Pulpitis is among the most common causes of orofacial pain. Irreversible pulpitis is characterized by a painful pulpal response to thermal stimuli that does not subside immediately after the removal of the stimulus. Pain is an unpleasant experience associated with actual or potential tissue damage. It is a subjective concept, and the pain threshold varies among individuals. Cold and heat tests are widely used in clinical practice for the diagnosis of symptomatic irreversible pulpitis. Irreversible pulpitis mainly arises due to infection caused by dental caries or the loss of restoration seal and microleakage. Dental trauma, pulpal exposure, and cracks can also lead to severe pulpitis. Pain associated with irreversible pulpitis accounts for more than 45% of emergency dental visits.
A detailed history of pain is essential, and it is often described as severe, dull, and throbbing; this pain may intensify with thermal or postural changes and can result in sleep disturbance. It tends to persist for prolonged periods (minutes to hours) and is generally unresponsive to analgesics. Patients also frequently report spontaneous and unprovoked sharp pains.
Achieving successful pulpal anesthesia during endodontic treatment of teeth with symptomatic irreversible pulpitis is critical for patient pain and stress management; however, this remains particularly challenging in mandibular teeth due to the inability of the inferior alveolar nerve block (IANB) to consistently provide profound anesthesia. Increased acidity in the inflamed pulp reduces the amount of basic anesthetic penetrating the nerve membrane, thereby delaying or preventing pulpal anesthesia.
Lip numbness, which typically occurs after anesthesia (i.e., loss of tactile sensation due to A-beta fiber blockade), is commonly regarded as an indicator that pulpal pain fibers (C and A-delta fibers) are also anesthetized and that the patient is ready for treatment. However, while tactile sensation is mediated by A-beta fibers, pain is transmitted via C and A-delta fibers. Local anesthetics block thick myelinated A-beta fibers and thin myelinated A-delta fibers at much lower concentrations than unmyelinated C fibers. Local anesthetics thus preferentially block myelinated fibers. Therefore, in healthy patients, the presence of lip numbness may be misleading for assessing pulpal anesthesia success. In patients with irreversible pulpitis, this method of assessment is even more unreliable.
\*\*Several theories have been proposed to explain anesthetic failure. However, no studies have investigated the relationship between systemic inflammation and anesthetic success. The systemic immune-inflammation index (SII) is a novel biomarker for inflammation and is calculated as (neutrophil count × platelet count) / lymphocyte count. In our study, SII and other inflammatory markers will be evaluated. These additional inflammatory indices are as follows:
Aggregate index of systemic inflammation (AISI) = neutrophil count × monocyte count × platelet count / lymphocyte count
Platelet-to-lymphocyte ratio (PLR) = platelet count / lymphocyte count
Systemic inflammatory index (SII) = neutrophil count / PLR
Neutrophil-to-lymphocyte ratio (NLR) = neutrophil count / lymphocyte count.\*\*
Moreover, although NLR has been used as an indicator of the inflammatory response in numerous diseases, there are insufficient data regarding its effects on postoperative pain, which is closely associated with acute inflammation. The aim of this study is to investigate the effects of systemic inflammatory markers, particularly SII and NLR, on the success of inferior alveolar nerve block anesthesia and postoperative pain.
