warfarin (Coumadin, Jantoven). Whether using these drugs alone or in combination, prescribers must be aware of the potential safety concerns associated with all analgesic medications,
especially in light of new information promoting lower doses, shorter treatment durations, and decreased maximum recommended doses (Medical Letter, 2018).
Figure 1: Stepwise Guidelines in the Diagnosis of Orofacial Pain
THE PATHOPHYSIOLOGY OF OROFACIAL PAIN
Tissue damage stimulates the release of inflammatory mediators (such as prostaglandins, kinins, leukotrienes, substance P, and histamine) at the site of injury (Hersch & Dionne, 2016). These mediators help to initiate and subsequently magnify pain impulses that are transmitted to the central nervous system to create the perception of pain. Among these mediators, prostaglandins are especially important for sensitizing peripheral neurons. Prostaglandins are also synthesized in the spinal cord and higher brain centers in response to pain impulses and enhance pain sensitivity by recruiting additional secondary neurons that respond to the primary stimulus (Hersch & Dionne, 2016). Aspirin and related NSAIDs work at the site of tissue damage, along the spinal cord, and in the higher brain centers, preventing prostaglandin formation by inhibiting cyclooxygenase (COX) activity. COX mediates the conversion of arachidonic acid to prostaglandins. Inhibiting this enzyme essentially inhibits the inflammatory triad process of pain, inflammation, and fever. Unfortunately, arachidonic acid is converted to
cytoprotective prostaglandins as well; as a result, aspirin and related NSAIDs have side effects that include delayed wound healing, gastrointestinal mucosal damage, an increased risk of cardiovascular events, and prolonged bleeding (Hersch & Dionne, 2016). With the exception of acetaminophen, which has only minimal anti-inflammatory effects in most settings, these drugs exert a combination of analgesic, antipyretic, and anti- inflammatory effects. There are two well-known subtypes of tissue COX: COX-1 and COX-2. COX-1 is a constitutive form that promotes hemostasis (in which synthesis of the prostaglandin analogue thromboxane A2 increases platelet degranulation and adhesion), stomach mucosal integrity (where synthesis of prostaglandins protects against acid damage), and kidney function (where prostaglandins help regulate normal renal blood flow). COX-2 is a largely inducible form that promotes the formation of pro-inflammatory prostaglandins and plays a major role in mediating inflammation, pain, and fever.
PHARMACOTHERAPY FOR NOCICEPTIVE OROFACIAL PAIN: ODONTOGENIC, MUCOSAL, AND MUSCULOSKELETAL CONDITIONS
There are three major categories of nociceptive orofacial pain: odontogenic conditions (e.g., pulpitis, apical periodontitis), mucosal conditions (e.g., ulcers, lichen planus, herpes simplex), and musculoskeletal conditions (e.g., myofascial pain, temporomandibular joint capsulitis, and arthritis). With the limited exception of myofascial pain, these conditions result Preferred drugs and dosing While nociceptive orofacial pain can resolve spontaneously once the underlying cause (e.g., inflamed pulp, carious lesion, abscessed gingiva) is definitively treated, a pharmacological approach to pain management may be considered the standard of care (Figure 2; Moore & Hersch, 2013; American Dental Association, 2020).
from an identifiable source of tissue injury and inflammation and nociceptor sensitization. Pain resulting from inflammation may also have an underlying infectious etiology; therefore, both anti- inflammatory analgesics and antimicrobial medications may be required.
Based on current evidence, the drugs of choice for treating nociceptive orofacial pain are acetaminophen and an NSAID that acts by inhibiting cyclooxygenase enzymes responsible for the formation of prostaglandins that promote pain and inflammation (Aminoshariae et al., 2016). A list of currently available NSAIDs in the United States is included in Table 1 (Donaldson & Goodchild, 2019a).
EliteLearning.com/ Dental
Book Code: DHFL2624
Page 161
Powered by FlippingBook