probe tip is retracted by an electromagnet; a red light on a control panel goes on, and the applied force is released. The 51
handle of the probe is about the size of a fountain pen and is connected by a flexible electrical lead to the control panel. The probe force is controlled within Âą 1 gram. Calibration is carried out by using a top loading balance to relate probe meter readings in microamperes with probe force in grams. In a dentinal sensitivity test, the probe force can be increased in steps of 5 grams until the subject experiences discomfort. That point is taken as the pain threshold. If a maximum force of 70 grams is reached with no discomfort, the tooth is scored as non-sensitive. The probe emits a buzzing sound when a predetermined pressure is applied. Thermal : 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. Room air is cooler than the teeth, and cooling by this means can be easily detected as pain if the teeth are sensitive. Blowing air on a tooth also involves drying, which as pointed out above could also be stimulatory. Air stimulation has been standardized in a number of studies as a 1second blast from the air syringe of a dental unit, where its temperature is set generally between 650 and 700 F and at a pressure of 60 psi. usually, the air is directed at right angles to the test surface near the cemento-enamel junction and/or exposed root surface, with adjacent teeth usually isolated by the operatorâ&#x20AC;&#x2122;s fingers. Responses are assessed on a severity scale such as 0 where there is no discomfort, 1 if there is some discomfort but no severe pain, 2 if severe pain is felt during application of the stimulus, and 3 if severe pain occurs during and persists after stimulus application. The temperature of room air is about 20 0C and when gently blown over a hypersensitive site at about 320C, the temperature of the site decreases. By using a miniature thermistor connected to a multi-channel recorder, Thrash and associates found that the temperature could be easily 52
measured. Measurement of the drop in temperature is usually repeated three times and the average taken. Tactile stimuli are applied before thermal stimuli if the two are being used in the same subject. Ash, the temperature of the probe tip was measured with a thermistor embedded in the tip. A flow of current in one direction was used to cool the probe tip from room temperature to 12 0C; current flow in the other direction heated the tip to 820C. the temperature was controlled by regulating the intensity of the current to the probe from a power supply. The initial temperature for thermal sensitivity testing was set at 37.50C. For cold stimulation, the temperature was reduced in decrements of approximately 10C. at each lower decrement, the instrument was shut off and the stimulator tip was then placed in contact with the root surface. The subject raised his or her hand when pain was first detectable. Testing with heat was carried out in exactly the same way except that the temperature of the stimulating tip was increased from the initial temperature of 37.50C in increments of 10C to the point at which pain could be felt. Osmotic : The subjective pain response to a sweet stimulus was used by McFall and Hamrick to measure the effect of several test dentifrices on dentinal sensitivity. This was done by preparing fresh a saturated solution of sucrose and allowing it to reach room temperature. After isolation of the test tooth with cotton rolls, a cotton applicator was saturated with the sucrose solution and then applied to the root surface of the tooth and allowed to remain in place for 10 seconds or until discomfort was perceived. The subject rated the sensation as no pain or pain, which was recorded as 0 or 1, respectively. The osmotic challenge was stopped by rinsing with warm water. Electrical :
53
Electrical measurements differ from the 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. Until recently, instruments for applying electrical stimuli of increasing intensity, generally referred to as pulp testers, were used mainly to determine whether a pulp is vital or not. The answer determined the treatment that would be carried out. Instrument improvement led to better quantification of the electrical stimulus and discovery that a condition of â&#x20AC;&#x153;pre-painâ&#x20AC;? 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. The pre-pain sensation has been attributed to the larger, more rapidly conducting, nerve fibers located at or in the pulp reacting sooner, than the smaller diameter nerve fibers that are also present. The presence of a pre-pain zone of stimulation makes it possible to obtain threshold stimulation levels without hurting the patient. This results in less or no apprehension; such apprehension can have an adverse effect on readings. Instruments for stimulating a tooth electrically have as their basic constituents an electrode or probe to apply the electrical stimulus to the test tooth, a power source, a means of varying the electrical stimulus so that its magnitude can be progressively increased, an a means of completing the electrical circuit. Because of the high resistivity of teeth, toothpaste or a similar material with high electrical conductivity is necessary to facilitate transmission of the electrical stimulus to the tooth. In some cases, the operator serves as a means of completing the circuit, with the finger of one hand in contract with the patientâ&#x20AC;&#x2122;s mouth and the other hand in contract with the casing of the probe. With the present need of the operator to wear protective gloves, this method is not satisfactory. Also, alternate pathways of current flow are more likely to occur if the operator is part of the 54
electrical circuit. Elimination of the operator from the circuit was accomplished by Stark, who used as a reference electrode a saliva ejector connecting the patient to a pulp-stimulating instrument that he called the pulp stethoscope. As an alternative, the reference electrode can be applied to the skin as in ECG measurements. The electrical resistance of the skin can vary from 1000 ohms for damp skin to 1 million ohms for dry skin. By using a conducting gel, this difference largely disappears. This method is better than the saliva ejector method of Stark because there is less likelihood of interruption of the electrical circuit during a measurement. Alternate pathways of current flow that are of some concern are those that can occur via the gingival adjacent to the site of electrode placement on the tooth, via other oral; soft tissues such as the cheek or tongue, or via saliva. All of these can be eliminated by carefully isolating and thoroughly drying the tooth being tested and by having the insulation of the stimulating probe extend right up to its tip. Fortunately, the sensation felt by a patient when the gingival, tongue, or cheek is inadvertently touched with the probe tip is very different and easy to distinguish from the sensation felt when only the tooth is controlled and the pulp is stimulated. By trial and error, an electrical stimulus consisting of a direct current pulsed voltage between 0 and 150 (Digilog Pulp Tester) or between 0 and 300 volts (Analytic Technology Pulp Tester; Redmond, WA) has been found suitable for eliciting a pulp response. If an alternating current supply is used to power the unit generating the electrical stimulus, then for safety reasons, it must provide for patient isolation. Although alternating currentpowered units are bulkier and less portable than direct current-powered instruments, they do allow for easier addition of printers and other recording devices, which are extremely useful for recording such information as the tooth stimulated and the magnitude of the electrical stimulus that elicited a pulpal response. 55
For safety reasons, any electrical current that is applied should be limited to less than 1 milliampere, preferably 0.5 milliampere or less, which is in the approximate range of the human bodyâ&#x20AC;&#x2122;s threshold of current perception for 1 second hand-to-hand contact. The voltage of an electrical stimulus should be in the from of pulses to avoid summation and a chance of reaching voltage levels that might result in pain rather than pre-pain. Pulses with a width of 0.05 to 0.20 millisecond each and spaced at 5 to 10 millisecond intervals will provide a stimulus of pre-pain instead of pain. With a commercial digital pulp tester that contains this feature of automatic ramping (Analytical Technology Pulp Tester), an indicator light comes on when the probe tip contacting the surface of a tooth encounters a circuit resistance below 5 million ohms. Method use in studies : It seems from the numerous studies that have been carried out on tooth hypersensitivity that different types of teeth in the human dentition and teeth of different ages and history will vary considerably in their response to pain-producing stimuli so that testing of homologous pairs of teeth would be prudent. To assess effects of an agent on dentinal sensitivity, there need to be relatively large numbers of subjects with sensitive and nonsensitive teeth in a cell. In general, we have found this number to be a minimum of 25 but preferably 35. Conclusion : Hypersensitivity apparently affects one in seven dental patients. It is a problem that should not be ignored because many of such teeth may become non-vital with time. Now that such measurements are becoming possible, practitioners should be able to monitor teeth that are sensitive to determine whether they are getting better or worse following treatment. A chronically sensitive tooth should be a warning sign that a pulp is under continual trauma. With the aging of the population, greater retention of teeth, and 56
greater root surface exposure because of gingival recession and periodontal surgery, one can expect the number of sensitive teeth to rise.
