Pain from tissue insult involves a complicated array of physiologic and chemical changes that lead to perception in the brain.
Understanding the terminology and physiology and managing oral pain in our patients is the focus of this series.
This month, the concepts of nociception, peripheral sensitization and central sensitization will be discussed as they relate
to patient management.
These mechanisms allow the practitioner to make analgesic choices for individual patients, taking into account the type, duration
and severity of the pain. Consistent, reliable results can be obtained using pre-emptive and multimodal analgesia
The second part of the series will provide a detailed description of regional nerve blocks for oral surgery. The third will
describe agents commonly used for analgesia. A discussion of chronic-and cancer-pain management and clinical use of constant-rate
infusions will conclude the series.
Nociception involves the processing of noxious stimuli, resulting in the brain's perception of pain (Figure 1). Transduction,
transmission and modulation are the components.
Figure 1: Transduction, transmission and modulation are components of nociception, the processing of noxious stimuli, which
results in the brain's perception of pain.
The conversion of a noxious stimulus (mechanical, chemical or thermal) into electrical energy by a peripheral nociceptor or
free afferent nerve ending is termed transduction. The propagation of the impulse from the site of oral injury through primarily
trigeminal afferents is referred to as transmission. The nerve fibers responsible for sharp pain are the fast A-delta fibers.
Dull, throbbing pain is caused by stimulation of slow C fibers. A-beta nerve fibers are tactile and consequently have a much
lower threshold. Neurons from these fibers synapse with nociceptive-specific and wide-dynamic-range neurons in the medulla's
nucleus caudalis, resulting in modulation. Nucleus caudalis tissue is very similar to that of the spinal cord dorsal horn
that modulates pain from areas other than the oral cavity. Exitory neuropeptides, like glutamate and substance P, are active
in the synapse and facilitate the pain signals by binding to their receptors on these neurons. Concurrently, endogenous (opioid,
serotonergic and noradrenergic), descending analgesic systems serve to decrease the nociceptive response.
Following surgical manipulation of the oral cavity we can expect a greatly enhanced postoperative nociceptor response to any
additional stimulation. The resulting enhanced response is termed peripheral sensitization (hyperalgesia).
Primary hyperalgesia is the term for peripheral hyperalgesia at the actual site of the injury. The damaged tissue releases
a number of compounds, including ATP, potassium ions, hydrogen ions, prostaglandins, bradykinin and nerve growth-factors.
Lymphocytes, monocytes, macrophages and mast cells are attracted to the site. These inflammatory cells then release cytokines
that amplify and potentiate inflammation. Histamine is among the list of cytokines released that enhance vasodilation, causing
plasma extravasation into surrounding tissues. As a result this "sensitizing soup" of substances extends beyond the actual
site of tissue injury into the surrounding normal tissue, producing secondary hyperalgesia. Now even non-noxious stimuli,
such as touch, can produce pain at and around the site of injury (allodynia).
Left untreated, peripheral sensitization produces similar changes in the wide dynamic range neurons of the nucleus caudalis
producing a state called central sensitization or "windup."