Pulp Response to Periodontal Disease: Novel Observations Help Clarify the Processes of Tissue Breakdown and Infection

This study evaluated the pulp response to periodontal disease of increasing severity.

The material comprised human teeth affected by moderate (n = 16) to severe (n = 48) periodontal disease and no clinically identified caries lesions. Specimens were obtained by extraction and were processed for histopathologic and histobacteriologic methods.

In 13 of 16 teeth with moderate periodontal disease and vital pulp, no frank accumulations of inflammatory cells were observed. In 22 of 32 teeth with severe periodontal disease and vital pulps, no distinct inflammatory cell accumulations were observed in any portion of the pulp when there was an intact or minimally damaged cementum layer in the corresponding areas. Intravascular bacterial aggregations were detected in pulp blood vessels in 6 teeth with symptomatic pulpitis and severe periodontal disease, which had not reached the root apex in 4 of them. Focal areas of infection and varying accumulations of acute and chronic inflammatory cells were observed throughout the pulp tissue and surrounding these infected blood vessels. When the periodontal pocket reached the apex of single-rooted teeth, the entire canal space was necrotic and colonized by bacteria, often forming biofilms. In multirooted teeth, the pulp response varied according to the root(s) affected. Intrapulpal calcifications were observed in 91% of the teeth. The pulp and cementum of the control teeth showed no pathologic changes or bacteria.

The pulp showed a significantly detectable response when the cementum coverage was lost or when the periodontal pocket reached the root apex. In the former condition, the pulp response was usually discrete, whereas in the latter, severe reactions usually developed. In some teeth, vessels with a compromised blood flow may serve as avenues for bacteria to invade the pulp via apical or lateral foramina. This indicates that in some teeth the pulp may undergo severe inflammation and necrosis even before the periodontal disease reaches the apical root segment.