DESIGNING HYPERSENSITIVITY CLINICAL STUDIES :
57
A clinical dentinal tooth hypersensitivity study is first and foremost a clinical pain study. Critical design factors include proper selection of investigator, subjects, hypersensitivity test measurement devices, agents to be tested, and statistical analysis. Investigator : The central aspect of hypersensitivity studies is the investigator. The investigator
must
know
and
understand
the
neurophysiologic
explanations for cause and effect of dentinal hypersensitivity. The design and implementation of a research protocol require comprehension of the proposed mechanism. The investigator should be capable of designing a thorough and efficient hypersensitivity study protocol. Sufficient time must be allocated to manage every aspect of a hypersensitivity study. The test site must be adequately staffed with trained auxiliary personnel. The best plans have little chance to translate into a well executed study when crammed into a busy schedule. The investigator must understand that the sensitive region of the tooth can be very specific. Not every exposed cervical dentin area not all points within a known sensitive area will be hypersensitive. The investigator must be thoroughly trained and experienced in the use of the test devices. In becoming proficient, the investigator will develop an intuitive feel for the sensitivity of the measuring device and when it is being correctly applied to suspected sensitive areas.
58
The investigator should be adept in evaluating prospective study subjects fro their genuine interest in participating in the study. He or she should be able to determine that each subject is properly relating when sensitivity is first perceived, or when a subject is just giving answers to get through the study for one reason or another. Most importantly, the investigator must be capable of developing rapport with subjects so they will be able to relax during hypersensitivity test examinations. A relaxed, professional atmosphere will give subjects a chance to provide accurate and reliable responses during the hypersensitivity testing procedures. Overall design : Principles of good clinical design must be followed in order to attain reliable conclusions. When performing a dentinal hypersensitivity study this usually means double-blind, parallel, randomized or stratified, and comparative study designs. In a double-blind study, neither the investigator (including research personnel) nor the subject knows the identity of the test product assigned to the subject. In a parallel study, all test materials/products should be assigned to separate subject groups/ cells and used by the respective subject cells. Thus, each subject group tests only one product. In a cross-over design, each subject uses one of the study products for a specified use-time. At the end of the product use-time, the subjects use no study product for a brief period to â&#x20AC;&#x153;wash outâ&#x20AC;? the effect of the first study product. This wash-out period is then followed by use of a second study product by each subject. The product-use and wash-out period sequence is followed by the subjects until they have used all study products. Cross-over designs are contraindicated because the wash-out period is not usually known for most desensitizing agents. 59
A comparative study compares one product to another. The simplest study design tests an active product to a placebo control. More complicated studies might compare two or more active products with each other and with the placebo. Subject recruitment, experimental design and statistical analysis become more difficult as the number of cells is increased.
Test materials : The dentifrice with the active agent (active dentifrice) should be compared with the same dentifrice without the active agent (placebo or negative control). It must be emphasized that the placebo dentifrice should possess the same color, taste, consistency and ingredients as the active dentifrice except for the active agent. The clinical dentinal hypersensitivity literature is replete with reports demonstrating efficacy for the placebo dentifrice. This is common referred to as the “placebo effect”. The use of a placebo control dentifrice will not only enable demonstration of desensitizing efficacy by the active agent alone; it will also rule out an additional potential placebo effect within the active product itself. Comparison of two or more desensitizing dentifrices is a frequent objective of clinical hypersensitivity studies. One of the dentifrices might be a well known and documented desensitizing product. This dentifrice could be referred to as a “positive” control and lead the investigator to rationalize that negative or placebo control is not necessary. A placebo control (negative) should be included in studies comparing two active products to verify that the design and conditions of the study will allow active agents to overcome a placebo effect and demonstrate their potential efficacy. 60
Subject selection : Subject selection is the most demanding part of a clinical hypersensitivity study.
Specific subject selection criteria should be
written into the protocol and strictly adhered to. The study should be designed to answer a question with regard to an identified population. The study subjects should be a representative sample of that population. Usually, the study subject population represents the general population of those bothered with dentinal hypersensitivity. Occasionally, the primary objective of the study is subset of the population, such as post-periodontal surgery patients. People troubled by hypersensitivity were found to range from 15 to 69 years of age. The greatest concentration were in their 20s and 30s. sensitivity has also been reported to be evenly distributed in males and females. Ideal subjects should be : 1. Cooperative and relatively relaxed in the dental chair 2. Experienced in interacting with dentists as dental patients 3. Reliable in their responses to test measurements, use of assigned product, and attendance at appointed examinations. Prospective subjects should not be troubled with active periodontal disease in the areas of their hypersensitivity teeth. Prospective subjects should not have undergone periodontal surgery within 6 months prior to the initiation of the study. Dental hypersensitivity is a particular problem in the post-periodontal surgery patient. A study designed specifically to investigate hypersensitivity in post-periodontal surgery patients would be appropriate. Teeth with cracked tooth structure, large carious lesions, or restorations should not be acceptable study teeth.
61
Prospective subjects should be in good general health. They should not be suffering from a chronic debilitating disease or a chronic disease that is associated with daily episodes of pain, such as arthritis. Such conditions would
most
probably
interfere
with
obtaining
representative
hypersensitivity pain data. An important final consideration for subject selection would be the level of hypersensitivity appropriate for inclusion in the study. For example, the tactile sensitivity of a prospective study tooth should not be too close to the tactile sensitivity of a prospective study tooth should not be too close to the “low end” of tactile sensitivity, which precludes the opportunity to demonstrate potential improvement, that is, non-responsive. On the other end of the sensitivity range, it might not be appropriate to include a tooth that is on the “high end” of tactile sensitivity. It might be difficult to distinguish between pulpal and dentinal pain for those subjects. It is also infinitely more difficult to reliably measure hypersensitivity pain at this end of the range of pain. Hypersensitivity measurement : Whatever stimulus is used, the stimulus should be quantifiable and reproducible. The stimulus should also elicit dentinal pain and not pulpal pain. Dentinal pain is usually rapid in onset, sharp in nature, and of short duration. Dentinal pain is produced by stimuli such as tactile, cold, heat, and osmotic, which are applied to exposed dentin. A general principle for all studies, clinical or laboratory, is to use accepted methods. Unfortunately, acceptable devices/techniques have not yet been established for measuring hypersensitivity. Thus, a large share of the undertaking of a clinical hypersensitivity study is transformed from a science to an art. Tactile sensitivity :
62
A dental explorer is passed over exposed dentin on the labial cervical areas of suspected sensitive teeth. Subjects will then report their sensitivity or lack of sensitivity to the examiner. Once sensitive teeth have been designated and subjects enrolled in a clinical study, the dental explorer is frequently used to measure tactile sensitivity levels throughout the study. Subjects will then evaluate their level of tactile sensitivity to the explorer using a verbal rating scale (VRS). A typical VRS might appear like this to the subject: 0 = No discomfort, but aware of stimulus 1 = Mild discomfort 2 = Marked discomfort 3 = Marked discomfort that lasted more than 10 seconds Measurement of tactile sensitivity by this method has two limitations. First, the investigator should test all sensitive areas on all teeth of all subjects during all examinations with the same tactile pressure. This would be an almost impossible task. Second, the VRS offers a restrictive choice of words that may not represent pain experience with sufficient precision for all subjects. An electronic pressure-sensitive probe (Yeaple probe) has been used to measure levels of tactile sensitivity. The primary advantage of the probe is that tactile sensitivity can be reported in terms of a quantified reproducible grams force. The probe tip (dental explorer) can also reach all tooth surfaces in all areas of the mouth. Care must be exercised that the force is applied gradually so that the applied force will not go beyond the point at which the subject actually perceives sensitivity. The investigator may â&#x20AC;&#x153;sweepâ&#x20AC;? a suspected sensitive area with a tactile probe several times before finding just one spot within the area that elicits sensitivity by the subject. Patience is a virtue in these situations. 63
Thermal sensitivity : The cold stimulus appears to be the strongest and causes the greatest problems to those troubled by dentinal hypersensitivity. A method often reported in the literature for measurement of cold sensitivity is the 1-second air blast at about 700F from a dental unit air syringe. There are several problems associated with this apparently simple quantifiable technique that render it difficult to reproduce accurately. First, there always exists the problems of proper control f the temperature of the air emanating from the syringe. The usual practice is to report a temperature range of 680 to 730 F. such a relatively wide range has the danger of crossing back and forth over the threshold temperature of cold air sensitivity for each subject. The intensity of the stimulus could also vary in accordance with variances in pressure (usually reported at 60 psi), the distance of the syringe tip from the tooth being tested, and the actual duration of the 1-second air blast. The latter of these two intensity factors are investigator controlled and could easily vary from one test to another. The question of an â&#x20AC;&#x153;air dryingâ&#x20AC;? effect on the exposed dentin area from the air blast has not been resolved. Immediately after the cold air blast, the subject usually reports the level of sensitivity via a VRS as discussed for tactile sensitivity.
