When caries reaches within 0.5 mm of the pulp, the immune system responds to the bacterial advance by recruiting inflammatory cells. These inflamma-tory cells migrate to the dental pulp, typically resulting in irreversible pulpitis, at which point nonsurgical endodontic therapy is the preferred treatment. But achieving an accept-able level of anesthesia in these cases is difficult.
Several studies have recommended the presurgical administration of various drugs, including dexamethasone, indomethacin and ketorolac, in addition to the usual local agents to achieve more profound anesthesia. The most popular proposed strategy involves the use of nonsteroidal anti-inflammatory drugs (NSAIDs)—in particular, ibuprofen. NSAIDs inhibit the synthesis of prostaglandins, which theoretically should increase the efficacy of local anesthetics. Not all studies have supported this hypothesis; however, these results have been based solely on clinical assessments of pain when accessing the teeth or in response to pulpal vitality tests.
Nguyen et al from the University of Washington attempted to determine the mechanism of ibuprofen on various inflammatory markers at the tooth site. They believed that identifying how ibuprofen worked in these contexts, rather than relying merely on patient feedback, would allow endodontists to make better treatment decisions in patients with irreversible pulpitis.
Their study included 38 patients (aged 21–65 years) with a diagnosis of symptomatic irreversible pulpitis in a maxillary or mandibular premolar or molar. A control group was created from 4 patients with normal, vital pulp who required endodontic treatment solely for restorative purposes. The remaining 34 patients were randomly allocated into 1 of 2 groups:
patients who took 600 mg of ibuprofen 1 hour before the initial treatment
patients who refrained from taking any NSAIDs the day of the procedure
After all caries was removed and the pulp exposed, blood from the exposed surface of the pulp was collected and assayed for levels of 6 inflammatory cytokines: prostaglandin E2 (PGE-2), interleukin-1β (IL-1β), IL-2, IL-6, tumor necrosis factor alpha (TNF-α) and interferon gamma (IFN-γ). The authors requested that patients record their level of postoperative pain (0–4 hours after anesthesia wore off) on a scale of 0 (no pain) to 10 (severe pain).
Patients who took preoperative ibuprofen had significantly lower levels of PGE-2, IL-6, TNF-α and IFN-γ than did patients who did not take preoperative NSAIDs. In some cases, levels were lower in the treatment group than in the control group. However, the 2 test groups did not demonstrate any significant difference in the level of postoperative pain.
The fact that preoperative ibuprofen reduced levels of inflammatory markers but did not affect the patients’ postoperative pain level seems curious. The study did not control for the amount of local anesthetic and the type of needle used, which may have influenced the amount of pain felt by individual patients. These results demonstrating the effect of ibuprofen on inflammatory cytokines, however, may prove valuable to practitioners in treatment planning for patients with symptomatic irreversible pulpitis.
Nguyen V, Chen Y–W, Johnson JD, Paranjpe A. In vivo evaluation of effect of preoperative ibuprofen on proinflammatory mediators in irreversible pulpitis cases. J Endod 2020;46: 1210-1216.