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Hypersensitive teeth. Part I: Etiology
RETENTION
2.
3.
4. i
6. 7
8.
9.
AND
RESISTANCE
Kaufman EC;, Coelho 4G, Colin L: Factors influencing the rrtentmn of cemented gold castings. J PR~STHET DENT 11:487, 1961. Craig RG. El-Ebrashi MK, Peyton FA: Experimental stress analysis of dental restorations. Part II: Two-dimensional photoelastic stress analysis of crowns. J PROSTHET DENT 17:292, 1907. Lorey RE, Myers GE: The retentive qualities of bridge retainerr J Am Dent Assoc 76:568, 1968. Reisblck MH, Shillingburg HT Jr: Effect of preparation geometry on retention and resistance of cast gold restorations. Calif Dent Assoc J 3:51, 197’1. Ohm E, Silness J: The convergence angle in teeth prepared for artificial crowns. J Oral Rehabil 5:371, 1978. Eames WB. O’Neal SJ, Monteiro J, Miller C, Roan JD Jr, Cohen KS: Techniques IO improve the seating of castings. J Am Dent Assoc. 96:432. 1978. Mack PJ: .\ theoretical and clinical investigation into the taper nchieced on crown and inlay preparations. J Oral Rehabil 7:255, 1980. Woolsey GD, Matich JA: The elect of axial grooves on the rcslstancr lorm of cast restorations. J Am Dent Assoc 97:978, 1978.
Hypersensitive Jack T. Kramer,
10.
11.
12.
13. 14.
15.
Potts RG, Shillingburg HT Jr. Duncanson XI<, Jr: Retention and reststance of preparations for I‘.ISI rrs~or‘.~t;~;ns, .J PRWTIIE I DENT 43:303, 1980. Chan KC, Hormati AA, Boyer DR. Artx:liarv rctetltion loi complete crowns provided by cemrnt kf,y>,, j ~‘ROSt.fll:T. D5.X I 45:152, 198 I. Kishimoto M, Shillingburg H’T Jr, D~nc,mwn MC;: Inlluence of preparation features on retentrrm and iisiatance. Part 11: Three-quarter crowns. J PROSTH~.I DENT 49: 188, 198 i. Shillingburg HT Jr, Hobo S, Whitsett LD Fundamentals oi Fixed Prosthodontics. Chicago. 1978. Quintesrrnw Books. p 67 Owen CP: Factors influencing thr rwentim~ and resistance of preparations for cast intracoronal rrq:!ornIi:>ni J PKO~.I.HK.I DEN.~ 55:674, 1986. Hegdahl T, Silness .J: Preparation arras reslstine d~splaccrnent of artificial crowns. J Oral Rehabil 4:201 IO-
Rejmni rque.\f\ ir,. DR. C. P. OWEN FAC:ULTY oti DENTISTRY PRIVATE BAG X 12 TYGERBERC; 7505 REPURLIC 01: SWTH AFRICA
teeth. Part I: Etiology
D.M.D.
North Palm Beach, Fla.
P
reservation of the natural dentition in a state of comfort, health, and function is the primary goal of the dental profession. Although great progress has been made in the restoration of function and health, attention to comfort has often been overlooked. Hypersensitive teeth are a source of chronic irritation that affects eating, drinking, and breathing. Severe hypersensitivity may even result in an emotional change that causes an altered daily lifestyle. The objective of this two-part article is to present a review of hypersensitive teeth and to include the etiologies, symptoms, theories of pain production, and methods of treatment. Management of hypersensitive dentin tends to be empirical because precise knowledge about the mechanism of pain transmission within the dentin is absent. The dentin is a highly sensitive tissue that differs from other sensitive tissues in the body. In skin, for example, four different sensations, cold, heat, touch, and pain, can
Presented at the Pacific B.C.. Canada. THE
JOURNAL
Coast
OF PROSTHETIC
Society
of Prosthodontists,
DENTISTRY
Vancouver,
be perceived. In dentin, different stimuIi cause only pain. When the pulp is removed, dentin is no longer sensitive, which indicates that sensory nerves in the pulp may extend into the dentin and respond when dentin is stimulated. Although it is well established that pulpal nerves carry the sensation of dental pain to higher centers, it is still unclear how the dentin transmits the varied stimuli to these nerves. Evidence suggests that sensitive exposed dentin exhibits patent tubules. Most histologic sections indicate, however that nerve fibers from the pulp only penetrate a limited distance along some dentinal tubules.’ Graf and Galasse2 reported pain arising from exposed dentin in as many as one in seven adult patients. According to Kanapka,3 sensitive teeth afflict some 40 million Americans at one time or another and more than 10 million report chronic hypersensitivity. Little has been accomplished to alleviate this painful problem. Exposure of hypersensitive dentin arises from either the removal of the coronal enamel or a denudation of the root surface by loss of cementum and the overlying 153
KRAUSER