64
The pain threshold approach has also been used test sensitivity to cool/cold air. A temperature-controlled stream of air was directed to the exposed dentin of a sensitive tooth via a disposable plastic tip. The initial air temperature of 1000F was reduced until the subject first experienced sensitivity or until a lower limit of 700F was reached. The air stream was generated by a compressor at 10 psi. the air temperature was controlled by an intricate device and was monitored at all times by a temperature probe just prior to the existing of the air through the tip. This technique would appear to be quantifiable and reproducible, but it may have the advantage of drying and sensitizing a test tooth as the investigator proceeds down through a temperature range. The thermocouple device used to test thermal sensitive provides a continuous application of heat or cold via a probe tip to a point on the tooth. The device has the advantage of precise control of temperature, but it suffers from a lag between probe and tooth surface temperature. changes in temperature must be made slowly so that a temperature threshold of sensitivity is not bypassed. In addition, sensitivity measurement by this device may not be representative of real world thermal sensitivity experienced by subjects. Subjects usually complain of cold air or cold liquids and not cold objects. Cold air or cold liquids produce sudden changes in dentin temperature and thereby, sudden shifts in dentinal fluid in the tubules result in hypersensitivity pain as described by the hydrodynamic theory. The thermocouple would most likely produce more gradual changes in dentinal temperature and dentinal tubule fluid movement.
65
A cold water testing technique was developed and later modified to include the use of different temperatures of water placed directly on the exposed dentin. Plastic impression syringes were filled with water from thermal insulated containers with temperatures equilibrated to 20 0, 100 and 00C. the investigators used the syringes to flow water over the exposed root surface fro 3 seconds or until a positive response was noted by the subject. Testing began with water at 20 0C and proceeded to 100 and 00 or until a positive response was obtained. The intensity of pain perceived by the subject at the temperature that first produced a positive response was not evaluated. This method is, in effect, a threshold technique and should include several more temperatures of water between 200 and 00C. to add more temperatures would require more thermal insulated water containers. The requirement of numerous water baths would make the technique considerably more equipment intensive. Another concern about this technique would be controlling the amount of water flowed over the exposed dentin during each challenge. Chemical sensitivity : Chemical stimuli have been used in clinical hypersensitivity studies. The stimulus is not conductive to threshold measurement because repeated applications of the chemical stimulus reduce the sensitivity of the exposed dentin. Problems such as inconvenience, difficulty in administering and controlling the stimulus, and possible injury to the adjacent soft tissue de-emphasize the chemical stimulus as a practical measurement of hypersensitivity in clinical studies.
Electrical sensitivity :
66
Application of electrical stimuli to either enamel or exposed dentin has not been shown to result in any noticeable effect on tubule fluid movements. The electrical stimulus would appear to be more appropriate for measuring pulp vitality than dentinal sensitivity. Subject assessment : Word descriptors that patients use to describe their hypersensitivity pain have not been documented. Clinical hypersensitivity studies should provide an opportunity to indicate the key words that best describe hypersensitivity pain throughout the use of an assigned product. The subjects quantitative assessment of their own overall perception of hypersensitivity pain has been used in clinical studies. When this method of evaluating the level of hypersensitivity is used, subjects are asked to rate the severity of sensitivity that they have been experiencing during their everyday routine. They are to include stimuli from cold air, hot/cold foods or drink, sweet and sour food, toothbrushing and so on in their overall sensitivity evaluation. When provided a suitable method for evaluation of perceived sensitivity, subject assessment of hypersensitivity during a clinical study provides meaningful information. The visual analogue scale is an acceptable method for providing this assessment. Visual analogue scale : A visual analogue scale (VAS) is a line, usually 10 cm in length. The extremes of the line represent the limits of pain a subject might experience during a dentinal hypersensitivity episode. One end could be labeled “no discomfort” or “no pain”, whereas the other end could be labeled “severe discomfort” or “severe pain”. Subjects are asked to place a “mark” on the 10cm line at a location between the no pain and sever pain ends that best indicates their current level of hypersensitivity. When the VAS is properly explained to subjects, they can easily understand its use and successfully use it to indicate their level of pain response to a hypersensitive stimuli. The 67
Vas offers a continuum between what the subjects would perceive as the extremes of pain (none to severe). The VAS also offers a greater capacity to change in response to a hypersensitive stimulus. On the other hand, the verbal rating scale (VRS) is restrictive in that it does not offer enough descriptions that can be placed in a continuous and ascending (or descending) order of severity of pain. Use of the VAS has been found to be reproducible because a very high correlation between successive measurements of pain severity has been noted. Application of stimuli : When more than one stimulus is used, the application order of the stimulus is very important. Care should be taken to insure, as much as possible, that each stimulus does not interfere with other stimuli used in the measuring procedure. The least disturbing stimulus should be used first, with the most disturbing stimulus used last. Depending on which stimuli are used, testing should begin with subject assessment and then followed by tactile, heart and cold stimuli. Control of extraneous factors that could potentially influence subject response is important. Standardized instructions and stimulus demonstration should be given. The examination room should be free of distractions caused by noise, music, lights, temperature and so on. Avoid fear-generating procedures. The subject should be allowed to adjust to the examination room environment. Test product assignment : Subject assignment : The first consideration in subject assignment should be the establishment of two subject groups (cells) with equivalent level of dentinal hypersensitivity. Treatment of equivalent levels of hypersensitivity is very important for a meaningful comparison of the active dentifrice with the
68
control dentifrice and the establishment of a desensitizing efficacy by the active dentifrice. Random assignment of subjects to treatment groups is the simplest scheme to implement. By this method, however, an investigator is always at risk of ending up with groups of different levels of hypersensitivity by this method. The risk becomes greater as the group size is decreased, whereas the risk is lessened as the group size is increased. One easy method of stratification involves maintaining a cumulative sum of the cold sensitivity measurements from the baseline examination of subjects. Subjects are assigned to the two groups with the guideline of maintaining equivalent sums of cold sensitivity data between the two groups. The stratification process can be made more intricate by also maintaining equivalent tactile sensitivity sums between the two groups in addition to maintaining equivalent cold sensitivity sums. The second consideration is subject group assignment based on â&#x20AC;&#x153;real worldâ&#x20AC;? population variables. Generally, the subjects within each group should be in the age range of 20 to 50. This age range should also be equally represented between the two groups. Whenever possible, males and females should be equally represented in each group. Achieving the ideal representation of these population variables is often very difficult because of the usual limited availability of hypersensitivity subjects. Product assignment : The active and control dentifrices should be assigned to the subjects so that the investigator, subject, and any other office staff do not know which product each subject is using (double blind). The active and control dentifrices should be packaged in plain dentifrice tubes and properly coded for identity. A third person who has no investigator or subject contact should be the only one who knows the code. 69
Study length/examination periods : The length of time subjects brush with their assigned dentifrice can be a critical factor of dentinal hypersensitivity studies. Subjects should use their assigned dentifrice over a sufficient time period to : 1. Demonstrate clinical efficacy on the part of the active desensitizing dentifrice as compared to the control or placebo dentifrice. 2. Rule out a â&#x20AC;&#x153;placebo effectâ&#x20AC;? on efficiency as compared with the active dentifrice. It has been the experience of the authors that a placebo effect by the control dentifrice usually runs its course in about 6 weeks of treatment. In order to confirm the course of the placebo effect, hypersensitivity measurement should be obtained after 8 and 12 weeks of use of the study dentifrices. Thus, a suggested examination/length of study format would be two baseline hypersensitivity examinations 1 week apart, begin use of study dentifrice immediately upon completion of the second baseline examination, and hypersensitivity examinations obtained upon completion of 2, 4, 8 and 12 weeks of dentifrice use. Statistical analysis : Sound statistical principles of study design and analysis must be considered at the outset of the trial, not at the conclusion. Failure to do so could weaken the scientific validity of the study and lead to inaccurate conclusions. Important factors to consider include representativeness of the subject sample, number of subjects needed, treatment group allocation methods, and selection of appropriate analytic methods. The clinical investigator should not turn to the statistician after a study has, been completed without prior consultation and expect the statistician to derive statistical meaning from the data.
