Australian Dental Journal 1997;42:(5):302-6

The cur r ent status of low level laser ther apy in dentistr y. Par t 2. Har d tissue applications
L. J. Walsh*
laser-induced changes to neural transmission networks within the dental pulp, rather than alterations to the exposed dentine surface, as is the case with other treatment modalities.3,4 There have been several studies of the effect of LLLT on DH. Most studies have used GaAlAs laser treatment, and have demonstrated desensitization of hypersensitive cervical dentine, with an efficacy rate of approximately 90 per cent.5-7 LLLT is efficacious when either the tooth crown or the root apex is irradiated. In a recent double blind study,7 subjects with DH received LLLT involving both the apex and the cervical areas of the tooth. Treatment was repeated at one week, two-week and eight-week intervals. There was a reduction in both tactile and thermal sensitivity, and these were even more marked in the second and eighth weeks. There is also evidence that LLLT delivered using HeNe lasers can reduce DH. In a randomized, double-blind clinical study involving 19 subjects, 8 hypersensitivity was assessed using a mechanical stimulus (a sharp explorer), and a thermal stimulus (a blast of cold air from a dental syringe), while pulpal vitality was measured using an electrical stimulus. Immediately following laser treatment and for three months thereafter, the subjects perceived level of discomfort decreased. HeNe laser treatment reduced dentine hypersensitivity to air by 63 per cent and to mechanical stimulation by 61 per cent over three months. All teeth remained vital after laser treatment, with no adverse reactions or complications. Based on a consideration of the optical properties of tooth structure, the phenomenon of laser desensitization must be as a direct result from effects of LLLT on neural networks within dental pulp, rather than any accompanying thermal effects.9 Since dentine and enamel are partly transparent to near infrared laser wavelengths,10 the majority of the deposited laser energy is transmitted through to the pulp, rather than dissipated at the tooth surface or at other optical boundaries.
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Abstr act While most applications of low level laser therapy (LLLT) in dentistry are directed toward soft tissues, in recent years there has been increasing interest in tooth-related or hard tissue applications of LLLT. This report provides an overview of applications of LLLT in the treatment of dentine hypersensitivity and pain arising from the periodontal ligament, and describes the phenomenon of lethal laser photosensitization and its applications in the treatment of dental caries. Technical aspects of LLLT equipment and safety concerns are also discussed.
Key words: Low level laser therapy, dentine, laser thermal effects, photosensitization, dental caries. (Received for publication May 1996. Accepted August 1996.)

Intr oduction While high power surgical lasers (such as CO2, argon, Nd:YAG and Er:YAG lasers) now have an accepted place in the armamentarium of dental practice, the value of low power semiconductor diode lasers is less clear. In Part 1 of this series, issues relating to the use of these lasers for low level laser therapy (LLLT) applications on soft tissues were discussed. 1 In this paper, the emphasis will be on hard tissue or tooth related applications of the same laser technology. Concerns regarding the effects of deliberate irradiation of teeth on the vitality of the dental pulp will also be addressed. The paper concludes with a brief description of the equipment used to deliver LLLT. Dentinal hyper sensitivity Dentinal hypersensitivity (DH) is one of the most common causes of dental pain. 2 LLLT for the treatment of DH has been developed. This relies upon

*Department of Dentistry, The University of Queensland.

