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Abstract
A successful treatment of periodontitis depends largely on the successful elimination of the periodontopathogens during non-surgical and surgical mechanical debridement. In this retrospective study, data collection was conducted from 2017 to 2021. The retrospective study included 128 patients with 128 sites of localized periodontitis with pocket depths > 5 mm. The included data were based on sites that received conventional mechanical debridement followed by different adjunctive approaches. In total, 30 patients did not receive any additional treatment (SRP group), 30 patients received SRP + 980 nm diode laser irradiation only (SRP + laser), 30 patients received SRP + 3% hydrogen peroxide irrigation (SRP + H2O2) only and 30 patients received a combined treatment of 3% hydrogen peroxide and 980 nm diode laser irradiation (SRP + H2O2 + laser). Total bacterial counts (TBC) in the periodontal pocket collected for all participants before treatment, immediately after treatment, 6 weeks after treatment, 12 weeks after treatment and 6 months after treatment were statistically analyzed and compared. When the laser was used, irradiation parameters were 10 μsec/pulse duration, 10 kHz, pick power of 10 W, average power of 1 W, irradiation time of one minute with inward and outward movements, and fiber diameter of 320 μm. The irradiation was repeated 3 times/pocket. When hydrogen peroxide was used, the irrigation was conducted for one minute and repeated 3 times. The maximum reduction in TBC was obtained when SRP was coupled with 3% H2O2 irrigation followed by 980 nm diode laser irradiation. After six months of follow-up, a significant reduction in TBC was obtained for the group of SRP + H2O2 + laser when compared to all the other groups, from 7.27 × 107 before intervention to 3.21 × 107 after six months. All three approaches to SRP showed a significant reduction in TBC immediately after treatment. Values were 3.52 × 107, 4.01 × 106, 9.58 × 106, 1.98 × 106 for SRP alone, SRP + diode, SRP + H2O2 and SRP + H2O2 + diode laser, respectively. At 6 months, we saw no significant difference between SRP + laser and SRP + H2O2 with 4.01 × 107 and 4.32 × 107, respectively. This retrospective study reveals that after SRP, irrigation with 3% hydrogen peroxide and irradiation with a 980 nm diode laser within specific treatment protocol can be used as an additional approach to conventional SRP to increase the disinfection of the periodontal pockets > 5 mm.
Highlights
Periodontitis is a multifactorial, biofilm-induced chronic inflammatory disease affecting and leading to a destruction of the periodontium and tooth loss [1,2].Periodontitis has a major negative impact on the patient’s quality of life and has been well documented to be associated with systematic conditions such as cardiovascular disease, rheumatoid arthritis, diabetes mellitus, respiratory disease, pregnancy and others [2]. investigations continue, the exact mechanism of action of the periodontal pathologies, notably periodontitis and the transition from gingivitis to periodontitis, is still not fully understood [3–5]
After six months of follow-up, the most significant reduction in Total bacterial counts (TBC) was obtained for the group scaling and root planning (SRP) + H2 O2 + laser with a statistically significant reduction when compared to the other three groups
2 alone after conventional SRP alone. This finding confirms that the 980 nm diode laser alone coupled with SRP, or the H2O2 alone coupled with SRP can lead to a better disinfection out of the range of root surface instrumentation achieved in the SRP
Summary
Periodontitis is a multifactorial, biofilm-induced chronic inflammatory disease affecting and leading to a destruction of the periodontium and tooth loss [1,2].Periodontitis has a major negative impact on the patient’s quality of life and has been well documented to be associated with systematic conditions such as cardiovascular disease, rheumatoid arthritis, diabetes mellitus, respiratory disease, pregnancy and others [2]. investigations continue, the exact mechanism of action of the periodontal pathologies, notably periodontitis and the transition from gingivitis to periodontitis, is still not fully understood [3–5]. It is agreed on today that the shift from stable gingivitis to periodontitis requires both dysbiotic microbiota and a susceptible host [6–8]. It is the interaction between dysbiotic microbiota and the host response that leads eventually to a complex inflammatory exchange including synergistic interactions of the microbiota for enhanced colonization, nutrient procurement and persistence in an inflammatory environment that promotes their adaptive fitness [6–9]. A better disinfection after mechanical debridement of the supra- and subgingival calculus inside the periodontal pocket should theoretically result in a better perturbation of the dysbiotic environment essentially controlled by anaerobic periodontopathogens, principally Porphyromonas Gingivalis, Aggregatibacter actinomycetemcomitans, Prevotella intermedia and Tannerella forsythia
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