The Effects of Low Level Laser Irradiation on Gingival Inflammation

Abstract

Objective: The goal of this study was to analyze the effects of low level laser irradiation treatment and conservative treatment on gingival inflammation. Background: It is widely accepted today that the primary etiological factor for the onset of periodontitis is dental plaque, although the exact mechanism of damage remains unknown. Inflammation is a basic response of periodontal tissue to damage and serves as a fast first line of defense against damage and infections. The treatment of gingivitis and periodontitis has gone through various stages: from the simplest, classical treatment methods, through improved radical interventions, to a new era marked by laser technology. Low level laser irradiation has an anti-inflammatory effect, both general and local. Materials and methods: The research was done on patients who had chronic periodontal disease (mild periodontitis) with expressed clinical symptoms of gingival inflammation. All patients in the study underwent conservative treatment. After conservative therapy, the patients from the experimental group were subjected to 10 low level laser treatment sessions. Both groups underwent regular follow-up visits 1, 3, and 6 months after treatment, which involved only clinical examination using plaque index (PI), gingival index (GI), and bleeding on probing index (BOP index). Results: A considerable decrease in all three indexes after the application of both therapies was noticed. The follow-up visits revealed the difference in index values. With laser therapy, the values of indexes decreased steadily, whereas with conservative therapy they increased up to a certain point, but did not reach the pre-therapy values. Conclusions: A general conclusion can be drawn that low level laser irradiation (semiconductor, 670 nm) can be used as a successful physical adjuvant method of treatment, which, together with traditional periodontal therapy, leads to better and longer-lasting therapeutic results.

Introduction

P eriodontal disease is defined as an “inflammatory disease of supporting tissues of the teeth caused by specific microorganisms which lead to progressive destruction of periodontal membrane and alveolar bone with formation of periodontal pockets and gingival recession.”¹ It is currently accepted that dental plaque is a primary etiological factor for the onset of periodontitis, although the exact mechanism of damage is still unknown.² It is always preceded by gingivitis with extreme inflammation.^3,4

Inflammation is a primary response of the periodontal tissue to damage. It is a fast-working first line of defense against infections. In periodontitis, inflammation is manifested by increased gingival fluid, which rinses plaque products, while neutrophils and macrophages, which pass through the tissue into the gingival sulcus, aim at destroying the plaque bacteria.⁵ This can happen only with small quantities of dental plaque. In the case of accumulation of dental plaque, the inflammatory mechanisms react in the opposite way and can lead to periodontal tissue destruction.⁶ Therapy which eliminates inflammation can lead to improvement and disease regression.

The treatment of gingivitis and periodontitis has gone through various stages: from the simplest, classical treatment methods, through improved radical interventions, to a new era marked by laser technology. Low level laser irradiation has an anti-inflammatory effect, which can be both general and local.⁷ Laser irradiation induces an increase in nonspecific protection factors such as complement,⁸ interferon, and others. Phagocyte activity of microphages and macrophages also increases,⁹ and production of immunoprotein-interferon grows, which means that the adaptive protecting mechanisms amplify as well.¹⁰ Microcirculation is also activated.¹¹ Laser irradiation decreases interstitial and intracellular swelling by improving blood circulation in the damaged tissue, and in some cases this can lessen the pain at the site of injury.¹² Laser irradiation decreases histamine and serotonin, which are mediators in the inflammation process and have vasodilating effects. Laser irradiation also decreases the porousness of blood vessels, thus preventing alteration-exudative processes. Clinically, this causes a decrease in swelling.¹³

Inflammation develops in several phases and includes the release of biochemical mediators which are secreted through membranes of the inflamed cells.¹⁴ Some of these mediators include prostaglandins.^15,16 It is possible that the laser directly affects the blockage of these mediators.¹⁷ The anti-inflammatory effects of laser irradiation are confirmed by a decrease in the number of clinical inflammation signs and lower values of acute phase proteins, as well as by a decrease in the circulation of immune complexes.¹⁸ In dentistry, low level laser has mainly been used for pain relief in oral mucous membranes and hypersensitive dentine.^19,20,21 It has rarely been used in periodontology.

