M. Hutchins, J. Suchina, J. Patten
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Figure 1
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Crown fractures involving dentin initially cause localized pulpal inflammation (1,2). Protective mechanisms exist in healthy pulp to avoid "self strangulation" (1, 3, 4).
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Figure 2
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INTRODUCTION:
The human dental pulp plays a role in both tooth formation and maintenance. Pulpal inflammation can occur from microbial, mechanical, or chemical irritants. The presence of microorganisms exerts a major role in the induction of pulpal inflammation. The pulp may be exposed to microorganisms suddenly due to trauma or more slowly by an advancing carious lesion. The bacteria present in a carious lesion cause pulpal effects long before they physically invade the pulp proper. Bacterial byproducts, diffusing through the dentinal tubules into the pulp, cause the local infiltration of chronic inflammatory cells, such as macrophages, lymphocytes and plasma cells. As bacteria actually invade the pulp, pulpal inflammation becomes acute with polymorphonuclear leukocytes the dominant inflammatory cell. Depending upon the severity of the pulpal insult, the pulp may exhibit a transient inflammation (reversible pulpitis).
The local response of the pulpal microvasculature allows the pulp to avoid self strangulation from the collapse of apical vessels. If pulpal protective mechanisms are overwhelmed, a irreversible pulpitis will occur which will proceed to total necrosis. The ability of the pulp, through physiologic mechanisms, to respond to a less than overwhelming assault is reviewed on the following one-page graphic illustration. True/False questions are provided for self-assessment.
Content questions should be directed to: Dr.
Max Hutchins
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The University of Texas Health Science Center at Houston (UT-Houston)
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