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| ORIGINAL ARTICLE |
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| Year : 2015 | Volume
: 9
| Issue : 1 | Page : 31-37 |
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Clinical efficacy of low-level laser therapy as an adjunct to nonsurgical treatment of chronic periodontitis
Uma Sudhakar, Satyanarayana, Sivasankari Thilagar, Snophia Suresh
Department of Periodontics, Thai Moogambigai Dental College and Hospital, Chennai, Tamil Nadu, India
| Date of Web Publication | 22-May-2015 |
Correspondence Address:
Dr. Uma Sudhakar
Thai Moogambigai Dental College and Hospital, Mugappair, Chennai - 600 017, Tamil Nadu
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/0976-2868.157597
Aims and Objective : In recent years, there has been a growing interest in the use of dental lasers for the treatment of periodontal diseases. The purpose of this randomized, split-mouth clinical trial was to evaluate the clinical efficacy of low-level laser therapy (LLLT) as an adjunct to conventional scaling and root planning (SRP). Materials and Methods: A total of 10 patients with untreated chronic periodontitis were randomly assigned in a split-mouth design to receive SRP with or without adjunctive LLLT. Clinical parameters including plaque index, gingival index, probing pocket depth were recorded at baseline, 1 st month and 3 rd month after the treatment. Gingival crevicular fluid (GCF) was collected for the assay of interleukin-1b (IL-1b) levels at baseline, 1 st week and 1 st month. Results: Both laser and control sides showed a significant reduction in IL-1b levels in GCF at 1 st week and 1 st month (P < 0.001). On comparing, laser sides showed a significant reduction in IL-1b levels at 1 st week (P = 0.041). No significant difference in IL-1b levels were found between laser and control sides at 3 rd month (P = 0.450). All the clinical parameters showed a significant difference (P < 0.05) at 1 st and 3 rd month after the treatment between laser and control sides. Conclusion: The present study suggests that LLLT could be a beneficial adjunct to nonsurgical treatment of chronic periodontitis on a short-term basis. Keywords: Chronic periodontitis, gingival crevicular fluid, interleukin, lasers
How to cite this article:
Sudhakar U, Satyanarayana, Thilagar S, Suresh S. Clinical efficacy of low-level laser therapy as an adjunct to nonsurgical treatment of chronic periodontitis. J Dent Lasers 2015;9:31-7 |
How to cite this URL:
Sudhakar U, Satyanarayana, Thilagar S, Suresh S. Clinical efficacy of low-level laser therapy as an adjunct to nonsurgical treatment of chronic periodontitis. J Dent Lasers [serial online] 2015 [cited 2023 Nov 29];9:31-7. Available from: http://www.jdentlasers.org/text.asp?2015/9/1/31/157597 |
| Introduction | |  |
Chronic periodontitis is initiated by microbial plaque, which accumulates on the tooth surface at the gingival margin and induces an inflammatory reaction resulting in the destruction of periodontal tissues. [1] Release of cytokines like interleukin-1b (IL-1b) in gingival crevicular fluid (GCF) is predominant of chronic periodontitis and the levels of IL-1b serve as a biomarker in monitoring the disease activity and also in assessing the response to treatment. [2]
The basic goal of periodontal treatment is to restore the biocompatibility of the periodontally diseased root surface for subsequent attachment of periodontal tissues to the treated root surfaces. Debridement of the diseased root surface is usually performed by scaling, and root planning (SRP) using manual or power driven instruments. Conventional mechanical debridement using curettes is still technically demanding and time consuming and power scalars might be uncomfortable to the patient from the noise and vibrations. Even access to areas such as furcation and grooves is limited owing to the complicated root anatomy.
There has been growing interest in recent years to search for a new machine driven therapeutic device which are capable of improving and simplifying mechanical root surface management. Low-level laser therapy (LLLT) is one such novel technique which has been increasingly used in recent years.
Low-level laser therapy is also known as soft laser therapy or biostimulation. The use of it in health care has been documented in the literature for more than three decades. The major interest in this technique clinically has been for accelerated wound healing or decreased pain.
Clinical application of LLLT is diverged. This field is characterized by a variety of methodologies and uses of various light sources (laser, light emission diodes) with different parameters (wave length). LLLT promotes proliferation of the multiple cells, mainly through the activation of mitochondrial respiratory chain and the initiation of cellular signaling. Red to near infrared light is thought to be absorbed by the mitochondrial respiratory chain component, resulting in the increase of ROS-reactive oxygen species and adenosine tri-phosphate (ATP)/cyclic adenosine-monophosphate and initiating a signaling cascade which promotes cellular and cytoprotection.
