So does lack of pulpal anesthesia following an IANB indicate that the injection technique was inadequate or that the block was “missed”? In most cases, especially when positive lip sign has been achieved, the answer is no. Studies using ultrasound and radiographs to assure accurate positioning of the needle next to the neurovascular bundles targeted for anesthesia have shown that even with perfect needle placement, pulpal anesthesia is sometimes not achieved. In other words, don’t beat yourself up if your patient doesn’t get numb with a well placed IANB.
Several factors may contribute to continued sensitivity even following an accurate IANB. According to the authors, the best explanation may be simple anatomy. The inferior alveolar nerve that supplies innervation to all the mandibular teeth on its respective side of the jaw is arranged in layers. As the nerve travels through the mandible, the layers sequentially branch off to supply the molars, followed by the bicuspids, and finally the anterior teeth. This means that at the site of anesthetic delivery, the nerves that supply anterior teeth are in the center or at the core of the nerve bundle and are insulated to some degree from the anesthetic solution. This explanation is consistent with experimental results that show higher IANB failure rates in anterior teeth.
Several other factors that affect the successful achievement of profound numbness are related to the unique aspects of inflamed tissues. One theory posits that the increased acidity of inflamed tissues inhibits the formation of the base form of the anesthetic solution which is needed to cross the membrane of the nerve cells. The possible effect of this phenomenon when delivering local infiltration anesthesia is clear, however its relationship to IANB failures is unclear since with the IANB the solution is usually delivered at some distance from the focus of inflammation. Additionally, nerves in inflamed tissues have decreased excitability thresholds which can result in the inability of anesthetic solution to prevent impulse transmission in the nerves.
Another factor contributing to anesthesia failure in areas of inflammation has to do with the types and quantities of ion channels in the membrane of the neuron. Studies have shown that nerve cells in pulps with irreversible pulpitis show a greater expression of sodium channels than nerves in non-inflamed pulps thereby affecting their excitability. And a specific class of sodium channels called Tetrodotoxin-resistant (TTXr) channels has been shown to resist the action of local anesthetics. Lastly, patients in pain are often apprehensive. Though the mechanism is not completely understood, this apprehensiveness has been shown to actually decrease pain thresholds.
So as the preceding points make clear, there are many factors affecting our ability as clinicians to help our patients achieve profound anesthesia prior to restorative or endodontic procedures. In our next post we will address multiple helpful strategies for overcoming inadequate anesthesia as well as debunk some other common misconceptions.
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