Critically Appraised Topic: Antibiotics & Dental Pain

Background:

Dental pain constitutes >2,000,000 ED visits each year, and approximately 40% of patients return to the ED after their initial visit. 

Dental pain can represent a range of clinical presentations, from reversible pulpitis (ie when patients' symptoms resolve in the absence of a stimulus) to diagnoses that present with clear signs of infection such as acute apical periodontitis and acute apical abscess (which are normally treated with antibiotics). 

Those that present with irreversible pulpitis (ie fairly severe dental pain that is provoked by a stimulus but remains in the absence of that stimulus) should not have any signs of overt infection (ie fevers, swelling, purulent drainage, trismus), yet are often prescribed antibiotics in addition to analgesic medications in the ED. 

Summary of methods/findings:

Study #1 (Nagle et al): Prospective, randomized, double blind, placebo controlled study. Compared PCN 500mg PO QID x7 days with placebo (lactose) in patients with symptomatic irreversible pulpitis. Primary endpoint was reduction in pain score. Secondary endpoint was total doses of analgesia. Patients also received ibuprofen 600mg q4-6h PRN with acetaminophen with codeine 60mg q4-6h for breakthrough pain. Recorded pain scores (0-3) in diary (at rest & w/ tooth percussion) for 7 days. N=40, 20 randomized to each group, none lost to follow up (100% retention rate). No significant difference in sum pain intensity differences (p = 0.776), sum percussion pain intensity differences (p = 0.290), or total doses of analgesia (p = 0.839 for ibuprofen, 0.325 for acetaminophen with codeine). More females were randomized to the placebo group, and the study did not include development of infection as an endpoint. 

 

Study #2 (Runyon et al): Prospective, randomized, double blind, placebo controlled study. Compared PCN 500mg PO QID x7 days with placebo in patients presenting to the ED with dental pain, without overt signs of infection. Primary endpoint was reduction in pain score. Secondary endpoints were development of adverse events (including infection) at follow-up and total doses of analgesia. Patients also received 20 capsules of ibuprofen and 15 capsules of acetaminophen with hydrocodone 500/5mg to use PRN for breakthrough pain. N=195 (98 PCN group, 97 placebo group); 134 patients had follow up data available from 5 to 7 days later (68.7% retention rate, ie nearly 1/3 of patients were lost to follow up). Some follow up data was obtained from return visits or scheduled appointments, but a majority was extrapolated from a 'care everywhere' type of charting system. No significant difference in mean pain score between treatment and placebo groups (p = 0.80); no significant difference in total doses of analgesia (p = 0.94 for ibuprofen, 0.87 for acetaminophen with codeine); similar rates of infection in both groups (7 patients ie 10% in placebo group & 6 patients ie 9% in treatment group; p values: 0.24 for trismus, 0.43 for extraoral swelling, 0.49 for fever, 1.00 for intraoral swelling, 1.00 for purulence). 

Conclusions

  • Several limitations exist in each study, and neither study had a notably large sample N, especially in comparison to the annual incidence of ED visits for dental pain.   
  • Neither study demonstrated a clinically significant effect in terms of pain score reduction, total doses of analgesia, or adverse outcomes reported at follow-up. 
  • Ultimately, more prospective, blinded, placebo controlled trials are necessary to truly determine whether antibiotics reduce adverse outcomes associated with dental pain in ED patients without overt signs of infection. 

References