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The purpose of this study was to determine whether use of transmitted laser light would enable a better assessment of human pulpal vitality than back-scattered light does (LDF: laser Doppler flowmetry). The experiments were carried out on ten upper central incisors in six subjects aged 23-28 years; five of the teeth were vital with no restoration, and five were non-vital. For use with transmitted laser light, the fibers within the probe of a conventional LDF apparatus were used, one for transmitting light onto the buccal surface, the other for receiving it at the palatal surface of the same tooth. For LDF, the probe was fixed at the buccal surface. Blood flow was measured at three different locations on each experimental tooth: the incisal third, the center and the cervical third of the tooth crown. In non-vital teeth, 1) output signals with transmitted laser light all registered zero, and no oscillation could be seen in recordings from any location on the tooth, but 2) LDF signals were above zero, there were regular oscillations related to heart rate, and passive increases in blood flow (corresponding to blood pressure increases) were recorded from both the center and the cervical third of the tooth, indicating that LDF registered blood flow of non-pulpal origin. In vital teeth, LDF signals were significantly higher than in non-vital teeth at each location on the tooth. At the central site on vital teeth, the output signals for transmitted laser light were about twice those seen with LDF, and passive blood flow changes corresponding to blood pressure increases were more clearly observed. These results indicated that transmitted laser light would be useful for the assessment of tooth pulp vitality both because the blood flow signals did not include flow of non-pulpal origin, and because its output signals and response to blood flow changes were clear and could easily be monitored.

Sympathetic regulation of periodontal ligament blood flow (PLBF) is well-attested; however, vasodilator responses mediated by parasympathetic nerve fibers have yet to be conclusively demonstrated in the periodontal ligament (PL). The present study was designed to determine whether parasympathetic vasodilator mechanisms do or do not exist in the cat PL. In our cats, the cervical sympathetic trunks were sectioned bilaterally prior to any stimulation in order to eliminate sympathetic effects on the vascular beds under study. Dynamic changes in PLBF, with mandibular lip blood flow (LBF) recorded for comparison, were investigated in cat mandibular canine teeth using laser Doppler flowmetry. The peripheral cut ends of the facial and glossopharyngeal nerve roots, which have been reported to contain parasympathetic nerve fibers to the oral tissues, were electrically stimulated intracranially. Such stimulation caused blood flow to increase in the ipsilateral PL and lip, without an increase in systemic blood pressure. These vasodilator responses in the PL and lip were sensitive to ganglion blockade (with hexamethonium), indicating vasodilation via activation of parasympathetic vasodilator fibers. In contrast, although intracranial stimulation of the trigeminal nerve root also induced increases in both PLBF and LBF, these were unaffected by hexamethonium, but reduced by tripelennamine, indicating antidromic vasodilatation via the trigeminal sensory nerve. These results suggest that parasympathetic vasodilator mechanisms do exist in feline PL.

The existence and nature of parasympathetic nerve fibers in the dental pulp have long been a subject for discussion; indeed, vasodilator responses mediated by such nerve fibers have yet to be conclusively demonstrated in the dental pulp. This study was designed to determine whether parasympathetic vasodilator mechanisms do or do not exist in the cat dental pulp. Dynamic changes in pulpal blood flow (PBF), with mandibular lip blood flow (LBF) recorded as a control, were investigated in cat mandibular canine teeth by means of laser Doppler velocimetry. Peripheral trigeminal afferents (see below) were stimulated electrically to confirm that somato-parasympathetic reflex vasodilatation could be induced. The peripheral cut ends of the facial and glossopharyngeal nerve roots, which have been reported to contain parasympathetic nerve fibers to the oral tissues, were then stimulated intracranially. Electrical stimulation of trigeminal afferents (in the infraorbital nerve or the maxillary buccal gingiva) caused no change in PBF but did increase ipsilateral LBF. Neither facial nor glossopharyngeal nerve root stimulation caused a PBF increase, though both elicited increases in ipsilateral LBF. The vasodilator responses in the lip were sensitive to ganglion blockade (with hexamethonium), indicating vasodilatation via activation of parasympathetic vasodilator fibers. In contrast, intracranial stimulation of the trigeminal nerve root induced increases in both PBF and LBF which were reduced by pre-treatment with tripelennamine, indicating antidromic vasodilatation via the trigeminal sensory nerve. These results suggest that a parasympathetic vasodilator mechanism is not present in feline dental pulp.

