Keywords
chronic periodontitis - diode laser - periodontal flap surgery - matrix metalloproteinase-8
Introduction
Periodontitis is a chronic inflammatory disease of bacterial etiology from dental
plaque.[1] Inflammation of the gingiva is a consequence of the initial lesions of the gingival
epithelium caused by dental plaque microorganisms and triggering a range of reactions,
such as cell infiltration, vascular changes, and changes in connective tissue elements
and intercellular matter.[1]
[2] It is important to detect initial signs of periodontitis for preventing the progression
of this disease.[3]
[4] Saliva is a reliable medium that reflects periodontal health and is easily accessible
by identifying periodontal biomarkers. Thus, saliva is a very useful tool for monitoring
not only oral but also systemic health. Periodontal tissue consists mainly of type
I collagen.[5]
[6]
[7] Periodontitis is characterized by loss of connective and bone tissues, which is
mainly initiated by a group of enzymes called matrix metalloproteinases (MMPs).[8]
[9] Therefore, laboratory detection of MMP-8 in gingival exudate enables differentiation
of the inflammatory condition and degradation of periodontal tissues.[10] The MMP family is divided into six groups of proteases: collagenases (MMP-1, MMP-8,
and MMP-13), gelatinases (MMP-2 and MMP-9), stromelysins (MMP-3, MMP-10, and MMP-
11), matrixes (MMP-7 and MMP-26), MMPs of the type (MMP-14, MMP-15, MMP-16, MMP-17,
and MMP-12), and other unclassified MMPs, given their auxiliary contrasts.[11] MMP activities are inhibited and regulated by endogenous natural tissue inhibitors
of matrix metalloproteinases (TIMPs) and α2-macroglobulin. Inequality between MMP
and TIMP often results in devastating irreversible periodontal pathology. The proteolytic
enzyme responsible for periodontal soft and hard tissues degeneration is the MMP-8,
also known as collagenase-2 or neutrophils.[12]
[13]
[14]
[15] After the diagnosis, the treatment is planned, which includes all therapeutic procedures
which are applied over a long period, and the success of the treatment is achieved
by applying all the necessary actions.[16]
[17] Traditional methods of treating periodontal injuries are mainly based on the removal
of pathological contents from periodontal pockets mechanically through nonsurgical
interventions—scaling and root planning.[18]
[19]
[20] However, it has been argued that even after clinically successful healing, there
is the possibility of reinfection by dental plaque biofilm residues.[21]
[22]
[23]
[24] Therefore, in the last two decades, studies on semiconductor lasers or so-called
diode lasers have been deepened to achieve a better therapeutic result.[25]
[26]
[27] Clinical evidence to date points to the therapeutic advantages of using diode lasers
as the first choice in the treatment of chronic periodontitis.[28]
[29] The diode lasers have an advantage compared with the mechanical processing of periodontal
tissue, as it removes all the altered epithelium then the biological stimulatory effect
normalizes cell function, increasing microcirculation, stimulating fibroblasts, osteoblasts,
odontoblasts, and increasing collagen formation.[30] The laser also allows us better access to surfaces where it is anatomically difficult
to reach with manual instruments.[31] The study aimed to evaluate the level of MMP-8 in chronic periodontitis before and
after treatment with two therapeutic methods: 980 nm diode laser and modified Widman
flap (MWF).
Materials and Methods
This was a prospective randomized single-blinded clinical study. One hundred patients
older than 18 years, with generalized (more than 30% of affected sites) stage III
periodontitis (previously classified as generalized chronic periodontitis), with periodontal
probing depth 4 to 6 mm deep, were included in this study. Excluded from the research
were patients younger than 18 years, pregnant women, lactating women, patients currently
treated with antibiotics for any other pathology, patients with addictions such as
smoking, alcohol, and patients with parafunction.[26] All patients were comprehensively informed about the content and purpose of the
study before being part of the research. The study protocol was approved by the Ethics
Committee of the Faculty of Medicine at the University of Prishtina under the Declaration
of Helsinki.
Evaluation of Periodontal Clinical Parameters
Clinically, the condition of the periodontium was assessed using periodontal indices,
such as pocket probing depth (PPD), gingival index (GI),[32] and clinical attachment level (CAL).[33] These measurements were performed using a standardized periodontal probe on six
surfaces of the examined dentition: mesiovestibular, vestibular, distovestibular,
mezioral, oral, and distooral. To define the extent and severity of the periodontal
disease, the updated classification of periodontal and peri-implant diseases and conditions
was used.[34] Evaluation of clinical parameters was done before periodontal treatment, 3 and 6
months after.
Matrix Metalloproteinase-8 Analysis
The presence of bone destruction mediator MMP-8 was assessed by dipstick immunoassay
test. The gingival exudate was taken from the periodontal pocket with the paper standing
for 30 seconds, then placed in the buffer tube and the result was read after 5 minutes.
Either positive or negative result was recorded. Evaluation of MMP-8 obtained from
periodontal pocket exudate was done before treatment and 6 months after the treatment.