This study was designed to compare the clinical efficacy of LLLT as an adjunct to SRP with SRP alone, on various clinical parameters and GCF IL-1b in the treatment of patients with chronic periodontitis.
| Materials and Methods | | |
Patients selected for the study were from the out-patient pool, attending Department of Periodontics, Thai Moogambigai Dental College and Hospital. Ten patients with chronic periodontitis were included in the study. The ethical committee approval was obtained, and the patients were informed about the study, and informed consent was obtained [Figure 1].
Patient aged 35 years and above with healthy systemic condition and presentation of untreated chronic periodontitis with at least two teeth on each side of the mouth having a pocket depth of ≥5 mm and radiographic signs of alveolar bone loss is included in the study. Subjects who are smokers, who are pregnant, having a systemic disease, subjects using immunosuppressive agents, antibiotics and antiinflammatory are excluded from the study.
The proposed study was a randomized, split-mouth clinical trial. Treatment for each side was decided using coin toss method. Control side received conventional scaling and root planning. Laser side received conventional scaling and root planning plus adjunctive LLLT [Figure 2] [Figure 3] [Figure 4].
Baseline gingival index (G.I), plaque index (P.I) and probing pocket depth (PPD) were recorded for all the subjects.
Collection of gingival crevicular fluid
Detailed case history, clinical examination and supragingival scaling were done 1-day before the collection of GCF. On the subsequent day, after drying the area with a blast of air, supragingival plaque was removed without touching the marginal gingival and GCF was collected.
A standardized volume of 1 ml was collected from each site with extracrevicular approach using volumetric capillary pipettes [Figure 5].
Treatment procedures
On baseline
All the periodontal parameters (P.I, G.I, PPD) were evaluated and full mouth supragingival scaling was done.
On 1 st day
Gingival crevicular fluid samples were collected from both the sides. SRP was performed for both the groups under LA using hand instruments. On completion of SRP, laser side received LLLT using a diode laser.
Diode laser-picaso laser is a class IV diode laser, with an active semiconductor medium (gallium, aluminium, arsenide) with a wavelength of 810 nm provided with an optical fiber thickness of 300 m.
The laser was fixed at the orifice of the gingival margin at a distance of 1 cm, using a setting of 1.5 W as a continuous wave. Each tooth received 5-10 s of exposure.
- On the 4 th day, the patient returned after 3 days for the final LLLT on the laser side
- On the 7 th day, GCF samples were collected from the control and laser side
- On the 30 th day - Reevaluation of clinical parameters and GCF samples were collected
- On the 90 th day - Reevaluation of clinical parameters was done.
Immunological assessment of IL-1b using ELISA. Orgenium laboratories IL-1b. ELISA is an enzyme-linked immunosorbent assay for the quantitative detection of human IL-1b in a buffered solution, cell culture supernatants and human serum. This assay employs an antibody specific for human IL-1b coated on 96 well plates [Figure 6] [Figure 7] [Figure 8].
| Results | | |
The clinical parameters were assessed on baseline, 1 st month and 3 rd month. These include P.I, G.I and PPD. Immunological parameters were assessed on the 0 th day, 1 st week and 1 st month using ELISA procedure. The data were analyzed statistically to find the mean, standard deviation and test of significance of mean values of various parameters. Independent samples t-test and dependent t-test for paired samples were used to assess the statistical data.
In the present study, the mean values of IL-1b showed a significant reduction at 1 st week and 1 st month (P ≤ 0.001) in both laser and control sides after the treatment. On comparing IL-1b mean values at 1 st week, between both the sides, laser side (229.20 ± 50.83) showed a significant difference (P = 0.041) with the control side (281.60 ± 55.50). However, there is no significant difference (P = 0.450) in mean IL-1b levels between laser and control sides at 1 st month. Comparisons of IL-1b mean and standard deviation values at three different time points of laser and control sides is depicted in [Table 1] and [Table 2]. | Table 1: Comparison of mean IL-1ß levels between laser and control sides
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 | Table 2: Comparing the IL-1ß mean values between time points in laser and control sides
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Comparison of clinical parameters (P.I, G.I, PPD) between the laser and control sides are depicted in [Table 3]. All the clinical parameters showed nonsignificant values between laser and control sides at the baseline. However after treatment, at 1 st month and 3 rd month, all the clinical parameters showed significant differences between laser and control side [Table 4]. | Table 3: Comparison of P value of P.I, G.I, PPD between the laser and control sides
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 | Table 4: Paired sample t-test to compare the P.I, G.I, PPD mean values between time points in laser and control sides
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Mean value of P.I scores showed significant differences at baseline - 1 st month and 1 st month and 3 rd month in both control and laser side. In Laser side, G.I mean scores between baseline and 1 st month showed a highly significant difference and G.I between 1 st month and 3 rd month were nonsignificant. In the control side, both the pairs showed a significant difference.