Based on the stated facts, the aim of this study was to analyze the effectiveness of low level laser irradiation on gingival inflammation.

Materials and Methods

Selection of patients

Patients who suffered from mild forms of periodontitis with obvious symptoms of gingival inflammation (PI < 2, BOP index-1.7, CAL < 4) were examined. Periodontal disease was diagnosed by classical methods: case history, clinical features, radiology, and the application of indexes of the oral hygiene status of the gingivae.

All patients with mild periodontitis were recruited from the Department of Periodontology and Oral Medicine of the Dental Clinic in Nis, Serbia. The study excluded patients under 18 years of age, pregnant women, patients with blood diseases, patients with acute or chronic infections, patients with autoimmune diseases, patients undergoing immunosuppressive treatment or phototherapy, photosensitive persons, and persons receiving antibiotic therapy. The patients from this study were between 19 and 60 years of age, predominantly between 30 and 60, and they were divided into two groups of 30 patients. The first group (30 patients) underwent a combined therapy which included conservative treatment methods followed by low level laser irradiation. The control group (30 patients) received only conservative treatment following the same principles and in the same order as the first group, but without the subsequent laser treatment.

Clinical examinations

All of the patients from the first group were examined before and after the conservative and laser treatments, and the patients from the second group were examined before and after the conservative therapy. Regular controls were carried out one, three, and six months after treatment, and included clinical examination using the Green-Vermilion plaque index (PI), Löe-Silness gingival index (GI), and the Cowell bleeding on probing index (BPO Index).²²

Conservative therapy

After the clinical examination, all participants in the study received detailed instructions concerning dental and gingival hygiene. Patients of both groups underwent conservative therapy which included the following methods:

dental plaque removal – scaling

calculus removal – root planing

periodontal pockets treatment – soft tissue curettage

deep rinse of detritus from periodontal pockets by hydrogen peroxide.

Scaling and root planing were carried out according to the patients' individual needs, using a variety of hand instruments. In the course of conservative therapy, common periodontal instruments were used, such as small and large sickle scalers for removing hard deposits, and periodontal curettes for soft tissue curettage of periodontal pockets (gingival tissue). Conservative treatment methods were applied to all teeth (single root/multiple root).

Low level laser irradiation

One week after conservative therapy, the patients from the first group received low level laser treatment. Laser irradiation therapy was conducted every day for 10 days after the classical instrumental treatment of periodontal pockets. The laser system used for the treatment was the “Scorpion”-SM-405-7A system (OPTIKA-LASER, Sofia, Bulgaria). The system is a semiconductor laser for oral usage, with a wavelength of 670 nm. The beam was applied via an optical cable, and the spot diameter was 3 mm. The beam was moved manually.

For anti-inflammatory effects, the following parameters were set: power density of 150 mW/cm² with two-minute field exposure per session. Laser irradiation was performed daily, within the period of 10 days, following the classical, instrumental treatment of periodontal pockets.

The inflamed gingiva around all periodontopathic teeth was radiated buccally and lingually. The laser beam (irradiated spot was 0.565 J/mm²) was at a right angle to the gingival surface and at a vertical distance of 2 mm from the surface. In order to reduce inflammation (and pain, if present), during the first five applications, the power density was set to 150 mW/cm², energy density to 18 J/cm². During subsequent applications, a presumed optimal dose of 100 mW/cm² was used.

Statistical analysis

First, standard descriptive parameters for all groups were measured – mean value, standard deviation (SD), variation coefficient (CV), minimum, and maximum.

Because the variation coefficient in the majority of the measured values was more than 30%, which indicates non-homogeneity of the groups with regard to index values, we applied the Mann-Whitney-Wilcoxon test and calculated Z values and probability p. Based on these, the significance of differences in index values was established. The testing was done using the SPSS 10.0 package for statistical analysis (SPSS, Inc., Chicago, IL).

A consent form was signed by each patient after a thorough explanation of the nature of the study. The study was allowed by the Scientific Ethical Committee of Medical Faculty.

Results

According to the goals set and methodology applied, the following results were obtained (Tables 1 –4).

Table 1.

