Clinical Effects of Nd:YAG Laser Applications During Nonsurgical Periodontal Treatment in Smoking and Nonsmoking Patients with Chronic Periodontitis

Abstract

Objective: The purpose of this study was to compare the clinical efficacy of nonsurgical periodontal treatment with and without Nd:YAG laser (NDL) applications in smoking and nonsmoking patients with moderate chronic periodontitis (CP). Materials and methods: The study population consisted of 52 patients with generalized moderate CP. The study compared the clinical effects of scaling and root planing (SRP) and SRP plus NDL in periodontal pockets measuring between 4 and 6 mm of smoking and nonsmoking patients with CP. The study patients were divided into four groups: Group 1: test teeth in smoker patients (ST; n=52 teeth); Group 2: placebo teeth in smoker patients (SP; n=52 teeth); Group 3: test teeth in nonsmoker patients (NST; n=52 teeth); and Group 4: placebo teeth in nonsmoker patients (NSP; n=52 teeth). Clinical examinations were performed immediately before SRP (the baseline) as well as 1 month (R1) and 6 months (R2) after treatment. Results: The recovery for pocket depth (PD), gingival index (GI), and gingival crevicular fluid (GCF) volume in the NST group was higher than in both smoker groups (p<0.05). Additionally, the changes for each of these parameters in the NSP group were higher than for the SP group (p<0.05) at R1 and R2. SRP plus NDL application versus SRP application alone did not lead to significant differences in any clinical parameters or in GCF volume between the two groups of patients who smoked (p>0.05), whereas statistically significant differences existed for PD between nonsmoker groups at R1 and R2 (p<0.05). Conclusions: Our results supported the idea that NDL applications provide additional benefits in the periodontal treatment of smokers.

Introduction

T he initiation and progression of periodontal disease arise as a consequence of the host's immune inflammatory response to oral pathogens. Progressive periodontal disease leads to the destruction of the tissues supporting the teeth, such as periodontal ligaments and bone.^1,2 Although periodontal diseases are caused by dental plaque,³ risk factors can modify the periodontal response to microbial aggression.⁴

Cigarette smoking is considered to be a significant risk factor in the pathogenesis of periodontal disease and is also associated with disease progression.⁵ Previous studies have found that tobacco smoking is strongly associated with deeper pocket depths; a larger number of deep pockets; and a greater degree of clinical attachment loss, including greater gingival recession, increased alveolar bone loss, reduced gingivitis, and decreased bleeding on probing.^6,7 Early studies have indicated that smokers have higher levels of periodontitis, poor levels of oral hygiene, and higher levels of calculus.^8,9 Smoking not only increases the risk of developing disease but also impairs the response to periodontal therapy.⁹

Periodontal therapy consists of treatment modalities that are aimed at arresting infection, regeneration of lost periodontal tissues, and maintaining the achieved therapeutic objectives.¹⁰ Numerous clinical and microbiological studies have confirmed that nonsurgical mechanical treatment consisting of plaque control and mechanical debridement is effective in reducing the bacterial load, thereby resulting in clinical improvement in periodontal treatment outcomes,¹¹ in conjunction with the application of hand instruments and power-driven scalers for subgingival mechanical debridement.¹² However, although this method has a well-documented success rate, certain limitations to its use exist, such as access to areas such as furcations, concavities, grooves, and distal sites of molars.^13,14 Therefore, in recent years, in order to improve the effectiveness of removing the subgingival biofilm and calculus, laser radiation has been recommended as an alternative or an adjunctive treatment to mechanical periodontal therapy.^14
–16 Neodymium-doped yttrium aluminum garnet (Nd:YAG) lasers (NDL)may attain excellent tissue ablation with strong bactericidal and detoxification effects. Moreover, they can reach sites that conventional mechanical instrumentation cannot.^14,17 For these reasons, lasers such as Nd:YAG, CO₂, diodes, ermium-doped YAG (Er:YAG), erbium/chromium-doped yttrium scandium gallium garnet (Er,Cr:YSGG), argon, excimer, and alexandrite are currently used to treat periodontal pockets.^14
–16

