Bupivacaine Versus Lidocaine on Inflammatory Regulation

We hypothesize that the use of the LLA bupivacaine will promote local inflammation leading to increased pain and central sensitization as evaluated by increase in pain at later time points. Hence our main hypothesis to be evaluated and statistically tested for our primary endpoint (Aim 1) is:

HO: There is no difference in mean levels of biochemical mediators of inflammation between groups.

HA: The bupivacaine group has higher levels of biochemical mediators following surgery.

Inclusion criteria

• Male or female volunteers referred for endodontic surgery willing to undergo 2 visits: 1 surgical appointment, and 1 follow-up research-related appointment
• Ages of 18 and older
• Willing to undergo observation for 1/2 hour post-operatively
• Willing to complete a 100 mm visual analog scale and record analgesic intake over 48 hrs period
• Willing to have a preoperative and postoperative biopsy on the day of surgery
• Willing to return at 48 hours post-operation to turn in completed pain diaries and for the third biopsy

Exclusion criteria

• Allergy to or other contraindications to use of aspirin, sulfites, amide anesthetics, or acetaminophen
• Chronic use of medications confounding the assessment of the inflammatory response or analgesia, for example, NSAIDS, COX-2 inhibitors, antihistamines, steroids, antidepressants
• Medications contraindicated with bupivacaine: MAO inhibitors and anti-depressants
• Diseases such as diabetes mellitus, liver disease, chronic infections, rheumatoid arthritis or any other systemic disease that compromises the immune system
• Unusual surgical difficulty