Rap nov cox

Physiology of dentine
hypersensitivity: clinical
By Charles Cox DMD, PhD, FADI
Charles Cox discusses possible causes of
nerve - less, cannot be, per se, sensitive, though capable dentine sensitivity and the treatment of
of conducting or transmitting by reason of its unique such problems.
physical and anatomical characteristics, thermal, tactile, surface tension and electrical impulses to the pulp.
Dentine is not alive, nor is it dead like enamel, it serves Brännström’s (1966) hydrodynamic explanation of den- as an intermediate tissue between the external enamel tine sensitivity is based on scientific data, which demon- and the internal living pulp, it does not generate sensa- strate that fluid filled dentine tubules are subject to cer- tions but transmits through its tubes impulses of various tain stimuli - cold, ice or a rapid air flow directed onto kinds to the pulp’. Fish (1927) speculated ‘there is a open tubules, causing a rapid bi-directional movement of lymphatic fluid in the dentinal tubule and that tubules fluid perceived as acute, immediate pain by the patient.
terminate with a lymphatic plexus, providing a continu- In 1900 Dr Gysi, a London prosthodontist, wrote ‘a pres- ous lymphatic flow through the various tubules and the sure or a drawing exercised upon the aqueous content pulp’. Later, Fish suggested ‘if the injury to the dentine of the dentinal canalicule (tubule) that opens into a car- reached a cer tain level, a coagulation process of the ious cavity is directly transmitted to the other end of the tubule contents of the will star t at the injured site and dentinal canalicule where it is loosely closed by the simulate the neighbouring tubules to do the same - odontoblasts and are densely interwoven with nerves to resulting in deposition of secondary dentine at the pul- feel the pressure or drawing as a sensation of pain’.
Although other colleagues were aware of his theory, Gysi was ‘right on the money’ and in tune with today’s A CASE FOR THE ODONTOBLAST
Orban (1940) speculated that restorative treatment caused mechanical compression of the dentine, resulting HISTORICAL PERSPECTIVE
in displacement odontoblasts and pulp cells into the A case for fluid flow - In 1856, Tomes suggested ‘the tubules. Ivory & Kramer (1952) showed aspiration of dentinal tubes are, in some way, the medium through odontoblasts under self-polymerising acr ylic resin which sensation of pain is distributed through the tissue.
restorations when placed without a lining agent, with no The dentine tubes are constantly filled by fluid, and the cell aspiration under restorations with liners - explaining pulp at their inner extremities feels pressure made upon that proper sealing of the dentine prevented the the fluid at the exposed ends of the tubes’. Whit (1870) exothermic reaction from acrylic polymerisation to stated ‘the pain arising from the contact with sensitive reach the pulp. Kramer (1955) considered the relation- dentine cannot be conveyed by direct contact with the ship between dentine hypersensitivity and movement of ultimate fibres of the dentine nerve, but through some tubule contents - speculating on the relationship intermediary agent. Beers (1893) stated ‘There is no doubt, but sensitiveness is due to the presence of the Charles Cox DMD, PhD, FADI is
tube contents, whether nerve fibres enter or not.
professor and vice chair at the
Dentine is nothing but [a] passive matrix, in which lie the UCLA School of Dentistry, Los
sources of sensation’. Hopewell-Smith (1923) stated that ‘I have come to the conclusion that dentine, being RESTORATIVE & AESTHETIC PRACTICE VOLUME 4 NO. 9 NOVEMBER 2002 CLINICAL - HYPERSENSITIVITY
generally become plugged due to formation of an Anderson (1958) thought that the sensation of dentine organic biofilm. Once a plug forms, it slows or stops the was not directly due to stimulation of nerve fibrils in the bi-directional fluid flow and the pain simply stops.
tubules, but from a disturbance, that passed through the Clinicians have sometimes referred to the sudden abla- tubules to stimulate the dentine and then to the nerves tion of dentine pain with non-treatment as a placebo in the pulp. He thought the receptors responsible for effect. However, it is due to normal salivary physiological pain sensations were in the pulp, rather than the dentine.
events that lead to tubule blockage.