The medium of the NDL is a crystal of yttrium aluminum garnet, doped with neodymium.¹⁶ This free-running pulsed-wave laser has a wavelength of 1,064 nm.¹⁸ The NDL has a low absorption in water, and the energy scatters or penetrates into biological tissues. It penetrates to various degrees in pigmented tissues, reaching depths ranging from 0.5 to 4 mm, as a function of optical scattering, minimal absorption and reflection, and the mode of delivery.¹⁶ The photothermal effect of the NDL is useful in soft-tissue surgery. In dentistry, soft-tissue surgery that utilizes the NDL is widely accepted.^19,20 The United States Food and Drug Administration (FDA) approved the removal of soft tissue by means of a pulsed NDL in 1990, and approved the process of sulcular debridement by means of a pulsed NDL in 1997.²¹ The NDL is easily delivered using a flexible optical fiber with a contact tip suitable for pocket insertion. Basic research and clinical trials have been performed on periodontal pocket curettage and root surface debridement.^14,22,23

The use of a dental laser in the treatment of chronic periodontitis (CP) is based on the purported benefits of its antimicrobial and anti-inflammatory properties. It has been shown that use of the laser could contribute to significant reduction in bacterial populations and control of periodontal inflammation.^24
–26

Because the NDL beam is well absorbed in pigmented tissues, including melanin, and in pigmented bacteria,²⁴ it may lead to improved periodontal treatment outcomes in smokers, who have increased melanin production and pigmented tissue.²⁷ However, no data currently exists in the literature regarding NDL applications in smokers, although cigarette smoking is one of the most important risk factors in the pathogenesis of CP and impairs the healing response. The purpose of this study was to evaluate the clinical efficacy of nonsurgical periodontal treatment with and without NDL in smoker patients, and to compare the clinical response to a treatment combining scaling and root planing (SRP) plus NDL in smokers and nonsmokers with CP.

Materials and Methods

Patient selection

The patient population consisted of 52 patients with CP (26 smokers and 26 nonsmokers) with a mean age of 43.5 years old (range: 32–52 years) who were referred to the Department of Periodontology of Ataturk University in Erzurum, Turkey. All of the patients who were approached agreed to participate in this study and signed an informed consent form approved by Ataturk University's Local Ethics Committee.

Inclusion criteria were as follows: (1) Patients with generalized moderate CP with the presence of at least 2 teeth with PD between 4 and 6 mm and radiographic signs of bone loss per quadrants were included. Subjects were diagnosed in accordance with the clinical criteria for CP, agreed upon by consensus at the World Workshop in Periodontics in 1999.²⁸ (2) Smokers were identified as smoking>10 cigarettes per day for>5 years, whereas nonsmokers were identified as never having smoked.

Exclusion criteria of the study were as follows: (1) had received periodontal therapy within the last 12 months; (2) had systemic diseases that could affect periodontal treatment outcomes; (3) had taken systemic and/or topical antibiotics within the last 6 months; (4) had taken systemic and/or topical steroidal or nonsteroidal anti-inflammatory drugs within the last 6 weeks; (5) currently pregnant or breastfeeding; and (6) had teeth with restorations such as crowns, bridges, or fillings that could affect periodontal treatment outcomes.

Study design

The study was designed as a randomized, controlled, single-blind, split-mouth clinical trial with data obtained at a single center to compare the clinical effects of SRP and SRP+NDL on the periodontal pockets of smoking and nonsmoking patients with CP.

This study was performed on 208 teeth (with PD between 4 and 6 mm) from 52 patients with CP (26 smokers/26 nonsmokers). Two test teeth and two control teeth were randomly selected from each patient (one tooth from each quadrant). The quadrants were randomly assigned to “placebo” or “test,” as determined by a coin toss at the study baseline. Quadrants were equally distributed between treatment modalities (upper/lower, left/right), smokers and nonsmokers, and men and women (Fig. 1). The present study was performed on four groups:

• Group 1 (test teeth in smoking patients) (ST) received periodontal therapy, including SRP+1 W (100 mJ, 10 Hz) NDL (n=52)

• Group 2 (placebo teeth in smoking patients) (SP) received periodontal therapy, including SRP (n=52)

• Group 3 (test teeth in nonsmoking patients) (NST) received periodontal therapy, including SRP+1 W (100 mJ, 10 Hz) NDL (n=52)

• Group 4 (placebo teeth in nonsmoking patients) (NSP) received periodontal therapy, including SRP (n=52)

FIG. 1.

