|Year : 2017 | Volume
| Issue : 2 | Page : 45-51
Comparative assessment of prostaglandin E2 levels in gingival crevicular fluid after diode laser pocket therapy: A clinico-biochemical study
Siddharth Gautam1, Sushama Galgali2, Ashank Mishra1
1 Department of Periodontics, Sri Sai College of Dental Surgery, Vikarabad, Telangana, India
2 Department of Periodontics, VS Dental College and Hospital, Bengaluru, Karnataka, India
|Date of Web Publication||29-Dec-2017|
Dr. Ashank Mishra
Department of Periodontics, Sri Sai College of Dental Surgery, Vikarabad, Telangana
Source of Support: None, Conflict of Interest: None
Introduction: Conventional periodontal therapy in form of scaling and root planing (SRP) has its own limitations when used in deep pockets. Various studies have reported adjunctive use of laser therapy as a promising modality to overcome limitations of SRP. Aim and Objectives of the Study: The aim of this study was to assess the adjunctive effect of 810-nm diode laser on clinical parameters and prostaglandin E2 (PGE2) levels in gingival crevicular fluid (GCF). Materials and Methods: The present study was a split-mouth clinical study, which included 48 sites from patients diagnosed with moderate-to-severe chronic periodontitis. Test group consisted of 24 sites that received diode laser (810 nm, 2.5 W) therapy as an adjunct to SRP whereas control group consisted of 24 sites, which received SRP only. Gingival index (GI) was assessed clinically whereas Florida Probe was used to record bleeding on probing (BOP), pocket probing depth (PPD), and clinical attachment level (CAL) at baseline, 3 months, and 6 months. GCF PGE2levels were measured at baseline and 3 months post therapy using commercially available ELISA kit (Neogen™). Results: Test group showed a significant reduction in GCF PGE2levels at the end of 3 months when compared to control sites. However, the primary clinical parameters (CAL and PPD) from baseline to 3 and 6 months did not show statistically significant improvement in the test group. Conclusion: Application of diode laser resulted in a significant reduction in PGE2levels compared to SRP alone. Thus, diode laser therapy as an adjunct to SRP appears to be a promising treatment modality to reduce or modify the host response.
Keywords: Laser therapy, prostaglandin E2, scaling and root planing
|How to cite this article:|
Gautam S, Galgali S, Mishra A. Comparative assessment of prostaglandin E2 levels in gingival crevicular fluid after diode laser pocket therapy: A clinico-biochemical study. J Dent Lasers 2017;11:45-51
|How to cite this URL:|
Gautam S, Galgali S, Mishra A. Comparative assessment of prostaglandin E2 levels in gingival crevicular fluid after diode laser pocket therapy: A clinico-biochemical study. J Dent Lasers [serial online] 2017 [cited 2018 Mar 24];11:45-51. Available from: http://www.jdentlasers.org/text.asp?2017/11/2/45/221997
| Introduction|| |
The goal of periodontal therapy is to arrest the progression of periodontal disease by suppressing or eradicating subgingival microflora and modifying the destructive host response triggered through subgingival biofilm. Although scaling and root planing (SRP) can control periodontal disease in a majority of population, it is unlikely to be sufficient in preventing progression of periodontal disease in all categories of patients., New adjunctive approaches are therefore being developed to overcome the limitations of SRP. Laser has been proposed as one such alternative or adjunctive treatment to conventional periodontal therapy.
Laser phototherapy is based on the premise that it completely removes the pocket epithelium while the conventional therapy leaves behind significant epithelial remnants. Removal of chronically inflamed epithelial lining is a crucial event in reduction of probing depth and improvement in clinical attachment, which could result in faster resolution of inflammation. Histological studies have shown that diode laser (810–980 nm, 2–4 W) removes pocket epithelium completely and facilitates establishment of new connective tissue attachment., Diode lasers have bactericidal and biostimulatory effects.,,
Data from clinical studies have shown not only bactericidal and detoxifying effects of the diode laser but also its ability to modify or reduce the host destructive response.,, Most of these studies have used low-level laser irradiation, and there is a paucity of studies evaluating the diode laser in surgical mode on the biomarkers of host immunoinflammatory response.
