Background: The aetiology and pathogenesis of periodontal disease may involve dysfunctions in the cellular immune responses. The aim of the present study was to study the phenotypic and functional activities of peripheral blood mononuclear cells (PBMC) from 16 patients with generalised aggressive periodontitis (G-AP), 13 patients with chronic periodontitis (CP) and 20 periodontally healthy subjects (H).
Methods: The relative counts of CD3+, CD4+, CD8+ T cells, T cells exhibiting HLA DR antigen and interleukin-2 receptor, CD19+ B cells and natural killer cells were determined by two colour flow cytometry using monoclonal antibodies. Blastogenic response of PBMC to mitogen phytohemagglutinin (PHA) was assessed after 96 h incubation by measuring 3(H)-thymidine incorporation and the results were expressed as net counts per minute. Spontaneous PBMC proliferation was also evaluated in unstimulated culture and the results were reported as mean counts per minute. Comparisons of G-AP, CP and H groups were performed using the Kruskal-Wallis and Bonferroni-corrected Mann-Whitney U test.
Results: No significant differences in the relative counts of PBMC subsets were found between G-AP, CP and H groups (P > 0.05) with the exception of lower relative amount of CD3+ T cells found in the CP group compared with healthy subjects (P = 0.0048). Blastogenic response to PHA was significantly suppressed in G-AP and CP groups relative to that of H group (P < 0.02). However, there was no significant difference in the blastogenic response to PHA between G-AP and CP groups (P > 0.05). Spontaneous proliferative response of G-AP and CP groups was also significantly lower compared to that of H group (P < 0.02). Similarly, no significant difference in spontaneous PBMC response was observed between G-AP and CP groups (P > 0.05).
Conclusions: Although G-AP and CP patients have similar amount of immune cells compared to healthy subjects, reduced functional activities of these cells may suggest the existence of defective cellular immune mechanism for the susceptibility to periodontal disease. One has to keep in mind that periodontal diseases have a genetic basis and the present functional analysis might not be connected to the actual genetic predisposition to the disease.