The dental hygienist’s guide to dental pain and pain management

Editor’s note: This is part one of a two-part series. Read part two here.

For more than 25 years, I have had the pleasure of working with and teaching dental hygienists. It has been an amazing experience and an honor to be among some of the most talented and caring health-care professionals as they perform procedures to restore their patients to good oral health. So, I must admit it surprises me that some people still avoid visiting their dental hygienist on a regular basis. Why? 

Pain is a powerful motivator and demotivator for patients to seek treatment from their dental hygienist. Pain, or fear of pain, keeps some patients from seeing us, which leads to poor oral health outcomes and adherence to dental hygiene treatment plans. Thus, proper management of dental pain and fear is essential to ensure our patients’ therapeutic success.

More by Tom Viola:

• Just breathe! Why asthma matters to the dental hygienist
• Antineoplastic agents and their oral adverse effect

But managing pain requires an understanding of its complexity and the factors that determine its expression. In this two-part column, we will explore the challenges of effectively and efficiently managing dental pain. In this installment, we will discuss the concept and physiology of pain and the pharmacology of the agents used in its management.

What is pain?

Pain is often described as an unpleasant sensory and emotional experience that results from either actual or perceived tissue damage and is the result of a variety of physical and psychological responses to that tissue damage. Since most dental procedures involve damage to the oral tissues, pain and inflammation are inevitable results of dental therapy.¹ Analgesic agents are often prescribed to dental patients to relieve that pain and inflammation. While analgesics are typically prescribed for use after procedures, these agents are sometimes also prescribed before procedures to reduce postprocedural pain. So, how do they work?

How does pain occur?

The process by which pain impulses are transmitted to the brain occurs via specialized receptors called nociceptors. Nociceptors are afferent sensory neurons that respond to mechanical stimuli, including pressure, temperature, and chemical stimuli (from inflammatory mediators). Nociceptors normally have a high depolarization threshold. To activate, nociceptors would have to experience strong stimuli that would normally damage otherwise healthy tissue.

How do prostaglandins make this worse? Prostaglandins amplify the pain message by increasing the sensitivity of nociceptors so that they are activated at lower-intensity stimuli.² Pain impulses are transmitted from the site of tissue damage along ascending peripheral nerve fibers to the dorsal horn in the spinal cord, where they synapse with central neurons to transmit the message to the brain stem. Transmission is assisted by excitatory neurotransmitters, such as substance P. The pain impulse is then transmitted to the brain stem and thalamus and then sent to the somatosensory cortex and limbic system, where perception of pain takes place.

The somatosensory cortex is the first level of conscious pain perception and is responsible for the perception and interpretation of pain impulses, as well as identifying both the location and intensity of the pain. The limbic system is responsible for the emotional response to pain. Both the somatosensory and limbic systems assist in comparing the current pain impulse to past painful experiences.

How is pain reduced?

Interestingly, transmission of pain to the brain may be downregulated by the release of inhibitory neurotransmitters that block the transmission of pain impulses, and therefore produce pain relief. These inhibitory neurotransmitters include endogenous opioids, serotonin, gamma-aminobutyric acid (GABA), and endogenous cannabinoids.^3,4 This endogenous pain regulation may explain the high degree of variability among patients with respect to perception of pain and emotional response to pain when undergoing similar dental procedures. Ultimately, pain is very subjective and difficult to measure.

The role of NSAIDs

Nonsteroidal anti-inflammatory drugs (NSAIDs) have long been considered first-line agents in treating dental pain. While they are rapidly absorbed with relatively quick onset, the duration of action can vary greatly depending on the agent. Ibuprofen is typically dosed every four to six hours, while naproxen is typically dosed every 12 hours. NSAIDs inhibit the formation of cyclooxygenase-2 (COX-2), the enzyme responsible for producing prostaglandins, which produce pain and inflammation.⁵ However, NSAIDs may also inhibit the formation of cyclooxygenase-1 (COX-1), the enzyme responsible for producing other prostaglandins that provide numerous beneficial effects, such as protection of the gastrointestinal mucous lining, adequate blood flow to the kidneys, bronchodilation, and regulation of clotting.

Ibuprofen is still considered the gold standard against which all other analgesics for dental pain are compared. NSAIDs with shorter durations of action, such as ibuprofen, are preferred for treating acute inflammatory pain (such as dental pain), since they allow more flexible dosing to accommodate the seeming ebb and flow of pain, in addition to episodes of breakthrough pain. Other NSAIDs with longer durations of action, such as meloxicam, are preferred for treating chronic inflammatory pain (such as pain from osteoarthritis), since they offer steady-state pain control and the convenience of once or twice daily dosing.

