Functionality of Orofacial Branches Feeding: Salivary Glands, Dental Pulp and Intraoral Anesthetic Field

Abstract

Branches of the external carotid artery support the integrity and functionality of oral tissue beds with critical impact in both health and disease. Stenosis or occlusion of the common carotid artery or of the tributaries – facial, maxillary, lingual arteries and dental pulp arterioles – contribute to the etiology of disease, in particular in the setting of ischemic and metabolic syndrome disorders of orofacial tissues. Blood flow through salivary glands is largely controlled via autonomic innervation, and endothelium-derived vasodilating and vasoconstricting substances. Endothelial cells actively regulate basal vascular tone and vascular reactivity in physiological and pathological conditions. In the resting state, blood flow in rat submandibular gland is largely controlled by sympathetic nerves, but vascular resistance is rapidly lowered by parasympathetic activity. Increase in blood flow during parasympathetic stimulation, through co-release of the neurotransmitters Ach and VIP, has been attributed to the release of endothelium-derived NO, prostacyclin and EDHF. In the glandular branch of rabbit facial artery, Ach provokes endothelium-dependent vasorelaxation, mediated by NO and prostacyclin, while VIP induces an endothelium-independent vasorelaxant effect, mediated by cAMP from vascular smooth muscle and neuronal NO. In the human submandibular artery, both transmitters produce endothelium-dependent vasodilation with different mechanisms, release of NO and prostacyclin for Ach and release of NO and EDHF for VIP. Endothelial dysfunction is commonly attributed to impaired endothelium-dependent vasorelaxation and increased vascular tone. In diabetic rat salivary glands, parasympathetic stimulation causes increased blood flow with delayed initial response. Carotid artery occlusion decreases the responsiveness of the glandular branch of the rabbit facial artery to Ach and VIP, with altered endothelial, smooth muscle and neuronal signaling. The dental pulp is a highly vascularized tissue, richly supplied with vasomotor nerves of sensory and sympathetic origin. A major difference between the vascularization of the pulp versus other tissues is the low-compliance since in the pulp vasodilation might lead to necrosis due to secondary vasoconstriction, whereas vasodilation typically in other tissues promotes survival during inflammation. Catecholamines are an important element in neuronal and humoral regulation of pulpal blood flow. Administration of catecholamines with local anesthetics causes sufficient vasoconstriction to disturb the pulpal microcirculation in dental patients. Endothelial NOS was detected in endothelium of the rat pulp microvasculature and it is likely that NO regulates pulpal vasodilation through a cGMP-dependent mechanism. NO synthesized from nerve fibers and odontoblasts could also reach endothelial and vascular smooth muscle cells of the pulp to regulate blood vessel function. In contrast to vasoconstriction of pulpal blood vessels, vasoconstriction of maxillary artery branches is useful for effective and long intraoral anesthesia. Local anesthetics are vasodilators, leading to decreased anesthetic effect, except ropivacaine which exert vasoconstriction on isolated infraorbital branches of human maxillary artery. To oppose the vasodilatory action of local anesthetics epinephrine is added to local anesthetic solutions. However, because of its absorption from injection sites, there are some limitations in the cardiovascularly compromised patients. It has been shown that clonidine, an alpha 2 adrenergic agonist, is a safer vasoconstrictor than epinephrine, providing hemodynamic stability due to its central hypotensive action.