Dental deafferentation and brain damage: A review and a hypothesis.

In the last few decades, neurobiological and human brain imaging research have greatly advanced our understanding of brain mechanisms that support perception and memory, as well as their function in daily activities. Knowledge of the neurobiological mechanisms behind the deafferentation of stomatognathic systems has also expanded greatly in recent decades. In particular, current studies reveal that the peripheral deafferentations of stomatognathic systems may be projected globally into the central nervous system (CNS) and become an associated critical factor in triggering and aggravating neurodegenerative diseases. This review explores basic neurobiological mechanisms associated with the deafferentation of stomatognathic systems. Further included is a discussion on tooth loss and other dental deafferentation (DD) mechanisms, with a focus on dental and masticatory apparatuses associated with brain functions and which may underlie the changes observed in the aging brain. A new hypothesis is presented where DD and changes in the functionality of teeth and the masticatory apparatus may cause brain damage as a result of altered cerebral circulation and dysfunctional homeostasis. Furthermore, multiple recurrent reorganizations of the brain may be a triggering or contributing risk factor in the onset and progression of neurodegenerative conditions such as Alzheimer's disease (AD). A growing understanding of the association between DD and brain aging may lead to solutions in treating and preventing cognitive decline and neurodegenerative diseases.

The role of endothelial nitric oxide in the Substance P induced vasodilation in bovine dental pulp.

Vasodilation, an important response in neurogenic inflammation, involves release of Substance P (SP) from the sensory nerve endings. It is now well known that SP causes edema formation and vascular relaxation in nondental tissues, however, the SP vasodilatory mechanism in the dental pulp is not completely understood. Endothelium-dependent relaxation is mediated by nitric oxide (NO) release with consecutive intracellular cyclic-GMP elevation in many vascular preparations. Recently, it has been shown in different vascular systems that SP-induced vasodilation is mediated by cyclic-GMP production through different pathways involving endothelial NO or direct endothelial-independent pathways. In the present study, the role of endothelial NO in SP induced vasodilation in the dental pulp was investigated to better understand the inflammatory mechanisms. Freshly extracted bovine dental pulp was used to measure NO production. Sodium nitroprusside (SNP), L-NAME and SP were utilized to induce and to inhibit NO production in endothelial cells. Released NO byproducts were measured with chemiluminescence assay technique. The present data demonstrate that SP induces NO production by activating NOsynthase (NOS) in endothelial cells. The NOS inhibitor L-NAME blocks NO production completely. In conclusion, in the bovine dental pulp, SP-induced vascular relaxation can be mediated by inducing NOS, and subsequently NO production in endothelial cells.

Endodontic working width: current concepts and techniques.

Root canal morphology is a critically important part of conventional and surgical endodontics (root canal therapy). Many in vitro studies have recorded the scales and average sizes of root canals, but there have been few clinical attempts to determine the working width. In the absence of a study that defines what the original width and optimally prepared horizontal dimensions of canals are, clinicians are making treatment decision without any support of scientific evidence. This article provides definitions and perspectives on the current concepts and techniques to handle working width-the horizontal dimension of the root canal system-and its clinical implications.