Tooth Pulp Tissue Pressure and Hydraulic Permeability.

• If the pulp chamber of a tooth is penetrated, either by dental caries, or by a dental drill, inflammation and eventual death of the pulp tissue usually follows. While a long interval may elapse before degeneration is complete, necrosis is an almost inevitable consequence of pulpal penetration. A current explanation in the dental literature for this phenomenon is as follows. The application of noxious stimuli to the dental pulp is followed by inflammation of pulp tissue and release of fluid into the dental pulp canal. This is supported by histologic evidence of edema, polymorphonuclear leukocytic infiltration, and disorganization of the odontoblastic layer in pulp of teeth which have been diagnosed as suffering from acute pulpitis. The inability of the dental pulp to recover easily from noxious stimulation is claimed to be due to the rigidity of the dentin walls surrounding the pulp. This rigidity prevents swelling characteristic of soft tissue inflammation and thus leads to an increase in pulp tissue pressure. The pressure eventually becomes high enough to impede circulation, causing pulpal ischemia and subsequent tissue death. The vascular supply of the dental pulp enters and leaves through tiny foramina at the apex of the root and thus is particularly susceptible to the increased tissue pressure. While this hypothesis seems reasonable, it can neither be completely accepted nor rejected due to the lack of information about the mechanical and hydrostatic forces within the pulp chamber.