periodontal structures. The thin layer of cementum (20 to 50 pm) is easily removed by curettes, abrasive pastes, foods, and brushing. The loss of cementum is an opportunity for sensitivity. A review of dental anatomy reveals that in 60% of adult teeth the cementum covers the enamel at the cementoenamel junction (CEJ). Thirty percent of the teeth exhibit a butt joint at the CEJ, and in 10% of teeth, the enamel and cementum do not meet and a portion of the dentin is exposed. It is tempting to assume that these teeth are prone to sensitivity; however, there is currently no evidence that this is true. Enamel loss through occlusal wear, toothbrush abrasion, dietary erosion, and other parafunctional habits may also elicit a hypersensitive reaction. Denudation of the root surface may also be multifactorial; the main causes are gingival recession, aging, chronic periodontal disease, tooth position within the dental arch, periodontal surgery, incorrect toothbrushing habits, and root preparation. The preparation of the root surface is one of the most important factors in regaining periodontal health. Chemical and mechanical means are generally used. Meticulous root preparation may, on the one hand, yield a superior environment for periodontal repair, but may also initiate a hypersensitive state. It is noteworthy that not all exposed dentinal surfaces exhibit hypersensitive symptoms. Factors such as age, rate of exposure, and the effect of naturally occurring or environmental desensitizing mechanisms affect the nature of the sensitivity. A psychogenic factor must also be considered. Ishikawa, however, observed patent tubules in areas of sensitive dentin but, in areas of occluded tubules the symptoms were absent.
THEORIES
OF DENTIN
SENSITIVITY
Although histochemical, autoradiographic, and electron microscopic studies have vividly described the relationship between the odontoblast and the neurofibers of the pulp, the exact mechanism of the transmission of the pain response from the dentin to the terminal nerve endings is only hypothesized. It is well established that the pulp is richly innervated and that the sensory nerves are present near the dentin between the odontoblast cells and in close contact with these cells. Since the 1950s the odontoblastic-receptor, direct nerve ending, and hydrodynamic theories of dentin sensitivity have been studied extensively.
Odontoblast-receptor
theory
Through its process within the dentinal tubules, the odontoblast receives and transfers stimuli to the nerve endings in the pul~.~ From an embryologic point of view, the odontoblast is thought to be of mesodermal origin and not neural origin. Various physiologic experiments studying membrane potential and electrical stimuli have given ambiguous results leading to neither acceptance 154
nor rejection of the odontoblast-receptor theory.6,7 Morphologic findings and electron microscopic findings by Frank et a1.8-‘o showed a close contact between the odontoblast and the nerve fibers in the pulp with a predentin and circumpulpal mineralized dentin. Frank et a1.8-‘0also observed a complex infolding of nerves in the odontoblastic process intratubularly. They concluded that a special functional relationship exists between the odontoblastic process and the nerve fibers and together they constitute a receptor complex. If this theory is to be accepted totally, it must be shown that the odontoblastic process extends from the pulp to the dentin-enamel junction. Light microscopy has revealed fibers within the tubules and minitubules that are assumed to be odontoblastic processes. In scanning electron microscopy, however, these intratubular fibers were seen as collagen fibers and not odontoblastic processes. Therefore, if the odontoblastic processes do not occupy the full length of the dentinal tubules, dental hypersensitivity cannot be fully explained on the basis of the odontoblast-receptor theory.
Direct nerve endings
theory
Unmyelinated sensory nerve endings exist within the dentinal tubules and conduct sensations to the pulp directly.5 This theory suggests the existence of nerve endings in the dentin that are of pulpal origin and can be directly stimulated. There is no doubt that nerves exist in the mineralized dentin. However, Frank et al.*-” showed nerves entering the tubules in the circumpulpal region that only extend to the inner one third of the mineralized dentin. Various physiologic studies indicated that there are nerves in the most pulpal portion of the dentin and none near the periphery.“-‘4 In prepared cavities, the placement of substances that could cause pain when applied to nerve endings (acetylcholine, potassium chloride, and bradykinin) resulted in no pain response in exposed dentin. However, these substances did cause intense pain when applied to the exposed pulp. It was also shown that neither local anesthetics nor protein-precipitating drugs eliminated dentinal sensitivity when inserted into the test cavity. Therefore, on the basis of microscopic and physiologic data, the existence of neural cells in the sensory portion of the outer dentin seems remote.
Hydrodynamic
theory
The interstitial fluid of the dentin and pulp exists as “dental lymph.” The changes in function, tension, or pressure at the surface of the tubules brings about a change in the hydrostatic equilibrium. This change causes a rapid fluid flow and a mechanoreceptor transfer to the sensory nerves in the subodontoblast nerve plexus. In 1900 Gysi15 first claimed that dentinal hypersensitivity is due to movement of a watery substance within AUGUST
1986
VOLUME
56
NUMBER
2
HYPERSENSITIVE
TEETH.