Of the various pro-inflammatory cytokines which are implicated in the pathogenesis of periodontal disease, host-produced prostaglandin E2 (PGE2) mediates much of the tissue destruction. Gingival crevicular fluid (GCF) as an inflammatory exudate of the periodontal tissues has a rich potential for its use as a diagnostic biologic fluid. It can be collected in a noninvasive manner from the site of interest repeatedly. Clinical studies have shown that concentrations of PGE2 in GCF can be used as a marker of clinical and subclinical disease., PGE2 levels within the crevicular fluid can serve as a static assessment of ongoing disease activity, i.e., rate of attachment loss and bone resorption. Lamster and Novak have shown the relationship of elevated PGE2 concentration in GCF to periodontal disease activity.
Thus, the aim of the present study was to assess the adjunctive effect of an 810-nm diode laser in surgical mode on clinical parameters and PGE2 levels in GCF.
| Materials and Methods|| |
This comparative clinical study was conducted on patients who reported to the Department of Periodontics, VS Dental College and Hospital, Bengaluru, Karnataka, India, from September 2014 to June 2015. Participation of individuals for the study was voluntary and written informed consent was obtained from those who agreed to participate. Ethical clearance was obtained from the Institutional Ethical Committee before the start of the study.
A total of fifteen participants suffering from moderate to severe chronic periodontitis were examined for the study. Chronic periodontitis was defined based on probing depth more than 4 mm in at least three sites contralaterally (anterior or posterior) and radiographs showing signs of bone loss. Systemically healthy, nonsmoker, and cooperative patients having age between 18 and 50 years were included in the study. Patients who gave a history of previous periodontal therapy within the past 6 months or having taken medications such as nonsteroidal anti-inflammatory drugs or antibiotics in the past 3 months were excluded from the study. Pregnant/lactating women or patients having mobile teeth/endodontically treated teeth were also excluded from the study [Figure 1].
A site-specific, split-mouth study was planned with three identical sites (same anterior/posterior sites) on each maxillary quadrant. Mandibular sites were not taken because of high chances of salivary contamination. Based on the inclusion/exclusion criteria, eight patients were included who contributed 48 sites for study. The selected sites were then divided into two groups [Figure 1].
Test group/(scaling and root planing + diode laser) group
It consisted of 24 sites in which laser phototherapy was used as an adjunct to SRP. SRP was performed in the same manner as in control group (using a combination of ultrasonics and standard Gracey curettes). Laser phototherapy was applied a day following SRP, and the procedure was repeated 3 days later [Figure 2] and [Figure 3].
|Figure 3: (a) Baseline clinical picture and corresponding Florida Probe charting. Mesiobuccal site of canine (13) was taken as test site. (b) Three-month follow-up clinical picture and corresponding Florida Probe charting. (c) Six-month follow-up clinical picture and corresponding Florida Probe charting|
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Control group/scaling and root planing group
It consisted of 24 sites in which only SRP was done. SRP was accomplished using a combination of ultrasonics (Dentsply, Cavitron Bobcat Pro) and standard Gracey curettes (Hu-Friedy Co.). Instrumentation was carried out until a hard, smooth calculus-free surface was obtained. Oral hygiene instructions were given [Figure 4].
|Figure 4: (a) Baseline clinical picture and corresponding Florida Probe charting. Mesiobuccal site of canine (23) was taken as control site. (b) Three-month follow-up clinical picture and corresponding Florida Probe charting. (c) Six-month follow-up clinical picture and corresponding Florida Probe charting. Note the relapse at control site|
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Clinical pro forma was used to collect data from all the participants. Gingival index (GI), bleeding on probing (BOP), probing pocket depth (PPD), and clinical attachment level (CAL) were recorded at baseline, 3 months, and 6 months., For measurement of BOP, PPD, and CAL, Florida Probe (FP 32, Version 6.6.2) was used.