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The mechanisms of the desensitizing effect at the cellular level have not yet been fully investigated; however, it is likely that inhibition of nociceptive signals arising from peripheral nerves11,12 is a major component of the therapeutic effect. Indeed, LLLT has been shown to block the depolarization of C-fibre afferents in dental pulp.13 It has been suggested that LLLT may elicit descending inhibition in the central nervous system, in addition to local effects on ner ve conduction,5 although this has yet to be proven. Per iodontal ligam ent pain dur ing tooth m ovem ent The effects of LLLT in reducing pain accompanying orthodontic movement of teeth have attracted little attention. In a recent double-blind clinical study of the efficacy of LLLT in controlling orthodontic post-adjustment pain,14 elastomeric separators were placed at the proximal contacts of one premolar in each quadrant of the dentition in 39 volunteers to induce orthodontic pain. The buccal gingiva at each site was irradiated, with the beam directed at the middle third of the root. Three different treatment durations of 15, 30, and 60 seconds and one placebo treatment of 30 seconds were tested within each subject. Pain experienced before and after laser applications over a 5-day period was quantified using a visual-analogue scale (VAS). At the group level, laser-treated sites showed lower levels of pain than placebo sites, according to an analysis of the VAS scores of pain. However, at the level of each individual subject, differences between active treatments and placebo were not always statistically significant. At least one component of the mechanism for a reduction in pain by LLLT in this system can be inferred from cell culture studies of periodontal ligament fibroblasts stretched to simulate orthodontic forces. These investigations have shown that LLLT impairs the secretion by fibroblasts of the highly pro-inflammatory molecules prostaglandin E2 and interleukin-1. 15 Destr uction of bacter ia by lethal laser photosensitization High-power heat-generating lasers, such as carbon dioxide and Nd:YAG surgical lasers, have well recognized destructive effects on bacteria, and this has led to the development of techniques for sterilizing wounds, cavity preparations and root canals.16-22 With heat-generating lasers, high irradiances (typically 100 J) are required for most sterilizing applications, and data from in vivo studies indicate that risks of thermal injury can be substantial, although this varies markedly according to the wavelength used.23,24 In contrast, if low power laser energy
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could be coupled (using dyes) into the bacterial cell wall, the energy required for destruction of bacteria would be quite small, and would pose little if any risk of injury to the pulp and periodontal ligament. The term lethal laser photosensitization (LLP) refers to the process whereby laser radiation emitted from a low power laser device activates a dye which in turn exerts a lethal effect on particular cells, such as bacteria. LLP is a specific interaction, in that treatment with the laser alone (i.e., in the absence of the enhancing dye), or with the dye alone, produces minimal effect. Similarly, treatment with laser followed by dye is without benefit. However, when exposure to the dye is followed by laser irradiation, there are changes within the dye which lead to dramatic chemical events within the target, with loss of viability as the end result. Since LLP relies on the use of the dye as an optically absorbing agent (or chromophore), it is essential to match the laser wavelength used with the chromophore, as well as to ensure that the chromophore itself does not exert toxic or irritant effects on the tissues. LLP is similar in principle to photodynamic therapy, in which laser energy activates otherwise non-toxic dyes producing reactive oxygen species that cause injury and death of tumour cells. Several laboratory studies have explored applications of LLP in dentistry. The visible red light emitted from a HeNe gas laser (wavelength 632 nm) can exert an inhibitory action on dental plaque micro-organisms when an appropriate dye is used. Streptococcus sobrinus is sensitive to LLP under these conditions, while Escherichia coli, a Gram-negative enteric micro-organism, is resistant.25 The effect on the cariogenic micro-organism S. sobrinus is rapid, with leakage of the bacterial membrane detectable after 2 minutes of laser exposure. The bactericidal action of LLP can be obtained with a range of blue, purple, and green dyes within the phenylmethane family, all of which are strong absorbers at 632 nm.25 Similar findings were obtained in a later study,26 which demonstrated destruction of biofilms of Streptococcus sanguis, Porphyromonas gingiva lis, Fusobacterium nucleatum and Actinobacillus actino mycetemcomitans on agar plates by LLP. Using a 7.3 mW HeNe gas laser, either toluidine blue O or methylene blue resulted in killing of all four target organisms after lasting for 30 seconds. These blue dyes are known to serve as potent sensitizers for a range of bacteria, for laser emissions in the visible red portion of the spectrum.27 In a more recent study, killing via LLP has been achieved for the cariogenic bacteria Streptococcus muta ns, S. sobrinus, Lactobacillus casei and Actinomyces viscosus, using toluidine blue O.28 For each organism, suspensions containing 106 colony forming units could be inactivated by irradiation for
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60 seconds. It has since been demonstrated that longer exposure times can result in kills exceeding 107 colony forming units.29 These investigations, conducted using cultures on agar plates, provide a clue as to the possible value of LLP for destruction of cariogenic bacteria. However, there are several important limitations of these studies which should be recognized. First, the experimental situations used have not replicated those encountered clinically, and the problems of bacteria present on smear layers or in dentinal tubules have not been addressed. As well, the use of HeNe gas lasers as a source of laser energy is less than ideal for a clinical application because these devices require optical systems and power supplies which are complex. Their conversion efficacy (electrical energy to laser energy) is not high. By comparison, indium:gallium:arsenide:phosphorus (InGaAsP) semiconductor diode lasers generate emissions of similar wavelength to HeNe lasers; however, their smaller size, higher efficiency, lower cost, and more versatile nature makes them better suited for LLP. Low power versions of these devices are used in lecture theatre pointers. There is considerable current interest in developing LLP techniques using visible diode