Influence of Type 2 Diabetes on Levels of GCF Inflammatory Biomarkers

Method: GCF samples were obtained from 40 T2DM patients (with and without periodontitis) and 20 systemically healthy controls with periodontitis. T2DM patients were recruited from Jaber Abol’ez Diabetes Center in Khartoum-Sudan. The non-diabetic controls were recruited from the outpatient dental clinic at Khartoum Dental Teaching Hospital. Individuals were diagnosed as having chronic periodontitis if there was at least one site with pocket depth ≥4mm. GCF samples were processed using cytokine multiplex fluorescent microbead immunoassay.

Result: Inflammatory biomarkes (IL-7, IL-9, Eotoxin, INF-ɤ, IP-10), chemokines (MCP-1, MIP-1α, RANTES) and molecules involved in healing (IL-4, IL-5, FGF, PDGF) were significantly increased among non-T2DM controls with periodontitis compared to T2DM cases with periodontitis. T-helper 1 (IL-2+INF-ɤ), T-helper 2 (IL-4+IL-5+IL-6+IL-10+IL-13) and growth and cellular biomarkers (IL-2+IL-7+IL-17+IL-13+ GM-CSF) were significantly increased among non-T2DM controls compared to T2DM cases with periodontitis. Moreover, the anti-/pro-inflammatory ratio (IL-4+IL-10+IL-13/IL-1β+IL-8+IL-12+TNF-α) was higher among non-T2DM controls with periodontitis compared to their T2DM counterparts.

Conclusion: Data from multiplex analysis of inflammatory and resolution biomarkers revealed less host immune response to periodontitis among T2DM patients compared to systemically healthy controls. Our results support the fact that T2DM might not be a direct cause for periodontitis but may deteriorate the per-existing infection by disturbing the balance between inflammatory and resolution molecules.