It is accepted worldwide by dental clinicians and researchers that “Periodontal disease comprises a group of inflammatory conditions of the supporting tissues of the teeth that are caused by bacteria.” 1 The oral cavity harbors numerous microorganisms, both pathogenic and saprophytic.2 Several bacteria have been involved with the initiation, establishment, and progression of periodontal diseases, and the most common bacterial species isolated from periodontal pockets are Gram-negative obligate or facultative anaerobes.
Sophisticated bacteriological techniques used in research laboratories, such as detection of DNA hybridization and/or cultivation, have allowed the oral microbiologist to identify the most common bacteria in periodontal pockets: microorganisms such as Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and Prevotella intermedia, among others. These microorganisms have been associated with particular forms of periodontal diseases, and furthermore, have peculiar pathogenic characteristics, such as invasion of the connective tissues adjacent to periodontal pockets (eg, A. actinomycetemcomitans).3
Regardless of each specific factor, these bacteria have been identified as having a major role in the etiology of periodontal diseases.4-6 Some periodontal pathogens have also been associated with the correlation between periodontal diseases and cardiovascular diseases, as shown in studies by Noack, et al7 and Harasthzy, et al.8 In light of the current knowledge of the relationship between periodontopathic bacteria and systemic diseases, and based on an understanding of the deleterious effects of such microorganisms on the periodontal structures, it is of fundamental importance to know how to treat periodontal infections.
It has been the objective of periodontal therapy to halt the progression of periodontal infection by suppressing or eliminating the subgingival microflora. Typical and conventional methods to achieve this goal include scaling and root planing either manually or with automated devices such as ultrasonics. According to Pattison and Pattison, the primary goal of scaling and root planing is to restore gingival health by completely removing elements that provoke gingival inflammation (ie plaque, calculus, and endotoxins).9
However, despite the excellent clinical results from scaling and root planing, bacteria are still present in the pocket and may recolonize and be detectable within a short length of time.10-12 In addition to scaling and root planing, local antimicrobials in the form of slow-release devices have been used in combination with irrigation or automated instrumentation.
In the past decade, one additional tool available to the dentist to treat periodontal infections has been the diode laser or soft-tissue laser, as demonstrated in recent publications.14-15 The diode laser is used following conventional mechanical periodontal therapy, including scaling and root planing, and should therefore be considered as an adjunct to mechanical instrumentation of the affected root surfaces.
DIODE LASER IN PERIODONTAL THERAPY: LITERATURE REVIEW
A recent study by Fontana, et al16 on 40 rats with induced periodontal disease demonstrated that a diode laser at 810-nm wavelength induced considerable bacterial elimination. In this study, bacterial samples were taken from periodontal pockets before and after subgingival laser irradiation. The microbiological analysis showed that bacteria such as Prevotella spp., Streptococcus beta-hemoliti-co, Fusobacterium spp., and Pseudomonas spp. were significantly reduced.
An in vitro study published by Kreisler, et al17 in the Journal of Clinical Periodontology on the proliferation rate of human periodontal ligament fibroblasts demonstrated interesting findings on the biological effects of a soft-tissue laser. Human periodontal ligament fibroblasts were cultured and irradiated with an 809-nm wavelength diode laser. The rate of proliferation, determined by relative fluorescence units (RFU), was checked at 24, 48, and 72 hours after irradiation. The results indicated that cells in the test group (irradiated) demonstrated a considerably higher proliferation activity than the controls. The differences were discernible up to a 72-hour observation time, and those differences were statistically significant. The same authors suggested that the laser treatment may be beneficial in regenerative periodontal therapy.
The fact that laser therapy is effective in periodontal regeneration was demonstrated in early studies by Crespi, et al,18,19 both in an animal model and in humans. In these studies, a CO2 laser in a defocused mode was used.18,19
A different aspect in the field of basic science applied to clinical periodontology has been investigated by Sakurai, et al.20 It is well accepted that periodontal diseases are an inflammatory condition caused by the presence of bacteria. Part of the complex series of events triggered by the micro-organisms is the production by the host of prostaglandins (PGE2) and cyclooxygenases (COX), which have been involved in bone resorption in periodontal and endodontic lesions. These authors challenged human gingival fibro-blasts with lipopoly-saccharides of bacterial origin. After irradiation with a diode laser, the amount of PGE2 was detected by radioimmunoassay, and levels of mRNA were detected. The results indicated that the irradiated cells did produce considerably less PGE2 and COX, indicating the possible anti-inflammatory role of the diode laser, which may have a therapeutic effect on the aggravation of gingivitis and periodontitis.20
Clinical studies on humans with an 810-nm diode laser have been conducted and published by Moritz, et al.21 Fifty patients with adult periodontitis were randomly subdivided into 2 groups. Subgingival bacteria samples were collected in all patients. Patients were treated either with laser or subgingival irrigations of H2O2. After 6 months, the final values of the periodontal indices and further microbiologic samples were measured. The total bacterial count, as well as specific bacteria (eg, A. actinomycetemcomitans, P. intermedia, and P. gingivalis), were assessed in a semiquantitative manner. The sites that received the subgingival laser treatment exhibited a much lower bacterial count. Furthermore, the reduction of values of bleeding on probing was 96.9% in the laser group compared to 66.7% in the control group. The authors concluded that diode laser treatment following scaling and root planing had a bactericidal effect and reduced inflammation.
