Aggressive periodontitis: A clinico-hematological appraisal

Area of Science:

• Immunology
• Periodontology
• Genetics

Background:

• Aggressive periodontitis (AP) is associated with polymorphonuclear leukocyte (PMN) dysfunction.
• The role of monocyte subsets in AP pathogenesis remains underexplored.
• Human leukocyte antigens (HLA) are investigated as potential genetic risk markers for AP.

Purpose of the Study:

• To assess the association between defective PMN adhesion and beta-2 integrin expression in AP subjects.
• To evaluate defective neutrophil migration and actin polymerization levels in AP.
• To determine the expression of ABO blood group and HLA antigens, and the percentage of CD14+CD16+ and CD45RA monocytes in AP patients compared to controls.

Main Methods:

• Study included 45 subjects (15 healthy, 15 chronic periodontitis (CP), 15 AP) aged 20-50 years.
• Peripheral blood samples were analyzed for ABO grouping, HLA typing, beta-2 integrin expression, actin polymerization, and monocyte subsets (CD14+CD16+, CD45RA) via fluorescence-activated cell sorter analysis.
• Parameters were compared across the three groups.

Main Results:

• AP subjects showed significantly lower average beta-2 integrin and actin levels compared to healthy subjects (P < 0.001).
• The mean percentage of CD14+CD16+ monocytes was highest in CP, followed by AP, then healthy subjects.
• The mean percentage of CD45RA monocytes was highest in AP, followed by CP, then healthy subjects.

Conclusions:

• Leukocytic functional defects, including altered monocyte subsets, were identified in aggressive periodontitis (AP) subjects.
• A statistically significant difference in CD14+CD16+ and CD45RA monocyte percentages was observed in AP patients compared to healthy and CP groups.
• A definitive association between ABO blood groups or HLA phenotypes and periodontal diseases requires further investigation.