Local anesthetics are drugs that are deposited directly in the vicinity of the target nerve fibers (precisely in the local area) and act by blocking the sodium channels intercalated on the path of neuronal axons. This inhibits the transmission of information from everything in the vicinity such as the pulp of all the teeth of an arch.
As already considered in previous works, pH plays a critical role in the pharmacodynamics of local anesthetics. Local dental anesthetics are marketed in the form of a 1.8 mL tube. The pH of the anesthetic solution contained therein is set at an acidity level 1000 times higher than the physiological level (4.5) to prolong the preservation of the product.
The pharmacological molecule is present in the vial tube in a water-soluble cationic form (RNH+) and in a fat-soluble deionized form (RN). The latter is the only one able to cross the membranes. The actual action on the channels, on the other hand, again requires the cationic form.
The relationship between the basic form and the ionized form is linked to the dissociation constant (pKa) of the compound, which is a measure of the affinity to hydrogen ions. When pKa is at the same level as pH, the two forms are also in equilibrium at 50%. The Henderson-Hasselbalch equation expresses the relationship between pH and pKa. In an acidic environment such as that of the vial tube, a strong imbalance in favor of the ionized form is observed. The interaction with the nerve fiber is, therefore, mediated by the action of the organism’s buffer systems, and this leads to an extension of the onset time. In the case of an acidic tissue environment, typically undergoing inflammation, the process is further hindered.
The acidity of the solution would also be related to another discomfort, i.e., the typical feeling that accompanies the urethra administration of the drug.
On this basis, several studies have suggested acting on the pH of the solution, typically adding sodium bicarbonate (in a ratio of 1 mL for every 9 mL of solution) just before administration. The buffering would lead to a reduction in latency and also in the burning perceived by the patient.
Some studies also argue that the CO2 released by the reaction induced by the addition of bicarbonate would even enhance the action of the molecule, through 3 distinct mechanisms: direct action on the nerve, concentration of the molecule, and reduction of local pH (as mentioned, the deionized molecule must be converted back into ionized form).
Recently, Kattan and colleagues have wondered if buffering can be an effective method in the framework of the most unfavorable onset anesthesia or inflammation of the pulp.
The authors have carried out a systematic review of the literature, updated at the end of 2016 (and interesting for the previous 10 years) and published in early 2019 in the journal of the American Dental Association (JADA).
The final evaluation was carried out in 5 randomized clinical trials and established that buffered local anesthesia was more effective than non-buffered anesthesia on the dental elements of the upper or lower jaw, with pulpal involvement. A likelihood ratio of 2.29 was also defined, meaning that the probability of achieving effective anesthesia doubles with the addition of a buffer.