Ages of the Patients

		Patient age
	Number	<21	>20	>30	>40	>50
First group	30	–	6	8	9	7
Control group	30	1	4	9	7	9
TOTAL	60	1	10	17	16	16

Since the group of patients under 21 years of age included only one patient, the group was not taken into account in further analyses.

Table 2.

Mean Plaque Index Values for Patients in Both Groups

	Laser + conservative therapy			Conservative therapy only
Index	X ± SD		CV	X ± SD		CV
PI before	1.48	0.63	42.87	1.61	0.64	40.08
PI after	0.07	0.23	308.55	0.01	0.04	271.73
PI₁ control	0.44	0.58	133.09	0.90	0.57	63.63
PI₂ control	0.47	0.62	132.40	1.28	0.47	36.65
PI₃ control	0.29	0.43	150.28	1.43	0.47	32.88

X, mean value; SD, standard deviation; CV, variation coefficient; PI before, values before treatment; PI after, values after treatment; PI₁ control, values after one month; PI₂ control, values after three months; PI₃ control, values after six months.

Table 3.

Mean Gingival Index Values for Patients in Both Groups

	Laser + conservative therapy			Conservative therapy only
Index	X ± SD		CV	X ± SD		CV
GI before	1.65	0.44	26.39	1.59	0.48	29.87
GI after	0.33	0.39	117.44	0.41	0.34	83.01
GI₁ control	0.13	0.22	167.65	0.66	0.45	67.72
GI₂ control	0.11	0.15	134.66	0.91	0.24	26.16
GI₃ control	0.09	0.13	144.38	0.91	0.26	28.99

X, mean value; SD, standard deviation; CV, variation coefficient; GI before, values before treatment; GI after, values after treatment; GI₁ control, values after one month; GI₂ control, values after three months; GI₃ control, values after six months.

Table 4.

Mean Bleeding Index Values for Patients in Both Groups

	Laser + conservative therapy			Conservative therapy only
Index	X ± SD		CV	X ± SD		CV
BOPI before	1.37	0.40	29.20	1.45	0.50	34.80
BOPI after	0.24	0.30	122.70	0.28	0.25	89.92
BOPI₁ control	0.10	0.18	171.09	0.50	0.37	74.06
BOPI₂ control	0.09	0.12	138.27	0.71	0.25	35.27
BOPI₃ control	0.07	0.11	150.77	0.70	0.25	36.36

X, mean value; SD, standard deviation; CV, variation coefficient; BOPI before, values before treatment; BOPI after, values after treatment; BOPI₁ control, values after one month; BOPI₂ control, values after three months; BOPI₃ control, values after six months.

A considerable decrease in all of the indexes was noticed after the application of both therapies. The controls revealed the differences in index values between the two groups; with laser therapy, the index values decreased steadily, whereas with conservative therapy they increased up to a certain point, but did not reach pre-therapy levels.

To compare the two applied therapies, Z scores and p values for each index were calculated. The results are shown in Tables 5, 6, and 7.

Table 5.

Test Results for Plaque Index Values of Experimental and Control Groups

	Conservative-only therapy vs. conservative + laser therapy
Group	Z	p
PI before	0.385	p > 0.05
PI after	0.992	p > 0.05
PI₁ control	3.739	p < 0.001
PI₂ control	5.391	p < 0.001
PI₃ control	6.644	p < 0.001

PI before, values before treatment; PI after, values after treatment; PI₁ control, values after one month; PI₂ control, values after three months; PI₃ control, values after six months.

Table 6.

Test Results for Gingival Index Values of Experimental and Control Groups

	Conservative-only therapy vs. conservative + laser therapy
Group	Z	p
GI before	0.838	p > 0.05
GI after	0.960	p > 0.05
GI₁ control	6.015	p < 0.001
GI₂ control	7.059	p < 0.001
GI₃ control	7.057	p < 0.001

GI before, values before treatment; GI after, values after treatment; GI₁ control, values after one month; GI₂ control, values after three months; GI₃ control, values after six months.

Table 7.