Research outline. All subjects made three visits, at baseline, and 1 and 6 months after treatment. Clinical data were recorded at all visits.

The power of the test

The sample size calculation determined that each group was to be composed of 18 subjects, and the test was calculated to provide 80% power (α=0.05). Eight additional subjects were included per group in order to compensate for possible dropouts during the study period.

Clinical assessments

A medical history was taken for each patient and age, gender, and smoking status were recorded. All clinical examinations of patients were performed immediately prior to SRP (baseline) as well as 1 month (R1) and 6 months (R2) after treatment. The examination involved assessing the plaque index (PI),²⁹ gingival index (GI),³⁰ pocket depth (PD), and clinical attachment level (CAL). PD was measured as the distance between the gingival margin and the deepest aspect of the pocket. CAL was measured as the distance between the cementoenamel junction of the tooth and the deepest aspect of the pocket.

All clinical parameter measurements were conducted by means of a manual periodontal probe. PD and CAL measurements were taken on six surfaces per tooth, whereas PI and GI measurements were assessed on four surfaces per tooth.

Measurements at all of a given subject's visits were made by one calibrated examiner who was not involved in providing treatment during the study (RO). Before the study began, the examiner was trained to strive for adequate levels of accuracy and reproducibility when recording the clinical parameters and indices.

Treatment procedure

All patients received initial periodontal therapy consisting of thorough oral hygiene instructions and full-mouth supragingival and subgingival SRP with the combined use of hand and ultrasonic instruments under local anesthesia in the same session. Subsequently, the periodontal pockets of the teeth on the test side (n=52 teeth in smokers/52 teeth in nonsmokers) were operated on with a 1.0 W NDL (wavelength 1,064 nm, 100 mJ, 10 Hz), whereas those on the control side (n=52 teeth in smokers/52 teeth in nonsmokers) were operated on with a placebo.

The laser beam was applied at settings in accordance with the instructions given by the manufacturer. A clinical NDL delivered by optic fiber inside the periodontal pocket was selected for the treatment. Laser application was performed by inserting the contact fiber tip at the bottom of the periodontal pocket. This tip was slowly moved from apical to coronal in a sweeping motion during laser light emission. The procedure was conducted mesially, distally, buccally, and lingually during an exposure time of 120 sec. All treatment procedures were performed by an investigator well trained in periodontal treatment (AE). During the laser application, protective eyeglasses were worn by the patient, the operator, and the assistants.

Collection of gingival crevicular fluid (GCF)

The GCF samples were taken from the control and test teeth for each patient at baseline and at R1 and R2. In total, 624 GCF samples were taken. GCF samples were used to determine the volume of GCF. The GCF samplings were conducted in the same manner.

Each clinical evaluation was preceded by the collection of GCF, as previously described, from the mesiobuccal surfaces (PD>4 mm) of all teeth included in the study.³¹ The teeth were air dried and isolated with cotton rolls, supragingival plaque was gently removed, and GCF was collected by means of prefabricated paper strips (PerioPaper, Oraflow, Smithtown, NY.), which were inserted into the pockets until resistance was felt, and kept there for 30 sec. The fluid volume of the strips was measured with a calibrated Periotron 8000. In cases of visible contamination with blood, the strips were discarded.

Statistical analysis

Shapiro–Wilk tests were computed for each variable in order to assess whether the variables were distributed normally. Kruskal–Wallis and Mann–Whitney U tests were performed in order to explore differences among the groups. Friedman and Wilcoxon tests were used to evaluate the effect of treatment within the groups. p Values<0.05 were considered statistically significant. All statistical analysis was performed using the SPSS for Windows version 15.0 software.

