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C H A P T E R 15

Pharmacotherapy of acute orofacial pain


Yair Sharav and Rafael Benoliel

Introduction 349 Dipyrone 365


Modes of Action of NSAIDs 351 Omega-3 Fatty Acids 365
Adverse Effects of NSAIDs 351 Opioids 365
Efficacy of NSAIDs 356 Analgesic Drug Combinations 367
Paracetamol (Acetaminophen) 363 Strategy of Pharmacotherapy of Acute Orofacial Pain 370

1. Introduction analgesics should have, at least, three major aims (Camu


et al 2003):
The aim of drug therapy for acute orofacial pain is to a. Prevention of sensitization of peripheral nociceptors;
relieve pain with maximum efficacy and minimum side b. Interruption of the neuronal transmission of
effects. Ideally an analgesic drug provides significant nociceptive signals; and
relief across all pain severities, has minimal side effects, c. Attenuation of the nociceptive message in the spinal
has few drug interactions and is convenient to administer cord and other parts of the CNS.
(e.g. single daily oral dose, pleasant tasting and rapid
absorption). However, ideal drugs do not exist and when Acute pain is usually activated by an inflammatory
administering an analgesic consideration should be given process, so the initial strategy to attain analgesia normally
to pain severity, the patient’s medical background, involves the use of anti-inflammatory drugs. However,
susceptibility to the various side effects (e.g. gastrointesti- the sole inhibition of inflammation may not be sufficient
nal, cardiac, renal) and the fact that patients may differ to obtain adequate analgesia. NSAIDs, including selective
genetically in their response to analgesics (Lotsch and cyclo-oxygenase enzyme (COX)-2 inhibitors, combine
Geisslinger 2006). The orofacial pain practitioner needs anti-inflammatory effects with analgesic actions on periph-
to thoroughly understand the different classes of analge- eral and central neural targets (Cashman 1996). The clinical
sics and their mechanisms of actions and appreciate that success of NSAIDs has resulted in their widespread use,
drug actions and interactions change with the patient’s and it is estimated that over 30 million patients ingest these
age and medical status (Kim et al 2004). Analgesics also for the treatment of pain and inflammation on a daily basis
have gender-specific adverse events and complex phar- (Singh and Triadafilopoulos 1999).
macological interactions with other medications that the
patient may be taking. This chapter reviews the clinical
1.1. The Inflammatory ‘Soup’
pharmacology of drugs usually employed in the treat-
ment of acute orofacial pain. Since long-term nonsteroidal The ‘inflammatory soup’ is a mixture of bioactive mole-
anti-inflammatory drugs (NSAIDs) and opioids are some- cules (bradykinin, histamine, prostaglandins, neurotro-
times employed in the management of persistent or recur- phins and interleukins) produced in response to a variety
ring orofacial pain conditions, relevant ‘chronic’ adverse of stimuli and tissue injury. These molecules may act per-
effects are also discussed. ipherally on primary afferents by direct and/or indirect
The pathogenesis of acute and chronic pain involves effects. Direct effects include activation of primary afferent
peripheral as well as central mechanisms of sensitization nociceptors and sensitization of nociceptors that result in
that are associated with plasticity in primary sensory increasing responses to various stimuli. Indirect effects
and dorsal horn neurons (Woolf and Salter 2000). The are mediated by leukocytes and the sympathetic nervous
local inflammatory response leads to heightened sen- system. These effects may involve increased excitability
sitivity and activity of local nociceptors and to distant of dorsal horn neurons (DHNs), leading to altered des-
effects at the level of the central nervous system (CNS). cending pain control mechanisms and adaptive changes
A mechanism-based strategy for pain control with in the thalamus, cortex and higher centres (Millan 1999).