Test Results for Bleeding Index Values of Experimental and Control Groups

	Conservative-only therapy vs. conservative + laser therapy
Group	Z	p
BOP before	1.388	p > 0.05
BOP after	0.871	p > 0.05
BOP₁ control	5.825	p < 0.001
BOP₂ control	6.939	p < 0.001
BOP₃ control	6.997	p < 0.001

BOPI before, values before treatment; BOPI after, values after treatment; BOPI₁ control, values after one month; BOPI₂ control, values after three months; BOPI₃ control, values after six months.

It can be concluded from the tables above that, for all three indexes (GI, BOP index, PI), no statistically significant differences in values prior to and just after therapy were seen between the conservative-only group and conservative + laser group. However, there was a statistically significant difference in index values between the two groups after the first, second, and third control periods. In other words, both groups of patients had similar index values before therapy, and after the first application of two different therapies they displayed similar index values as well (both the first and the second therapy were successful). However, the controls revealed a difference between the applied methods of treatment, with the conservative + laser treatment group showing significantly better and longer-lasting effects than the conservative-only treatment group.

Discussion

Recent findings have proved that, besides age and the presence of deposits, gingival inflammation presents a very important factor in periodontal disease progression. The subgingival curettage technique is performed to reduce pocket depth by decreasing the inflammatory process, thus speeding up recovery. Bonan²³ states that people with decreased gingival inflammation could have a better regenerative response, provided they maintain good oral hygiene. He also emphasizes that the level of oral hygiene is an important indicator of the healing process, both for conventional and regenerative periodontal surgery, because it decreases inflammation of the gingiva and the anti-inflammatory effect enables tissue regeneration.

This study provided significant findings concerning the gingival index change. The results showed that the mean GI values in patients from both groups before therapy were similar (I-1.65; II-1.59). After the application of both therapies there was a considerable decrease in GI values (I-0.33; II-0.41), which was a result of the direct effect of the therapy on the gingiva. Applied conservative therapy, which included periodontal pocket treatment with pathologically modified tissue removal, had a considerable influence on the improvement of the gingival condition, with notable decreases in GI values.

The controls revealed that, for the combined laser therapy group, GI values steadily decreased (I-0,13; II-0,11; III-0.09) as time progressed. In contrast, for the conventional treatment only group, GI values increased slightly (I-0,66; II-0,91; III-0,91). As with the PI values, the GI values did not reach the pre-therapy level, which can be explained by continuous maintenance of oral hygiene.

No statistically significant differences in GI values were seen between the two groups of patients before and immediately after therapy, but there was a statistically significant difference in GI values for the first, second, and third controls (p < 0.001).

When conservative therapy alone was applied, a statistically significant difference in values before and after the therapy was noted (p < 0.001). However, in the values obtained after the control, the difference was diminished (p <0.05), though GI values never reached the pre-therapy levels. Comparative analysis of GI values in the combined laser group showed statistically significant decreases (p > 0.001) compared with GI values in the conventional-only group.

Nakova et al.²⁴ and Angelov et al.²⁵ also investigated the effects of low level laser irradiation on the treatment of gingivitis and periodontitis. Their results are in accordance with the results of this study.

Bleeding is an alarming signal of inflammation and a sign of disease exacerbation. It is directly dependant on inflammation. Excessive inflammation causes profuse bleeding, which is consequently decreased by the reduction of inflammation. Further research in this study was directed at examining BOP changes as indicators of the degree of inflammation during the laser treatment, as compared to conservative therapy only. Average BOP index values for both groups of patients are displayed in Table 4, which clearly shows that pre-therapy BOP index values were similar in both groups (I-1.37; II-1.45). After the therapy, there was a considerable decrease in BOP index for both groups (I-0.24; II-0.28). As with the other indexes, the controls revealed that in combined laser therapy the values continued to decrease, whereas in conservative-only therapy they rose, but did not reach the pre-therapy levels (I-0.11; II-0.70). Z-scores and p values for BOP index values in the combined laser group as compared to the conventional-only group are shown in Table 6. They indicate that BOP index values before and immediately after treatment do not show statistically significant differences between the groups (p > 0.05). However, the controls revealed a significant difference (p < 0.001).