Antidromic stimulation of sensory nerves has been shown to increase blood flow in the tissue they innervate. This study was designed to determine if antidromic vasomotor responses occur in feline dental pulp and if they are mediated by branched axons supplying both tooth pulp and gingiva. Dynamic changes in pulpal blood flow (PBF) elicited by electrical stimulation, pinching, heating, and capsaicin application to the gingivae were investigated in cat mandibular canine teeth by means of Laser Doppler Velocimetry. All inferior alveolar nerve bundles and the cervical sympathetic trunk had been previously sectioned to avoid the occurrence of brainstem reflexes, e.g., somato-autonomic vasomotor reflexes. Increases in PBF were observed in seven out of 12 cats when a restricted gingival area adjacent to the canine teeth was stimulated as described, but the increases were abolished after the sensitive gingival area was painted with lidocaine jelly, a surface anesthetic. These vasodilator responses, remarkably reduced following repeated application of 30 mM of capsaicin, are considered to be induced via antidromic activation of capsaicin-sensitive nociceptive nerve fibers, presumably by axon reflex mechanisms, suggesting that nerve terminals supplying the gingiva originate from parent axons which have collaterals that innervate the canine tooth pulp.

The purpose of the present study was to investigate the nervous control of gingival blood flow in cats. Gingival blood flow was measured by laser Doppler flowmeter in 75 cats during electrical stimulation and cutting or ligation of the inferior alveolar nerve and cervical sympathetic nerve without sympathectomy or pretreatment with adrenoceptor blocking agents. Three different patterns of responses in gingival blood flow were observed following electrical stimulation of the inferior alveolar nerve in cats. In 45 cats there was an increase in blood flow, in 4 cats a decrease in blood flow, and in 7 cats a biphasic change consisting of an initial decrease and a successive increase in blood flow. The vasodilator effect was significantly reduced by pretreatment with (D-Pro2, D-Trp7.9)-substance P. tripelennamine, and methysergide. Pretreatment with cimetidine, atropine, hexamethonium, phentolamine, or propranolol had no effect on vasodilatation. The vasoconstrictor response was completely inhibited by pretreatment with phentolamine; in this case the vasodilator response appeared after stimulation of the inferior alveolar nerve. Ligation or cutting of the inferior alveolar nerve always elicited an increase in gingival blood flow. Cutting the cervical sympathetic nerve had no effect on gingival blood flow in 8 of 10 cats and caused an increase in gingival blood flow in 2 cats; however, electrical stimulation of the cervical sympathetic nerve always caused a decrease in gingival blood flow in the cats investigated. The present results suggest that cat gingival blood flow is controlled by sympathetic alpha-adrenergic fibers for vasoconstriction and by sensory fibers and mast cells for vasodilatation.

Dynamic changes of pulpal blood flow (PBF) and gingival blood flow (GBF) induced by intra-venous injection of two kinds of vasoactive drugs were observed in dogs by means of Laser Doppler Velocimetry. Intra-venous injection of norepinephrine caused PBF to increase, corresponding to the blood pressure (BP) increase, while GBF decreased. Orciprenaline sulfate caused PBF to decrease parallel to the BP decrease, as compared with a GBF increase. The effects of these vasoactive drugs lasted longer on GBF than on PBF and BP. These results indicate that the regulation of blood flow in the dental pulp is more dependent on systemic blood pressure than on local vasoconstriction or vasodilation.

This study was carried out to investigate the nervous control of the blood flow in the periodontal ligament measured by laser Doppler flowmeter. Ten adult cats were anesthetized with pentobarbital sodium (initial dose of 30 mg/kg, i.v. and maintenance dose of 5 mg/kg, i.v.). After enucleating the left eye ball, the superior alveolar nerve was exposed. The bone overlying the labial aspect of the left maxillary canine tooth root was pared away until a transparent layer of bone was left covering the periodontal ligament. A laser light from a probe of the flowmeter fixed at the tooth was beamed through the thinned bone. Three different patterns of responses were observed following the electrical stimulation of the distal end of the cut superior alveolar nerve: an increasing, a decreasing and a biphasic change of blood flow. The application of capsaicin onto the superior alveolar nerve reduced the response of blood flow increase but had no effect on the response of blood flow decrease. On the other hand, the response of blood flow decrease was completely inhibited by the pretreatment with phentolamine while the response of blood flow increase was not affected. The present results suggest that blood flow in the periodontal ligament of cats is controlled by sympathetic alpha-adrenergic fibers for vasoconstriction and by sensory fibers for vasodilation.