Results

Subjects visited the clinic at the time of randomization (baseline) and at the intervals of 1 and 6 months. Fifty-two patients were recruited and included in this study; all patients completed the 6-month evaluation (Table 1).

Table 1.

Characteristics of the Subjects

	Smokers	Nonsmokers
n	26	26
Gender (female/male)	13/13	13/13
Mean age (mean±SD)	42.7±5.1	44.1±4.9
Age range	32–51	34–52
Cigarette day (mean±SD)	17±6	0

At baseline, the mean PD, CAL, and PI were similar among the four groups (p>0.05) (Tables 2 –4); however, the GI and GCF volume were lower for the smoker groups than for the nonsmoker groups (p<0.05) (Tables 5 and 6).

Table 2.

Inter- and Intra-Group Comparison of Plaque Index (PI) at Baseline and at 1 and 6 Months After Treatment (Mean±SD)

	Smokers		Nonsmokers
	Placebo group (n=52)	Test group (n=52)	Placebo group (n=52)	Test group (n=52)
Baseline	1.7±0.6	1.9±0.6	1.8±0.5	1.7±0.8
R1	0.4±0.6^a	0.5±0.6^a	0.4±0.6^a	0.4±0.6^a
R2	0.7±0.5^b	0.8±0.5^b	0.6±0.5^b	0.6±0.4^b

R1, 1 month after treatment; R2, 6 months after treatment.

p<0.001.

p<0.01.

p Values represent changes from baseline within each group.

Table 3.

Inter- and Intra-Group Comparison of Pocket Depth (PD) at Baseline and at 1 and 6 Months After Treatment (Mean±SD)

	Smokers		Nonsmokers
	Placebo group (n=52)	Test group (n=52)	Placebo group (n=52)	Test group (n=52)
Baseline	5.4±0.7	5.4±0.8	5.3±0.8	5.3±0.7
R1	4.0±0.6^a	3.8±0.5^b	3.5±0.6^b,c	3.1±0.5^b,c,d,e
R2	4.2±0.5^b	3.8±0.6^b	3.6±0.5^b,c	3.1±0.5^b,c,d,e

R1, 1 month after treatment; R2, 6 months after treament.

SP, placebo group with smokers; ST, test group with smokers; NSP, placebo group with nonsmokers.

p<0.05 and ^b p<0.01; p values represent changes from baseline within each group.

p<0.05; p values represent differences from SP group.

p<0.05; p values represent differences from ST group.

p<0.05; p values represent differences from NSP group.

Table 4.

Inter- and Intra-Group Comparison of Clı̇nı̇cal Attachment Level (CAL) at Baseline and at 1 and 6 Months After Treatment (Mean±SD)

	Smokers		Nonsmokers
	Placebo group (n=52)	Test group (n=52)	Placebo group (n=52)	Test group (n=52)
Baseline	6.6±1.2	6.7±1.1	6.1±0.9	6.1±1.1
R1	6.4±1.1	6.4±1.1	5.8±1.0	5.7±1.1
R2	6.5±1.1	6.4±1.1	5.8±1.0	5.6±1.0

R1, 1 month after treatment; R2, 6 months after treament.

Table 5.

Inter- and Intra-Group Comparison of Gingival Index (GI) at Baseline and at 1 and 6 Months After Treatment (Mean±SD)

	Smokers		Nonsmokers
	Placebo group (n=52)	Test group (n=52)	Placebo group (n=52)	Test group (n=52)
Baseline	1.53±0.5	1.44±0.5	1.91±0.6^c,d	1.89±0.7^c,d
R1	0.77±0.6^a	0.73±0.6^a	0.81±0.5^b,c	0.74±0.4^b,c,d
R2	0.80±0.5^a	0.74±0.5^a	0.86±0.6^b,c	0.72±0.5^b,c,d

R1, 1 month after treatment; R2, 6 months after treament.