| Discussion | | |
Destruction of the osseous support of the dentition is a hallmark of chronic periodontitis. [3] This tissue destruction appears to result from a complex interaction between these bacteria and hosts immune and inflammatory responses. Proteolytic activities of these bacteria, including collagenase, may participate in collagen degradation. [1] Activation and over expression of host matrix metalloproteases (MMPs) caused by periodontal pathogens such as Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis and by inflammatory cytokines have been reported [2],[4],[5],[6],[7]
Interleukin-1b is the major inflammatory cytokine occurring in the gingiva associated with periodontitis. It is formed and released in response to several immune-stimulatory agents such as lipopolysaccharides (LPSs) and tissue degradation products and can activate endothelial cells to upregulate ICAM-1 and E-selectin expression, which may increase the diapedesis of leukocytes. [8] Kornman et al. showed that patients with periodontitis have a significantly higher frequency of an IL-1 genotype that has been associated with increased production of IL-1. [9]
Lasers have been increasingly been used in modern dentistry for more than 30 years. A wide range of laser such as CO 2 , Nd: Yag and Er: Yag used in the field of periodontology for soft and hard tissue ablation, detoxification of root surfaces, pocket debridement, bacterial elimination and various other surgical approaches. [10]
There is another less known type of laser called low-level lasers, they work in the milliwatt range with wavelengths in the red (or) infrared spectrum (400-900 nm). [11] Low-level lasers do not cut (or) ablate the tissues. The basic principle of LLLT is based on the biostimulation (or) bio modulation effect. [12] Which consists of the fact that irradiation at a specific wavelength is able to alter the cellular behavior. This effect is achieved by acting on the cellular mitochondrial respiratory chain [13] or on membrane calcium channels. [14] This action subsequently promotes an increase in cell metabolism and proliferation. In vivo and in vitro data suggest that LLLT facilitates fibroblasts and keratinocyte cell motility, collagen synthesis, angiogenesis and growth factor release which lead to increased wound healing. [12]
Scaling and root planning is the one of the most commonly utilized procedures for the treatment of periodontal diseases and has been used as the gold standard therapy against which other have been compared. [15],[16] Most of the beneficial effects of SRP appeared to occur within the first 3 months. While SRP is considered to be fundamental periodontal treatment, it is not always completely successful, and adjuvant therapies have been suggested.
The purpose of the present study was to determine the efficacy of LLLT in the treatment of chronic periodontitis, its effect on clinical parameters as well as on the GCF IL-1b levels, when used as an adjunct to SRP and to compare those with treated only with SRP.
On the comparison of P.I scores in laser and control sides, statistically significant difference was observed from the baseline to 1 st month and 1 st month and 3 rd month. The decrease in P.I score was greater on the laser side, which agrees with the study done by Qadri et al. It is uncertain whether this is because of a reduction in degree of gingival inflammation (or) the laser irradiation per second. However our results are contrary to the study by Lui et al. [17] which showed no significant difference in P.I scores between test and control.
We found that additional irradiation with low-level laser was better than SRP alone. Its effect was greatest on the G.I and PPD. Significant decrease in G.I and PPD has also been reported by Kiernicka et al. [18] Laser therapy following SRP reduced gingival inflammation and MMP-8 expression while histological examination showed a decrease in inflammatory cells. [19] Our study showed a significant difference (P < 0.05) in G.I scores between laser and control sides at 1 st and 3 rd month suggesting beneficial effects of LLLT on reducing inflammation.
On the comparison of mean PPD in laser and control sides, there was statistically significant difference observed from baseline to 1 st month and 1 st month to 3 rd month. Laser side demonstrated a higher reduction in PPD values when compared to the control group. This is because of the adjunctive use of laser, as laser irradiation reduces prostaglandin E2 [20] and stimulates cellular ATP. [21] However our results are contrary to the study by [17] which showed no significant difference. It is difficult to offer a comprehensive explanation for greater improvement of periodontal status at the laser irradiated sites. The reduction in PPD might be attributed to the improved maintenance of oral hygiene. This could be possible because of the better comfort and less pain on the laser side.
