## 4 Discussion  
Periodontitis may result in a dysbiosis of the biofilm and host, eventually causing inflammation and destruction of periodontal tissues [34; 35]. The conventional treatment of periodontitis entails root surface debridement to allow for a recovery of the symbiosis between the host and the oral microbiome [36; 37]. This therapy may be supported by pharmacological treatment of the inflammation using NSAID. The aim of the present study was to assess the evidence for the benefits of such an adjuvant pharmacological therapy in the literature in terms of PD and the secondary parameters CAL level, PI, and BOP. Twelve studies were initially identified and further assessed in terms of their suitability and quality. Seven studies met the inclusion criteria and provided numerical data on at least the main outcome parameter, PD. The results of this systematic review showed that in two of the seven included studies, there was a significant reduction of PD with adjunctive NSAID treatment than with just conventional scaling and root planing. In two studies, the opposite was the case, where PD showed a larger reduction in the control group than in the NSAID group, while for two studies, the changes in PD were comparable. However, taking the data from these seven studies together, there were no significant differences in terms of the PD reduction between patients who received NSAID and those that did not. Overall, the reduction in PD was only 0.11 mm larger in the NSAID group compared to the controls. The largest average reduction was observed in the study by [PERSON] et al. [33], with a 1.38 mm greater PD reduction in the NSAID group compared to the control group. Nonetheless, the PD reduction also showed the widest range in this study, with an estimated 95% confidence interval of \(-\)3.00 to 5.76 mm, indicating that there were large differences between the patients. The studies assessed the probing pocket depth at three different follow-up timepoints: 10 days, 4 weeks, and 12 weeks. This extended time span could have an impact on the PD results, as one might expect a larger reduction after a longer time-period and hence a longer intake of NSAIDs. Nonetheless, there were no obvious differences or trends between these different follow-up periods. In fact, the study by [PERSON] et al. [28] with a follow-up period of only 10 days found a larger reduction of the PD in the NSAID group, while the study by [PERSON] et al. [31], assessing patients after a 12-week follow-up period, found a larger reduction in the control group. A systematic review published by [PERSON] et al. [38] investigated the adjunctive use of host modulators in non-surgical periodontal therapy. Among drugs, such as bisphosphonate, sub-antimicrobial doxycycline, and probiotics, NSAIDs applied locally and systemically were evaluated. Due to the heterogeneity of the NSAIDs being used and dosage no metanalysis was directed. \begin{table}
\begin{tabular}{c c c c c c c} \hline \hline
**Study and Groups** & **Non-NSAID (\(n\))** & **NSAID (\(n\))** & \begin{tabular}{c} **API Non-NSAID** \\ **(SD)** \\ \end{tabular} & \
\begin{tabular}{c} **API NSAID** \\ **(SD)** \\ \end{tabular} &
\begin{tabular}{c} **Follow-up** \\ **(SD)** \\ \end{tabular} & **Max. Dose/Day (\%)** \\ \hline [PERSON] et al., 2007 & 17 & 17 & \(-\)0.7 (0.23) & \(-\)1.41 (0.18) & 6 weeks & 46 \\ [PERSON] et al., 2008 & 10 & 10 & \(-\)65.82 (12.9) & \(-\)57.83 (20.2) & 30 days & 100 \\ [PERSON] et al., 2010 & 20 & 20 & \(-\)74 (12.2) & \(-\)74 (34.9) & 10 days & 50 \\  & & & \(-\)71 (11.2) & \(-\)64 (35.8) & 4 weeks & \\ [PERSON] et al., 2007 & 15 & 14 & \(-\)1.48 (0.29) & \(-\)1.3 (0.53) & 10 days & 33.3 \\ [PERSON] et al., 2014 & 16 & 16 & \(-\)0.79 (0.57) & \(-\)0.82 (0.56) & 4 weeks & 50 \\ [PERSON] et al., 2003 & 10 & 10 & \(-\)0.75 (0.12) & \(-\)0.7 (0.35) & 12 weeks & 50 \\ [PERSON] et al., 2008 & 47 & 54 & \(-\)18.6 (25.0) & \(-\)20.9 (27.4) & 12 weeks & 50 \\ \hline \hline \end{tabular}
\end{table} 
Table 6: Plaque index in comparison of non-NSAID and NSAID groups.