70
Designing hypersensitivity study is in effect a clinical experiment of testing the null hypothesis that the â&#x20AC;&#x153;activeâ&#x20AC;? desensitizing dentifrice is no different than the control dentifrice in reducing hypersensitivity. The ability to separate treatments in a statistical analysis is partly a function of the statistical tests used. A desirable statistical test has a small probability of rejecting the null hypothesis when it is true and a large probability or rejecting it when it is false. Parametric tests usually have higher probabilities of rejecting the null hypothesis when it is false than non-parametric tests. When appropriately used, both parametric and nonparametric tests have low probabilities of rejecting the null hypothesis when it is true. The choice of which of these two statistical techniques and which specific tests should be used depends on several factors and assumptions. A good study should include enough subjects to have adequate power. That is , the study should be able to identify, with high confidence, when there is a meaningful difference between the treatment groups. This is especially important when interpreting studies that show no statistically significant difference between the treatment groups. For studies with an adequate number of subjects, this result can be interpreted to mean that the treatments are unlikely to differ by a meaningful amount. In studies with too few subjects, the failure to differentiate treatments may simply be due to insufficient power. OVER-THE COUNTER DENTIFRICES IN THE TREATMENT OF TOOTH HYPERSENSITIVITY : Traditionally, a dentifrice has been defined as a substance used with a toothbrush to aid in cleaning the accessible surfaces of the teeth. Pader has expanded this definition to recognize the pharmacologic role of anticaries therapeutic dentifrices by defining a dentifrice that falls into this category as an abrasive-containing dosage from for delivering anticaries agents to the teeth. A dentifrice formulated to alleviate or treat the symptoms of tooth 71
hypersensitivity can be defined as an abrasive-containing dosage form for delivering desensitizing agents to the affected teeth. It is important to note that in the United Stages and many other countries, dentifrices that claim to treat the symptoms of tooth hypersensitivity are regulated as drugs and thus must meet strict standards of safety and effectiveness. Dentifrice as a delivery vehicle : Toothpaste, by far the commonest form of dentifrice, is apparently a simple product but is actually quite complex in formulation terms. On the one hand, consumers expect a toothpaste to extrude from its container easily, spread onto and stick to the toothbrush, but then break apart and foam almost instantly when brushing starts. Users also expect a pleasant and refreshing flavor, a certain level of foam, and a lack of stringiness and grittiness. Conversely, manufacturers must provide a product that is stable and retains its rheologic characteristics for 2 or ideally 3 years and more important, retains effective drug availability and delivery potential for this length of time, often under less than ideal storage conditions. Dentifrice
components
include
abrasive,
surfactant
(foamer),
humectant, thickener, flavor, sweetener, coloring, and water. Therapeutic dentifrices contain drug agents in addition to the other items. Desensitizing dentrifices are, for the most part, standard in formulation except that a concern for abrasivity exists because the condition is associated with exposed cementum or dentin, structures that are much softer than enamel. Abrasives are solid particles that clean or polish the tooth surface. compounds used for this purpose include various insoluble calcium salts (e.g., phosphate, pyrophosphate, and carbonate), sodium metaphosphate, and alumina. In recent years, a shift toward silicas has occurred because of their compatibility with fluoride, and their utility in formulating clear or opacified gel dentifrices. In the United States the abrasiveness (abrasivity) of a dentifrice is commonly determined by an in vitro procedure in which 72
radioactive dentin is mechanically brushed with a standardized slurry of dentifrice under a standard protocol developed by the American Dental Association (ADA). The amount of radioactive material removed is compared with that removed by a standard abrasive, which is given a value of 100; hence, this scale is commonly referred to as the RDA 100 (radioactive dentin abrasivity) scale. Most toothpastes that are available today, including desensitizing pastes, have RDA values from about 50 to 150. this is well within the estimate of a safe and effective level of abrasiveness, 50 to 200 RDA, provided by Pader after extensive review. Dentifrice abrasives are essential to prevent tooth staining. Because clinical studies have shown that the degree of stain formation is inversely proportional to the abrasivity level, a certain degree of abrasiveness in a dentifrice is cosmetically essential. Clinicians, however, have sometimes noted wedge-shaped lesions or defects at the cementoenamel junction, and the question has arisen as to the role of dentifrice abrasives in the etiology of this condition. The results of a clinical study designed to answer this question showed that the action of brushing contributed substantially to the amount of dentin removed, whereas the contribution of dentifrice abrasivity was not a major factor in the progression of cervical lesions. A second cosmetic attribute of dentifrices that is essential to successful treatment of tooth hypersensitivity is flavor. In fact, the taste of a dentifrice is one of the most important factors related to the continuous use of a particular dentifrice, and, perhaps somewhat surprisingly, market research has shown that most consumers will not continue to use a particular dentifrice solely for its therapeutic benefit. Most desensitizing toothpastes have a taste that is different from that of conventional toothpastes because they incorporate therapeutic agents. When recommending or prescribing a product, clinicians should explain this to the patient. The fact that a taste is different does not mean that it is unacceptable. The pleasantness of a taste is 73
a cultural, subjective, and personal phenomenon, and adaptation can rapidly occur. If a patient reports that the flavor of a particular brand is unacceptable for continued use, then the dentist should recommend another brand that incorporates a different active system. Using an in vitro dentin disc system, Pashley and co-workers found that dentifrice components could occlude tubules, and that products differed in their ability to produce this effect. Clinically, Addy and Co-workers related decreased tooth sensitivity to an in vitro observation that the fine silica abrasive particles in some toothpastes readily occluded open dentinal tubules. Interactions among several potential dentifrice components affect their uptake by dentin, and these interactions may have advantageous or negative consequences for treatment. RATIONALE FOR OTC TREATMENT OF TOOTH HYPERSENSITIVITY Up to one in seven adults screened in an office practice in Switzerland had tooth hypersensitivity. In view of this incidence, home-use OTC-desensitizing products appear to be the most realistic and practical means of treating most patients with tooth hypersensitivity and should be the first step in routine management. This presupposes that the diagnosis of hypersensitivity has been made and the patient educated as to the proper preventive measures to adopt. First, they are readily and widely available, especially in pharmacies. Second, the products are cost-effective. Repeated dental office visits for desensitization treatments are costly in terms of time and money. Third, the OTC products are simple to use and noninvasive. Fourth, the habit of tooth brushing is almost universal in economically developed societies, the patient is not required to do anything he or she would not normally do, thus easing problems with regimen compliance. In 1981, the Council on Dental Therapeutics of the American Dental Association established a category for 74
