Opioid addiction has reached epidemic proportions in the United States and it is thought that the problem started with the prescription for legal pain medications by health care professionals, particularly for treating patients who had undergone surgery. To reduce the reliance on opioids in dental pain management, increase use of nonsteroidal anti-inflammatory drugs (NSAIDs) and other adjunctive techniques have emerged. The use of NSAIDs, transdermal and transmucosal patches are presented. Understanding the rational for these different approaches requires a basic knowledge of the molecular biology of dental pain.
Approaches to reduce the use of opioids for pain control in the dental patient.
Transdermal, transmucosal and other agents that can be used in the safe management of dental pain.
Pharmacology, dosages and principles of using NSAIDs to control dental pain.
Opioid addiction has reached epidemic proportions in the United States. It is thought that the problem started with the prescription for legal pain medications by health care professionals, particularly for treating patients who had undergone surgery. Since 2018, there has been an increased effort by the US Justice Department to identify and prosecute physicians involved in overprescribing opioids. Several states have passed legislation limiting opioid prescriptions. In New York State a practitioner may not initially prescribe more than a 7-day supply of an opioid medication for acute pain. There is also a mandatory online course on pain management for all licensed health care professionals in New York, with the emphasis on decreasing opioid prescription. The opioid addiction situation and new laws have led to a paradigm shift in the management of pain, particularly acute pain. This article presents strategies for pain management for dentists that will de-emphasize the reliance on opioids.
The International Association for the Study of Pain defines pain as an unpleasant sensory and emotional experience associated with actual or potential tissue damage. In reality, it is a complex neurologic condition that can be both psychologically and physically debilitating to the patient. Dental problems, from whatever cause, is commonly associated with pain that will have a significant effect on the oral health quality of life. One study reported that dental pain is the most common type of orofacial pain. Toothache appears high on many different listings of the most excruciating painful conditions experienced by humans. The fact that dental pain is intense and constant is believed to be the main reason why toothache is considered one of the worst pains a human has to endure.
Molecular bases of dental pain
Dental pain is associated with inflammatory reactions that involve different molecular mechanisms. Peripheral pain mechanisms associated with odontogenic painful conditions are similar to the mechanisms observed in all other body parts. These similarities include the type of sensory neurons involved as well as the different molecules that play a role in these processes. The pain signal is transmitted via thin fibers of unmyelinated C fibers and myelinated A fibers of primary sensory neurons to secondary order neurons in the spinal cord and finally to the S1 and S2 areas of the cortex via a relay in the thalamus. The A fibers transmit pain directly to the thalamus, generating a fast, sharp pain that can be easily localized. The C fibers reach the thalamus slower and result in a slow pain that is generally characterized as dull and aching.
Evidence shows that neuropeptides are considerably involved in the molecular mechanisms underlying dental pain. One such neuropeptide that plays a significant role in dental pain and inflammation is substance P (SP), which is found in large concentrations in the fibers that innervate the dental pulp and dentin. SP is released from C fiber nerve terminals and is involved both in inflammation and in pain. Nearly all pathologic conditions that affect oral tissues increase the production and release of SP and it plays a major role in the development and maintenance of dental pain and inflammation. In fact, extracellular levels of SP are increased in symptomatic pulp tissue diagnosed as irreversible pulpitis. The 2 key components of pulpal inflammation are microcirculation and the activation of nerve fibers. The excitation of the A∂ fibers seems to have an insignificant effect on the pulp blood flow, whereas the activation of the C fibers enhances the blood flow and causes pain by the action of neurokinins, especially SP. The dental pulp is encased within a hard firm structure and cannot expand, therefore the inflammation increases the intrapulpal pressure significantly, lowering the pain threshold of nerve endings in the pulp.
Although SP plays a major role in pulpal pain it is not the only inflammatory mediator involved in the pain mechanism. Tissue injury results in the release of inflammatory mediators from damaged cells, including ions (K + , H + ), bradykinin, histamine, 5-hydroxytryptamine, adenosine triphosphate, and nitric oxide. Activation of the arachidonic acid pathway leads to the production of prostanoids and leukotrienes. Prostaglandins are important mediators of inflammation, fever, and pain. In some situations prostaglandins contribute to pain by directly activating nociceptors, but they are generally considered to be sensitizing agents. Prostaglandins increase levels of cyclic adenosine monophosphate and may enhance nociceptor sensitization by reducing the activation threshold for tetrodotoxin resistance sodium channels via a protein kinase A pathway. They sensitize primary afferent neurons to bradykinin and other mediators and are likely to be involved at multiple sites along the nociceptive pathway.
The anxiety of having to see the dentist and the fear of dentistry can activate the pituitary-adrenal axis, leading to an increased experience of pain.
