By Lynda Williams, Senior medwireNews Reporter
Scientists have detected significant differences in the cytokine and chemokine make up of gingival crevicular fluid (GCF) taken from chronic periodontitis patients with uncontrolled Type 2 diabetes and those without.
“[U]ncontrolled type 2 [diabetes] modulated the local levels of several cyto/chemokines at healthy and diseased sites in favour of a proinflammatory profile,” report Poliana Duarte (Guarulhos University, São Paulo, Brazil) and co-workers in the Journal of Clinical Periodontology.
“These findings may partially explain the greater susceptibility of diabetic subjects to periodontal breakdown.”
The only clinical dental examination characteristic that significantly differed between the 26 patients with Type 2 diabetes that had not responded to treatment and the 20 individuals without diabetes was probing depth; patients with diabetes had significantly deeper full-mouth probing depth than controls, at 3.6 versus 3.3 mm.
However, GCF samples taken at healthy sites from patients with diabetes had significantly higher levels than controls of eotaxin, macrophage inflammatory protein (MIP)-1α, granulocyte–macrophage-colony stimulating factor (GM-CSF), interleukin (IL)-6, tumor necrosis factor (TNF)-α, and IL-12, after adjusting for multiple comparisons.
Patients with diabetes also had a trend toward higher levels of IL-7, IL-8, and granulocyte- colony stimulating factor, but lower concentrations of IL-2 and IL-10, an important anti-inflammatory cytokine.
Diabetes patients also had significantly higher levels at diseased sites of eotaxin, , MIP-1α, GM-CSF, IL-6, TNF-α, and IL-12 than controls, with a tendency toward higher levels of IL-8 and lower levels of IL-2 and IL-10.
While acknowledging the limited study size, Duarte et al suggest: “Together, these findings may suggest the role of hyperglycemia in intensifying the periodontal immunoinflammatory responses by increasing the levels of relevant proinflammatory markers in the presence as well as absence of disease.
“It is hypothesized that the imbalance in the levels of pro- and anti-inflammatory mediators at healthy sites may be a risk for future periodontal breakdown, as soon as bacterial challenge begins.”
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