Ga-Al-As diode laser (AMD Lasers; PICASSO Model) of 810 nm at a power output of 2.5 W in pulsed mode (30 Hz, pulse duration 30 ms) was used as an adjunct to SRP to remove the diseased pocket epithelium. The optic fiber of 300 μm was used in light contact, sweeping mode for pocket debridement. The procedure was repeated after 3 days.
GCF was collected with the help of microcapillary pipettes from the selected sites. The sites to be sampled were isolated with cotton rolls, gently air dried before the placement of micropipettes (Sigma-Aldrich Co.) at the entrance of gingival sulcus (extrasulcular method of GCF collection). GCF was collected from selected sites a day following full-mouth supragingival scaling for the assessment of PGE2. This was done at baseline and at 3 months in both the groups. GCF samples were stored at −80°C until further analysis. PGE2 levels were assessed using the commercially available ELISA kit (Neogen ™ Elisa kit). The concentrations were reported in ng/ml.
All the analysis was done using the Statistical Package for the Social Sciences (SPSS, IBM, Chicago, Illinois, USA) version 18. P < 0.05 was considered statistically significant. Mean values for GI, BOP, PPD, and CAL were calculated. Tooth site was taken as a unit of analysis. Normality assumption was checked using Shapiro–Wilk test. As the data followed a normal distribution, parametric tests were used to compare data.
| Results|| |
Eight patients with mean age of 37.5 ± 7.4 years were included in the study. All patients completed study period. The follow-up period was uneventful and no complications occurred. Out of the 48 sites, 8 sites went undetected in ELISA PGE2 analysis. Hence, only 40 sites were taken into consideration for statistical analysis.
There were no statistically significant differences between the two groups at baseline indicating homogeneity between the groups. The comparison of the clinical parameters in intra- and inter-group is summarized in [Table 1] and [Table 2]. On intragroup comparison, all the clinical parameters showed statistical significant difference (P < 0.05) from baseline to 3 and 6 months. On intergroup comparison, the primary clinical parameters (CAL and PPD) from baseline to 3 and 6 months did not show statistical significance in the test group.
|Table 1: Intragroup comparison of clinical parameters and prostaglandin E2 at various time intervals|
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|Table 2: Intergroup comparison of clinical parameters and prostaglandin E2 at various time intervals|
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The reduction in PGE2 concentration in both the groups was statistically significant (P < 0.05) at the end of 3 months. Furthermore, a statistically significant difference in PGE2 concentrations was observed between the groups at the end of 3 months (P < 0.05) [Table 1].
The mean difference in the clinical parameters from baseline to 3 months and baseline to 6 months is shown in [Table 3].
|Table 3: Intergroup comparison of difference (baseline-3 or 6 months) using independent sample t-test|
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| Discussion|| |
Periodontal inflammation is initiated by bacteria, however, the tissue breakdown events that lead to clinical signs of disease result from host immunoinflammatory response. SRP is the cornerstone of periodontal therapy and the first recommended approach in the management of periodontitis. However, SRP has limitations, especially in pockets >5 mm, where it is inefficient in eradicating all subgingival pathogens and reducing gingival inflammation. It is, therefore, logical that application of laser phototherapy as an adjunct to SRP may enhance the clinical benefits and healing through modulation of host immunoinflammatory response. Diode laser is indicated for the treatment of soft tissues but does not ablate calculus on the root surface. Therefore, it can only be used as an adjunct to SRP.,
Improvements observed in clinical parameters in both the groups are comparable to those reported in literature.,,,,,, The results obtained at the end of 6 months in this study were superior to what was achieved by Borrajo et al. that had a short follow-up period of only 6 weeks and that of Kamma et al. which examined aggressive periodontitis patients., In contrast to our observations, Kreisler et al. and Dukic et al. demonstrated superior results with laser phototherapy., These differences may be attributed to variations in the laser wavelength, number of applications, and the duration of the studies. In general, the mean changes in PPD following nonsurgical therapy have been reported to be in the range of 1.2–2.7 mm, and the results of our study are in accordance with their study.,
It is a noteworthy observation that in terms of clinical parameters, there were no significant differences between the test and control group at any time point during the study. This could be attributed to the limitation of the nonsurgical periodontal therapy with or without adjunctive laser phototherapy in treating deep pockets due to inaccessibility and cumbersome instrumentation. However, changes in test group were significantly better at all time intervals compared to control group (intragroup comparison) indicating the ability of laser phototherapy in preventing the progression of disease possibly through improving adhesion of fibroblasts to root surface and maintaining the pocket in an inactive state., The result of the present study is in accordance with the American Academy of Periodontology statement.
