Macrophage activity is associated with gingival inflammation: Soluble CD163 in an experimental gingivitis study

Aim: This study aimed to investigate the association between gingival inflammation and levels of soluble CD163 (sCD163), a macrophage-specific marker associated to inflammation, in young adults participating in an experimental gingivitis study. Methods: Forty-two university students volunteered to participate in the study, which comprised three phases: a two-week Hygiene Phase (clinical examination and professional cleaning); a three-week Induction Phase (absence of oral hygiene); and a two-week Resolution Phase (reestablishment of oral hygiene). Clinical recordings of plaque (Modified Quigley and Hein Plaque Index) and gingival inflammation (Modified Gingival Index) were collected weekly during the Induction Phase, and after two weeks during the Resolution Phase. Levels of sCD163 from gingival crevicular fluid (GCF) were collected during Induction and Resolution Phases and measured by ELISA. Group-based-trajectory-modeling (GBTM) was used to model patterns of sCD163 throughout the Induction Phase. Mixed-effects multilevel models were used to estimate the effect of gingival inflammation on sCD163 over time. Results: Levels of sCD163 increased steadily over time, however, sCD163 showed a lagged response to gingival inflammation. GBTM analysis identified two groups for sCD163: one with a linear trajectory of sCD163 over the Induction Phase (n = 35), and another with a quadratic (n = 7) increase of sCD163 at the end of the Induction Phase. Stratified analysis by the sCD163 groups revealed that linear sCD163 growth was associated with both GCF volume and gingival inflammation but lagged in time, while a quadratic growth was associated with gingival inflammation and time. Conclusions: Macrophage activity is associated with gingival inflammation and can be detected at early stages of gingivitis. However, while in most participants a linear trajectory of sCD163 over the development of gingival inflammation was observed, among few individuals an exacerbated increase of sCD163 levels in GCF was noticed particularly at the end of the Induction Phase.