This research did not include detailed examination or description of the dental plaque structure. Dental plaque was only examined with the aim of selecting patients for this study according to maintenance of oral hygiene. Examination of dental plaque values showed that both groups had similar plaque values before the therapy (I-1.48; II-1.64). There was a considerable decrease in PI values for both groups after the application of therapy (I-0.07; II-0.01). The decrease in plaque index was a result of patients' education in oral hygiene maintenance, which resulted in the elimination of the inflammatory effects that microbes and their products have on gingival tissue.

The controls revealed differences in index values between the two groups. In the combined laser group, values continued to decrease, but in the group that received conservative therapy only, the values increased relative to the post-therapy values.

Persistence of the anti-inflammatory effects of laser treatment can also have an impact on the decrease of plaque formation. This assumption was confirmed by the plaque index values shown in Table 5, which indicates no statistically significant differences in PI values before and immediately after the two treatments (p > 0.05), but statistically significant differences in index values between the two groups during the first, second, and third controls (p < 0.001). The application of combined laser therapy led to a significant decrease in PI, which showed a decreasing tendency after all three controls compared with conservative therapy, where PI values decreased immediately after the therapy, but rose significantly at controls, approaching the pre-therapy values. The research conducted by Angelov has also shown a decrease in plaque index.²⁵

The mechanism of inhibition of dental plaque caused by laser is not clear. Further experimental studies are needed to examine the effects of laser on vital cells in dental plaque. This may help explain the laser beam effects on gingival inflammation and the decrease in plaque bacteria.²¹

The anti-inflammatory effects of laser treatment were also examined and the results are shown as gingival index and gingival bleeding index values. They are in accordance with the results of other authors,²⁵ who have concluded that laser therapy brings about improvement of a protective reaction in the zone of application. This hypothesis can be used to explain the results obtained during the controls.

According to the results of this study, the improvements obtained with combined laser therapy lasted longer in comparison with conservative-only therapy. Laser application resulted in better protective-adoptable processes, resulting in longer-lasting anti-inflammatory effects than conservative therapy.

Anti-inflammatory effects and edema reduction can partially be explained by improved circulation or stimulation immediately after laser therapy. The increase in blood flow caused by low level laser application is not the result of a heat effect, but of an increase and normalization of homeostasis in tissue metabolism.^26,27,28,29 Other authors' opinions emphasize that anti-inflammatory effects may be the result of the inhibition of mast-cell degranulation.³⁰ Frenzen and Koort,³¹ as well as other authors,^32,33 suggest that laser treatment increases microcirculation, causing vasoconstriction of blood vessels, which directly affects the inflammatory process.

It has been previously shown that lipopolysaccharides from periodontal pathogenic bacteria can penetrate into gingival tissue and stimulate production of prostaglandin PgE₂.³⁴ Clinical observations suggest that low level laser may influence growth factors, prostaglandin E₂ production, and cellular function.^35,36

In addition, with regard to the anti-inflammatory effects of laser treatment on the inflamed gingiva, it should not be forgotten that laser irradiation, according to some authors, can reduce inflammation by directly affecting the oral biofilm bacteria.

The hypothesized mechanisms underlying anti-inflammatory reactions after the application of low level laser (semiconductor 670 nm) are also partly confirmed by histopathological examinations of gingival tissue, which has been reported earlier.^37,38

The published literature^39,40,41 reports varying results of low level laser application depending on the types of laser and parameters of laser irradiation, but the clinical effects have been confirmed.

Conclusion and Summary

Based on the analysis of the obtained results we can conclude the following:

Upon application of laser therapy, a decrease in plaque values can be noted, but the decrease is not statistically significant.

There is a statistically significant improvement in values of gingival index and bleeding index obtained after laser application, especially over a longer period of time, which was revealed by the controls three and six months after irradiation.

This study clearly shows that the number of laser applications is important for obtaining better results with the irradiated tissue. Namely, after the fifth application, a considerable anti-inflammatory effect was achieved.

Based on the reported results, we can reach a general conclusion that low level laser therapy (semiconductor, 670 nm) can be used as a successful adjuvant, physical method of treatment which, combined with traditional periodontal therapy, ensures better treatment results and longer-lasting therapeutic results.

Author Disclosure Statement

No competing financial interest exists.