acceptance of desensitizings agents. Products that meet the association’s criteria for safety and effectiveness are allowed to display the ADA “seal of acceptance” on the product and packaging, provided the manufacturer also agrees to adhere to the association’s standards in promotion and advertising. Currently, the council has accepted formulations containing three active ingredients for OTC dentifrice use : potassium nitrate, strontium chloride hexahydrate, and dibasic sodium citrate in a pluronic gel. Clinical methods of efficacy assessment : It is important to note that the ultimate criterion of success for a hypersensitivity treatment is, in fact, the subjective opinion of the clinician and patient : the former will not use a procedure or recommend a treatment that is perceived to be ineffective, whereas the latter will not allow a treatment regimen that does not alleviate the pain encountered in everyday situations. Nevertheless, the unreliability of subjective opinions alone necessitates that well-designed, double-blind, controlled clinical trials be conducted to establish scientifically the effectiveness of hypersensitivity treatment procedures before dissemination to the dental profession and the public at large. Pain perception, however, depends on several variables including among other factors the significance of the pain, individual personality, psychological factors, cultural attitudes, anticipation of pain, and the degree of apprehension. That fact, along with other negative study design factors including lack of stimulus standardization among investigators, led to inconclusive or contradictory results in many studies in which the intensity of pain perceived was the primary measurement criterion. An ad hoc advisory committee on dentinal hypersensitivity appointed by the ADA recommended the following study design features ; 1) the test data should be quantifiable and reproducible ; 2) the threshold of response should be established, preferably quantified, and correlated to a clinically 75
definable intensity ; 3) the relationship between the experimental stimulus and the defined area of hypersensitivity must be established by controlled clinical research ; 4) if more than one stimulus is used, then these stimuli should be reproducible, and interference between them must be minimized ; and 5) appropriate statistics should be used, and these should be justified according to the experimental design. The committee recommended, in addition to sound clinical and statistical design, the use of variable stimulus level-fixed threshold response as opposed to the earlier method of fixed stimulus level-variable response for the evaluation of tooth hypersensitivity. In evaluating the results of clinical desensitization studies, the clinician should carefully determine how close the methodology used is in conformance with the preceding guidelines and give greater credence to results obtained with newer methods. Note that the terms “old methods” and “new methods” are used for convenience; many studies conducted decades ago essentially confirm to the guideline, whereas some studies conducted recently do not. CLINICAL RESULTS Strontium chloride Dentifrices Dentifrices containing 10% strontium chloride hexahydrate as the desensitizing agent have been widely available for three decades. Sensodyne tooth paste for Sensitive Teeth was the product tested; at least one other brand (Thermodent Sensitive Teeth Toothpaste, Mentholatum Company, Buffalo, New York) incorporating strontium chloride hexahydrate is available commercially. Ross in 1961 reported the results of a monadic study conducted among 78 office patients who were instructed to use this dentifrice at home. Subjectively, 73% of the subjects reported complete relief of the condition, and this was confirmed by the clinician who observed the subjects’ involuntary response to artificially induced tactile and thermal stimuli. 76
Alleviation of symptoms usually occurred within 1 month of use. Similar results were reported in other monadic studies by Cohen, Skurnik, Meffert and Hoskins, Zelman. Although these early monadic studies showed that the use of a strontium chloride dentifrice had a potential benefit, they did not establish the efficacy of the drug agent itself because a placebo control was not used. Subsequently, as clinical methodology evolved, several double-blind, placebo-controlled clinical studies, were conducted two double-blind, placebo-controlled clinical studies were conducted two double-blind studies comparing the effectiveness of a strontium chloride dentifrice against that of a placebo control, or placebo and monofluorophosphate-containing controls. In the study against placebo, after 4 weeks of use, 68% of the sensitive teeth in 38 subjects had improved in the active group as compared with 53% in the 38 subjects using the placebo. This difference was significant at the 95% confidence level. After 8 weeks of use, however, although the percentage of improved teeth in both the active and placebo groups continued to increase (76 vs. 71% respectively) the differences were no longer significant. Subjects using the monofluorophosphate dentifrice experienced the same degree of benefit in comparison with the placebo as did subjects using the strontium chloride product. Blitzer conducted a double-blind 1-month study in which the patients subjectively rated their response to either an active (20 subjects) or placebo (17 subjects) dentifrice into the categories of complete disappearance of hypersensitivity, partial relief, or no improvement. In the active group, 75% of the subjects rated their improvement as complete in comparison with 24% in the placebo group. The intergroup difference was significant at the 99% confidence level. Smith and Ash conducted a double-blind, placebo-controlled study over 60 days in 20 subjects using qualitatively applied thermal and 77
mechanical stimuli to elicit a response. Subjects also self-rated their hypersensitivity condition. The results showed that no improvement occurred in either group regarding any of the parameters tested. Johnson and co-workers found that after 12 weeks of unsupervised twice daily use, 28 subjects using the strontium chloride dentifrice demonstrated an increase in the ability to tolerate a cold water stimulus of 5.33 0C, whereas an identical number of subjects using a conventional stannous fluoride dentifrice showed a smaller increase of 3.040C. The intergroup difference was significant at the 99% confidence level. Addy and coworkers found that a strontium chloride dentifrice was significantly superior to a placebo dentifrice when measured by the graded responses using the classical cold air method, but was inferior to the placebo in terms of the number of sensitive teeth responding to a thermoelectric probe set at 00C and 50C. Minkoff and Axelrod : Uchida and co-workers studied the effectiveness of a strontium chloride dentifrice in treating hypersensitivity following periodontal surgery. In the active group, the pain score (a summary of pain responses to mechanical, cold water, and cold air stimuli) increased from 1.2 to 2.6, 1 week postoperatively, and then decreased to 0.6 (76%), 8 weeks postoperatively or 7 weeks after the start of treatment. In the placebo group, the pain score also increased from 1.0 to 2.2, 1 week postoperatively, but at the end of treatment the value was still 1.4, a 34% reduction. The significance of the Uchida study lies in the fact that the results quantitatively confirmed the clinical impression that periodontal procedures often induce tooth hypersensitivity, and, additionally, that a strontium chloride dentifirce is effective in relieving the condition.