Causes of dental pain
The dental pulp, when stimulated, has only one response, which is pain. The sensory nerve fibers within the dental pulp are afferent endings of the trigeminal nerve. These nerve fibers transmit only pain. The fibers are divided into 2 categories—A∂ (myelinated) and C (unmyelinated)—based on their diameter, conduction velocity, and function. The myelinated A∂ fibers have a fast conduction speed and low stimulation threshold, are located at the dentinopulpal junction, transmit pain directly to the thalamus, and generate a sharp and stabbing pain that is easily localized. They are the first nerve fibers to transmit the pain impulse from the tooth. C fibers are unmyelinated and have a smaller diameter, slower conduction velocity, a higher threshold, and are located within the core of the pulp.
Tooth pain is caused by exposed dentinal tubules following bacterial (caries), chemical, or mechanical erosion of enamel and/or gingival recession. External stimuli causes dentinal fluid movements that transfers the stimulation to the underlying dental pulp via odontoblasts through their apical extension into the dentinal fluid running in the tubules; or via a dense network of trigeminal sensory axons intimately related to the odontoblasts. Bacterial, chemical, or mechanical stimuli can cause inflammation within the pulp. A variety of endogenous chemical mediators have been associated with inflammation and pain; these include histamine, bradykinin, 5-hydroxytryptamine, prostaglandins, and neuropeptides. These chemical mediators will cause irreversible pulpitis, pulp necrosis, and possibly periapical inflammation/infection.
Chronic periodontitis is also associated with orofacial pain. The inflammation associated with periodontitis is related to a lowered pain threshold. Periodontal pockets are a source of subgingival biofilm and function as a reservoir of periopathogenic gram-negative bacteria. The biofilm is the source of proinflammatory mediators that can lead to dull, throbbing, and persistent pain.
Like periodontal disease, pericoronitis will also present with local inflammation associated with food impaction and persistent pain.
Treatment of dental pain
The treatment of dental pain will always require a dental or oral surgical procedure, and pharmaceutical intervention will be an adjunct. Even the strongest pain medication will not produce optimal and continuous pain relief to the patient if the underlying cause of pain is not removed. The underlying cause of dental pain is the inflammatory response, which activates the pain-producing mediators ( Table 1 ). If the patient comes to the dentist with pain, there will be existing inflammation and the cause has to be removed or controlled. Generally, procedures on hard tooth structures that do not involve the pulp create little or no inflammatory response, but, when soft tissues are traumatized, a pain response can be expected
|Irreversible pulpitis||Endodontic treatment or exodontia, analgesics|
|Periapical infection||Endodontic treatment or exodontia, analgesics|
|Infection involving fascial spaces||Remove the source of infection, incision and drainage if fluctuance is present, Antibiotics and analgesics|
|Periodontitis||Root planning and scaling, adjunctive periodontal treatment, analgesics|
|Dental trauma||Tooth repositioning/reimplantation, endodontics, restoration of fractured tooth, analgesics|
|Facial trauma||Close soft tissue wounds, reduction and fixation of facial bone fractures, analgesics, antibiotics for compound fractures|
|Temporo-mandibular joint/myofascial pain||Diagnosis, analgesics, anti-inflammatory agents, muscle relaxants, dental splint, physical therapy|
|Acute necrotizing ulcerative gingivitis||Superficial debridement, antibiotics (metronidazole), chlorhexidine mouthwashes, nutritional support|
|Dry socket||Local anesthesia, irrigation, dry socket dressing, analgesics|
Apart from myofascial pain, the vast majority of dental pain will be acute pain; therefore, the management of pain in the average dental patient is not likely to be affected by central neurophysiological plasticity as it would be in the chronic pain situation. Although dental pain is usually acute pain, it is important, however, for the dentist to screen the patient for chronic pain elsewhere in the body, for example, arthritis, back pain, migraine. The patient with chronic pain problems may not respond to the treatment of dental pain as would the pain-free patient and may require adjustments to routine analgesics.
A 2011 systematic review of treatment of acute pain in adults with moderate to severe pain after oral surgery in which single-dose therapy of a single drug has been published. Several drug/dose combinations were found to reduce the postsurgical pain by over 50% (pain of 8 on the visual analog scale going to 4). Drugs and doses were: ibuprofen 400 mg, diclofenac 50 mg, etoricoxib 120 mg, acetaminophen 1000 mg plus codeine 60 mg, celecoxib 400 mg, and naproxen 500/550 mg. The longest duration of action (≥8 hours) was found to occur with etoricoxib 120 mg, diflunisal 500 mg, acetaminophen (paracetamol) 650 mg plus oxycodone 10 mg, naproxen 500/550 mg, and celecoxib 400 mg. It should be noted that all the effective drugs were NSAIDs ( Table 2 ).