## 1 Introduction  
Periodontal disease (PD) is highly prevalent worldwide. Approximately 50% of the adults present PD [1; 2; 3]. PD can be defined as chronic multi-factorial inflammatory diseases, depending on the composition of dental plaque biofilm, and characterized by the deterioration of tooth-supporting tissues [4; 5]. The American Academy of Periodontology(AAP) and the European Federation of Periodontology (EFP) provided a new classification scheme for periodontal and peri-implant diseases during the 2017 World Workshop, identifying three forms: Necrotizing periodontal disease, periodontitis as a manifestation of systemic condition, and periodontitis. Regarding this last group, four stages (based on severity and complexity of management) were identified: Initial (stage I) and moderate (stage II) periodontitis, severe periodontitis with potential for additional tooth loss (stage III) and with potential for loss of the dentition (stage IV). The risk of disease progression was classified into slow (grade A), moderate (grade B), and rapid (grade C) [6; 7; 8; 9; 10; 11; 12]. Gingivitis and periodontitis represent two different conditions, showing different phenotypes: Gingivitis, the mildest form of PD, presents itself as a reversible gingival inflammation, it arises due to the presence of bacterial biofilm deposits, and it is characterized by the absence of periodontal attachment apparatus destruction [13; 14]. The combination of bacterial infection and persistent inflammatory response can progressively destroy the deeper periodontal tissues, leading to periodontitis, which is represented by the loss of alveolar bone and clinical attachment and by the onset of periodontal pocket [15]. The progression of periodontitis causes tooth mobility and, if not treated, can result in tooth exfoliation. Periodantal inflammation may induce low-grade systemic inflammation, damaging the function of other organs [16; 17]. Periodontitis represents a condition that occurs because of the chronic inflammatory process proper to gingivitis, although it is essential to note that gingivitis does not necessarily progress to periodontitis [18; 19]. The onset of periodontitis is associated with the presence of periodontal pathogenic microorganisms, individual genetic factors, immune pathways and lifestyle, which may enable bacteria to express their pathogenic potential [20; 21].  
Periodontal treatment aims to avoid the progression of periodontitis by resolving oral infection and thus preserving the natural dentition, restoring tissues that have been damaged, and preventing its recurrence [22; 23; 24]. These goals may be achieved by eliminating supragingival and subgingival biofilms: As literature widely reported, the prevention of periodontal disease may be achieved by performing non-surgical therapy (scaling and root planning) and maintaining adequate oral hygiene [25; 26; 27; 28; 29]. However, SRP alone does not permit to control the disease since it could only provide a temporary change of the subgingival bacteria, maintaining the presence of periodonotrophic microorganisms and, therefore, allowing the recolonization of the periodontal sites. Limitations of SRP may derive from the presence of bone defects, limited access to the periodontal tissues, and complex tooth anatomy [30; 31]. Adjunctive use of new therapies can provide a further advantage in managing the disease: The literature showed that laser therapy can improve the healing of treated sites [32; 33; 34; 35].