In reviewing these theories, some were closer to the scientific truth of hydrodynamics than others. In the final ENAMEL DEFECTS
analysis, we owe a debt of gratitude to Dr Mar tin Defects, often show as small cracks - especially when Brännström and colleagues by using sound scientific data the enamel dries from prolonged placement of a rubber to answer clinical questions raised by early colleagues.
dam, excessive blasts from an air-chip syringe, or mouth breathers. Enamel tufts and spindles are organic geolog- TOOTH SUBSTRATES - ENAMEL - DEVEL-
ical remnants, which persists between adult enamel rods OPING & MATURE
that rise from the EDJ and project upward into the Enamel is a non-vital tissue that develops from epithelial enamel for a shor t distance. Lamellae are inter-rod cells. It is a 96% mineralised substrate with a 4% water faults, which extend from the EDJ - through the sub- and organic protein.The basic structural unit of enamel is strate of enamel - to the oral surface. Generally, tufts a rod, tightly packed and mechanically adherent to other and lamellae are of little clinical significance. However, enamel rods, its hardness comparable to brittle steel.
with time they become channels, which permit Each rod follows an undulating course from the enamel- microleakage and eventual sensitivity following acid dentine junction (EDJ) to the oral surface - never follow- etching and improper hybridisation. For restorative ing the course of the adjacent rod’s course of travel. The restoration, acid etching achieves the immediate organic component of enamel exists as a fine lacy protein removal of the organic biofilm plaque - along with a few network - seen only in carefully processed sections. This outer micrometers of the prepared tooth surface.
lacy organic network is seen as widened spaces between However, for restorative success, enamel and dentine individual enamel rods. Enamel is attached to subjacent must be immediately hybridised as dentine adhesion is a dentine by a micro-mechanical interlocking EDJ - scal- micro-mechanical interlocking mechanism within the loped ridges which interdigitate along the interface with inter tubular dentine below the etched collagen. In one a micro-mechanical biological bond of approximately impor tant feature, dentine hybridisation of moisture dependent, while enamel etching is easily attained - all Enamel defects are present - the result of minor physiological or pathological changes to ameloblasts dur- ing their ‘cell’ stage, due to childhood diseases that leave SENSITIVITY FROM AESTHETIC BLEACH-
‘bands’ of organic defects, which become embedded within the mineral substrate during the systemic distur- Many patients are now interested in achieving a bance (disease). Ameloblasts return to their normal phys- ‘Hollywood white’ smile, and clinicians may now provide iological effor t upon recovery. High doses of fluoride or bleaching treatments in their clinical theatres as well as tetracycline also cause unsightly changes to the matrix of provide patients with home bleaching devices. In the enamel - leaving large patches of dark hypo-mineralised dental clinic, various ‘power’ forms such as heat or light pigmented bands, to small spots of brown/grey mottled activation may accelerate bleaching. In order to gain aes- thetic success - prolonged aggressive bleaching with cer- tain organic solutions such as carbamide peroxidase or AGE CHANGES OF ENAMEL
hydrogen peroxide are known to dissolve the organic Enamel may be thought of as a semi-permeable mem- debris within the enamel defects - resulting in increased brane - allowing passage of fluids and small molecules porosity when left untreated. This has been repor ted in through the organic defects between enamel crystals. It is patients who abuse their home bleaching by wearing easily worn away with advanced age, becoming dis- their bleaching apparatus for extended time periods - by coloured and its permeability (fluid flow through enamel) abusing their treatment time, the organic biofilm is dis- becoming altered. With advancing age, organic channels solved resulting in open enamel channels. Without any RESTORATIVE & AESTHETIC PRACTICE VOLUME 4 NO. 9 NOVEMBER 2002 CLINICAL - HYPERSENSITIVITY
clinical treatment to close the remaining fluid fault, these as the ‘hydrodynamic’ theory. Närhi, Hayaras-Tonder, patients then repor t to the clinician with post-bleaching Pashley and others have confirmed this theory as scien- hypersensitivity to cold and air stimuli. Treatment regi- tific fact by physiological testing in animals. Stimuli by the tactile probing of exposed dentine with an instrument causes mechanical deformation and fluid movement in DENTINE - THE SECOND HARDEST SUB-
the tubule complex The direction of an air blast, a cold STRATE IN THE HUMAN BODY
stimuli or placement of salt or sugar on the fluid - all Dentine is a vital tissue that develops from mesenchyme cause activation of mechano-receptors within the - composed of 70% mineral and 20% proteins, harder odontogenic layer. Air, cold, osmotic are valid stimuli to than bone, weaker than enamel - providing an elastic test for enamel or dentine hypersensitivity. Until recent- ‘give’ - preventing tooth fracture.The basic structural unit ly, few clinical treatments of enamel-dentine hypersensi- of dentine is a tubule (approx. 3.5µm) at the pulp wall tivity were permanent - only temporarily effective at to approx. 0.06µm diam at the EDJ. Each tubule is gen- erally filled with an odontoblast process, collagen, fluid Perhaps the most complex factor in measuring and occasional nerves from the pulp.Today’s science val- enamel-dentine hypersensitivity is the exact degree of idates the premise that fluid movement is the responsi- pulp inflammation. In case of symptomatic or asymptot- ble for dentine hypersensitivity. Following cavity prepara- ic pulpitis, it is known that an inflamed dental pulp pre- tion, cutting debris remains on the surface also being sents a differential physiologic response to pulp testing.
forced into each cut tubule for several microns and fluid Many current clinical methods of diagnosis fail to differ- may flow from the pulp through the tubules and smear entiate between pulp inflammation and dentine hyper- layer onto the cavity floor. It is this fluid ‘wetness’, which sensitivity resulting from fluid flow within tubules.
may complicate the clinical success of dentine bonding.