PART
I: ETIOLOGY
the dentinal tubules from the surface to the odontoblastic layer, which is interwoven with nerves. The pressure change associated with this fluid movement would yield pain.15 Brannstrom et a1.‘6-26gathered support for this hydrodynamic theory with in vivo experiments demonstrating that the tissue fluid within the tubules may seep through the tubules onto an exposed dentinal surface. This movement of fluid occurs with a speed calculated at 2 to 4 mm per second. This speed indicates that empty tubules could fill in a few seconds. If this assumption is correct, the hydrodynamic theory may be valid inasmuch as quick fluid flow may occur in the dentinal tubules under certain conditions. In addition, all stimuli that cause pain must cause a rapid fluid flow in the dentinal tubules. Dehydration of dentin is the clearest example of understood dental pain. The outward movement of fluid into the dehydrating source through a mechanoreceptor principle would stimulate the odontoblast and sensory nerves and cause pain. Cold and hypertonic or hyperosmotic solutions act in a similar manner in causing an outward flow from the tubules. The influence of heat-causing pain is more complicated. Application of dry heat apparently causes evaporation of the fluid from the surface and a shift of movement toward the pulp. The pressure buildup would then be recognized as pain. The hydrodynamic theory is gaining support and seems to explain dentinal sensitivity on the basis of mechanical stimulation of nerves in the dentin-pulp interface. This mechanical stimulation is a result of a rapid fluid flow in the dentinal tubules caused by pain-provoking irritants.‘6*26
obliterated dentinal tubules. The sclerotic zones beneath the region of attrition were occluded by peritubular, dentin-like material. This finding supports the view that the oral environment controls the development of dentinal sclerosis and that the obliteration or blockage of the patent tubules prevents the passage of’ painful impulses.
DIFFERENTIAL
Pain arising from dentin exposed to chemical, thermal, tactile, or osmotic stimuli varies in frequency and severity. Seltzer and Bender3’ have explored the di:+gnostic features of the many causes of pain that should be ruled out before the diagnosis of dentin hypersensitivity. Attempts to correlate pulpal pathology with clinical signs and symptoms of dentin hypersensitivity have failed to produce significant findings.
SUMMARY Although several theories have been suggested for hypersensitive dentin, it appears that the hydrodynamic theory is most plausible. If a clinical diagnosis of dentin hypersensitivity can be made, occlusion of the patent tubules would result in a reduction of hypersensitivity by the rapid fluid shift within the tubules. The naturally occurring defense mechanisms would wall off the narrow tubules producing the fluid flow, thus reducing the pain associated with hypersensitivity. In Part II of this article the current treatment modalities for dentin hypersensitivity will be discussed. REFERENCES 1.
NATURAL
PULPAL
DEFENSE MECHANISMS
The pulp has several natural defenses to protect itself from irritating stimuli.
2.
Calcification
3.
Pulpal calcification and the formation of secondary dentin, peritubular dentin, and dentinal sclerosis have been demonstrated by Ha112’ and Bernick.28 This natural occlusion of the peritubular dentin by calcium crystals is the tooth’s physiologic response to dentinal sensitivity. The tooth may naturally desensitize itself with a peritubular dentin mineralization.
4. 5.
6.
Bacterial plaque Another defense mechanism that may decrease dentinal sensitivity is the formation of plaque in the acquired salivary pellicle material coupled with salivary occlusion. In a dog study, Karlson and Penny29 found that plaque decreased sensitivity.
7. 8.
9.
Sclerosis Electron microscopic studies by Brannstrom3’ on teeth with incisor attrition revealed partially or completely THE
JOURNAL
OF PROSTHETIC
DENTISTRY
DIAGNOSIS
10.
Tronstad L: The anatomic and physiologic basis for dentinal sensitivity. Compendium of Continuing Education in Dentistry. Suppl No. 3, 1982, page S99. Graf H, Galasse R: Morbidity, prevalence and intraoral distribution of hypersensitive teeth. J Dent Res :Sperial iwx A) 62:56,2, 1983. Kanapka J: A new agent. Compendium 01 Coniinumg Education in Dentistry. Suppl No. 3, 1982, S118. Ishikawa S: A clinico-histological study on the hypersensitivity of dentin. J Japan Stomatol Sot 36~68, 1969. Fearnhead RW: The histological demonstration of nerve fibers in human dentin. In Anderson DJ, editor: Sensory Mechanisms in Dentin. Oxford, England, 1962, Oxford Pergamon Press, pp 15-26. Naylor MN: Studies on the mechanism of sensation to cold stimulation of human dentin. In Anderson DJ, editor: Sensory Mechanisms in Dentin. Oxford, England. 1963, Oxford Pergamon Press, pp 80-87. Tronstad L: Ultrastructural observations on human coronal dentin. Stand J Dent Res 1981:101, 1973. Frank RM: Ultrastructural relationship between the odontoblast, its process and the nerve fiber. In Symons N, editor: Dentinc and Pulp: Their Structure and Reaction. London, 1968, Livingstone, pp 115-l 45. Frank RM: Attachment sites between the ndontoblast process and the intradentinal nerve fiber. Arch Oral Rio1 13:833, 1968. Frank RM, Sauvage C, Frank P: Morphologlcai basis of dental sensitivity. Int Dent J 22:1, 1972.