Study Groups
Patients were randomly divided into two groups:
The basic therapy for both groups consisted of debridement of supragingival hard and
soft deposits, as well as scaling and root planning as a nonsurgical preparation for
further interventions.
Laser therapy for patients of group I was performed using a diode laser (Laser HF,
Hager-Werken, Germany) with the application of laser light inside the periodontal
pocket of depth up to 6 mm, and exposure of light of wavelength 980 nm with 10 mW
power within 1 minute.
Standard surgical procedure using MWF for debridement of periodontal pockets was used
for patients of group II.[35] It was performed by a nonauthor of this article to exclude any bias.
Statistical Analysis
Data processing was done with the statistical package SPSS 22.0. The obtained data
are presented in [Tables 1]
[2]
[3]
[4]
[5]
[6]
[7] to [8].
Table 1
CAL before the treatment in both groups of patients
Baseline CAL
|
Laser treatment
|
Surgical treatment
|
N
|
50
|
50
|
Average (mm)
|
4.42
|
4.38
|
SD
|
1.03
|
0.99
|
SEM
|
0.12
|
0.11
|
Minimum
|
2.77
|
2.87
|
Maximum
|
7.32
|
7.21
|
Abbreviations: CAL, clinical attachment level; SD, standard deviation; SEM, standard
error of the mean.
Note: Kruskal–Wallis' test, p-value KW = 4.15, p = 0.056.
Table 2
CAL 6 months after the treatment in both groups of patients
CAL after 6 mo
|
Laser treatment
|
Surgical treatment
|
N
|
50
|
50
|
Average (mm)
|
3.18
|
3.29
|
SD
|
0.89
|
0.83
|
SEM
|
0.10
|
0.10
|
Minimum
|
2.01
|
2.00
|
Maximum
|
6.01
|
5.79
|
Abbreviations: CAL, clinical attachment level; SD, standard deviation; SEM, standard
error of the mean.
Note: Kruskal–Wallis' test, p-value KW = 6.55, p = 0.036.
Table 3
PPD before the treatment in both groups of patients
Baseline PPD
|
Laser treatment
|
Surgical treatment
|
N
|
50
|
50
|
Average (mm)
|
4.18
|
4.14
|
SD
|
0.66
|
0.58
|
SEM
|
0.06
|
0.06
|
Minimum
|
2.24
|
2.46
|
Maximum
|
6.25
|
5.82
|
Abbreviations: PPD, periodontal pocket depth; SD, standard deviation; SEM, standard
error of the mean.
Note: Kruskal–Wallis' test, p-value KW = 5.63, p = 0.058.
Table 4
PPD 6 months after the treatment in both groups of patients
PPD after 6 mo
|
Laser treatment
|
Surgical treatment
|
N
|
50
|
50
|
Average (mm)
|
2.78
|
2.95
|
SD
|
0.53
|
0.50
|
SEM
|
0.06
|
0.06
|
Minimum
|
2.00
|
2.00
|
Maximum
|
5.73
|
5.64
|
Abbreviations: PPD, periodontal pocket depth; SD, standard deviation; SEM, standard
error of the mean.
Note: Kruskal–Wallis' test, p-value KW = 26.8, p < 0.0001.
Table 5
GI before the treatment in both groups of patients
Baseline GI
|
Laser treatment
|
Surgical treatment
|
N
|
50
|
50
|
Average (0–3)
|
2.07
|
2.10
|
SD
|
0.26
|
0.33
|
SEM
|
0.03
|
0.04
|
Minimum
|
1.24
|
1.02
|
Maximum
|
3.00
|
3.00
|
Abbreviations: GI, gingival index; SD, standard deviation; SEM, standard error of
the mean.
Note: Kruskal–Wallis' test, p-value KW = 2.55, p = 0.235.
Table 6
GI 6 months after the treatment in both groups of patients
GI after 6 mo
|
Laser treatment
|
Surgical treatment
|
N
|
50
|
50
|
Average (0–3)
|
0.16
|
0.28
|
SD
|
0.40
|
0.45
|
SEM
|
0.04
|
0.05
|
Min
|
0.00
|
0.00
|
Max
|
2.33
|
2.20
|
Abbreviations: GI, gingival index; SD, standard deviation; SEM, standard error of
the mean.
Note: Kruskal–Wallis' test, p-value KW = 11.0, p = 0.004.
Table 7
MMP-8 before the treatment in both groups of patients
Baseline MMP-8
|
Laser treatment
|
Surgical treatment
|
N
|
50 (%)
|
50 (%)
|
Negative
|
10 (20)
|
9 (18)
|
Positive
|
40 (80)
|
41 (82)
|
Total
|
50 (100)
|
50 (100)
|
Abbreviations: MMP-8, matrix metalloproteinase-8; SD, standard deviation; SEM, standard
error of the mean.
Note: Chi-square test, p-value chi-square = 0.07, p = 0.7988.