Blockage of defects and sclerotic dentine tubule occlu- The rate of fluid flow in the dentine tubule complex may sion may occur via physiological deposition of mineral be as high as 2-4mm per second, with an inter-pulp pres- salts, but this a slow and limited occurrence. The ideal sure of vital pulps varying from 15 to 30mm Hg.
goal to prevent and treat hypersensitivity is placement Consequently, with 30.000 dentine tubules per square of a permanent clinical seal to the defect (Kolker et al, mm along the pulp wall, an open dentine tubule on a 2002). Nakabayashi likened this as an extension of the cavity floor could empty itself at least ten times each day.
enamel seal along the restoration interface. A clinical Thus, displacement of few thousandths of a millimetre of seal may be accomplished by one of several treatment fluid movement within the dentine tubule complex Over the counter products such as tooth pastes contain agents that provide a transient blockage of the TYPES OF PATIENT PAIN
tubule complex, or they may provide a supposed neur- Dentine pain may be considered as acute pain, such as al alteration to pulp nerves. At best, these agents are when an ice cold drink or a rapid air stimuli are placed only palliative - no better than the placebo effect, which on the tooth surface. It is usually a signal of rapid fluid forms a plaque biofilm that rapidly covers the open movement within the dentine or enamel channels - dis- tubules. If left undisturbed, the biofilm will thicken and appearing as fast as it may have occurred. Whereas mineralise as a calculus and provide a nidus for bacteri- chronic pain generally tends to be a lingering dull throb- al colonisation and potentially resulting in caries.
bing pain, which signals either a pulpal or a periapical Office treatments may use placement of an adhe- sive to cover the open tubules, generally relying upon Acute pain is a result of fluid movement within the removal of the smear layer along with application of a dentinal complex from fluid movement within the chan- primer to the tooth substrate. Adhesives generally work nel defects within enamel. Gysi (1900) repor ted that his by covering the tubules to provide a transient blockage patients felt pain when he removed fluid from the floor of fluid flow. However, adhesives should not be placed of the cavity preparation. Brännström later described this on root dentine following periodontal surgery as cer- fluid movement phenomenon within the dentine tubules tain components will inhibit the periodontal tissue heal- RESTORATIVE & AESTHETIC PRACTICE VOLUME 4 NO. 9 NOVEMBER 2002 ing following repositioning of the surgical flap. In addition, which supposedly drive agents directly into the defect or cer tain adhesives contain various agents (i.e. HEMA,TEG- tubule complex. Generally they employ fluoride to sup- DMA) that are cytotoxic and immunogenic to the heal- posedly alter the sensory mechanism of the nerves in ing response, causing sloughing of the normal epithelial the tubules and subjacent pulp. Again, these devices are expensive and need some safety attachments when An early traditional treatment regimen relied upon treating the patient to prevent electrical.
placement of a varnish over the prepared surface to coat More recently, chelating agents as various mineral the defect or the open dentine tubules. Some varnishes salts are available which actually work with the chemistry contained supposed antimicrobial agents. Varnishes only of the tooth to form insoluble chemical precipitates with provide a palliative effect, which simply coats the surface, the natural chemistry of the peritubular dentine sub- much like painting a wet wall with an oil-based paint.
strate within the tubule complex. No light curing or etch- Because they are non-adhesive, varnishes will become ing treatment steps are needed. Super Seal is one such dislodged within a shor t time resulting in areas for bac- agent (Figure 1) that works by stopping fluid flow - with- terial colonisation as well as resulting in recurring patient out irritation to gingival tissues or to the healing of a tis- hypersensitivity. This type of palliative treatment general- sue flap following surgical root treatment. Application of ly needs repeated agent application to provide relief dur- Super Seal is simply achieved by rubbing the offending cavity dentine and exposed root cementum and dentine Other clinical treatments include placement of agents surfaces with a cotton pellet saturated with Super Seal.