155
KRAUSER
11.
12. 13. 14.
15. 16.
17. 18.
19. 20. 21. 22.
23.
Anderson D J: The pulp as a sensory organ. In Finn SB, editor: Biology of the Dental Pulp Organ. Birmingham, Ala, 1968, University of Alabama Press, pp 273-280. Anderson DJ, Naylor MN: Chemical excitants of pain in human dentine and dental pulp. Arch Oral Biol 7~413, 1962. Branstrom M: The elicitation of pain in human dentine and pulp by chemical stimuli. Arch Oral Biol 7:59, 1962. Dellow PG, Roberts ML: Bradykinin application to dentine: A study of a sensory receptor mechanism. Aust Dent J 11:384, 1966. Gysi A: An attempt to explain the sensitiveness of dentin. Br J Dent Sci 14~685, 1900. Brannstrom M: Dentinal and pulpal response, II. Application of an airstream to exposed dentine, short observation period. Acta Odontol Stand l&17, 1960. Brannstrom M: Observations on exposed dentine and corresponding pulp tissuue. Odont Revy 13:235, 1962. Brannstrom M: Some experiments with heat and pressure illustrating the movement of odontoblasts into the dentinal tubules. Oral Surg 15~203, 1962. Brannstrom M, Astrom A: A study on the mechanism of pain elicited from the dentine. J Dent Res 43~619, 1964. Berggren G, Brannstrom M: The rate of flow in dentinal tubules due to capillary attraction. J Dent Res 44~408, 1965. Brannstrom M: Sensitivity of Dentine. Oral Surg 21:512, 1966. Brannstrom M, Linden LA, Astrom A: The hydrodynamics of the dental tubule and of the pulp fluid. Caries Res 1:310, 1967.
Inlay repair of a broken T. Milton University
Skeeters, D.M.D.,” of Kentucky,
College
Hugh
of Dentistry,
25. 26.
27.
28. 29. 30. 31.
Reprint
requests
to:
DR. JACK T. KRAMER 824 U.S. HIGHWAY ONE NORTH
PALM BEACH,
FL 33408
solder joint
N. Burkett, Lexington,
24.
Brannstrom M, Linden LA, Johnson G: Movement of dentinal and pulpal fluid caused by clinical procedures. J Dent Res 47~679, 1968. Brannstrom M, Johnson G: Movements of the dentine and pulp liquids on application of thermal stimuli. Acta Odontol Stand Z&59, 1970. Johnson G, Brannstrom M: Dehydration of dentin by some restorative materials. J PROSTHET DENT 26~307, 1971. Brannstrom M, Astrom A: The hydrodynamics of the dentine: Its possible relationship to dentinal pain. Int Dent J 22~219, 1972. Hall DC: Pulpal calcifications-A pathologic process. In Symons NB, editor: Dentin and Pulp: Their Structure and Reaction. Dundee, Scotland, 1968 DC Thomas and Co, pp 269-273. Bernick S: Age changes to the blood supply to human teeth. J Dent Res 46~544, 1967. Karlson UL, Penny DA: Natural desensitization of exposed tooth roots in dogs. J Dent Res 54~982, 1975. Brannstrom M, Gageroglio R: Occlusion of dentinal tubules under superficial attrited dentin. Swed Dent J 4~86, 1980. Seltzer S, Bender IB: The nerve supply of the pulp and pain perception. In Seltzer S, Bender IB, editors: The Dental Pulp. Philadelphia, 1975, JB Lippincott Co, pp 131-151.
D.M.D.,**
and Thomas R. Mee, D.D.S.***
Ky.
C
linical repair of a broken solder joint in a fixed partial denture can be advantageous for patient and dentist alike. Miller and Thayer’ have described a method using a parallel pin retained casting for the intraoral repair of fixed partial dentures. An inlay can often provide a simple solution to the clinical problem. This article describes a technique and its clinical application.
TECHNIQUE A six-unit maxillary anterior fixed partial denture (FPD) replacing the central incisors, with a broken *Associate **Former ***Former ry.
156
Professor, Associate Assistant
Department of Restorative Dentistry. Professor, Department of Restorative Dentistry. Professor, Department of Restorative Dentist-
Fig. 1. Fractured solder joint between maxillary central incisors on a six-unit FPD.