References

Caton

1989. Periodontal diagnosis and diagnostic aids; consensus report, in: Proceedings of the World Workshop in Clinical Periodonics, American Academy of Periodontology. Ann. Periodontol., 3:1–32.

David

M.W.

, Fransis

J.H.

, Edward

W.O.

2003. Pathology of Periodontal Disease. London: Oxford Medical Publications, 25–54.

Marriotti

1999. Dental plaque-induced gingival diseases. Ann. Periodontol., 4:54–56.

Linde

1983. Text book of Clinical Periodontology. Copenhagen, (Denmark): Manusgaard, 66–98.

Pejčić

2005. Comparative analysis of low level laser therapy and conservative therapy of gingival inflammation. [Master thesis] Nis.: University of Nis, Medical Faculty, 78.

Genco

R.J.

, Slots

1984. Host responses in periodontal disease. J. Dent. Res., 63:441–451.

Mirković

, Živković

, Kojović

, Pejčić

2002. Laser therapy in oral medicine. Acta. Stom. Naissi., 27:45–47.

Bjordal

J.M.

, Lopes-Martines

R.A.B.

, Iversen

V.V.

2006. A randomised, placebo controlled trial of low level laser therapy for activated Achilles tendinitis with microdyalisis measurement of peritendinous prostaglandin E₂ . Br. J. Sports Med., 40:76–80.

Vladimirov

Y.A.

, Osipov

A.N.

, Klebanov

G.I.

2004. Photobiological principles of therapeutic applications of laser radiation. Biochemistry, 69:81–90.

10.

Oron

, Oron

, Streeter

et al. 2007. Low level laser therapy applied transcranially to mice following traumatic brain injury significantly reduces long-term neurological deficits. J. Neurotrauma., 24:651–656.

11.

Ishan

F.R.M.

2005. Low level laser therapy accelerates collateral circulation and enhances microcirculation. Photomed. Laser Surg., 23:289–294.

12.

Peševska

, Nakova

, Pejčić

, Ivanovski

, Angelov

, Minđova

2006. Biostimulative laser therapy: base for favorized and accented results in dentistry. Acta Fac. Med. Naiss., 23:75–78.

13.

Maričić

, Mady

, Hraste

, Zuza

1987. Laser analgetic effect in dental therapy. Acta. Stom. Crot., 21:291–302.

14.

Wilton

J.M.A.

, Johnson

N.W.

, Curtis

M.A.

et al. 1991. Specific antibody response to subgingival plaque bacteria as aids to the diagnosis and prognosis of destructive periodontitis. J. Clin. Periodontol., 18:1–15.

15.

Shimizu

, Jamaguchi

, Goseki

1995. Inhibition of prostaglandin E₂ and Interleukin 1-β by low power laser irradiation in streatch human periodontal ligament cells. J. Dent. Res., 74:1382–1388.

16.

Pejčić

, Peševska

, Grigorov

, Bojović

2006. Periodontitis as a risk factor for general disorders. Acta Fac. Med. Naiss., 23:59–65.

17.

Meikle

M.C.

, Heath

J.K.

, Reynolds

J.J.

1986. Advances in understanding cell interactions in tissue resorption. Relevance to the pathogenesis of periodontal disease and a new hypothesis. J. Oral Pathol., 15:239–250.

18.

Funk

J.O.

, Kruse

, Kirchner

, Neustock

1993. Helium-Neon laser irradiation induces effects on cytokine production at the protein and mRNA level. Exp. Dermatol., 2:75–83.

19.

Nakova

, Simonovski

, Ivanovski

, Popovska

1995. Laser and SDAR (solcoseryl dental adhesive pasta) in treatment of Stomatitis aphthosa and Ulcera decubitalis. Maced. Dent. Review, 19:37–42.

20.

Goteiner

, Vogel

, Deasy

1986. Periodontal and caries experiance in children with insulin-dependent diabetes mellitus. J. Am. Dent. Assoc., 113:277–279.

21.

Iwase

, Saito

, Hara

, Morioka

1989. Inhibitory effect of He-Ne laser on dental plaque deposition in hamsters. J. Period. Res., 24:282–283.

22.

Greenstein

1984. The role of bleeding upon probing in the diagnosis of periodontal disease. A literature review. J. Periodontol., 56:684–687.