that contain a tissue fixatives such as glutaraldehyde. This Its unique chemistry alters the tubular chemistry to agent is a biological fixative that acts by binding to vari- decrease dentine fluid flow and providing clinical relief of ous tissue fluid proteins that denature (coagulate) the the patient’s pain. Super Seal is unique in that it will not proteins in the tubules and the superficial cells of the sub- interfere with either transitional or definitive cementa- jacent pulp. However, any of glutaraldehyde or HEMA tion - with conventional zinc phosphate cements, or with containing agents, which contain a fixative cannot be a glass ionomer or the newer resin modified glass placed on or near gingival epithelium, as they cause local ionomer cements. More impor tantly, for those clinicians tissue necrosis, causing loss of gingiva as well as loss of who are using the newer adhesive systems for bonding the physiological biological attachment mechanism. In their restorations to the prepared dentin substrate, addition, protective eyewear must be worn by the patient Super Seal does not interfere with the formation of a hybrid layer formation (Figure 2). The unique effect of Power assist devices using iontophoresis are available, Super Seal is its capacity to complex with the calcium Figure 1: Super Seal is
one such agent that
works by stopping fluid
flow-without irritation to
gingival tissues or to the
healing of a tissue flap
following surgical root
Figure 2: Super Seal does
not interfere with the
formation of a hybrid
layer formation
rich zone of peritubular dentin to form a crystal plug and Science 227: 1059-1061
thereby shut down dentin sensitivity at near 100% levels (Kolker et al, 2002). That independent university study Gangarosa L, Park NH (1978). Practical considerations in ion- compared five current commercially available desensitis- tophoresis of fluoride for desensitizing hypersensitive er agents. Their study demonstrated that Super Seal was dentin. J Prosthet Dent 39: 173-178
consistently at 97.5% effective while the next agent was only effective at 54.2% of the time. In addition, the study Greenhill JD, Pashley DH (1981). The effects of desensitizing by Niazi demonstrated there was no soft tissue irritation agents on the hydraulic conductance of human dentin in or inflammation when Super Seal was placed onto the vitro. J Dent Res 60: 686-698
gingival when treating hypersensitive root surfaces - whereas other agents result in tissue irritation and Gysi A (1900). An attempt to explain the sensitiveness of den- sloughing and recurring hypersensitivity.
tine. Brit J Dent Res 43: 865-868
Hirvonen TJ, Narhi MVO, Hakumaki MOK (1984). The excitabil- Brännström M (1966). Sensitivity of dentine. Oral Surg 21: 517-
ity of dog pulp nerves in relation to the condition of dentin surface. J Endod 10(7): 294-298
Brännström M (1979). The transmission and control of dentinal Hume WR (1984) An analysis of the release and diffusion pain. In: Mechanism and control of pain. LI Grossman, Ed.
through dentin of eugenol from zinc oxide-eugenol mix- tures. J Dent Res 63(6): 881-884
Chapman CR, Casey KL, Dubner R et al (1985). Pain measure- Lutins ND, Greco GW, McFall WT (1984). Effectiveness of sodi- ment: an overview. Pain 22: 1-31
um fluoride on tooth hypersensitivity with and without ion- tophoresis. J Periodontol 55: 285-288
Dayton RE, De Marco TJ, Swedlow D (1974). Treatment of hypersensitive root surfaces with dental adhesive materials.
Kidd EA (1976). Microleakage in relation to amalgam and com- J Periodontol 45(12): 873-878
posite restorations. A laboratory study. Br Dent J 141(10):
Dvorak HF, Senger DR, Dvorak AM et al (1985). Regulation of extravascular coagulation by microvascular permeability.
of dentin desensitizing agents on dentin permeability. J Dent 13(2): 75-96
Res (IADR abstract #0295), San Diego 2002. Accepted for publication, Journal of Cosmetic Dentistry Niazy HA, Alagili D, Hafez AA, Cox CF (2000). The effect of desensitizing systems on dentin hypersensitivity following McGrath PA (1986). The measurement of human pain. Endod crown preparation. J Dent Res 79: 518, #2998
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Pashley DH, Nelson R, Williams EC et al (1981). Use of dentine- Mumford JM (1982). Orofacial pain. Third edition. Churchill fluid protein concentrations to measure pulp capillary reflection coefficients in dogs. Arch Oral Biol 26(9): 703-706 Pashley DH, Kepler EE, Williams EC, O'Meara JA (1984). The Desensitisation of dentin by resin impregnation: a clinical effect on dentine permeability of time following cavity and light-microscopic investigation. ASDC J Dent Child preparation in dogs. Arch Oral Biol 29(1): 65-68
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