Faculty Bibliography

Crown fractures and luxations occur most frequently of all dental injuries. An appropriate treatment plan after an injury is important for a good prognosis. Guidelines are useful for delivering the best care possible in an efficient manner. The International Association of Dental Traumatology (IADT) has developed a consensus statement after a review of the dental literature and group discussions. Experienced researchers and clinicians from various specialties were included in the group. In cases where the data did not appear conclusive, recommendations were based on the consensus opinion of the IADT board members. The guidelines represent the current best evidence, based on literature research and professional opinion. In this first article of three, the IADT Guidelines for management of fractures and luxations of permanent teeth will be presented.

Pain sensitivity varies substantially among humans. A significant part of the human population develops chronic pain conditions that are characterized by heightened pain sensitivity. We identified three genetic variants (haplotypes) of the gene encoding catecholamine-O-methyltransferase (COMT) that we designated as low pain sensitivity (LPS), average pain sensitivity (APS) and high pain sensitivity (HPS). We show that these haplotypes encompass 96% of the human population, and five combinations of these haplotypes are strongly associated (P=0.0004) with variation in the sensitivity to experimental pain. The presence of even a single LPS haplotype diminishes, by as much as 2.3 times, the risk of developing myogenous temporomandibular joint disorder (TMD), a common musculoskeletal pain condition. The LPS haplotype produces much higher levels of COMT enzymatic activity when compared with the APS or HPS haplotypes. Inhibition of COMT in the rat results in a profound increase in pain sensitivity. Thus, COMT activity substantially influences pain sensitivity, and the three major haplotypes determine COMT activity in humans that inversely correlates with pain sensitivity and the risk of developing TMD.

The aim of this study was to investigate the associations among 4 measures of pain induction procedures in 244 healthy women. The procedures were (1) pressure pain threshold assessed over the temporalis muscles, masseter muscles, temporomandibular joints, and the wrists; (2) C fiber-mediated heat pain threshold/tolerance assessed on the skin over the forearm, cheek, and dorsal aspect of the foot; (3) temporal summation of C fiber-mediated heat pain; and (4) ischemic pain threshold/tolerance. Strong associations among pressure pain thresholds at the 4 sites examined (rho = 0.7 to 0.8, P values < or = .001) and among heat pain threshold/tolerance values at the 3 sites examined (rho = 0.6 to 0.9, P values < or = .001) were observed. Pressure pain threshold was moderately correlated with each of the heat pain threshold/tolerance values (rho = 0.2 to 0.4, P values < or = .001). Ischemic pain threshold/tolerance was moderately associated with each of the pressure and heat pain measures (rho = 0.2 to 0.3, P values < or = .05 to .001). Derived measures of the temporal summation of heat pain did not correlate strongly with threshold or tolerance measures of pressure, ischemic, or heat pain. We concluded (1) that for a specific pain modality, the correlation between threshold and tolerance values across anatomic sites is high, and (2) that measures of pressure, ischemic, and thermal pain threshold/tolerance are significantly correlated, although the strength of these associations is moderate. These findings demonstrate that a battery of pain-assessing procedures is required to determine an individual's pain sensitivity profile or phenotype. PERSPECTIVE: By investigating the relationship between pain sensitivity produced by different forms of stimuli, this study demonstrates that a battery of tests should be used to assess an individual's pain sensitivity and one should be careful in making inferences about an individual's sensitivity to pain by using only one pain modality.

This study was conducted to determine the bacterial reduction using Profile GT files and a strict irrigation protocol utilizing 5.25% NaOCl and EDTA. The additive antibacterial effect of Ca(OH)2 was also evaluated. In addition, the study compared the bacterial reduction with the GT protocol versus larger instrumentation. Thirty-one subjects with apical periodontitis were recruited. Bacterial samples were taken upon access (S1), after instrumentation and a strict irrigation protocol (S2), and following >1 wk of Ca(OH)2 (SC). A log10 transformation of colony forming units was done since sample bacterial counts are not normally distributed. At S1, 93.55% of canals sampled bacteria. At S2, 52.72% of the cases sampled bacteria. At SC, 14% of the cases cultured bacteria. The McNemar test showed a significant reduction (p<0.0009) in bacteria between S1 and S2. This was also true between S2 and SC (p<0.0019). It was concluded the GT protocol significantly reduced the number of bacteria in the canal but failed to render the canal bacteria free in more than half of the cases Ca(OH)2 application significantly further reduced bacteria. Lastly, large apical instrumentation removed more bacteria than small apical instrumentation.

This study assessed the efficacy of a triple antibiotic paste in the disinfection of immature dog teeth with apical periodontitis. The canals were sampled before (S1) and after (S2) irrigation with 1.25% NaOCL and after dressing with a triple antibiotic paste (S3), consisting of metronidazole, ciprofloxacin, and minocycline. At S1, 100% of the samples cultured positive for bacteria with a mean CFU count of 1.7 x 10. At S2, 10% of the samples cultured bacteria-free with a mean CFU count of 1.4 x 10. At S3, 70% of the samples cultured bacteria-free with a mean CFU count of only 26. Reductions in mean CFU counts between S1 and S2 (p < 0.0001) as well as between S2 and S3 (p < 0.0001) were statistically significant. These results indicate the effectiveness of a triple antibiotic paste in the disinfection of immature teeth with apical periodontitis.

