No abstract

This article deals with blood flow and tissue pressure changes in the inflamed dental pulp. While detailed patho-physiological studies of the circulation in the inflamed pulp are still partly lacking, available data from studies of the normal pulp tissue are also discussed. Knowledge of the normal physiological adjustments may indicate which circulatory changes would take place during inflammation. One of the focal points in the present article is how a localized increased tissue pressure may persist in the inflamed area without a circumferential spread to the rest of the pulp. The article is organized in the following manner: First a short review is given of the vascular changes during inflammation in general. Then available data from morphological and functional studies of the pulpal circulation are treated in some detail. Particular attention is given to the transcapillary fluid flow and the so-called 'self-strangulation theory'. The effect of a localized increased tissue pressure on pulpal blood flow is thereafter discussed.

Blood flow in the external cartoid artery (ECBF) and dental pulp (PBF) was measured during arterial infusion of vasodilators (isoprenaline, papaverine, acetylcholine and bradykinin). Systemic arterial pressure (AP) and local arterial pressure of the teeth (LAP) were recorded in a femoral and the lateral nasal artery respectively. All four vasodilators were found to increase ECBF and simultaneously reduce lateral nasal arterial pressure--or in other words-to STEAL" PERFUSION PRESSURE FROM THE TEETH. AP remained practically unchanged whereas PBF was variably affected. During infusion of isoprenaline PBF decreased on average by 19% of control. Papaverine nearly doubled PBG, while bradykinin caused no consistent change. Great pulpal flow variations were often recorded during constant acetylcholine infusion rate. The variable effect of the four vasodilators on PBF could partly be explained by the fall in LAP. Calculated pulpal resistance (LAP/PBF) showed no consistent change during isoprenaline infusion, bradykinin caused a slight fall and papaverine reduced LAP/PBF by 49%. The experiments demonstrate that due to the "stealing" of dental perfusion pressure caused by vasodilation in the neighbouring tissues, the effect of vasodilators on pulpal resistance vessels cannot be estimated without knowledge of the pressure in the small arteries directly feeding the teeth.

The present summary is a review and a discussion of the following papers (I-V), submitted as partial fulfillment of the requirements for the degree of Doctor Odontologiae at the University of Bergen. I. Blood flow in the dental pulp in dogs measured by local H2 gas desaturation technique. Arch. Oral Biol. 1975, 20, 73-79. Co-author: K. Aukland II. The effect of variations in arterial blood pressure and baroreceptor reflexes on pulpal blood flow in dogs. Arch. Oral. Biol.1975, 20, 345-349 III. Effect of vasodilating drugs on external carotid and pulpal blood flow in dogs: "Stealing" of dental perfusion pressurE. Acta Physiol. Scand. 1976, 97, 75-87 IV. Nervous control of blood flow in the dental pulp in dogs. Acta Physiol. Scand. 1978, 104, 13-23. Co-author: G. Naess V. Microvascular pressure in the dental pulp and gingiva in cats. Acta Odontol. Scand. 1979, 37, 161-168. Co-author: G. Naess Other papers are referred to in the conventional manner.

Pressure in selected microvessels was measured directly on the exposed coronal or apical pulp in one of the upper canine teeth or on the gingiva in a total of 36 cats. The vessels were punctured with glass micropipettes, diameter 1-4 micrometer, and the pressure measured with a modified Wiederhielm servocontrolled counter-pressure technique. Pressures in corresponding vessels in coronal and apical pulp were similar. The pressure in pulpal arterioles, diameter 10-70 micrometer averaged 43 mm Hg, or 36% of mean systemic arterial pressure (PA), while pressure in the pulpal venules, diameter 10-80 micrometer, was on an average 19 mm Hg or 16% of PA. Capillary pressure measured in the coronal pulp averaged 35 mm Hg. Mean arterial systemic pressure was 124 mm Hg. The total vascular pressure drop within the pulp was only 20% of the total systemic arteriovenous pressure difference. Accordingly, only one fifth of the vascular resistance governing pulpal blood flow is situated within the pulp itself. This means that blood flow in the dental pulp in cats may be influenced by mechanisms located extrapulpally. In gingiva only venular pressure was measured, which averaged 19 mm Hg.