Characterization of Inflammatory Cell Infiltrate in Human Dental Pulp

Objectives: This study was undertaken to evaluate the characteristics and densities of CD4 T helper lymphocytes, CD45RO memory T lymphocytes, CD8 T suppressor lymphocytes, CD20 B lymphocytes and CD68 macrophages in the dental pulp in healthy and carious human teeth.
Methods: In this study we have examined 80 pulps of human teeth under different clinical conditions: healthy teeth, shallow cavities, deep cavities and with a clinical diagnosis of irreversible pulpitis. Teeth were extracted for various therapeutic reasons (mostly for orthodontic reasons), and immediately cut longitudinally; pulp tissue was extirpated and fixed in 10% buffered formalin for 24 hours at 4 °C. The specimens were embedded in paraffin, according to standardized laboratory procedure. Sections were cut at 5 μm thicknesses and stained by the streptavidin-biotin complex immunoperoxidase method. Cells were identified by using the following monoclonal antibodies: CD4, CD45RO, CD8, CD20 and CD68. Wilcoxon and Mann-Whitney tests were used for statistical analysis.
Results: T lymphocytes were observed in normal pulpal tissues with CD8 lymphocytes being predominant. Pulpal tissue in shallow cavities shows a focal accumulation of mononuclear inflammatory infiltrate, and more than 90% of the lymphocyte population were T lymphocytes with a CD4/CD8 ratio of 0.84. Higher numbers of CD45RO, CD4, CD8; and B lymphocytes were observed in the pulps from deep cavities. A ratio of 1.22 of CD4/CD8 lymphocytes was observed in the deep cavities. A B/T lymphocyte ratio of 1.81 suggested this ratio might be used as an index in the immunohistological diagnosis of irreversible pulpal pathosis.
Conclusions: Dental caries revealed distinct quantitative and qualitative differences in inflammatory cell infiltration. Results obtained in this study suggest about the regulatory functions of helper (CD4) and suppressor (CD8) T lymphocytes. The interaction of T and B lymphocytes and their products in the pathogenesis of pulpal disease is present.