78
Potassium Nitrate Dentifrices : In 1974, a potassium nitrate-containing dentifirce was reported as providing effective desensitization for 35 dental office patients who experienced slight to severe tooth hypersensitivity. The positive results for the agent provided by this type of quantifiable stimulation in double-blind controlled studies led to the acceptance by the ADA of several commercial products, Denquel Sensitive Teeth Toothpaste (Richardson-Vicks, Wilton, Connecticut), Sensodyne-F, and promise with Fluoride. Tarbet and co-workers compared the relative abilities of four active ingredients present in OTC dentifrices to desensitize hypersensitive teeth. They reported that 5% potassium nitrate was the most effective agent tested and rank ordered the relative effectiveness of the other agents tested as follows: strontium chloride, dibasic sodium citrate, formaldehyde. On an overall basis, the clinical evidence supports the efficacy of a 5% potassium nitrate dentifrice for the alleviation of the pain of tooth hypersensitivity. Dibasic Sodium Citrate Dentifrices Dibasic sodium citrate, formulated into a pluronic F-124 containing dentifrice (Protect) is the final ingredient currently recorgnized by the ADA as being safe and effective for the treatment of dentinal hypersensitivity. Formaldehyde Dentifrices : No longer sold in the united States, One brand, Emoform is available in the United Kingdom. Actually, dentifrices that contain 1.2 to 1.4% formaldehyde were the first widely available, commercially successful desensitizing dentifrices. Clinically, however, the results have been decidedly mixed. In early monadically designed studies, some investigators reported a favorable effect. The results for formaldehyde dentifrice have been generally negative. McFall and Morgan confirmed the negative tactile
79
finding but also found a significantly increased ability to tolerate a quantifiable cold stimulus. The ADA has not evaluated this agent to date. Fluoride and other dentifrices : One of the more popular early in-office treatments for treatment of hypersensitivity was burnishing the affected sites with fluoride-containing medicaments. The results of several studies, especially, those conducted with sodium monofluorophosphate in comparison with nonfluoride control, indicate a certain degree of effectivness. Kanouse and Ash found that after 3 months of use, subjects using the monofluorophosphate dentifrice had an increased tolerance to cold and hot of 1.70C and 1.30C, respectively, whereas subjects using a placebo showed increases of 0.5 0C for both stimuli. The intergroup differences were significant at the 95% confidence level. RECOMMENDATIONS FOR FUTURE STUDY DESIGN After reviewing the clinical desensitization literature of the last 30 years, one can conclude that a major obstacle impeding the development of more efficacious products to treat tooth hypersensitivity is the lack of standardization in study design. Clinical studies have been of varying duration, from 4 to 12 weeks; numbers of subjects per experimental cell vary widely; and the unit of data analysis has been the hypersensitive surface, hypersensitive tooth, and the individual. Fleiss and Kingman state that it is a mistake to employ statistical procedures that take individual sites as the units of analysis; the patient must be the unit of analysis. Although
intrastudy
comparisons
are
possible,
and
overall
assessments of drug efficacy are possible on the basis of the number of studies and their overall quality, interstudy comparisons cannot be made. Hence, questions such as the relative effectiveness of agents or the comparative times required to observe an effect cannot be answered reliably on the basis of published data. 80
Contrast this situation with that in anticaries clinical research. In this area, the units of measurements are well defined: decayed-missing-filled teeth or surfaces. Measurements are usually made at yearly intervals. Even the usual test population, school children, is well-defined because this age group is both prone to the disease and is readily accessible to clinical investigators. In earlier studies, the active products were compared with true placebos; currently, new products are compared with clinically verified positive controls. The net result of this has been the establishment of a large data base suitable for interstudy comparisons, which will allow for future advances in this area. Choice of stimulus will remain a difficult issue because different investigators have different opinions on this instrumentation. Nevertheless, some have adopted tactile stimulation because at least one instrument is widely available (Yeaple Probe, Vine Valley Research, Middlesex, NY). A review of Current Approaches to In-Office management of tooth Hypersensitivity : CLINICAL
CHARACTERISTICS
OF
DENTAL
HYPERSENSITIVITY The terms dentin sensitivity and dentin hypersensitivity are often used interchangeably, although the prefix hyper-denotes excessive sensitivity. Whereas dentin sensitivity is a normal response to stimulation of freshly exposed dentin, hypersensitivity may have a more pathologic basis. In virtually all cases of hypersensitivity, it is the vestibular surfaces of the teeth that are sensitive. Orchardson and Collins found that in different tooth types the relative frequency of hypersensitivity was: premolars, 38 percent; incisors, 26 per cent; canines, 24 per cent; and molars, 12 per cent. Dentinal hypersensitivity is subjective evidence that dentin has lost its investiture of cementum. However, about 10 per cent of teeth have no cementum covering the cervical portion of the root, and in these teeth 81
gingival recession alone may lead to hypersensitivity. Most hypersensitive teeth have associated gingival recession in excess of 1mm, and about 30 percent have cervical lesions. Gingival recession can be caused by periodontal disease, periodontal therapy (including oral prophylaxis), and improper tooth-brushing habits. Typically, the chief symptom of dentinal hypersensitivity is a sharp, sudden pain of short duration, although some patients complain of a dull, lingering sensitiveness. The most frequent complaint is sensitivity to cold, but pain may also be elicited by the use of a toothpick and /or brushing. In some cases, hot liquids and sweet or sour foods may evoke a response. Although most teeth are sensitive to more than one stimulus, not all hypersensitive teeth respond to the same stimulus. DIFFERENTIAL DIAGNOSIS : In attempting to determine the cause of discomfort, teeth should be examined for the presence of carious lesions, restorations, fractures, discoloration, periodontal disease, occlusal trauma, and exposed dentin that might be sensitive. Once the diagnosis of hypersensitivity has been established, it may be advisable to obtain a written dietary history in order to gather information regarding the possible etiologic role of acidic foods. Incomplete tooth fracture can be associated with a number of symptoms ranging from mild discomfort to severe pain. The most common complaint is pain to pressure. Tapping the teeth or having the patient bite down on an orangewood stick almost invariably evokes a sharp pain in the affected tooth. Application of a dye such as methylene blue to suspected tooth may aid in the diagnosis by disclosing the line of fracture. Exposure of dentin due to chipped enamel is usually obvious. Fractured restorations may be more difficult to visualize. Nevertheless, careful examination of the restoration will usually reveal the fracture.
82
Differentiating dentinal hypersensitivity from caries is realatively easy, particularly in the case of a deep carious lesion. However, it must be recognized that caries and dentinal hypersensitivity can coexist in the same tooth. Tooth sensitivity following a restorative procedure may resemble hypersensitivity in that the tooth is particularly sensitive to heat and cold and the evoked pain is generally of short duration and moderate intensity. Acute hyperfunction. A common example is the new amalgam or crown that has been placed without proper adjustment of the occlusion. Although the recent operative procedure may be partially at fault, hyperfunction alone can produce symptoms of pulpitis, Occlusal equilibration has been reported as a treatment modality for hypersensitive roots that did not successfully respond to accepted desensitizing methods. Teeth in acute hyperfunction are typically responsive to temperature changes and may mimic hypersensitive dentin, even though the investiture of these teeth ay be intact. Application of a saturated solution of CaCl 2 (8.8m) on a cotton pellet may be useful in identifying areas of hypersensitive dentin (Dr. David Pashley, personal communication). Saturated CaCl2, a highly soluble salt, is capable of evoking a sharp sensation by creating a strong osmotic pressure across dentin, thus producing fluid movement in the tubules. Diagnosis of pulpitis must be based on subjective and objective findings. Diagnostic aids include history of pain, percussion and palpation tests, inspection of the teeth and surrounding tissues, thermal and electric pulp tests, and radiographic examination. The dental history should cover the chronology, nature, location, radiation, and aggravating and alleviating factors that influence the pain. Dentinal hypersensitivity resembles reversible pulpitis in that pain is generally mild to moderate and fairly well localized to the tooth in question. 83
SPONTANEOUS REMISSION OF HYPERSENSITIVITY It is well known that hypersensitivity often abates without treatment. This is probably related to the fact that dentin permeability can decrease spontaneously. Natural processes contributing to desensitization include the formation of reparative dentin by the pulp, obturation of tubules by the formation of mineral deposits (dentinal sclerosis), and calculus formation on the surface of the dentin. It has been estimated that approximately 20 to 45 per cent of patients who receive no treatment or sham treatment experience relief. PLACEBO EFFECT A major factor in the establishment of a placebo response is the doctor-patient relationship. Individuals afflicted with real or imagined illness must have complete confidence in their doctor because patient expectations are critical for the induction of the placebo response. Illness and discomfort are perceived by the patient as threatening, and it is assumed that practitioners are able to decrease the peril. A positive doctor-patient relationship can motivate a patient to obtain relief. Furthermore, positive emotional and motivational behavioral responses can activate the bodyâ&#x20AC;&#x2122;s central pain-inhibiting system. this system modulates painful stimuli from the periphery through the release of endorphins centrally. PATIENT MANAGEMET Informing a patient in advance regarding the possibility of a potentially painful event can greatly strengthen the doctor-patient relationship, alleviate anxiety, reduce unnecessary emergency calls, lower the risk of litigation, and enhance the placebo effect. Proper patient management relies heavily on good communication skills. Every patient must be informed of the potential treatment risks, and post-treatment dentinal hypersensitivity is no exception.