Unfortunately, since some NSAIDs are available without a prescription, patients may be inclined to believe that they are insufficient for relieving moderate to severe pain, such as dental pain. However, studies comparing ibuprofen to placebo found that ibuprofen provided greater pain relief in patients with moderate to severe post-therapeutic dental pain.⁶ In addition, monotherapy with ibuprofen has been shown to be equal or superior to monotherapy with acetaminophen in managing dental pain.⁶ In a systematic review of 27 randomized, controlled trials, it was concluded that NSAIDs should be considered drugs of choice for managing dental pain—barring any contraindication—and if necessary could be combined with acetaminophen.⁷

Cautions with NSAIDs

Due to their ability to cause significant adverse reactions, NSAIDs should be used at the lowest therapeutic dose for the shortest duration of therapy. Since they inhibit the COX-1 enzyme, NSAIDs may cause gastrointestinal upset (by inhibiting production of the protective gastrointestinal mucosal lining), as well as increase the risk of gastrointestinal bleeding (by impairing platelet function).^8-10

NSAIDs may also increase the risk for serious cardiovascular thrombotic events, including heart attack and stroke.¹⁰ By decreasing the synthesis of prostaglandins, NSAIDs may cause fluid retention, exacerbating cardiovascular disease and decreasing the effects of antihypertensive agents; they can also interfere with the cardioprotective effects of low-dose aspirin.^8,11 NSAIDs can cause severe skin reactions, such as Stevens-Johnson syndrome, and may precipitate bronchospasm in susceptible patients with asthma.^8,12,13

The role of dental hygienists

Pain may serve as a demotivator for patients to seek dental hygiene treatment, leading to poor outcomes for those patients in maintaining oral health. However, dental hygienists can help patients conquer this fear and improve outcomes by understanding the complexity of pain, factors that determine its expression, and the agents employed in pain management.

In part two, we will explore the pharmacology of other agents used to manage dental pain, including acetaminophen, opioid analgesics, and anesthetic agents. 

Editor's note: This article appeared in the August 2022 print edition of RDH magazine. Dental hygienists in North America are eligible for a complimentary print subscription. Sign up here.

References

1. Hahn CL, Liewehr FR. Relationships between caries bacteria, host responses, and clinical signs and symptoms of pulpitis. J Endod. 2007;33(3):213-219. doi:10.1016/j.joen.2006.11.008
2. Bergenholtz G. Inflammatory response of the dental pulp to bacterial irritation. J Endod. 1981;7(3):100-104. doi:10.1016/S0099-2399(81)80122-7
3. Stein C. The control of pain in peripheral tissue by opioids. N Engl J Med. 1995;332(25):1685-1690. doi:10.1056/NEJM199506223322506
4. Guindon J, Hohmann AG. Cannabinoid CB2 receptors: a therapeutic target for the treatment of inflammatory and neuropathic pain. Br J Pharmacol. 2008;153(2):319-334. doi:10.1038/sj.bjp.0707531
5. Huber MA, Terezhalmy GT. The use of COX-2 inhibitors for acute dental pain: a second look. J Am Dent Assoc. 2006;137(4):480-487. doi:10.14219/jada.archive.2006.0220
6. Moore PA, Ziegler KM, Lipman RD, Aminoshariae A, Carrasco-Labra A, Mariotti A. Benefits and harms associated with analgesic medications used in the management of acute dental pain: an overview of systematic reviews. J Am Dent Assoc. 2018;149(4):256-265. doi:10.1016/j.adaj.2018.02.012
7. Aminoshariae A, Kulild JC, Donaldson M, Hersh EV. Evidence-based recommendations for analgesic efficacy to treat pain of endodontic origin: a systematic review of randomized controlled trials. J Am Dent Assoc. 2016;147(10):826-839. doi:10.1016/j.adaj.2016.05.010
8. Risser A, Donovan D, Heintzman J, Page T. NSAID prescribing precautions. Am Fam Physician. 2009;80(12):1371-1378.
9. Choi KH, Kim AJ, Son IJ, et al. Risk factors of drug interaction between warfarin and nonsteroidal anti-inflammatory drugs in practical setting. J Korean Med Sci. 2010;25(3):337-341. doi:10.3346/jkms.2010.25.3.337
10. Pelletier JP, Martel-Pelletier J, Rannou F, Cooper C. Efficacy and safety of oral NSAIDs and analgesics in the management of osteoarthritis: evidence from real-life setting trials and surveys. Semin Arthritis Rheum. 2016;45(4 Suppl):S22-S27. doi:10.1016/j.semarthrit.2015.11.009
11. Meek IL, Vonkeman HE, Kasemier J, Movig KLL, van de Laar MAFJ. Interference of NSAIDs with the thrombocyte inhibitory effect of aspirin: a placebo-controlled, ex vivo, serial placebo-controlled serial crossover study. Eur J Clin Pharmacol. 2013;69(3):365-371. doi:10.1007/s00228-012-1370-y
12. Simon RA. Adverse respiratory reactions to aspirin and nonsteroidal anti-inflammatory drugs. Curr Allergy Asthma Rep. 2004;4(1):17-24. doi:10.1007/s11882-004-0037-x
13. Kasemsarn P, Kulthanan K, Tuchinda P, Dhana N, Jongjarearnprasert K. Cutaneous reactions to nonsteroidal anti-inflammatory drugs. J Drugs Dermatol. 2011;10(10):1160-1167.