Penetration of Sodium Hypochlorite Modified with Surfactants into Root Canal Dentin

Abstract The aim of this study was to evaluate the effect of concentration, exposure time and temperature of sodium hypochlorite (NaOCl) added with surfactants on its penetration into dentinal tubules. Sixty-five extracted human permanent maxillary anterior teeth with single canals were prepared by ProTaper SX hand-operated instruments. The teeth were then sectioned perpendicular to the long axis. The crowns and apical thirds of all the teeth were removed. The remaining roots were processed into 4-mm-long blocks and stained overnight in crystal violet. One hundred and thirty stained blocks were further split into halves and treated by nine different types of NaOCl-based solutions. Three solutions were added with surfactants (Hypoclean, H6, Chlor-Xtra) and the others were regular hypochlorites at increasing concentrations (1%, 2%, 4%, 5.25%, <6%, 6% NaOCl) from different brands. The dentin blocks were exposed to the solutions for 2, 5, and 20 min at 20 °C, 37 °C and 45 °C, respectively. The depth of NaOCl penetration was determined by bleaching of the stain and measured by light microscopy at 20&#61472;&#61620; and 40&#61620;. Statistical comparisons were made by using a generalized linear model with Bonferroni's post-hoc correction. The shortest penetration (81±6.6 &#956;m) was obtained after incubation in 1% NaOCl for 2 min at 20 °C; the highest penetration (376.3±3.8 &#956;m) was obtained with Chlor-Xtra for 20 min at 45 °C. Varying NaOCl concentration produced a minimal effect while temperature and exposure time had a significant direct relationship with NaOCl penetration into dentinal tubules, especially those with lowered surface tension. The exposure time and temperature of sodium hypochlorite as well as the addition of surfactants may influence the penetration depth of irrigants into dentinal tubules

Reappraising neuropathic pain in humans—how symptoms help disclose mechanisms

Neuropathic pain--that is, pain arising directly from a lesion or disease that affects the somatosensory system--is a common clinical problem, and typically causes patients intense distress. Patients with neuropathic pain have sensory abnormalities on clinical examination and experience pain of diverse types, some spontaneous and others provoked. Spontaneous pain typically manifests as ongoing burning pain or paroxysmal electric shock-like sensations. Provoked pain includes pain induced by various stimuli or even gentle brushing (dynamic mechanical allodynia). Recent clinical and neurophysiological studies suggest that the various pain types arise through distinct pathophysiological mechanisms. Ongoing burning pain primarily reflects spontaneous hyperactivity in nociceptive-fibre pathways, originating from 'irritable' nociceptors, regenerating nerve sprouts or denervated central neurons. Paroxysmal sensations can be caused by several mechanisms; for example, electric shock-like sensations probably arise from high-frequency bursts generated in demyelinated non-nociceptive Aβ fibres. Most human and animal findings suggest that brush-evoked allodynia originates from Aβ fibres projecting onto previously sensitized nociceptive neurons in the dorsal horn, with additional contributions from plastic changes in the brainstem and thalamus. Here, we propose that the emerging mechanism-based approach to the study of neuropathic pain might aid the tailoring of therapy to the individual patient, and could be useful for drug development.Neuropathic pain - that is, pain arising directly from a lesion or disease that affects the somatosensory system - is a common clinical problem, and typically causes patients intense distress. Patients with neuropathic pain have sensory abnormalities on clinical examination and experience pain of diverse types, some spontaneous and others provoked. Spontaneous pain typically manifests as ongoing burning pain or paroxysmal electric shock-like sensations. Provoked pain includes pain induced by various stimuli or even gentle brushing (dynamic mechanical allodynia). Recent clinical and neurophysiological studies suggest that the various pain types arise through distinct pathophysiological mechanisms. Ongoing burning pain primarily reflects spontaneous hyperactivity in nociceptive-fibre pathways, originating from 'irritable' nociceptors, regenerating nerve sprouts or denervated central neurons. Paroxysmal sensations can be caused by several mechanisms; for example, electric shock-like sensations probably arise from high-frequency bursts generated in demyelinated non-nociceptive Aβ fibres. Most human and animal findings suggest that brush-evoked allodynia originates from Aβ fibres projecting onto previously sensitized nociceptive neurons in the dorsal horn, with additional contributions from plastic changes in the brainstem and thalamus. Here, we propose that the emerging mechanism-based approach to the study of neuropathic pain might aid the tailoring of therapy to the individual patient, and could be useful for drug development. © 2013 Macmillan Publishers Limited