Table 8
MMP-8 6 months after the treatment in groups of patients
MMP-8 after 6 mo
|
Laser treatment
|
Surgical treatment
|
N
|
50 (%)
|
50 (%)
|
Negative
|
48 (96)
|
40 (80)
|
Positive
|
2 (4)
|
10 (20)
|
Total
|
50 (100)
|
50 (100)
|
Abbreviations: MMP-8, matrix metalloproteinase-8; SD, standard deviation; SEM, standard
error of the mean.
Note: Chi-square test, p-value chi-square = 6.06, p = 0.0138.
Results
The research results show that both treatment methods have shown improvement compared
with the baseline values before treatment. But the treatment with diode laser showed
to be more effective in improvement of all clinical parameters, such as PPD, CAL,
GI, and the level of MMP-8.
Discussion
The key to the successful treatment of periodontal disease is early diagnosis, which
aids us to prevent disease progression, thus reducing the likelihood of periodontal
tissues' loss. The earlier diagnosis, the better prognosis of the disease. Following
the evidence of scientific literature, worldwide experiences, and the need for less
invasive treatment, this research evaluated the application of diode laser compared
with the surgical method of treatment of periodontal disease and analyzed the level
of MMP-8 in gingival exudate from the periodontal pocket.
In our surveyed patients before the treatment, around 80% of them appear to have the
presence of MMP-8 in gingival exudate taken from the periodontal pocket, a strong
correlation between clinical periodontal parameters and the presence of MMP-8 in gingival
exudate. Research by Räisänen et al (2021) demonstrated the association between periodontal
diagnostic clinical parameters (PPD) and the presence of MMP-8 in gingival exudate
in patients with chronic periodontitis.[31]
In our research, all analyzed periodontal clinical parameters improved in 6 months
after laser treatment compared with patients who were treated with periodontal surgery,
but with statistically important significance were PPD and CAL. In the MMP-8 assessment
at 6 months, 96% of laser treatment cases were negative compared with cases treated
with surgery (80%).
Khan et al (2021) evaluated the adjunct effect of 980 nm diode laser treatment of
periodontal surgical therapy (MWF) for the treatment of chronic periodontitis. Periodontal
surgical therapy together with laser therapy as an adjunct method led to a significant
improvement of clinical parameters such as periodontal pocket depth, CAL, and better
bactericidal effect 3 months after the treatment.[36]
Sezen et al (2020) evaluated the clinical and biochemical efficacy of laser treatment
(Er, Cr: YSGG) compared with nonsurgical periodontal treatment, in patients with periodontitis.
Both treatment modalities resulted in significant improvements in clinical parameters,
but laser treatment was shown to be more effective in reducing periodontal inflammation.
There were no statistically significant differences in interleukin (IL)-1β and MMP-8
levels between the groups (p < 0.05).[37]
Deshmukh et al (2018) in their study evaluated the clinical and microbiological parameters,
comparing the efficiency of periodontal treatment with diode laser and periodontal
flap surgery treatment. The laser-treated group was found to have a higher decrease
in the depth of periodontal pockets compared with the surgically treated group. The
bactericidal effect of the laser was also significantly clearer in the reduction of
periopathogens compared with the group treated with flap surgery.[38]
Karthikeyan et al (2019) in their research analyzed the effect of diode laser treatment
as adjunctive therapy with Kirkland flap surgery. Diode laser treatment as adjunctive
therapy in Kirkland surgery has resulted in a greater reduction of clinical and microbiological
parameters compared with Kirkland surgery alone, thus offering additional benefits
in treating patients with chronic periodontitis.[39]
Saglam et al (2014) in their research on the clinical and biochemical effects of diode
laser in the treatment of periodontitis showed significant improvements in clinical
parameters and reduction of the level of MMP-8 in laser-treated patients compared
with the group who were treated with scaling and root planning (SRP) only.[40]
Lobo and Pol (2015) investigated the adjunct effect of diode laser compared with periodontal
surgical treatment, based on clinical parameters (periodontal pocket depth, CAL, gingival
atrophy, plaque index, GI, and tooth mobility) in early, 3, and 6 months after treatment.
Their results showed a significant improvement of all periodontal clinical parameters
after the therapy, but no statistically significant difference was encountered between
the two treatment groups, except for a more noticeable reduction in gingival inflammation
in the laser treatment group. Generally, patients regarded the laser treatment as
more acceptable.[41]
Conclusion
Concerning the periodontal clinical parameters of this research, it can be concluded
that in patients treated with diode laser, there was an increase in CAL 3 and 6 months
after treatment, a decrease in the depth of the periodontal pocket after 6 months,
and a decrease of the GI, compared with the group treated with periodontal surgery.
About the biological mediator of bone destruction, we have observed a decrease in
the level of MMP-8 with a statistically significant difference in the cases treated
with laser compared with the group treated with surgery. Based on these results, it
would be interesting to extend the application of laser in the treatment of chronic
periodontitis and apply clinical methods and protocols of this advanced technology.