Following therapy, both the intra- and inter-group comparison showed a statistically significant reduction in PGE2 levels by the end of 3 months. The reduction in PGE2 in control group is comparable to earlier studies but contrasts with study by Needleman who found no significant change in PGE2 levels in spite of using surgical therapy in combination with metronidazole gel.,,,,,, The reduction in test group observed was significant in our study but cannot be compared to any studies because the effect of laser on COX-2 gene expression and reduction in PGE2 has been only observed in in vitro studies and/or in vivo studies but with low-level laser therapy (LLLT).,,,, This is perhaps the first clinical study assessing the effect of diode laser (810 nm, 2.5 W) in a surgical mode on PGE2 levels.
Chronically inflamed proliferating epithelia are a potentially important source of PGE2 because of the presence of significant amounts of prostaglandin H synthase 2 in epithelial cell cytoplasm., PGE2 at sites of inflammation serves as a pluripotent inflammatory adjuvant. It acts synergistically with interleukin (IL-1β) and tumor necrosis factor-alpha in enhancing its bone resorptive response and with IL-1 in promoting collagenase production. As laser phototherapy removes the pocket epithelium, this could explain the significant reduction of PGE2 levels in test group.
The major limitation of the present study was small sample size. Based on the concept that periodontal disease is site specific, multiple sites from small number of patients were sampled and were considered as unit of analysis. One patient with many sites within the study may have greatly influenced the result. Furthermore, PGE2 levels might not simply represent site-specific inflammation but might be influenced by general inflammatory status of the body. Hence, there is a need to select one or two sites from a large number of periodontitis patients to confirm the findings.
Studies have shown a wide variation in laser power density settings (350 mW/cm 2 to 2830 W/cm 2), exposure time (3 to 90 s), frequency of laser treatments (1–6 times), and clinical assessment parameters indicating heterogeneity in literature making comparisons difficult and challenging. Delivering laser energy within the therapeutic treatment window remains an elusive treatment goal. Future studies need to be homogeneous in this respect, and standard protocols need to be developed.
| Conclusion|| |
Within the limitations of the present study, it was concluded that the application of diode laser provided a significant improvement in PGE2 levels. Additional longitudinal, randomized control trials are necessary to evaluate the efficacy of diode laser on nonsurgical periodontal therapy.
We would like to thank the Principal, V. S. Dental College and Hospital, Bengaluru, for their permission and support to conduct the study. Furthermore, we are grateful to the technical staff of Department of Microbiology, KIMS, for their help in conducting the study.
Declaration of patient consent
The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
Financial support and sponsorship
Conflicts of interest
There are no conflicts of interest.
| References|| |
Dukic W, Bago I, Aurer A, Roguljic M. Clinical effectiveness of diode laser therapy as an adjunct to non-surgical periodontal treatment: A randomized clinical study. J Periodontol 2013;84:1111-7.
Gojkov-Vukelic M, Hadzic S, Dedic A, Konjhodzic R, Beslagic E. Application of a diode laser in the reduction of targeted periodontal pathogens. Acta Inform Med 2013;21:237-40.
