IADR Abstract Archives
Immunohistochemical Study of Inflammatory and Angiogenic Response of Dental Pulp
Objectives: This study was undertaken to examine the presence and quantitative changes of class II antigen-presenting cells, T and B lymphocytes, and endothelial cells in the dental pulp in healthy and carious human teeth.
Methods: In this study, we have examined 60 maxillary/mandibular premolars under 3 different clinical conditions: healthy teeth, and shallow and deep cavities. Teeth were extracted for various therapeutic reasons (mostly for orthodontic reasons), and immediately cut longitudinally; pulp tissue was extirpated and fixed in formalin for 24 hours at 4 °C. The specimens were embedded in paraffin, according to standardized laboratory procedures. 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: HLA-DR, CD68, CD45, CD20, and CD34.
Results: In the pulp of healthy teeth, HLA-DR-positive cells were distributed mainly under the odontoblast layer, with few CD68 positive cells located more coronary and with single CD45 and CD34 positive cells. Pulpal immunological response in shallow dentinal caries was characterized by a localized accumulation of HLA-DR antibody-positive cells. CD68 positive cells were present in a small number located coronary. The number of CD45 lymphocytes showed an increase in teeth with shallow dentinal caries. In the pulp of progressed caries, distinct quantitative and qualitative differences in inflammatory cell infiltration were observed with a marked increase of HLA-DR-positive, CD45, and CD20 positive cells. In carious teeth, CD34 positive cells subsequently coalesce to form solid vascular cords inside the connective tissue, which later aggregate with the progression of the carious lesion.
Conclusions: This study suggests that immune mechanisms play important role in pulpal infection resistance. Dental caries revealed distinct quantitative and qualitative differences in inflammatory cell infiltration. The presence of CD34 endothelial cells reveals the continuous adjustment of vessels in response to functional needs.
Methods: In this study, we have examined 60 maxillary/mandibular premolars under 3 different clinical conditions: healthy teeth, and shallow and deep cavities. Teeth were extracted for various therapeutic reasons (mostly for orthodontic reasons), and immediately cut longitudinally; pulp tissue was extirpated and fixed in formalin for 24 hours at 4 °C. The specimens were embedded in paraffin, according to standardized laboratory procedures. 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: HLA-DR, CD68, CD45, CD20, and CD34.
Results: In the pulp of healthy teeth, HLA-DR-positive cells were distributed mainly under the odontoblast layer, with few CD68 positive cells located more coronary and with single CD45 and CD34 positive cells. Pulpal immunological response in shallow dentinal caries was characterized by a localized accumulation of HLA-DR antibody-positive cells. CD68 positive cells were present in a small number located coronary. The number of CD45 lymphocytes showed an increase in teeth with shallow dentinal caries. In the pulp of progressed caries, distinct quantitative and qualitative differences in inflammatory cell infiltration were observed with a marked increase of HLA-DR-positive, CD45, and CD20 positive cells. In carious teeth, CD34 positive cells subsequently coalesce to form solid vascular cords inside the connective tissue, which later aggregate with the progression of the carious lesion.
Conclusions: This study suggests that immune mechanisms play important role in pulpal infection resistance. Dental caries revealed distinct quantitative and qualitative differences in inflammatory cell infiltration. The presence of CD34 endothelial cells reveals the continuous adjustment of vessels in response to functional needs.