In a previous pilot study,22 the same group of investigators determined that the presence of microorganisms such as A. actinomy-cetemcomitans was reduced in the group that received laser treatment. As described earlier, A. actinomycetemcomitans not only colonizes onto the periodontally diseased root surface, but also invades adjacent soft tissue; this makes eradication more difficult when using only mechanical periodontal instrumentation.
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| Figure 1. During periodontal surgery, the proximity of the roots and the limited surgical access made conventional instrumentation relatively cumbersome. | Figure 2. The laser fiber-optic, due to its small diameter, is inserted into the defect. |
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| Figure 3. The laser beam eliminates granulation tissue within the interproximal space. |
Diode lasers have also been used as adjuncts to periodontal surgery.23 In the case depicted in Figures 1 through 3, root proximity and very narrow interradicular space made thorough manual periodontal instrumentation impossible. A 0.4-mm laser fiber-optic (Odyssey, Ivoclar Vivadent) was easily introduced to reach the narrow bottom of a 10-mm periodontal defect, and the area was irradiated. In a short strokes/steps motion at 0.8 W, the granulation tissue was carefully ablated, most likely reducing bacterial presence in the area, and according to the literature previously cited, decreasing the level of inflammation.
PRACTICAL TECHNIQUE
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| Figure 4. Periodontal probing is performed to assess pocket depth after initial therapy. |
The typical protocol for the use of a diode laser as an adjunct to conventional periodontal therapy advocates its application following thorough mechanical and automated periodontal instrumentation (Figure 4).24 Ultrasonic instrumentation of the pocket should not be performed on patients with hearing aids or pacemakers.
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| Figure 5. Additional scaling and root planing are performed with horizontal strokes using a curette. |
At the re-evaluation of the therapy approximately 6 weeks following instrumentation in cases of recurrent deep pockets, the clinician could use the laser after additional scaling and root planing (Figure 5). To prepare the laser for use, cleave and strip the fiber, attach the handpiece and canula, and turn on the laser.24
The laser can be used in the continuous or pulsed mode, and the average power can range from 0.8 to 1.0 W. At this wattage, most patients do not require any form of anesthesia. If increased power is needed, anesthesia (ie, topical or local, as needed) is recommended; wattage should not exceed 1.2 W.
To calibrate the fiber and the tip, measure the length of fiber so it equals the pocket depth, minus 1 mm.24 Next, initiate the fiber at 400 um by touching the tip to articulating paper and “test firing.”24
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| Figure 6. The laser fiber-optic is inserted into the pocket. | Figure 7. Same view as Figure 6, without the use of the flash. The fiber-optic is inserted into the pocket to reach approximately 1.0 mm from the bottom of the defect. |
To begin sulcular debridement, insert the fiber in a vertical direction toward the bottom of the pocket with the laser tip oriented toward the soft tissue facing the pocket (Figures 6 and 7). Move the fiber in a horizontal and vertical fashion at a slow, moderate speed, keeping the fiber tip in contact with the epithelium and/or parallel to the root surface. Debride all granulation tissue, and as necessary, remove plume and debris with high-volume evacuation. A fine water spray can be used during the laser treatment for rinsing, and constant suction is required to aspirate the fumes that form during the ablation of the inflamed tissues.
There is no recommended time for the laser to be in the pocket; the total amount of time for the laser procedure is a function of the extent of the diseased soft tissue. However, in general, lase pockets 6 mm or less for approximately 30 seconds and those greater than 6 mm for 45 seconds. If the patient experiences noticeable discomfort, lower the power setting and administer anesthetic, if necessary.
CONCLUSION
While scaling and root planing remain the initial treatment modality in periodontal therapy, clinicians may also consider the use of a soft-tissue diode laser as an efficacious and helpful tool in their daily armamentarium. The laser should be used as an adjunct to conventional therapy both for its decontaminating and biostimulating effects.
References
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2. Roberts A. Bacteria in the mouth. Dent Update. 2005;32:134-142.
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17. Kreisler M, Christoffers AB, Willershausen B, et al. Effect of low-level GaAlAs laser irradiation on the proliferation rate of human periodontal ligament fibroblasts: an in vitro study. J Clin Periodontol. 2003;30:353-358.
18. Crespi R, Covani U, Andreana S, et al. CO2 laser therapy in periodontal disease [abstract]. J Periodontol. 1993;64:1103.
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Acknowledgement
The author would like to thank Drs. S. Yeh and G. Intini for their technical support in the development of this article.
Dr. Andreana graduated from the School of Dental Medicine at the University of Rome La Sapienza in Rome, Italy, and pursued his master’s in oral sciences in the University of Buffalo Department of Oral Biology in Buffalo, NY. Formerly the manager of the Applied Testing Cen-ter at Ivoclar Vivadent in Am-herst, NY, he is currently a clinical assistant professor and investigator at the departments of Periodontology, Endodontics, and Oral and Maxillofacial Surgery and Restorative Dentistry, School of Dental Medicine of the University at Buffalo. Dr. Andreana practices part time in periodontal offices in Italy, where he collaborates with practices involved in aesthetic dentistry. As well as being the president of the Buffalo chapter of the American Association for Dental Research, he is also an active member of the International Academy of Periodontology, Academy of Osseointegration, Academy of Laser Dentistry, and New York Academy of Sciences, and a member of the American Academy of Periodontology, American Association of Endodontics, ADA, and Academy of Dental Materials. He has more than 80 articles in nationally and internationally peer-reviewed journals in the fields of periodontology, endodontics, and implantology, and more than 60 research abstracts. He has also lectured extensively to dental professionals in Europe as well as in North, Central, and South America. He can be reached at (716) 829-3845.