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IN-OFFICE TREATMETN PROCEDURES : RATIONALE OF THERAPY Treatment of hypersensitive teeth should be directed toward reducing the functional diameter of the tubules so as to limit fluid movement. In order to accomplish this objective there are several possible approaches : 1. Formation of a smear layer by brushing the exposed root surface. 2. Topical application of agents that form insoluble precipitates within the tubules. 3. Impregnation of tubules with plastic resins. 4. Application of dental bonding agents to seal off the tubules. Although most agents that are effective in reducing dentinal hypersensitivity are also effective in partially occluding the dentinal tubules, potassium nitrate (KNO3) is an exception. SPECIFIC TREATMENT MODALITIES : Prior to treating sensitive root surfaces, hard or soft deposits should be removed from the teeth. Root planning with curettes or otherwise manipulating sensitive dentin may cause considerable discomfort, in which case teeth should be anesthetized prior to treatment. The teeth should be isolated and dried with warm air. When using desensitizing agents that have a caustic effect on sot tissue, care must be exercised to prevent them from contacting the alveolar mucosa. Cavity Varnishes : Dentin often becomes insensitive when open tubules are covered with a thin film of varnish. This may be an effective means of providing temporary relief. Wycoff advocates the use of a cavity varnish such as Copalite. For more sustained relief, a fluoride-containing varnish, Duraflor. Can be applied
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Corticosteroids : Mosteller reported that when a liner consisting of 1 per cent prednisolone in combination with 25 per cent para-chlorophenol, 25 per cent m-cresyl acetate, and 50 per cent gum camphor was applied to the walls of cavities, it was completely effective in preventing postoperative thermal sensitivity. It
has
also
been
reported
that
burnishing
an
ophthalmic
corticosteroids solution into sensitive root areas achieved some success. Studies involving the use of corticosteroids have provided little evidence that desensitization was due to the hormone, particularly when it was claimed that sensitivity was promptly relieved. Corticosteroids are not fast-acting drugs. Effects of Burnishing Dentin :
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Burnishing of dentin with a toothpick or orangewood stick results in the formation of a smear layer that partially occludes the dentinal tubules. Pashley and coworkers employed an in vitro method to study the effects of burnishing NaF, kaolin, and glycerin, alone or in various combinations, on dentin permeability. They observed that burnishing created a partial smear layer that reduce fluid movement across dentin by 50 to 80 per cent. Burnishing dentin with a dray orangewood stick was more effective in reducing dentin permeability than burnishing with glycerin alone. Formation of insoluble precipitants to block tubules : Certain soluble salts react with ions in tooth structure to form crystals on the surface of the dentin. In order to be effective, crystallization should occur within 1 to 2 minutes, and the crystals should be small enough to enter the tubules. The crystals must also be large enough to partially obturate the tubules. Although relatively large crystals such as calcium oxalate dihydrate (which form when potassium oxalate is applied to dentin) are very effective in reducing permeability smaller crystals such as CaF 2 are les apt to be effective. Although it is used infrequently today, AgNO3 is time-honored desensitizing agent. Numerous authors have attributed the effectiveness of AgNO3 to its ability to precipitate protein constituents of odontoblast processes (Tomesâ&#x20AC;&#x2122; fibers), thereby partially blocking the tubules. However, there are reasons to doubt this explanation.
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Gottlieb developed the zinc chloride â&#x20AC;&#x201C; potassium ferrocyanide impregnation method for desensitizing root surfaces and cavities. In this procedure a 40 per cent solution of aqueous zinc chloride was rubbed into the surface per cent aqueous solution of potassium ferrocyanide was vigorously rubbed onto the dentin surface until an orange, curdy precipitate formed. Scanning electron micrographs of this precipitate have revealed a highly crystalline deposit covering the dentin surface. As most of the crystals were too large to enter the tubules, it is doubtful whether this method would provide a more efficient means of desensitizing dentin than burnishing alone. Grossman proposed formalin as the desensitizing agent of choice in treating anterior teeth because, unlike AgNO 3, it does not produce an unsightly stain. Formalin has been used in the dental office in a concentration of 40 per cent (full strength) for topical application by means of cotton pellets or orangewood sticks. CALCIUM COMPOUNDS : Calcium hydroxide : Calcium hydroxide (Ca(OH2) has been a popular agent for the treatment of dentin hypersensitivity for many years, particularly after root planning. The exact mechanism of action is unknown, but evidence suggests that it may block dentinal tubules or promote peritubular dentin formation. Using SEM, Brannstrom observed a variable constriction of the dentinal tubules in the majority of teeth treated with Ca(OH) 2, but only to a depth of 0.1 mm Mjor employed microradiograph to compare Ca(OH)2 â&#x20AC;&#x201C; covered dentin with normal dentin and demonstrated increased radiodensity in the Ca(OH)2-covered dentin.
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Because increasing the concentration of calcium ions around nerve fibers can results in decreased nerve excitability Ca(OH)2 might be capable of suppressing nerve activity. However, Trowbridge and coworkers found that application of Ca(OH)2 to the walls of deep cavities in cat canine teeth had no effect on the excitability of nerve fibers in the underlying pulp. Levin and associates applied Ca(OH)2 paste to the necks of 118 teeth in 50 patients and found it to be immediately effective in reducing sensitivity in 98 per cent of the teeth. First, sensitive teeth were isolated and dried with cotton rolls. Next, a paste of Ca(OH) 2 and sterile distilled water was applied to the exposed root surfaces with a sable brush. The paste was allowed to remain on the tooth for 3 to 5 minutes. After removal of the paste, the tooth was tested sensitivity. If the dentin was still sensitive, the paste was re-applied. Pashely and coworkers found that Ca(OH)2 was effective in reducing the permeability of acid-etched dentin as well as smear layers. However, when 6 per cent citric acid was applied to the Ca(OH) 2-treated smear layer, dentin permeability returned to the initial acid-etched value. This would suggest that ingestion of acidic foods and beverages might result in removal of Ca(OH)2 from the dentin. Dibasic Calcium Phosphate : Hiatt and Johansen studied the effectiveness of burnishing CaHPO 4 into sensitive areas of roots with a round toothpick and found that 93 per cent to patient reported significant relief of discomfort, as compared with 25 per cent of the control group, which received burnishing only. FLUORIDE COMPOUNDS :
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Lukomsky was the first to propose sodium for fluoride (NaF) as a desensitizing agent. Later, Hoyt and Bibby developed a paste consisting of equal parts of NaF, kaolin, and glycerin. The paste was burnished into the exposed root surfaces with a porte polisher, an orangewood stick or a rubber cup for 1 to 5 minutes. Although this procedure was considered to be a success in decreasing sensitivity, at least part of the effect can be attributed to burnishing. More recently, fluoride gels have been developed for inoffice treatment of hypersensitivity. Because dentinal fluid is saturated with respect to calcium and phosphate ions, application of NaF to dentin leads to precipitation of CaF 2 crystals, thus reducing the functional radius of the dentinal tubules. The crystal size of CaF2 is very small (approximately 0.5 Âľm), and therefore as single application of NaF has less effect on dentin permeability than agents such as potassium oxalate that give rise to larger crystals. Furthermore, it has been shown that fluoride is lost fairly rapidly following application of NaF to dentin. This may explain why topical application of fluoride solutions is of limited effectiveness in reducing sensitivity on a long-term basis. Evidence suggests that a small fraction of the fluoride initially applied to dentin is retained in the insoluble apatitic form, thus making the lattice more stable and less soluble in acid. This could protect the dentin from dietary acids, which tend to open the tubules. Acidulated Sodium Fluoride : Laufer and colleagues observed that the concentration of fluoride in dentin treated with acidulated NaF was significantly higher than dentin treated with NaF. However, there was no difference after samples were washed with synthetic saliva. Sodium silicofluoride: 90
Bhatia claimed that application of saturated solution (0.6 per cent) of sodium silicofluoride for 5 minutes was much more potent than a 2 per cent solution of NaF in desensitizing painful cervical areas of teeth. Everett and associates postulated that silicic acid forms a gel with the calcium of the tooth, thus producing an insulating barrier. Stannous Fluoride : Blank and Charbeneau advocate burnishing a 10 per cent solution of stannous fluoride (SnF2) into sensitive root areas. Ellingsen and Rď&#x192;ślla. This observed a dense layer of tin- and fluoride-containing globular particles blocking the dentinal tubules. The dentinal tubules were totally covered even after treatment with relatively low concentrations of SnF2. Blong and associates found that a 0.4 per cent SnF 2 gel was an effective agent in the control of pain associated with hypersensitive dentin. However, prolonged use of the gel (up to 4 weeks) was necessary to achieve satisfactory results. Fluoride â&#x20AC;&#x201C; Inotophorises : Iontophresis is a term applied to the use of an electrical to transfer ions into the body for therapeutic pusposes. The object of fluoride iontophoresis is to drive fluoride ions more deeply of fluoride alone. In a histologic study, leflkowitz observed secondary (reparative) dentin in the pulps of teeth extracted soon after iontophoresis and concluded that iontophoresis stimulates dentin formation. This inference is highly suspect, as it takes several weeks for reparative dentin to form in human teeth. Iontophoresis is not a simple procedure. It involves the placement of a negative electrode to dentin and a positive electrode to the patientâ&#x20AC;&#x2122;s face or arm. If the negative electrode makes contact with salvia, gingival tissue or a metallic restoration, the flow of current will follow the path of least resistance and stream around the dentin rather than through. It for this, 91
reason, Gangarosa recommended that teeth be isolated with plastic strips and cotton rolls rather, than a rubber dam. He cautions that moisture can accumulate between the tooth and the rubber dam, thus providing a low resistance pathway for the current. Although a number of authors have reported a significant reduction in sensitivity with the use of iontophresis with 2 per cent NaF, Greenhill and Pashely- found that the use of AgNO3 or potassium oxalate produced significantly grater reductions in hydraulic conductance than fluoride iontophoresis. Although iontophoresis has gained some popularity, its effectiveness needs to be demonstrated in well-controlled clinical studies. Iontophoresis devices are expensive, somewhat difficult to use, and generally less costeffective than other treatment procedures. Strontium chloride : Kun found that (topical application of concentrated strontium chloride (SrCl2) on an abraded dentin surface produced a deposit of strontium that penetrated dentin to a depth of approximately 20 Âľ and extended into the dentinal tubules. It has been suggested that strontium deposits are produced by an exchange with calcium in the dentin resulting in recrystallization in the form of a strontium apatite complex. Gedalia and associates reported that topical application of 10 per cent SrCl2 prior to application of 2 pre cent NaF was more effective in decreasing sensitivity than NaF alone, as assessed 3 months following treatment. Oxalates : Since their initial development as a desensitizing agent, the oxalates have gained great popularity, particularly among periodontitis. They are relatively inexpensive, easy to apply, and well tolerated by patients.
