Subantimicrobial‐Dose Doxycycline and Cytokine‐Chemokine Levels in Gingival Crevicular Fluid

Abstract

These results show that SDD, as an adjunct to non-surgical periodontal therapy, stabilizes the inflammatory response by promoting the suppression of proinflammatory cytokines and increasing the anti-inflammatory cytokines. The chemokine activity would account for the regulation of the inflammatory response to SDD therapy.

Impact of periodontitis on chemokines in smokers

“…The total amount of RANTES in GCF in the CP group was found to be significantly higher when compared to the healthy control. The increase in RANTES was consistent with the literature on GCF [21,45,48,49] while tissue-level expression of RANTES was also not in parallel [50]. These data collectively suggest that CC chemokines can be potential biomarkers while their local levels in the GCF may be the sum of the locally produced and serum-derived content.…”

“…Collectively, the data on CC chemokines suggest that these markers are associated with activity and severity of periodontal disease. Detection of CC chemokines, in particular MIP-1α and MIP-1β, in the inflamed gingiva and GCF suggests that these chemokines are involved in inflammatory responses during periodontal disease [19,21,18,22].…”

Systematic review and meta-analysis on the nonsurgical treatment of chronic periodontitis by means of scaling and root planing with or without adjuncts

“…Compared with SRP alone, SRP plus SDD resulted in a 0.35-mm mean gain in CAL (95% CI, 0.15-0.56) (Figure 4). [31][32][33][34][35][36][37][38][39][40][41][42] We judged the overall level of certainty in the evidence to be moderate on the basis of the evidence profile in Table 3.…”

Effects of low-dose doxycycline on cytokine secretion in human monocytes stimulated with Aggregatibacter actinomycetemcomitans

“…However, it is unclear to what extent this low-doses of doxycycline is acting directly on MMP activity or if this reduced activity reflects a generalised anti-inflammatory effect (34)(35)(36)(37). Improving our knowledge of host cytokine regulation in response to bacterial challenge is fundamental to understanding the clinical course of the disease and developing novel treatment strategies for periodontitis (38,39).…”