Post-injury inflammation activates nociceptive systems and recruits normally non-nociceptive afferents into a pain processing role. During inflammation, Abeta low threshold mechanoreceptor afferents that usually mediate tactile sensation acquire properties of nociceptors, allowing them to participate in post-injury spontaneous pain and evoked abnormalities such as tenderness and pain to light touch. This study assessed the sensory consequences of post-injury inflammation following extraction of a single, lower third molar tooth. Extensive bilateral evaluations were performed in the territory of nerves assumed to be exposed to both inflammation and mechanical trauma, inflammation alone, or only the central consequences of peripheral inflammation. Testing at the distal termination of nerves assumed to be exposed to local inflammation (mental and lingual nerve territory) revealed decreased detection thresholds (P < 0.05) to electrical stimulation and to mechanical stimulation by sensitive, disposable filaments developed and validated for this application. Testing at sites of assumed inflammation and mechanical trauma (mental nerve territory) showed reduced pain thresholds to electrical stimulation. Thermal detection and pain thresholds were not altered at any location in patients, and no effects were observed in control subjects receiving only local anesthetic injections. These results in humans are consistent with recent experimental evidence that inflammatory processes alter the central consequence of activity in large-diameter Abeta touch primary afferents evoked under natural conditions by gentle mechanical stimulation. These effects result in hyperesthesia, increased sensitivity to light touch, and mechanical allodynia, pain evoked by normally innocuous stimulation of Abeta primary afferents.