The present study showed that laser side had a greater reduction in GCF IL-1b level compared with the control side, 1-week after the treatment implying that laser therapy might have a beneficial effect in controlling periodontal inflammation during the early healing period. However, the reduction does not reach the significance in 1-month. Our results are in accordance with the studies by. [17] Where as studies by Qadri et al. disclosed a difference between SRP and SRP with laser with respect to cytokines IL-1b level. Results by Makhlouf et al. [22] showed similar results.
Ozawa et al. 1997 [23] showed that laser photo therapy (LPT) significantly inhibits the increase of the plasminogen activator (PA) induced in human periodontal ligament cells in response to mechanical tension force, PA is capable of activating latent collagenase, the enzyme responsible for cleaving collagen fibers. In human gingival fibroblasts, LPT significantly reduced PGE2 production stimulated by LPS through a reduction of COX2 gene expression in a dose-dependent manner. Nomura et al. [24] reported that LPT significantly inhibited LPS stimulated IL-1b production in human gingival fibroblasts cells, and this inhibitory effect was dependent on radiation time.
Safavi et al. [25] evaluated the effect of LPT on gene expression of IL-1b, interferon-g (IFN-g) and growth factors (platelet-derived growth factor [PDGF], transforming growth factor-b [TGF-b] and basic fibroblast growth factor) to provide an overview of laser influence on their interactive role in the inflammatory process. The findings suggest an inhibitory effect of LPT on IL-1b and IFN-g production and a stimulatory effect on PDGF and TGF-b. Antiinflammatory effects of laser and irradiation and its positive influence on wound healing could be attributed to the above facts.
It is not always possible to select the optimal laser and treatment parameters for laser therapy because of lack of adequate studies. The parameters used in this study seem to have been within the "therapeutic window" of dosage but not optimal. Many studies have failed to find this window especially in studies performed in 1980s and early 1990s. Many authors used doses in the range of 0.001-0.01 J/cm 2 (Masse et al. 1993) although it had been suggested by Mester et al. 1971 that doses of about 1-2 J/cm 2 are necessary to heal wounds.
Limitations of the present study include small sample size, lack of established protocol adjunctive laser treatment with SRP. Long-term studies with layer sample size are required to evaluate the efficacy of LLLT in the treatment of chronic periodontitis.
| Conclusion | | |
Our study aimed to estimate GCF IL-1b levels in the subjects who underwent LLLT as an adjunct to conventional SRP. The results showed that the sites with additional laser therapy showed greater reduction in IL-1b levels than the SRP alone in the early healing period, suggesting LLLT might have a beneficial effect in controlling periodontal inflammation during early healing period. Additional well-defined randomized, blinded, controlled longitudinal studies are required to evaluate the long-term efficacy of LLLT in the treatment of chronic periodontitis.
| References | | |
| 1. | Armitage GC. Development of a classification system for periodontal diseases and conditions. Ann Periodontol 1999;4:1-6.  |
| 2. | Claesson R, Johansson A, Belibasakis G, Hänström L, Kalfas S. Release and activation of matrix metalloproteinase 8 from human neutrophils triggered by the leukotoxin of Actinobacillus actinomycetemcomitans. J Periodontal Res 2002;37:353-9. |
| 3. | Listgarten MA. Pathogenesis of periodontitis. J Clin Periodontol 1986;13:418-30. [ PUBMED] |
| 4. | DeCarlo AA Jr, Windsor LJ, Bodden MK, Harber GJ, Birkedal-Hansen B, Birkedal-Hansen H. Activation and novel processing of matrix metalloproteinases by a thiol-proteinase from the oral anaerobe Porphyromonas gingivalis. J Dent Res 1997;76:1260-70. |