AUGUST
1986
VOLUME
56
NUMBER
2
2.
3.
4. i
6. 7
8.
9.
AND
RESISTANCE
Kaufman EC;, Coelho 4G, Colin L: Factors influencing the rrtentmn of cemented gold castings. J PR~STHET DENT 11:487, 1961. Craig RG. El-Ebrashi MK, Peyton FA: Experimental stress analysis of dental restorations. Part II: Two-dimensional photoelastic stress analysis of crowns. J PROSTHET DENT 17:292, 1907. Lorey RE, Myers GE: The retentive qualities of bridge retainerr J Am Dent Assoc 76:568, 1968. Reisblck MH, Shillingburg HT Jr: Effect of preparation geometry on retention and resistance of cast gold restorations. Calif Dent Assoc J 3:51, 197’1. Ohm E, Silness J: The convergence angle in teeth prepared for artificial crowns. J Oral Rehabil 5:371, 1978. Eames WB. O’Neal SJ, Monteiro J, Miller C, Roan JD Jr, Cohen KS: Techniques IO improve the seating of castings. J Am Dent Assoc. 96:432. 1978. Mack PJ: .\ theoretical and clinical investigation into the taper nchieced on crown and inlay preparations. J Oral Rehabil 7:255, 1980. Woolsey GD, Matich JA: The elect of axial grooves on the rcslstancr lorm of cast restorations. J Am Dent Assoc 97:978, 1978.
Hypersensitive Jack T. Kramer,
10.
11.
12.
13. 14.
15.
Potts RG, Shillingburg HT Jr. Duncanson XI<, Jr: Retention and reststance of preparations for I‘.ISI rrs~or‘.~t;~;ns, .J PRWTIIE I DENT 43:303, 1980. Chan KC, Hormati AA, Boyer DR. Artx:liarv rctetltion loi complete crowns provided by cemrnt kf,y>,, j ~‘ROSt.fll:T. D5.X I 45:152, 198 I. Kishimoto M, Shillingburg H’T Jr, D~nc,mwn MC;: Inlluence of preparation features on retentrrm and iisiatance. Part 11: Three-quarter crowns. J PROSTH~.I DENT 49: 188, 198 i. Shillingburg HT Jr, Hobo S, Whitsett LD Fundamentals oi Fixed Prosthodontics. Chicago. 1978. Quintesrrnw Books. p 67 Owen CP: Factors influencing thr rwentim~ and resistance of preparations for cast intracoronal rrq:!ornIi:>ni J PKO~.I.HK.I DEN.~ 55:674, 1986. Hegdahl T, Silness .J: Preparation arras reslstine d~splaccrnent of artificial crowns. J Oral Rehabil 4:201 IO-
Rejmni rque.\f\ ir,. DR. C. P. OWEN FAC:ULTY oti DENTISTRY PRIVATE BAG X 12 TYGERBERC; 7505 REPURLIC 01: SWTH AFRICA
teeth. Part I: Etiology
D.M.D.
North Palm Beach, Fla.
P
reservation of the natural dentition in a state of comfort, health, and function is the primary goal of the dental profession. Although great progress has been made in the restoration of function and health, attention to comfort has often been overlooked. Hypersensitive teeth are a source of chronic irritation that affects eating, drinking, and breathing. Severe hypersensitivity may even result in an emotional change that causes an altered daily lifestyle. The objective of this two-part article is to present a review of hypersensitive teeth and to include the etiologies, symptoms, theories of pain production, and methods of treatment. Management of hypersensitive dentin tends to be empirical because precise knowledge about the mechanism of pain transmission within the dentin is absent. The dentin is a highly sensitive tissue that differs from other sensitive tissues in the body. In skin, for example, four different sensations, cold, heat, touch, and pain, can
Presented at the Pacific B.C.. Canada. THE
JOURNAL
Coast
OF PROSTHETIC
Society
of Prosthodontists,
DENTISTRY
Vancouver,
be perceived. In dentin, different stimuIi cause only pain. When the pulp is removed, dentin is no longer sensitive, which indicates that sensory nerves in the pulp may extend into the dentin and respond when dentin is stimulated. Although it is well established that pulpal nerves carry the sensation of dental pain to higher centers, it is still unclear how the dentin transmits the varied stimuli to these nerves. Evidence suggests that sensitive exposed dentin exhibits patent tubules. Most histologic sections indicate, however that nerve fibers from the pulp only penetrate a limited distance along some dentinal tubules.’ Graf and Galasse2 reported pain arising from exposed dentin in as many as one in seven adult patients. According to Kanapka,3 sensitive teeth afflict some 40 million Americans at one time or another and more than 10 million report chronic hypersensitivity. Little has been accomplished to alleviate this painful problem. Exposure of hypersensitive dentin arises from either the removal of the coronal enamel or a denudation of the root surface by loss of cementum and the overlying 153
KRAUSER
