A. Hypothesis:

As in other tissue, injury to the tooth pulp initiates inflammation. But, because the pulp is encapsulated in rigid walls of dentine and enamel, the normal response of edema is impossible and instead pulp tissue pressure rises. This increased tissue pressure causes compression of tooth pulp venules and veins, leading to a rise in postcapillary vascular resistance. The higher Rv in turn causes capillary hydrostatic pressure to increase, which leads to higher tissue pressure, which further increases R v , establishing a vicious cycle. The increased Rv will eventually cause ischemia, hypoxia (which will contribute to further tissue pressure increase), and, eventually, necrosis or pulp death.

B. Evidence For

1. The injured pulp often becomes necrotic even when the injury is only minor

2. Intrapulpal pressure can become very high (up to 80 mmHg) in pulpitis

C. Evidence Against

1. injured pulp sometimes recovers completely

2. the pressure rise away from the site of injury is less than at the injured site

3. If the pulp is large and healthy, the pulp pressure rises initially after injury but then declines to its normal level