lasers. Work in the authors laboratory is evaluating the feasibility of using InGaAsP laser diodes operating in the visible spectrum (wavelength 670 nm) in conjunction with methylene blue to sterilize a carious cavity and infected dentinal tubules containing a known bio-load of S. mutans. This would have obvious clinical relevance in terms of managing deep dentinal carious lesions. With the ability to rapidly and effectively sterilize the floor of deep carious lesions without significant heat, more conservative approaches to the removal of demineralized and infected tooth structure could be used. Of note, LLP is able to exert significant effects even when the cariogenic organisms are protected in a matrix of demineralized dentine.29 As mentioned previously, laser radiation in the red visible and near infrared region is able to pass through demineralized dentine. While LLP techniques can still be applied effectively to reach micro-organisms enmeshed in dentine, higher irradiances are required to exert the same destructive effect than when the microorganisms are on the surface (4.8 vs. 1.2 J). To achieve these irradiances in a clinically acceptable timeframe requires the use of higher power diode lasers and more efficient delivery systems, and current work is addressing these issues. Lethal laser photosensitization technology may also have application in the treatment of hypersensitive cervical dentine covered by dental plaque, where the technique would be used in tandem with desensitization of the dental pulp by LLLT. In terms
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of managing plaque on hypersensitive dentine, LLP has recently been shown to be a viable technique for killing bacteria in supragingival plaque.30 Following LLP with either HeNe or GaAlAs lasers, substantial reductions were demonstrated in the total anaerobic count as well as in the number of viable streptococci and actinomyces present in the samples. An irradiance of only 1.3 J resulted in log10 reductions of 3.0, 5.4 and 3.3 in the total anaerobic count, streptococci and actinomyces respectively. In addition to its use in the management of dental caries, the LLP technique has potential application for the destruction of microorganisms in the root canal system and in periodontal pockets, as an adjunct to conventional techniques. However, much further work is required to develop protocols which could be used in a clinical setting and to improve the laser delivery systems to permit access to all areas of the mouth. Ther m al changes accom panying har d-tissue LLLT Thermal insult to pulpal tissue is the major limiting factor to the use of any laser on dental hard tissues. It is essential that any thermal changes which do occur do not pose a risk to the vitality of the pulp. Parameters for thermal injury to dental pulp have been determined by in vivo studies which have examined pulp pathology following exposure of pulps to various non-laser heat sources.31 This work has defined a critical threshold for pulpal temperature rise of 10F (5.5C), above which an unacceptably high incidence of pulpal necrosis occurs. Below 5.5C, reversible and mild pulpitis occur. Below 4F (2.2C), no histological changes are discernible. The parameters which determine the nature of laser thermal effects in any given situation can be summarized as follows. Fixed parameters, which cannot be modified by the operator, include: laser wavelength, absorption and scattering coefficients for the tissue being irradiated, and internal cooling (blood flow). Variable factors, which can be modified by the operator at the level of the laser instrument or at the tissue interface, include: laser power, mode (continuous or pulsed), spot size (energy density), exposure time, and external cooling (i.e., water or air).23,24 In a recent study, thermal changes at the level of the dental pulp in human molar teeth irradiated in vitro with an 830 nm wavelength GaAlAs laser were measured.9 The laser was operated in pulsed or continuous modes at settings identical to those used clinically for desensitization by LLLT. Laser irradiation of teeth induced measurable temperature rises; however, neither the continuous wave mode of operation nor any of the pulsed modes induced
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temperature rises which exceeded the pulpal damage threshold (2.2C), even at energies of up to 9.0 J (30 mW/300 seconds). It should be noted that an irradiance of 9.0 J exceeds the exposure used commonly for laser desensitization by a factor of 5, and thus there is a significant margin of safety in terms of the threshold for significant pulpal injury. Thermal effects were more pronounced with longer laser exposure times (60 seconds vs 120 seconds). It can be concluded that thermal changes are induced by GaAlAs irradiation, but these are not of a magnitude which would be expected to cause pulpal inflammation or necrosis and thus are unlikely to be clinically significant. LLLT technology The major components of an LLLT system are the laser device itself, a delivery system, and a controller. All common commercially available LLLT systems use semiconductor diode lasers. These are generally variants of either Gallium: Aluminium:Arsenide (GaAlAs) which emit in the near infrared spectrum (wavelength 700-940 nm), or Indium:Gallium:Arsenide:Phosphorus (InGaAsP) devices which emit in the red portion of the visible spectrum range (wavelength 600-680 nm). Power outputs are typically 10-50 mW, when measured at the level of the diode laser itself, although the final useable output (from the handpiece) will be less because of losses in the delivery system. For this reason, calibration of the laser system using an external power meter is an important quality assurance measure. The output of diode lasers is controlled electronically, and in state-of-the-art equipment, microprocessor controllers are used. These allow the user to alter most aspects of the laser output other than wavelength (e.g., power, pulse frequency, exposure time). The diode laser device itself is quite compact, being approximately the size of an 8 mm diameter light emitting diode. The conversion efficiency (i.e., electrical energy to laser energy) is approximately 20 per cent, the remainder being dissipated as heat. Since the increased temperature of the laser device during operation alters both the output power (and to a lesser extent the wavelength), it is critical that the output of the laser diode is monitored so that the control circuitry can make the necessary adjustments to maintain a constant output. This is usually accomplished using a phototransistor which is fitted within the heatsink of the laser device. With an adequate heatsink and control system, the negative effect of temperature on laser output at the level of the treatment beam can virtually be eliminated.