periodontal structures. The thin layer of cementum (20 to 50 pm) is easily removed by curettes, abrasive pastes, foods, and brushing. The loss of cementum is an opportunity for sensitivity. A review of dental anatomy reveals that in 60% of adult teeth the cementum covers the enamel at the cementoenamel junction (CEJ). Thirty percent of the teeth exhibit a butt joint at the CEJ, and in 10% of teeth, the enamel and cementum do not meet and a portion of the dentin is exposed. It is tempting to assume that these teeth are prone to sensitivity; however, there is currently no evidence that this is true. Enamel loss through occlusal wear, toothbrush abrasion, dietary erosion, and other parafunctional habits may also elicit a hypersensitive reaction. Denudation of the root surface may also be multifactorial; the main causes are gingival recession, aging, chronic periodontal disease, tooth position within the dental arch, periodontal surgery, incorrect toothbrushing habits, and root preparation. The preparation of the root surface is one of the most important factors in regaining periodontal health. Chemical and mechanical means are generally used. Meticulous root preparation may, on the one hand, yield a superior environment for periodontal repair, but may also initiate a hypersensitive state. It is noteworthy that not all exposed dentinal surfaces exhibit hypersensitive symptoms. Factors such as age, rate of exposure, and the effect of naturally occurring or environmental desensitizing mechanisms affect the nature of the sensitivity. A psychogenic factor must also be considered. Ishikawa, however, observed patent tubules in areas of sensitive dentin but, in areas of occluded tubules the symptoms were absent.
THEORIES
OF DENTIN
SENSITIVITY
Although histochemical, autoradiographic, and electron microscopic studies have vividly described the relationship between the odontoblast and the neurofibers of the pulp, the exact mechanism of the transmission of the pain response from the dentin to the terminal nerve endings is only hypothesized. It is well established that the pulp is richly innervated and that the sensory nerves are present near the dentin between the odontoblast cells and in close contact with these cells. Since the 1950s the odontoblastic-receptor, direct nerve ending, and hydrodynamic theories of dentin sensitivity have been studied extensively.
Odontoblast-receptor
theory
Through its process within the dentinal tubules, the odontoblast receives and transfers stimuli to the nerve endings in the pul~.~ From an embryologic point of view, the odontoblast is thought to be of mesodermal origin and not neural origin. Various physiologic experiments studying membrane potential and electrical stimuli have given ambiguous results leading to neither acceptance 154
nor rejection of the odontoblast-receptor theory.6,7 Morphologic findings and electron microscopic findings by Frank et a1.8-‘o showed a close contact between the odontoblast and the nerve fibers in the pulp with a predentin and circumpulpal mineralized dentin. Frank et a1.8-‘0also observed a complex infolding of nerves in the odontoblastic process intratubularly. They concluded that a special functional relationship exists between the odontoblastic process and the nerve fibers and together they constitute a receptor complex. If this theory is to be accepted totally, it must be shown that the odontoblastic process extends from the pulp to the dentin-enamel junction. Light microscopy has revealed fibers within the tubules and minitubules that are assumed to be odontoblastic processes. In scanning electron microscopy, however, these intratubular fibers were seen as collagen fibers and not odontoblastic processes. Therefore, if the odontoblastic processes do not occupy the full length of the dentinal tubules, dental hypersensitivity cannot be fully explained on the basis of the odontoblast-receptor theory.
Direct nerve endings
theory
Unmyelinated sensory nerve endings exist within the dentinal tubules and conduct sensations to the pulp directly.5 This theory suggests the existence of nerve endings in the dentin that are of pulpal origin and can be directly stimulated. There is no doubt that nerves exist in the mineralized dentin. However, Frank et al.*-” showed nerves entering the tubules in the circumpulpal region that only extend to the inner one third of the mineralized dentin. Various physiologic studies indicated that there are nerves in the most pulpal portion of the dentin and none near the periphery.“-‘4 In prepared cavities, the placement of substances that could cause pain when applied to nerve endings (acetylcholine, potassium chloride, and bradykinin) resulted in no pain response in exposed dentin. However, these substances did cause intense pain when applied to the exposed pulp. It was also shown that neither local anesthetics nor protein-precipitating drugs eliminated dentinal sensitivity when inserted into the test cavity. Therefore, on the basis of microscopic and physiologic data, the existence of neural cells in the sensory portion of the outer dentin seems remote.
Hydrodynamic
theory
The interstitial fluid of the dentin and pulp exists as “dental lymph.” The changes in function, tension, or pressure at the surface of the tubules brings about a change in the hydrostatic equilibrium. This change causes a rapid fluid flow and a mechanoreceptor transfer to the sensory nerves in the subodontoblast nerve plexus. In 1900 Gysi15 first claimed that dentinal hypersensitivity is due to movement of a watery substance within AUGUST
1986
VOLUME
56
NUMBER
2
HYPERSENSITIVE
TEETH.
