Aggressive periodontitis: A clinico-hematological appraisal.

BACKGROUND

Human leukocyte antigens (HLA) have been considered a candidate of genetic risk markers for aggressive periodontitis (AP). AP has also been associated with polymorphonuclear leukocyte (PMN) dysfunction. The role of monocyte subsets in AP has also not been completely explored. Therefore, the present study was undertaken to assess in, AP subjects, the possible association between defective PMN adhesion and β2-integrin expression; defective neutrophil migration and actin polymerization level; the expression of ABO blood group and HLA antigen; and the percentage of CD14+ CD16+ monocytes and CD45RA monocytes. All these parameters have been compared with the subjects of chronic periodontitis (CP) and healthy controls.

MATERIALS AND

METHODS

A total of 45 subjects of the age group 20-50 years, free from any known systemic disease, were divided into three groups - Group I - periodontally healthy control (n = 15), Group II - CP (n = 15) and Group III - AP (n = 15). Peripheral blood samples were collected. ABO grouping and HLA typing were performed. β2-integrin expression, actin polymerization level and percentage of CD14+ CD16+ monocytes and CD45RA monocytes were estimated by fluorescence-activated cell sorter analysis.

RESULTS

Most of the subjects of AP belonged to the blood group AB, and an increased frequency of HLA-A30, CW1 and DR1 (P < 0.1) and B44 and DQ2 (P < 0.05) were also observed in this group. In the AP group, both average values (β2-integrin and actin level) were significantly less than those of normal subjects (P < 0.001). The mean percentage of CD14+ CD16+ monocytes was found to be maximum in CP, followed by AP, and then in healthy subjects, while the mean percentage of CD45RA was maximum in AP, followed by CP, and then in healthy subjects.

CONCLUSIONS

With the present state of knowledge from this study, a definite association of ABO blood groups and HLA phenotypes with periodontal diseases is yet to be established. Leukocytic functional defects were found in AP subjects. A statistically significant percentage of CD14+ CD16+ and CD45RA monocytes were found in AP subjects as compared with the normal control and CP groups.