Romanos GE, Henze M, Banihashemi S, Parsanejad HR, Winckler J, Nentwig GH, et al.
Removal of epithelium in periodontal pockets following diode (980 nm) laser application in the animal model: An in vitro
study. Photomed Laser Surg 2004;22:177-83.
Castro GL, Gallas M, Núñez IR, Borrajo JL, Varela LG. Histological evaluation of the use of diode laser as an adjunct to traditional periodontal treatment. Photomed Laser Surg 2006;24:64-8.
Moritz A, Schoop U, Goharkhay K, Schauer P, Doertbudak O, Wernisch J, et al.
Treatment of periodontal pockets with a diode laser. Lasers Surg Med 1998;22:302-11.
Caruso U, Nastri L, Piccolomini R, d'Ercole S, Mazza C, Guida L, et al.
Use of diode laser 980 nm as adjunctive therapy in the treatment of chronic periodontitis. A randomized controlled clinical trial. New Microbiol 2008;31:513-8.
Convissar R. Principles and Practice of Laser Dentistry. 1st
ed. St. Louis, Missouri, USA: Mosby Elsevier; 2011. p. 12-20.
Shimizu N, Yamaguchi M, Goseki T, Shibata Y, Takiguchi H, Iwasawa T, et al.
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.
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.
Offenbacher S, Odle BM, Van Dyke TE. The use of crevicular fluid prostaglandin E2 levels as a predictor of periodontal attachment loss. J Periodontal Res 1986;21:101-12.
Offenbacher S, Heasman PA, Collins JG. Modulation of host PGE2 secretion as a determinant of periodontal disease expression. J Periodontol 1993;64:432-44.
Offenbacher S, Collins JG, Heasman PA. Diagnostic potential of host response mediators. Adv Dent Res 1993;7:175-81.
Lamster IB, Novak MJ. Host mediators in gingival crevicular fluid: Implications for the pathogenesis of periodontal disease. Crit Rev Oral Biol Med 1992;3:31-60.
Loe H, Silness J. Periodontal disease in pregnancy. I. Prevalence and severity. Acta Odontol Scand 1963;21:533-51.
Ainamo J, Bay I. Problems and proposals for recording gingivitis and plaque. Int Dent J 1975;25:229-35.
Newmann MG, Takei HH, Klokkevold PR, Carranza FA. Carranza's Clinical Periodontology. 11th
ed. South Asia edition. New Delhi, India: Saunders Elsevier; 2012. p. 261.
Ishikawa I, Baehni P. Nonsurgical periodontal therapy – Where do we stand now? Periodontol 2000 2004;36:9-13.
Aoki A, Sasaki KM, Watanabe H, Ishikawa I. Lasers in nonsurgical periodontal therapy. Periodontol 2000 2004;36:59-97.
Harris DM, Yessik M. Therapeutic ratio quantifies laser antisepsis: Ablation of porphyromonas gingivalis with dental lasers. Lasers Surg Med 2004;35:206-13.
Cugini MA, Haffajee AD, Smith C, Kent RL Jr., Socransky SS. The effect of scaling and root planing on the clinical and microbiological parameters of periodontal diseases: 12-month results. J Clin Periodontol 2000;27:30-6.
Rabbani GM, Ash MM Jr. Caffesse RG. The effectiveness of subgingival scaling and root planing in calculus removal. J Periodontol 1981;52:119-23.
Sherman PR, Hutchens LH Jr. Jewson LG. The effectiveness of subgingival scaling and root planing. II. Clinical responses related to residual calculus. J Periodontol 1990;61:9-15.
Van der Weijden GA, Timmerman MF. A systematic review on the clinical efficacy of subgingival debridement in the treatment of chronic periodontitis. J Clin Periodontol 2002;29 Suppl 3:55-71.