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Potassium oxalate and forric 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. SEM revealed a high degree of tubule occlusion by crystals that almost completely covered the orifices of the tubules. Subsequent application of 6 per cent citric acid to the oxalate-treated dentin did not increase dentin permeability, indicating that calcium oxalate should be resistant to dietary acids. In the development of an effective desensitizing system, there oxalate compounds have been developed, 6 per cent ferric oxalate, 30 per cent dipotassium oxalate, and 3 per cent monohydrogen-monopatssium oxalate. Pashley and Galloway found that when reacting with ionized calcium, 30 per cent dipotassium oxalate produced fewer but significantly layer calcium oxalate crystals than those produced by 3 per cent monohydrogenmonopotasium oxalate. These investigators suggested that the larger crystals are only effective in obturating wide open tubules, whereas the smaller crystals are capable of obturating open as well as partially close tubules. Application of KHOx to the etched dentin reduced sensory nerve excitability to the level of unetched dentin. KHOx is commercially available under the name of Protect. It comes in a convenient unit-dose applicator tubules with a cotton tip that delivers KHOx to the dentin surface. Ferric oxalate is currently marketed under the Sensdodyne Sealant name. It is available as a professional desensitizing treatment for unit-dose application with a disposable contra-angled instrument. DENTAL RESINS AND ADHESIVES : The objective in employing resins and adhesives is to seal the dentinal tubules to prevent pain-producing stimuli form reaching the pulp. Several investigators have demonstrated immediate and enduring relief of 93
pain for periods of up to 18 months following treatment. although not intended for treatment of generalized areas of root sensitivity, this can be an effective method of treatment when other forms of therapy have failed. Brď&#x192;śnnstrď&#x192;śm and colleagues achieved excellent results by impregnating the dentinal tubules with a restorative resin material. in this procedure, the area of sensitive dentin was cleansed and etched with an acid conditioner for 5 seconds. The dentin was them dehydrated with a continuous blast of air for a at least 15 to 20 seconds in order to dry the outer part of the dentinal tubules. A drop of a Concise Enamelbond was then applied to the dentin. Before the resin on the surface hardened into a thin film it carefully removed to allow resin tags to occlude the outer part of the tubules without covering the dentin between the tubules with resin. The use of NTC-GMA and PMDM following ferric oxalate treatment of the dentin smear layer led to a sustained decrease in dentin permeability. This system spears to hold promise as a future treatment for dentinal hypersensitivity. Pashley and associates have shown that contamination of dentin with blood or salvia lowers the bond strength of composite resin. However, they found that contaminated surface could be removed with a high-speed bur. During a 6-weeks study, Javid and coworkers compared the effects of a single application of isobutyl cyanoacrylate with weekly applications of a 33 per cent NaF paste. The material is gradually lost, so that repeated cyanoacrylate applications may be necessary. Wycoff advocates the use of adhesives for severe cases of hypersensitivity that do not respond to other therapy. He prefers a glassionomer cement because it is hydrophilic acid conditioning is not required, the material adheres well, and it is esthetically pleasing. Copeland found that application of Scotchbond produced immediate and lasting relief from hypersensitivity. Clinically superior results were 94
obtained by covering the resin with a drop of dilute restorative material. Eighteen months following treatment, 89 per cent of 368 hypersensitive teeth remained free of pain. GLUMA- includes a 5 per cent gluteraldehyde primer and 35 per cent HEMA. It provides an attachment to dentin that is immediate and strong. GLUMA has been found to be highly effective when other methods of treatment failed to provide relief. It has been reported that the sequential use of GLUU<A followed by Scotchbond produced impressive bond strength. Because. GLU<A has excellent wetting characteristics, it should enhance bond strength of a resin when the dentin has been contaminated with blood or saliva. Recently Felton and coworkers have reported that GLUMA seems to prevent bacterial growth in tooth/restoration interfaces. This could have a beneficial effect in inhibiting plaque accumulation on sensitive root surfaces. PATIENT EDUCATION : Dietary counseling : Dietary counseling should focus on the quantity and frequency of acid intake and intake occurring in relation to tooth brushing. Any treatment may fail if these factors are not controlled. A written diet history should be obtained on patients with dentinal hypersensitivity in order to advise them concerning eating habits. Addy and associates found that red and white wine, citrus fruit juices, apple juice, and yogurt were capable of dissolving the smear layer in vitro. They also found that formic and tannic acids, low-pH carbonated drink, Coca-Cola and black currant cordial had no effect on smear layers. Tooth brushing in combination with decalcification of superficial dentin is capable of accelerating the loss of tooth structure. because loss of dentin is greatly increased when brushing is performed immediately after 95
exposure of the tooth surface to dietary acids, patients should be cautioned against brushing their teeth soon after ingestion of citrus foods. Tooth Brushing Techniques : Because incorrect tooth brushing appears to be an etiologic factor in dentin hypersensitivity, instruction in proper brushing techniques can prevent further loss of dentin and the resulting hypersensitivity. PLAQUE CONTROL : Saliva contains calcium and phosphate ions and is therefore able to contribute to the formation of mineral deposits within exposed dentinal tubules. The presence of plaque may interfere with this process, as plaque bacteria, by producing acid, are capable of dissolving any mineral precipitates that form, thus opening tubules. Periodontitis generally feel that patient who maintain effective plaque control complain less about hypersensitivity. Recurrent of root sensitivity has been noted in specific areas that were missed in home care. It is difficult for patients of undertake desensitizing procedures such as plaque control if the procedures cause pain. The goal of treatment is to reduce sensitivity so that the patient is able to burnish sensitive dentin surfaces with a toothpick, Stim-U-Dent, or abrasive-containing dentifrice. This keeps the dentin surfaces clean and at the same time forms a smear layer.
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