Periodontitis is a multifactorial chronic inflammatory disease that affects tooth-supporting soft/hard tissues of the dentition. The dental plaque biofilm is considered as a primary etiological factor in susceptible patients; however, other factors contribute to progression, such as diabetes and smoking. Current management utilizes mechanical biofilm removal as the gold standard of treatment. Antibacterial agents might be indicated in certain conditions as an adjunct to this mechanical approach. Studies suggest efficacy in the use of adjunctive antimicrobials in patients with grade C periodontitis of young age or where the associated risk factors are inconsistent with the amount of bone loss present. Meanwhile, alternative approaches such as photodynamic therapy and probiotics showed limited supportive evidence, and more studies are warranted to validate their efficiency.
Periodontitis is an inflammatory disease initiated by dysbiosis of the subgingival microbiome, with aberrant immune response, causing collateral damage to the tooth-supporting tissues and ultimately leading to tooth loss [1][2][15,16]. Dental plaque biofilm is considered as the primary etiologic factor for the majority of dental/periodontal diseases [3][17]. The gold standard of treatment for periodontitis is mechanical debridement of subgingival biofilm. Indeed, suppression of pathogenic microorganisms has for a long time been a keystone in regeneration and repair of periodontal tissues, which can be challenging using mechanical debridement alone, which must be complemented by patient-based plaque control programs [4][5][6][18,19,20]. For many decades, attempts have been made to improve the efficacy of mechanical treatment by introducing different adjuncts such as the use of antimicrobials/antibiotics at different dosages and routes of administration. However, the structural complexity of dental biofilm provides a shelter for many pathogenic microorganisms, making delivery to individual bacteria challenging [7][21]. In addition, due to the non-specificity of these drugs, they may target useful commensal species which counteract pathogenic biofilm development [8][22].
A number of studies using various antimicrobials against periodontal pathogens have been carried out. It is apparent that the antimicrobials can kill periodontal pathogens in in vitro biofilm models. However, some studies indicated that amoxicillin (AMX) + metronidazole (MET) were not efficient in reducing the bacterial count [30][31]. Nevertheless, most of the studies consistently reported that the combination of these two antibiotics was superior to using either of them alone, particularly against red complex bacteria [32][33][34][35]. Similar results with regard to these bacteria were obtained with other antibiotics including azithromycin (AZM) [32][35], minocycline [36], and active organic ingredients of mouthrinses [37][38][39]. However, it is important to acknowledge that owing to greater tolerance to antimicrobials, the minimum inhibitory concentration calculated in in vitro studies would purportedly be lower and would bear little relevance to in vivo situations [18][40]. Furthermore, the majority of these studies used laboratory strains in their biofilm models, which apparently differ from clinical strains in their behavior and resistance to antimicrobials [41].
Many studies have been conducted to evaluate the additional benefits of using antibiotics within the course of periodontal therapy. Results from some of these studies have concluded that antibiotics are important adjuncts to SD in specific situations [42][43][44]. The additional clinical benefits of antibiotics are more pronounced in molar sites than in non-molar sites [45]. Following SD, the administration of broad-spectrum antibiotics for three to seven days improves microbiological outcomes compared to SD alone [44]. In regenerative periodontal therapy, better clinical outcomes could be achieved when systemic antibiotics are prescribed for patients [46]. On the other hand, many studies have reported that the use of antibiotics as an adjunct to periodontal therapy has no additional clinical benefits. Following periodontal surgery, the adjunctive use of AMX alone [47] or in combination with MET [48] for more than one week postoperatively provides no additional clinical improvements after one year. Similarly, the use of AZM as an adjunct to SD for the treatment of periodontitis seems to have no role in improving clinical outcomes compared to SD alone [49] despite the reduction in the levels of periodontal pathogens in deep periodontal pockets [50]. Precaution in prescribing antibiotics for patients with periodontal disease is advised and should be limited to certain conditions. To date, available evidence suggest prescribing adjunctive antimicrobials in patients with grade C periodontitis of young age or where the associated risk factors are inconsistent with the amount of bone loss present.A number of studies using various antimicrobials against periodontal pathogens have been carried out. It is apparent that the antimicrobials can kill periodontal pathogens in in vitro biofilm models. However, some studies indicated that amoxicillin (AMX) + metronidazole (MET) were not efficient in reducing the bacterial count [66,67]. Nevertheless, most of the studies consistently reported that the combination of these two antibiotics was superior to using either of them alone, particularly against red complex bacteria [68,69,70,71]. Similar results with regard to these bacteria were obtained with other antibiotics including azithromycin (AZM) [68,71], minocycline [72], and active organic ingredients of mouthrinses [73,74,75]. However, it is important to acknowledge that owing to greater tolerance to antimicrobials, the minimum inhibitory concentration calculated in in vitro studies would purportedly be lower and would bear little relevance to in vivo situations [34,76]. Furthermore, the majority of these studies used laboratory strains in their biofilm models, which apparently differ from clinical strains in their behavior and resistance to antimicrobials [77].