**5. Failure of local anesthesia**

### **5.1 Anatomic factors**

While it's possible that the operator's inability to deposit anesthetic solution close to the targeted nerve would result in an insufficient blockade in both normal *Tackling Local Anesthetic Failure in Endodontics DOI: http://dx.doi.org/10.5772/intechopen.99316*

and non-inflamed states, it's also possible that a partial blockade would suffice in neurons that inflammatory mediators did not sensitize. It's crucial to understand the nerve supply to the anesthetized tissue and the anatomy of the injection site and any changes [14].

During a local infiltration at the root apex, however, the cortical bone of the body of the mandible can effectively block the anesthetic. The maxillary cortical bone is often thinner. Anesthetic diffusion is more easily achieved through this bone. Therefore, infiltration anesthesia, which is routinely used in the maxilla, would be less affected by anatomic variance. Block anesthesia is advised in the mandible because it is more predictable. Still, it demands a deeper awareness of the deep anatomy of the jaw and is more technique sensitive, which is why anesthetic failures in the mandible are more common. Inadequate local anesthetic has also been linked to accessory innervation of the mandibular teeth from various sources. The nerve to the mylohyoid muscle, in particular, has been linked to the transport of afferent fibers from the mandibular teeth [14]. The clinician has many alternatives for overcoming accessory innervations from the mylohyoid nerve, including using a blocking technique that deposits anesthetic solution higher in the pterygomandibular space.

#### **5.2 Inflammation and tissue pH**

The pH of the anesthetic solution determines the ratio of RN to RNH<sup>+</sup> . According to the Henderson–Hasselbalch equation, there are equal amounts of half-charged and half-uncharged molecules when the acid dissociation constant Pka equals the pH of the solution. In a cartridge of local anesthetic solution, both charged (RNH+ ) and uncharged (RN) molecules exist in equilibrium. The deionized lipid-soluble (RH) form penetrates the neuronal membrane and takes up H+ . RNH<sup>+</sup> within the nerve, resulting in RNH+ , which enters the sodium channel and blocks conduction. To produce anesthesia, the body buffers the pH-injected anesthetic solution to the physiological pH [15].

This becomes potentially critical since inflammation-induced tissue acidosis can cause local anesthetics to get "ion trapped." According to this theory, the low tissue pH causes a higher proportion of the local anesthetic to be held in the charged acid form of the molecule, preventing it from passing through cell membranes. This theory has been proposed as a primary cause of local anesthetic failures in situations like endodontic pain [16].

#### **5.3 Central sensitization**

Local anesthetic failures may be exacerbated by central sensitization. Increased sensitivity may enhance incoming sensory nerve impulses. There is a significant response to peripheral stimuli in central sensitization, and as a result, the IANB may allow adequate signaling to occur, leading to the experience of pain [16].

#### **5.4 Central core theory**

According to this hypothesis, the nerves on the exterior of the nerve bundle supply the molar teeth, while the nerves on the inside supply the anterior teeth. Even if the anesthetic solution is placed in the right location, it may not disperse enough into the nerve trunk to reach all nerves and cause a sufficient block. This concept may only apply to the increased failure rates associated with IANB in the anterior teeth, not the posterior teeth [17].