23.

Bonan

, Bill

1998. Multi-control Analysis of 24-month clinical outromes of Quidet Tissue Regeneration of Deep Periodontal Pockets. C.M.J., 39:1–7.

24.

Nakova

, Simonovski

, Popovska

, Ivanovski

, Peševska

1995. Laser in gingivitis and periodontitis therapy. Maced. Dental Review, 19:27–31.

25.

Angelov

, Simonovski

, Nakova

, Popovska

, Peševska

1998. Laser and local periodontal therapeutic effect in diabetic patients. II Dental Congress of Makedonia-Ohrid, 83–84.

26.

Schindl

, Schindl

, Schon

, Knober

, Havalec

, Schindl

1999. Low intensity laser irradiation improves skin circulation in patients with diabetic microangiopatia. Diabet. Care, 21:580–584.

27.

Gerschman

J.A.

, Ruben

, Gebart-Eaglemont

1994. Low level laser therapy for dentinal tooth hypersensitivity. Australian Dent. J., 39:353–356.

28.

Schaffer

, Bonel

, Sroka

2000. Effect of 720 nm diode laser irradiation on blood microcirculation preliminary findings on time dependent. Ti-weighed contrast-enhanced magnetic resonance imaging. J. Photochem. Photobiol. B. Biology, 54:55–60.

29.

Inone

, Nishioka

, Hukuda

1989. Altered lymphocyte proliferation by low dosage laser irradiation. Clin. Exp. Reumatol., 7:521–523.

30.

Albertini

, Aimbire

F.S.C.

, Correa

F.I.

et al. 2004. Effects of different protocol doses of low powers GaAlAs laser radiation (650 nm) on carragenan induced rat paw oedema. J. Photochem. Photobiol. B. Biology, 74:101–107.

31.

Frenzen

M.H.

, Koort

1990. Lasers in dentistry new possibilities with advancing laser technology. Int. Dent. J., 40:323–332.

32.

Gold

, Vilardi

M.A.

1994. Pulsed laser beam effect on gingiva. J. Clin. Periodontol., 21:391–396.

33.

Qadri

, Bohdanecka

, Tuner

, Miranda

, Altamash

, Gustafsson

2007. The importance of coherence length in laser phototherapy of gingival inflammation-a pilot study. Lasers in Med. Sci., 22:245–251.

34.

Lewis

G.P.

1976. The role of prostaglandins in inflammation. Wienna (Austria): Han Hiber, 213–221.

35.

Hsin

S.J.

, Nee

L.C.

, Chia

L.J.

, Jui

W.C.

, Gwo

S.C.

1996. Low Energy, Helium-Neon Laser Irradiation Stimulate Interleukin-1α and Interleukin-8. Release from Cultural Human Keratinocytes. J. Invest. Dermatol., 107:593–596.

36.

Conlan

M.J.

, Rapley

J.W.

, Cobb

C.M.

1996. Biostimulation of wound healing by low energy laser irradiation. A review. J. Clin. Periodontol., 23:492–496.

37.

Pejcic

, Zivkovic

2007. Histological Examination of Gingiva Treated with Low-level Laser in Periodontal therapy. J. Oral Laser Appl., 7:37–43.

38.

Hou

L.T.

, Liu

C.M.

, Liu

B.Y.

, Lin

S.J.

, Liao

C.S.

, Rossomando

E.F.

2003. Interleukin-1beta, clinical parameters and matched cellular-histopathological changes of biopsed gingival tissue from periodontal patients. J. Perio. Res., 38:247–254.

39.

Raskin

, Fany

R.R.

2004. Laser treatment for neovascular formation. Lasers Surg. Med., 34:189–192.

40.

Kreisler

, Kohnen

, Marinello

et al. 2003. Antimicrobial efficacy of semiconductor laser irradiation on implants surfaces. Int. J. Oral Max. Fac. Implants, 18:706–711.

41.

Maver-Biscanin

, Mravak-Stipetic

, Jerolimov

, Biscanin

2004. Fungicidal effect of diode laser irradiation in patients with denture stomatitis. Lasers Surg. Med., 35:259–262.