PART
I: ETIOLOGY
the dentinal tubules from the surface to the odontoblastic layer, which is interwoven with nerves. The pressure change associated with this fluid movement would yield pain.15 Brannstrom et a1.‘6-26gathered support for this hydrodynamic theory with in vivo experiments demonstrating that the tissue fluid within the tubules may seep through the tubules onto an exposed dentinal surface. This movement of fluid occurs with a speed calculated at 2 to 4 mm per second. This speed indicates that empty tubules could fill in a few seconds. If this assumption is correct, the hydrodynamic theory may be valid inasmuch as quick fluid flow may occur in the dentinal tubules under certain conditions. In addition, all stimuli that cause pain must cause a rapid fluid flow in the dentinal tubules. Dehydration of dentin is the clearest example of understood dental pain. The outward movement of fluid into the dehydrating source through a mechanoreceptor principle would stimulate the odontoblast and sensory nerves and cause pain. Cold and hypertonic or hyperosmotic solutions act in a similar manner in causing an outward flow from the tubules. The influence of heat-causing pain is more complicated. Application of dry heat apparently causes evaporation of the fluid from the surface and a shift of movement toward the pulp. The pressure buildup would then be recognized as pain. The hydrodynamic theory is gaining support and seems to explain dentinal sensitivity on the basis of mechanical stimulation of nerves in the dentin-pulp interface. This mechanical stimulation is a result of a rapid fluid flow in the dentinal tubules caused by pain-provoking irritants.‘6*26
obliterated dentinal tubules. The sclerotic zones beneath the region of attrition were occluded by peritubular, dentin-like material. This finding supports the view that the oral environment controls the development of dentinal sclerosis and that the obliteration or blockage of the patent tubules prevents the passage of’ painful impulses.
DIFFERENTIAL
Pain arising from dentin exposed to chemical, thermal, tactile, or osmotic stimuli varies in frequency and severity. Seltzer and Bender3’ have explored the di:+gnostic features of the many causes of pain that should be ruled out before the diagnosis of dentin hypersensitivity. Attempts to correlate pulpal pathology with clinical signs and symptoms of dentin hypersensitivity have failed to produce significant findings.
SUMMARY Although several theories have been suggested for hypersensitive dentin, it appears that the hydrodynamic theory is most plausible. If a clinical diagnosis of dentin hypersensitivity can be made, occlusion of the patent tubules would result in a reduction of hypersensitivity by the rapid fluid shift within the tubules. The naturally occurring defense mechanisms would wall off the narrow tubules producing the fluid flow, thus reducing the pain associated with hypersensitivity. In Part II of this article the current treatment modalities for dentin hypersensitivity will be discussed. REFERENCES 1.
NATURAL
PULPAL
DEFENSE MECHANISMS
The pulp has several natural defenses to protect itself from irritating stimuli.
2.
Calcification
3.
Pulpal calcification and the formation of secondary dentin, peritubular dentin, and dentinal sclerosis have been demonstrated by Ha112’ and Bernick.28 This natural occlusion of the peritubular dentin by calcium crystals is the tooth’s physiologic response to dentinal sensitivity. The tooth may naturally desensitize itself with a peritubular dentin mineralization.
4. 5.
6.
Bacterial plaque Another defense mechanism that may decrease dentinal sensitivity is the formation of plaque in the acquired salivary pellicle material coupled with salivary occlusion. In a dog study, Karlson and Penny29 found that plaque decreased sensitivity.
7. 8.
9.
Sclerosis Electron microscopic studies by Brannstrom3’ on teeth with incisor attrition revealed partially or completely THE
JOURNAL
OF PROSTHETIC
DENTISTRY
DIAGNOSIS
10.
Tronstad L: The anatomic and physiologic basis for dentinal sensitivity. Compendium of Continuing Education in Dentistry. Suppl No. 3, 1982, page S99. Graf H, Galasse R: Morbidity, prevalence and intraoral distribution of hypersensitive teeth. J Dent Res :Sperial iwx A) 62:56,2, 1983. Kanapka J: A new agent. Compendium 01 Coniinumg Education in Dentistry. Suppl No. 3, 1982, S118. Ishikawa S: A clinico-histological study on the hypersensitivity of dentin. J Japan Stomatol Sot 36~68, 1969. Fearnhead RW: The histological demonstration of nerve fibers in human dentin. In Anderson DJ, editor: Sensory Mechanisms in Dentin. Oxford, England, 1962, Oxford Pergamon Press, pp 15-26. Naylor MN: Studies on the mechanism of sensation to cold stimulation of human dentin. In Anderson DJ, editor: Sensory Mechanisms in Dentin. Oxford, England. 1963, Oxford Pergamon Press, pp 80-87. Tronstad L: Ultrastructural observations on human coronal dentin. Stand J Dent Res 1981:101, 1973. Frank RM: Ultrastructural relationship between the odontoblast, its process and the nerve fiber. In Symons N, editor: Dentinc and Pulp: Their Structure and Reaction. London, 1968, Livingstone, pp 115-l 45. Frank RM: Attachment sites between the ndontoblast process and the intradentinal nerve fiber. Arch Oral Rio1 13:833, 1968. Frank RM, Sauvage C, Frank P: Morphologlcai basis of dental sensitivity. Int Dent J 22:1, 1972.
