Australian endodontic journal : the journal of the Australian Society of Endodontology Inc
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This prospective study investigated the frequency and intensity of postoperative pain and identified associated factors in adolescents undergoing two-visit root canal therapy. Sixty-four patients aged 11 to 18 years old presenting with molars with pulp necrosis were assigned consecutively to two visits (plus an interappointment dressing using calcium-hydroxide paste). Pain intensity was recorded on a visual analogue scale (VAS) of 0-5. ⋯ Spontaneous preoperative pain (odds ratio (OR) = 6.60; 95% confidence interval (CI) = 1.61-26.97; P = 0.009) and absence of apical perodontitis (OR = 5.65; 95% CI = 1.34-23.87; P = 0.01) were associated with postoperative pain. The frequency of postoperative pain was high, but the intensity, in general, was low, including flare-ups. The presence of spontaneous preoperative pain and absence of apical periodontitis increase the probability of suffering from postoperative pain.
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Comparative Study
Evaluation of the root dentine cutting effectiveness of the HERO 642, HERO Apical and HERO Shaper rotary systems.
Different HERO rotary systems were evaluated by pre- and postoperative images of a cross-section of their mesiobuccal root thirds with a stereoscopic magnifier (45x). Fifty mesiobuccal canals of human mandibular first molars were divided into five groups: 1--HERO 642; 2--HERO 642 and HERO Apical; 3--HERO Shaper; 4--HERO Shaper and HERO Apical; 5--NitiFlex files. The perimeter of the canal was calculated using Image Tool software (UTHSCA). ⋯ The distribution of the values of the final canal perimeter for each instrumentation method was not statistically significant in any of the thirds (P = 0.174, cervical third; P = 0.874, middle third; and P = 0.631, apical third). An increase in canal perimeter was observed in all groups. In the cervical third the greatest increase was Group 5; in the middle third, Group 4, and in the apical third, Group 2.
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Biography Historical Article
Obituary. Ronald William Rankine-Nelson (1924-2006).
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Review Case Reports
Neuropathic orofacial pain. Part 2-Diagnostic procedures, treatment guidelines and case reports.
Neuropathic orofacial pain can be difficult to diagnose because of the lack of clinical and radiographic abnormalities. Further difficulties arise if the patient exhibits significant distress and is a poor historian regarding previous diagnostic tests and treatments, such as somatosensory local anaesthetic blockade. Valuable information can be obtained by utilising the McGill Pain Questionnaire that allows the patient to choose words that describe the qualities of his/her pain in a number of important dimensions (sensory and effective). ⋯ Attention to the patient's psychological status is crucial and requires the skill of a clinical psychologist and/or psychiatrist with pain clinic experience. Psychological variables include distress, depression, expectations of treatment, motivation to improve, and background environmental factors. Unnecessary dental treatment to "remove the pain" with dental extractions is contraindicated and aggravates neuropathic orofacial pain.
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Neuropathic pain is defined as "pain initiated or caused by a primary lesion or dysfunction in the nervous system". Neuropathic orofacial pain has previously been known as "atypical odontalgia" (AO) and "phantom tooth pain". The patient afflicted with neuropathic oral/orofacial pain may present to the dentist with a persistent, severe pain, yet there are no clearly identifiable clinical or radiographic abnormalities. ⋯ The aberrant developmental neurobiology leading to this pain state is complex. Neuropathic pain serves no protective function, in contrast to physiological pain that warns of noxious stimuli likely to result in tissue damage. The relevant clinical features of neuropathic pain include: (i) precipitating factors such as trauma or disease (infection), and often a delay in onset after initial injury (days-months), (ii) typical complaints such as dysaesthesias (abnormal unpleasant sensations), pain that may include burning, and paroxysmal, lancinating or sharp qualities, and pain in an area of sensory deficit, (iii) on physical examination there may be hyperalgesia, allodynia and sympathetic hyperfunction, and (iv) the pathophysiology includes deafferentation, nerve sprouting, neuroma formation and sympathetic efferent activity.