SP, placebo group with smokers; ST, test group with smokers.

p<0.01 and ^b p<0.001; p values represent changes from baseline within each group.

p<0.05; p values represent differences from SP group.

p<0.05; p values represent differences from ST group.

Table 6.

Inter- and Intra-Group Comparison of Gı̇ngı̇val Crevı̇cular Fluı̇d (GCF) Volume at Baseline and at 1 and 6 Months After Treatment (Mean±SD)

	Smokers		Nonsmokers
	Placebo group (n=52)	Test group (n=52)	Placebo group (n=52)	Test group (n=52)
Baseline	1.03±0.31	1.05±0.37	1.29±0.45^c,d	1.24±0.48^c,d
R1	0.54±0.29^a	0.45±0.24^a	0.58±0.33^b,c	0.50±0.30^b,c,d
R2	0.57±0.25^a	0.45±0.27^a	0.62±0.29^b,c	0.51±0.32^b,c,d

R1, 1 month after treatment; R2, 6 months after treament.

SP, placebo group with smokers; ST, test group with smokers.

p<0.01 and ^b p<0.001; p values represent changes from baseline within each group.

p<0.05; p values represent differences from SP group.

p<0.05; p values represent differences from ST group.

Intragroup analysis revealed that the mean change in the PI, GI, PD, and GCF volume for all groups showed statistically significant differences at R1 and at R2 (p<0.05). Only the changes in CAL for all groups proved to not be statistically significant at R1 and at R2 (p>0.05); no statistically significant changes between R1 and R2 were revealed by the intragroup analysis in all clinical parameters and GCF volume for all groups (p>0.05).

Intergroup analysis indicated that the mean changes for CAL and PI among all groups were not statistically significant throughout the study (p>0.05), and the average change in all clinical parameters and GCF volume among all groups did not change in a statistically significant fashion between R1 and R2 (p>0.05). At R1 and R2, the reductions in GI and GCF volume were higher in the NST than in both smoker groups (p<0.05). Whereas these changes in the NSP group were higher than in the SP group (p<0.05), no statistically significant difference existed between the NSP and ST groups (p>0.05).

SRP plus NDL application versus SRP application alone resulted in no significant differences for any of the clinical parameters or for GCF volume between smoker groups (p>0.05). Whereas SRP plus NDL application versus SRP application alone resulted in no significant differences in the PI, CAL, GI, and GCF volume between nonsmoker groups (p>0.05), there was a statistically significant difference for PD between nonsmoker groups at R2 in comparison with R1 (p<0.05).

Discussion

The present study was designed to evaluate the clinical effects of SRP plus NDL application in periodontal pockets of both smoking and nonsmoking patients with CP. SRP plus NDL application versus SRP application alone resulted in significant reductions in PD in nonsmokers, whereas no significant differences existed between groups for any of the clinical parameters and GCF volume in smokers.

Most of the clinical, inflammatory, and microbial changes occurred during the first 4 weeks following nonsurgical therapy.³² Additionally, several studies have demonstrated that the greatest changes in PD and CAL occur within the first 6 months following nonsurgical therapy.^33,34 For these reasons, the intervals of 1 and 6 months post-baseline were selected for outcome evaluation.

Smoking is recognized as a major risk factor for periodontal health. The observation that PD and CAL were greater in diseased sites in smokers than in nonsmokers confirmed that smoking might be associated with increased severity of disease.⁶ Furthermore, smokers exhibited greater bone loss than nonsmokers, and cigarette smoking was primarily associated with a greater decrease in gingival inflammation.⁶ Smoking has already been shown to have a similar negative impact in a study conducted by Haffajee and Socransky on a group of 289 adults with periodontitis.⁷ Current smokers had significantly more CAL (a fact that helped provide a valid estimate of the historical amount of periodontal destruction),³⁵ more missing teeth, deeper pockets, and fewer sites exhibiting bleeding upon probing than past smokers or nonsmokers.⁶ In the present study, smokers showed less GI and less GCF volume than did nonsmokers at baseline. At baseline, no significant differences were observed between smokers and nonsmokers for PD, CAL, and PI. Our results support previous reports of smokers showing less gingival inflammation than nonsmokers. Because this study included teeth with PD between 4 and 6 mm, no statistically significant differences existed in the mean PD and CAL, markers of tissue destruction, in smokers compared with nonsmokers at baseline.