| 5. | Okamoto K, Misumi Y, Kadowaki T, Yoneda M, Yamamoto K, Ikehara Y. Structural characterization of argingipain, a novel arginine-specific cysteine proteinase as a major periodontal pathogenic factor from Porphyromonas gingivalis. Arch Biochem Biophys 1995;316:917-25. |
| 6. | Ryan ME, Golub LM. Modulation of matrix metalloproteinase activities in periodontitis as a treatment strategy. Periodontol 2000 2000;24:226-38. |
| 7. | Chang YC, Yang SF, Lai CC, Liu JY, Hsieh YS. Regulation of matrix metalloproteinase production by cytokines, pharmacological agents and periodontal pathogens in human periodontal ligament fibroblast cultures. J Periodontal Res 2002;37:196-203. |
| 8. | Carlos TM, Harlan JM. Leukocyte-endothelial adhesion molecules. Blood 1994;84:2068-101. |
| 9. | Kornman KS, Crane A, Wang HY, di Giovine FS, Newman MG, Pirk FW, et al. The interleukin-1 genotype as a severity factor in adult periodontal disease. J Clin Periodontol 1997;24:72-7. |
| 10. | Cobb CM. Lasers in periodontics: A review of the literature. J Periodontol 2006;77:545-64. |
| 11. | Qadri T, Miranda L, Tunér J, Gustafsson A. The short-term effects of low-level lasers as adjunct therapy in the treatment of periodontal inflammation. J Clin Periodontol 2005;32:714-9. |
| 12. | Walsh LJ. The current status of laser applications in dentistry. Aust Dent J 2003;48:146-55. |
| 13. | Silveira PC, Streck EL, Pinho RA. Evaluation of mitochondrial respiratory chain activity in wound healing by low-level laser therapy. J Photochem Photobiol B 2007;86:279-82. |
| 14. | Alexandratou E, Yova D, Handris P, Kletsas D, Loukas S. Human fibroblast alterations induced by low power laser irradiation at the single cell level using confocal microscopy. Photochem Photobiol Sci 2002;1:547-52. |
| 15. | Pihlstrom BL, McHugh RB, Oliphant TH, Ortiz-Campos C. Comparison of surgical and nonsurgical treatment of periodontal disease. A review of current studies and additional results after 61/2 years. J Clin Periodontol 1983;10:524-41. [ PUBMED] |
| 16. | Lindhe J, Nyman S. Long-term maintenance of patients treated for advanced periodontal disease. J Clin Periodontol 1984;11:504-14. [ PUBMED] |
| 17. | Lui J, Corbet EF, Jin L. Combined photodynamic and low-level laser therapies as an adjunct to nonsurgical treatment of chronic periodontitis. J Periodontal Res 2011;46:89-96. |
| 18. | Kiernicka M, Owczarek B, Galkowska E, Wysokinska-Miszczuk J. Comparison of the effectiveness of the conservative treatment of the periodontal pockets with or without the use of laser biostimulation. Ann Univ Mariae Curie Sklodowska Med 2004;59:488-94. |
| 19. | Obradovic R, Kesic L, Mihailovic D, Antic S, Jovanovic G, Petrovic A, et al. A histological evaluation of a low-level laser therapy as an adjunct to periodontal therapy in patients with diabetes mellitus. Lasers Med Sci 2013;28:19-24. |
| 20. | Sakurai Y, Yamaguchi M, Abiko Y. Inhibitory effect of low-level laser irradiation on LPS-stimulated prostaglandin E2 production and cyclooxygenase-2 in human gingival fibroblasts. Eur J Oral Sci 2000;108:29-34. |
| 21. | Karu TI. Molecular mechanism of the therapeutic effect of low-intensity laser radiation. Laser Life Sci 1988;2:53-74. |
| 22. | Makhlouf M, Dahaba MM, Tunér J, Eissa SA, Harhash TA. Effect of adjunctive low level laser therapy (LLLT) on nonsurgical treatment of chronic periodontitis. Photomed Laser Surg 2012;30:160-6. |
| 23. | Ozawa Y, Shimizu N, Abiko Y. Low-energy diode laser irradiation reduced plasminogen activator activity in human periodontal ligament cells. Lasers Surg Med 1997;21:456-63. |
| 24. | Nomura K, Yamaguchi M, Abiko Y. Inhibition of interleukin-1beta production and gene expression in human gingival fibroblasts by low-energy laser irradiation. Lasers Med Sci 2001;16:218-23. |
| 25. | Safavi SM, Kazemi B, Esmaeili M, Fallah A, Modarresi A, Mir M. Effects of low-level He-Ne laser irradiation on the gene expression of IL-1beta, TNF-alpha, IFN-gamma, TGF-beta, bFGF, and PDGF in rat's gingiva. Lasers Med Sci 2008;23:331-5. |
[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8]
[Table 1], [Table 2], [Table 3], [Table 4]
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