###### Abstract  
This systematic review aimed to assess the literature on the benefit of adjuvant nonsteroidal anti-inflammatory drugs (NSAIDs) during conventional periodontal therapy in terms of probing pocket depth (PD). A literature search according to PRISMA guidelines in Medline (PubMed), Embase (Ovid), and Cochrane library identified seven studies to be included in this review. In terms of the main outcome, PD, three studies found a larger reduction after NSAID administration compared to non-NSAID control patients. In two studies, no difference in PD reduction between NSAID and placebo was found. Overall, the NSAID patients showed no significant difference with an estimated 0.11 mm larger reduction in PD than the control [95% CI: -0.22 mm, 0.44 mm]. The secondary outcomes, bleeding on probing (BOP) and clinical attachment gain, also showed comparable results in all studies between patients receiving NSAID and those that did not. The estimated additional PD reduction of 0.11 mm in the NSAID group is very small and not statistically significant. It is unlikely that PD can be improved by adjuvant NSAID treatment after root surface debridement, yet the evidence to date is limited and warrants further investigation.  
periodontitis; non-surgical periodontal therapy; systematic review; nonsteroidal anti-inflammatory drugs +
Footnote †: journal: Medical  
anti-inflammatory drugs (NSAIDs), which block proinflammatory pathways [12] and prevent tissue degradation.  
NSAIDs have an analgesic, antipyretic, and antiphlogistic effect [13]. They block the enzyme cyclooxygenase (COX) and thus the synthesis of prostaglandamins, which are involved in inflammatory processes and the development of pain and fever. Two types of cyclooxygenase are implied in different ways: COX-1 is constitutively expressed and is responsible for prostaglandin synthesis in the healthy organism, while COX-2 is mainly expressed in inflamed tissues. It is involved in physiological processes, such as cell proliferation and wound healing, and can be triggered very quickly in connection with inflammatory events. As a result, the intake of NSAIDs leads to pain relief and reduces inflammation [14].  
However, taking NSAID can also lead to undesirable side effects, especially with long-term use. The prostaglandin synthesis takes place physiologically in many organs; the blocking of COX induces side effects in these areas, such as the stomach (prostaglandin E2--necessary for regulation of gastric acid), kidney (increases the glomerular filtration rate), encephalopathy, or platelets (thromboxane A2). Since the majority of side effects are caused by blocking COX-1, selective COX-2 inhibitors allow management of anti-inflammatory therapy with reduced side effects [15; 16].  
Already in the 1970s and 1980s, studies were undertaken that revealed that prostaglandamins play a role in inflammatory processes and are relevant for the progression of periodontal disease [17; 18]. Several studies have been conducted in animals and humans to demonstrate the positive effect of NSAIDs on reducing periodontal inflammation [19; 20]. The group of non-steroidal anti-inflammatory drugs, especially COX-2 inhibitors, seems to be the most promising \"host-modulating agents\" to date [21].  
Therefore, the purpose of this study was to systematically assess the effect of NSAIDs on periodontal inflammation when used as an adjunct to scaling and root planning (SRP). We hypothesized that the intake of NSAID, in combination with conventional periodontal therapy, leads to a reduced PD compared to placebo-controlled conventional therapy.