To date, several studies have reported various advantageous characteristics of the use of laser beams, such as bactericidal effects against periodontopathic pathogens, removing epithelium lining of the periodontal pocket, and regeneration of periodontal tissue via biostimulative effects, all of which might lead to improved periodontal treatment outcomes.^14,15 Because of these features, in recent years the use of laser radiation has served as an alternative or an adjunctive treatment to conventional, mechanical periodontal therapy. Our previous study showed that SRP plus NDL treatment of periodontal pockets was more effective than SRP alone in reducing PD, CAL, GI, and GCF volume.³⁶ Several studies reported various degrees of success from SRP plus NDL applications in periodontal pockets.^23,37,38 Some authors, however, have reported that SRP plus NDL applications did not have beneficial effects when used to treat periodontal pockets.^22,39 Because the present study demonstrated that PD recovery was higher in the NST than in the NSP, our findings provide limited support to the results of previous studies that reported improvements in clinical healing via the antibacterial and biostimulative effects of the NDL beam.

The role of cigarette smoking in the pathogenesis of periodontal disease has been extensively studied and well documented by several investigators. Periodontal treatment outcome is often poorer in subjects who are smokers, with most refractory cases being found in smokers.^40,41 Smoking impairs the normal host defense mechanisms and stimulates destructive effects.^42,43 Smokers with periodontitis have been reported to have impaired granulocyte function.⁴⁴ In order to further elucidate the role of smoking in periodontal disease, investigations of the influence of smoking on the host response are needed. For example, nicotine has been shown to have a vasoconstrictive effect on gingival blood vessels, thereby reducing inflammatory response; this reduction is considered to be the result of a lower increase in the number of gingival blood vessels in smokers than in nonsmokers.⁴⁵ Additionally, the underlying mechanisms by which smoking is associated with the pathological conditions of the periodontium are still not fully understood. Conflicting results, however, have been reported on the subgingival microbiota in both smoking and nonsmoking patients with periodontal disease.^46,47

Gingival melanin pigmentation is a focal pigmentation of endogenous origin that occurs as a result of the excessive deposition of melanin.⁴⁸ Smoking is correlated with the stimulation of melanin production in gingival tissue.²⁷ The stimulatory effect could occur as a result of the high affinity function of nicotine and benzpyrene in tobacco smoke relative to melanin.^27,49 The color of the oral melanin pigmentation may vary from light to dark brown or black, depending upon the amount and localization in the tissue.⁵⁰ It is well known that the NDL is well absorbed by dark substances, and that India ink or other types of black pigment are often applied to increase the efficiency of ablation.^24,51 Our study suggests that NDL affects pigmented tissue to a greater degree, as it is preferentially absorbed in pigmented tissues. It also suggests that killing more pigmented bacteria might lead to improved periodontal treatment outcomes in smokers. We observed similar improvements in all clinical parameters and GCF volume between the NSP and ST groups, contrary to previous reports that cigarette smoking led to impaired periodontal treatment outcomes. These results supported the notion that NDL applications may provide additional benefits in the periodontal treatment of smokers.

Limitations

According to our results, NDL application may be helpful in the treatment of periodontal pockets in smokers, via effects in pigmented tissue and pigmented bacteria. In this respect, our study had two limitations: (1) the pigmentation degrees of tissues were not evaluated, and (2) pigmented bacteria effects of the NDL beam were not researched.

Conclusions

This study was the first to demonstrate the additional benefits of SRP plus NDL applications in periodontal pockets of smokers with CP. NDL application can reduce cigarette smoking's negative effects in terms of impairing periodontal treatment outcomes, especially with regard to PD improvement. However, further investigation of this issue is needed.

Footnotes

Author Disclosure Statement

No conflicting financial interests exist.

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