Dental Anesthesia in the Presence of Inflammation: Pharmacological Mechanisms for the Reduced Efficacy of Local Anesthetics - Abstract
Profound analgesia or pain control with local anesthetics is essential for most dental procedures in endodontic and restorative treatments, tooth extraction and minor oral surgery. However, dental clinicians frequently experience that it is difficult for infiltration and nerve block injections to achieve clinically acceptable local anesthesia in the presence of pupil and periapical inflammation. Local anesthetic failures are well documented especially when treating mandibular posterior teeth with inflamed pulps. Successful local anesthesia of patients with irreversible pulpitis is continually challenging in dentistry. A variety of mechanisms have been
hypothetically proposed for such reduced efficacy of local anesthetics. Among mechanistic hypotheses, technical injection errors, mandibular anatomical variations and psychological factors are not directly related to inflammation, whereas inflammation-relevant mechanisms include alterations in the peripheral vascular system, nociceptive neurons, drug targets and central nervous sensitivity. However, none of them explain all aspects of dental anesthetic failures. The reasons why inflammatory lesions affect local anesthetics to decrease their effects are not fully understood. This article reviews pharmacological mechanisms underlying the failures of dental local anesthesia by focusing on inflammatory acidosis, products and mediators which
would modify the properties of anesthetic agents and their targets. From a pharmacological point of view, different strategies to enhance the efficacy of local anesthetics are discussed about the drug selection based on structural and physicochemical characteristics, the buffering of injection solutions, the promotion of peripheral vasoconstriction, the premedication with anti-inflammatory drugs, the use of drug delivery systems, the application of new dental anesthetics, and the supplementary anesthesia.