Patients with aggressive periodontitis (AgP) are diagnosed as rapid and severe periodontal destruction commonly in younger systemically healthy individuals (Armitage, 1999). Although periopathogenic bacteria are essential for initiation, this alone does not be responsible for the manifestation and severity of the clinical status/phenotype (Offenbacher et al., 2008), suggesting an imbalance between host and bacterial load (Kinane et al., 2007). Response to bacterial biofilm is determined by the host immune system (Mahanonda and Pichyangkul, 2007, Amano, 2010) in which genetic and enviromental factors modify and may get individuals more susceptible or resistant to the periodontal diseases (Kulkarni and Kinane, 2014).~The role of whether an impaired or a hyperinflammatory host response is responsible for the progression of aggressive periodontitis has been a topic of discussion. Regarding to this topic Shaddox et al. (2016) studied the whole blood specimens collected from LAgP subjects and stimulated with plaque sample generated from healthy or diseased sites. And as a result, LAgP subjects displayed hyperinflammatory response regardless of contents of bacterial stimulus. In an another research hyperinflammatory responders LAgP subjects presented the lowest reductions in clinical parameters, on the contrary low responders showed the highest reductions after treatment (Allin et al., 2016). Similarly Garrison and Nichols (1989) reported that hyper-inflammatory monocyte phenotype can be deterministic in periodontal destruction. In the view of the aforementioned findings, the aim of this study is to estimate GCF MCP-1 levels of healthy and AgP subjects and to compare MCP-1 levels between LAgP and GAgP to establish its predictive value/role for distinguishing LAgP and GAgP development.~A total of 160 subjects including, 80 AgP and 80 age and gender matched periodontally healthy (H) controls were recruited in this cross-sectional study. Clinical periodontal measurements including plaque index (PI), gingival index (GI), proping depth (PD) and clinical attachment loss (CAL) were performed. GCF samples were collected from 160 patients including 50 LAgP, 30 GAgP and 80 H. Volume of GCF samples were measured by an electronic device (Periotron 8000, OroFlow Inc.) and GCF MCP-1 was measured by an enzyme-linked immunosorbent assay ELISA.
The aim of this study is to estimate GCF MCP-1 levels of healthy and Aggressive periodontitis (AgP) subjects and to compare MCP-1 levels between Localized AgP (LAgP) and Generalized AgP (GAgP) to establish its predictive value/role for distinguishing LAgP and GAgP development.