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The beam profile from a typical diode laser is rectangular (100 4 m) with a high divergence on the long axis (20 degrees from the centre axis), and a low divergence on the short axis (2 degrees). This gives a highly divergent sweep profile. To obtain a more useful beam, a series of lenses or a selffocusing graded index fibre can be used in front of the device to either deliver the treatment beam itself or to direct the laser output into a small diameter flexible optical fibre or a solid light guide (such as a curing light tip). Customized devices have been designed to achieve a sweeping pattern of the treatment beam across the treatment area,32 although these are not used commonly. Whatever the delivery system used, it is important that the components which come into direct contact with patients are able to be protected adequately with a laser-transmissive disposable barrier, or are themselves autoclavable or disposable. Similarly, it should be possible for the clinician to activate the laser into treatment mode without breaching asepsis. Some units employ footswitches or light-operated switches to allow hands-free use. Laser units used for LLLT are generally classified as Class III or Class IIIb in terms of the optical hazard which they pose to staff and patients.33 Because a low power treatment beam can be focused by the eye to give a high power density on the retina, the optical hazard is sufficiently great that laser safety standards (e.g., Australian Standards AS22111991 and AS4173-1994) mandate the wearing of appropriate protective glasses by patients and clinicians during treatment. Glasses are available which provide protection against common LLLT wavelengths in both the visible and near infrared spectrum. Conclusions The use of LLLT in the treatment of dentinal hypersensitivity and periodontal ligament pain during orthodontic tooth movement has been shown in clinical trials to be both safe and effective. There is accumulating evidence which indicates the potential of lethal laser photosensitization as a technique for the destruction of cariogenic and other microorganisms within the mouth without causing undue thermal stress to the tooth. Improvements in the design of LLLT equipment are necessary to enable these various techniques to be accomplished within an adequate timeframe and without breaching crossinfection control requirements. Given the lowtechnology, low-cost characteristics of LLLT, the future for hard tissue LLLT applications is
AS2211-1991:Laser safety. (Under revision as DR95239:Laser safety. Part 1:Equipment classification, requirements, and users guide.) AS/NZS4173-1994:Guide to the safe use of lasers in health care. 305

promising. As with soft tissue applications of LLLT, efforts should be directed toward investigating the precise dosimetry required for therapeutic laser effects, in order to achieve standardization of treatment protocols. Refer ences
01. Walsh LJ. The current status of low level laser therapy in dentistry. Part 1. Soft tissue applications. Aust Dent J 1997;42:247-54. 02. Dowell P, Addy M. Dentine hypersensitivity: a review. J Clin Periodont 1983;10:341-50. 03. Forrest-Winchester K, Walsh LJ. The effect of infrared laser radiation on dentinal permeability in vitro. Periodontol 1992;3:37-43. 04. Scherman A. Managing dentin hypersensitivity: what to recommend to patients. J Am Dent Assoc 1992;123:57-61. 05. Hoji T. Effects of soft laser irradiation on dentinal pain. Gifu Shika Gakkai Zasshi 1990;17:534-46. 06. Furuoka M, Yokoi T, Fukuda S, Usuki M, Matsuo S, Taniguchi K, Kitamura K. Effects of GaAlAs laser diode in the treatment of hypersensitive dentine. Fukuoka Shika Daigaku Gakkai Zasshi 1988;15:42-8. 07. Gerschman JA, Ruben J, Gebart-Eaglemont J. Low level laser therapy for dentinal tooth hypersensitivity. Aust Dent J 1994;39:353-7. 08. Gelskey SC, White JM, Pruthi VK. Reduction of dentin hypersensitivity by infrared laser irradiation. J Can Dent Assn 1993;59:377-86. 09. Sandford MA, Walsh LJ. Thermal effects during desensitisation of teeth with gallium-aluminium-arsenide lasers. Periodontology 1994;15:25-30. 10. Featherstone JDB, Nelson DGA. Laser effects on dental hard tissues. Adv Dent Res 1987;1:21-6. 11. Sato T, Kawatani M, Takeshige C, Matsumoto I. Ga-Al-As laser irradiation inhibits neuronal activity associated with inflammation. Acupunct Electrother Res 1994;19:141-51. 12. Tsuchiya K, Kawatani M, Takeshige C, Matsumoto I. Laser irradiation abates neuronal responses to nociceptive stimulation of rat-paw skin. Brain Res Bull 1994;34:369-74. 13. Wakabayashi H, Hamba M, Matsumoto K, Tachibana H. Effect of irradiation by semiconductor laser on responses evoked in trigeminal caudal neurons by tooth pulp stimulation. Lasers Surg Med 1993;13:605-10. 14. Lim HM, Lew KK, Tay DK. A clinical investigation of the efficacy of low level laser therapy in reducing orthodontic postadjustment pain. Am J Orthod Dentofacial Orthop 1995;108:614-22. 15. Shimizu N, Yamaguchi M, Goseki T, Shibata Y, Takaguchi H, Iwasawa T, Abiko Y. Inhibition of prostaglandin E2 and interleukin 1-beta production by low-power laser irradiation in stretched human periodontal ligament cells. J Dent Res 1995;74:1382-8. 16. Adrian JC, Gross A. A new method of sterilization: the carbon dioxide laser. J Oral Pathol 1979;8:60-1.