Fallah A. Effects of 980 diode laser treatment combined with scaling and root planing on periodontal pockets in chronic periodontitis patients. Proc SPIE 7549, Lasers in Dentistry XVI, 75490D (March 05, 2010). [Epub ahead of print]. [Doi: 10.1117/12.846838].
Lin J, Bi L, Wang L, Song Y, Ma W, Jensen S, et al.
Gingival curettage study comparing a laser treatment to hand instruments. Lasers Med Sci 2011;26:7-11.
Borrajo JL, Varela LG, Castro GL, Rodríguez-Nuñez I, Torreira MG. Diode laser (980 nm) as adjunct to scaling and root planing. Photomed Laser Surg 2004;22:509-12.
Kamma JJ, Vasdekis VG, Romanos GE. The effect of diode laser (980 nm) treatment on aggressive periodontitis: Evaluation of microbial and clinical parameters. Photomed Laser Surg 2009;27:11-9.
Kreisler M, Al Haj H, d'Hoedt B. Clinical efficacy of semiconductor laser application as an adjunct to conventional scaling and root planing. Lasers Surg Med 2005;37:350-5.
Kreisler M, Meyer C, Stender E, Daubländer M, Willershausen-Zönnchen B, d'Hoedt B, et al.
Effect of diode laser irradiation on the attachment rate of periodontal ligament cells: An in vitro
study. J Periodontol 2001;72:1312-7.
American academy of periodontology statement on the efficacy of lasers in the non-surgical treatment of inflammatory periodontal disease. J Periodontol 2011;82:513-4.
Preshaw PM, Lauffart B, Brown P, Zak E, Heasman PA. Effects of ketorolac tromethamine mouthrinse (0.1%) on crevicular fluid prostaglandin E2 concentrations in untreated chronic periodontitis. J Periodontol 1998;69:777-83.
Preshaw PM, Heasman PA. Prostaglandin E2 concentrations in gingival crevicular fluid: Observations in untreated chronic periodontitis. J Clin Periodontol 2002;29:15-20.
Mizrak T, Güncü GN, Caglayan F, Balci TA, Aktar GS, Ipek F, et al.
Effect of a controlled-release chlorhexidine chip on clinical and microbiological parameters and prostaglandin E2 levels in gingival crevicular fluid. J Periodontol 2006;77:437-43.
Kumar AK, Reddy NR, Babu M, Kumar PM, Reddy VS, Chavan CV, et al.
Estimation of prostaglandin E2 levels in gingival crevicular fluid in periodontal health, disease and after treatment. Contemp Clin Dent 2013;4:303-6.
] [Full text]
Sánchez GA, Miozza VA, Delgado A, Busch L. Salivary IL-1ß and PGE2 as biomarkers of periodontal status, before and after periodontal treatment. J Clin Periodontol 2013;40:1112-7.
Bliddal H, Hellesen C, Ditlevsen P, Asselberghs J, Lyager L. Soft-laser therapy of rheumatoid arthritis. Scand J Rheumatol 1987;16:225-8.
Heussler Needleman IG, Moles DR, Collins AM. Periodontal flap surgery with 25% metronidazole gel. (2). Effect on gingival crevicular fluid PGE2. J Clin Periodontol 2000;27:193-7.
Heussler JK, Hinchey G, Margiotta E, Quinn R, Butler P, Martin J, et al.
A double blind randomised trial of low power laser treatment in rheumatoid arthritis. Ann Rheum Dis 1993;52:703-6.
Johannsen F, Hauschild B, Remvig L, Johnsen V, Petersen M, Bieler T, et al.
Low energy laser therapy in rheumatoid arthritis. Scand J Rheumatol 1994;23:145-7.
Heasman PA, Lauffart BL, Preshaw PM. Crevicular fluid prostaglandin E2 levels in periodontitis-resistant and periodontitis-susceptible adults. J Clin Periodontol 1998;25:1003-7.
[Figure 1], [Figure 2], [Figure 3], [Figure 4]
[Table 1], [Table 2], [Table 3]