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Anderson D J: The pulp as a sensory organ. In Finn SB, editor: Biology of the Dental Pulp Organ. Birmingham, Ala, 1968, University of Alabama Press, pp 273-280. Anderson DJ, Naylor MN: Chemical excitants of pain in human dentine and dental pulp. Arch Oral Biol 7~413, 1962. Branstrom M: The elicitation of pain in human dentine and pulp by chemical stimuli. Arch Oral Biol 7:59, 1962. Dellow PG, Roberts ML: Bradykinin application to dentine: A study of a sensory receptor mechanism. Aust Dent J 11:384, 1966. Gysi A: An attempt to explain the sensitiveness of dentin. Br J Dent Sci 14~685, 1900. Brannstrom M: Dentinal and pulpal response, II. Application of an airstream to exposed dentine, short observation period. Acta Odontol Stand l&17, 1960. Brannstrom M: Observations on exposed dentine and corresponding pulp tissuue. Odont Revy 13:235, 1962. Brannstrom M: Some experiments with heat and pressure illustrating the movement of odontoblasts into the dentinal tubules. Oral Surg 15~203, 1962. Brannstrom M, Astrom A: A study on the mechanism of pain elicited from the dentine. J Dent Res 43~619, 1964. Berggren G, Brannstrom M: The rate of flow in dentinal tubules due to capillary attraction. J Dent Res 44~408, 1965. Brannstrom M: Sensitivity of Dentine. Oral Surg 21:512, 1966. Brannstrom M, Linden LA, Astrom A: The hydrodynamics of the dental tubule and of the pulp fluid. Caries Res 1:310, 1967.
Inlay repair of a broken T. Milton University
Skeeters, D.M.D.,” of Kentucky,
College
Hugh
of Dentistry,
25. 26.
27.
28. 29. 30. 31.
Reprint
requests
to:
DR. JACK T. KRAMER 824 U.S. HIGHWAY ONE NORTH
PALM BEACH,
FL 33408
solder joint
N. Burkett, Lexington,
24.
Brannstrom M, Linden LA, Johnson G: Movement of dentinal and pulpal fluid caused by clinical procedures. J Dent Res 47~679, 1968. Brannstrom M, Johnson G: Movements of the dentine and pulp liquids on application of thermal stimuli. Acta Odontol Stand Z&59, 1970. Johnson G, Brannstrom M: Dehydration of dentin by some restorative materials. J PROSTHET DENT 26~307, 1971. Brannstrom M, Astrom A: The hydrodynamics of the dentine: Its possible relationship to dentinal pain. Int Dent J 22~219, 1972. Hall DC: Pulpal calcifications-A pathologic process. In Symons NB, editor: Dentin and Pulp: Their Structure and Reaction. Dundee, Scotland, 1968 DC Thomas and Co, pp 269-273. Bernick S: Age changes to the blood supply to human teeth. J Dent Res 46~544, 1967. Karlson UL, Penny DA: Natural desensitization of exposed tooth roots in dogs. J Dent Res 54~982, 1975. Brannstrom M, Gageroglio R: Occlusion of dentinal tubules under superficial attrited dentin. Swed Dent J 4~86, 1980. Seltzer S, Bender IB: The nerve supply of the pulp and pain perception. In Seltzer S, Bender IB, editors: The Dental Pulp. Philadelphia, 1975, JB Lippincott Co, pp 131-151.
D.M.D.,**
and Thomas R. Mee, D.D.S.***
Ky.
C
linical repair of a broken solder joint in a fixed partial denture can be advantageous for patient and dentist alike. Miller and Thayer’ have described a method using a parallel pin retained casting for the intraoral repair of fixed partial dentures. An inlay can often provide a simple solution to the clinical problem. This article describes a technique and its clinical application.
TECHNIQUE A six-unit maxillary anterior fixed partial denture (FPD) replacing the central incisors, with a broken *Associate **Former ***Former ry.
156
Professor, Associate Assistant
Department of Restorative Dentistry. Professor, Department of Restorative Dentistry. Professor, Department of Restorative Dentist-
Fig. 1. Fractured solder joint between maxillary central incisors on a six-unit FPD.
AUGUST
1986
VOLUME
56
NUMBER
2