17. Zakariasen KL, Dederich DN, Tulip J, DeCoste S, Jensen SE, Pickard MA. Bactericidal action of carbon dioxide laser radiation in experimental dental root canals. Can J Microbiol 1986;32: 942-6. 18. Dederich DN, Pickard MA, Vaughn A, Tulip J, Zakariasen KL. Comparative bactericidal exposures for selected oral bacteria using carbon dioxide laser radiation. Lasers Surg Med 1990;10:591-4. 19. Powell GL, Whisenant BK. Comparison of three lasers for dental instrument sterilization. Lasers Surg Med 1991;11:69-71. 20. Rooney J, Midda M, Leeming J. A laboratory investigation of the bactericidal effect of a NdYAG laser. Br Dent J 1994;176:61-4. 21. Whitters CJ, MacFarlane TW, MacKenzie D, Moseley H, Strang R. The bactericidal activity of pulsed Nd-YAG laser radiation in vitro. Lasers Med Sci 1994;9:297-303. 22. Moshonov J, Orstavik D, Yamauchi S, Pettiette M, Trope M. Nd:YAG laser irradiation in root canal disinfection. Endodont Dent Traumatol 1995;11:220-4. 23. Walsh LJ. Pulpal safety parameters for irradiation of dental hard tissues with carbon dioxide lasers. Aust Endodont Newsl 1993;19:21-5. 24. Sandford MA, Walsh LJ. Differential thermal effects of pulsed vs. continuous CO2 laser radiation on human molar teeth. J Clin Laser Med Surg 1994;12:139-42. 25. Okamoto H, Iwase T, Morioka T. Dye-mediated bactericidal effect of He-Ne laser irradiation on oral microorganisms. Lasers Surg Med 1992;12:450-8. 26. Dobson J, Wilson M. Sensitization of oral bacteria in biofilms to killing by light from a low-power laser. Arch Oral Biol 1992;37:883-7. 27. Bazhanov NN, Ragimov CR, Kasymov AI. The efficacy of using a helium-neon laser, ascorbic acid and methylene blue in the combined treatment of patients with maxillofacial phlegmons. Stomatologiia Mosk 1990;5:35-7. 28. Burns T, Wilson M, Pearson GJ. Sensitisation of cariogenic bacteria to killing by light from a helium-neon laser. J Med Microbiol 1993;38:401-5. 29. Burns T, Wilson M, Pearson GJ. Effect of dentine and collagen on the lethal photosensitization of Streptococcus mutans. Caries Res 1995;29:192-7. 30. Wilson M, Burns T, Pratten J, Pearson GJ. Bacteria in supragingival plaque samples can be killed by low-power laser light in the presence of a photosensitizer. J Appl Bacteriol 1995;78:56974. 31. Zach L, Cohen G. Pulp responses to externally applied heat. Oral Surg Oral Med Oral Pathol 1965;19:515-30. 32. Sommer A, Franke RP. LILAB, a new system for superficial application of low intensity laser beams in medicine. Biomed Tech Berlin 1993;38:168-71. 33. Makinson OF. Soft lasers and dentistry. Current Note No. 63. Aust Dent J 1986;31:139.

Address for correspondence/reprints: Dental School, The University of Queensland, 200 Turbot Street, Brisbane, Queensland 4000.

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