Substantial research suggests that coping strategies, especially catastrophizing, play an important role in shaping adjustment to chronic pain. Although laboratory and clinical studies both suggest that catastrophizing enhances pain, the interaction of catastrophizing and clinical pain on pain sensitivity has received little attention. The present study evaluated the extent to which catastrophizing influenced laboratory thermal pain responses during and after the resolution of acute dental pain. Thermal pain threshold and tolerance, as well as self-reported catastrophizing, were determined in 46 dental patients (15 men and 31 women) experiencing pain as a result of acute pulpitis. All subjects participated in 2 experimental sessions; the first took place immediately before endodontic treatment for relief of pulpal pain, and the second session occurred when patients were pain free, approximately 1 to 2 weeks later. Thermal pain thresholds increased on resolution of acute dental pain, whereas levels of catastrophizing did not change from pretreatment to post-treatment. Catastrophizing was unrelated to thermal pain responses in the presence of acute dental pain (ie, during the first session). Once patients were pain free, catastrophizing showed significant inverse associations with measures of thermal pain threshold and tolerance. In addition, catastrophizing was a robust predictor of changes in thermal pain responses across sessions, with higher baseline catastrophizing predicting reductions or relatively smaller increases in pain threshold and tolerance after successful treatment of acute pain. These data suggest that catastrophizing is prospectively associated with enhanced sensitivity to and reduced tolerance for thermal pain. The use of catastrophizing as a coping strategy might interfere with the resolution of sensitization after cessation of an acutely painful condition, or it might be associated with magnified experimental pain responses across time. PERSPECTIVE: The findings of the present study suggest that, in some instances, different ethnic groups and genders may use the same descriptors to report different levels of pain. In the context of clinical pain assessment, it may be important to consider the possibility that descriptions of painful sensations reflect, in part, demographic characteristics.

OBJECTIVE: Incremental placement and curing of resin composites has been recommended. However, this requires longer operating time, and therefore, increased risk of contamination. The purpose of this study was to evaluate the effects of blood contamination on microtensile bond strengths (microTBS) between resin interfaces and to determine the best decontamination method to re-establish the original resin-resin bond strength. MATERIALS: The top surfaces of 64, 4-mm composite blocks (Z-250, Renew, APX, Pertac II) were untreated as the control, or were treated as follows: blood applied and dried on the surface (Treatment 1), blood applied, rinsed, dried (Treatment 2), blood applied, rinsed, and an adhesive applied (Single Bond, One-Step, Clearfil SE, Prompt L-Pop) (Treatment 3). Fresh composite was applied and light-cured in 2-mm increments. After 24 h storage in water, the specimens were sectioned into 0.7-mm thick slabs, trimmed to a cross-sectional area of 1 mm(2), and loaded to failure at a crosshead speed of 1 mm/min using an Instron universal testing machine. Data were analyzed using two-way ANOVA and Fisher's PLSD test (p<0.05). RESULTS: Control values ranged from 45.1 MPa for Pertac II to 71.5 MPa for APX. Untreated blood contamination resulted in resin-resin bond strengths of only 1.0-13.1 MPa. Rinsing raised bond strengths to over 40 MPa for each material. Use of an adhesive further increased bond strengths except for Pertac II. SIGNIFICANCE: Rinsing blood from contaminated surfaces increases the resin-resin bond strength significantly and the application of an appropriate adhesive increases the bond strength to control levels.

This study investigated the effect of topical antibiotic treatment on pulp revascularization in replanted teeth. Thirty-four immature teeth were selected from three young dogs. Baseline radiographs and laser Doppler flowmetry (LDF) readings were obtained. Specimens were randomly divided into four groups: Thirty-eight teeth were extracted, kept dry for 5 min, and either (Group 1) covered with minocycline mixture (G1, n = 11), (Group 2) soaked in doxycycline (G2, n = 11), or (Group 3) soaked in saline (G3-negative control, n = 6), and replanted. Teeth in Group 4 were not extracted (positive control, n = 6). Postoperative radiographs and LDF readings were obtained for 2 months after replantation. After sacrifice, the jaws were collected and processed for light microscopy. Pre- and postreplantation LDF readings and radiographs, and histologic findings were analyzed to assess revascularization. Pulp revascularization occurred in 91% (G1), 73% (G2), and 33% (G3) of the specimens. In conclusion, minocycline facilitates pulp revascularization in replanted immature teeth after replantation.

BACKGROUND: Extraction and endodontic therapy are treatment options for irreversible pulpitis. Extraction often is chosen for financial reasons. The authors conducted a study to investigate an alternative interim therapy. METHODS: The authors recruited patients (N = 73) with irreversible pulpitis and whose teeth were restorable but who opted for extraction owing to financial reasons. After undergoing pulpotomy, the teeth were restored by random assignment with one of two intermediate restorative materials: Caulk IRM (Dentsply Caulk, Milford, Del.) (Group I, n = 38) or an IRM base with glass ionomer core (Fuji IX GP, GC America, Alsip, Ill.) (Group II, n = 35). The authors monitored the teeth over six and 12 months for pain, integrity of restoration and radiographic periapical status by densitometric analysis. RESULTS: By six months, 10 percent of subjects remaining in the study (Group I, n = 27; Group II, n = 25) reported pain; by 12 months, 22 percent (Group I, n = 22; Group II, n = 18) reported pain. A two-tailed Fisher exact test showed no significant difference (P > or = .05) between groups at either time interval. No apical radiographic change was noted in 49 percent of teeth at six months (Group I, n = 18; Group II, n = 19) and 42 percent at 12 months (Group I, n = 16; Group II, n = 15). Chi2 analysis demonstrated no significant differences (P > or = .05) between groups. Seven of 22 restorations in Group I and four of 18 in Group II required repair at 12 months with no statistical difference (chi2 analysis, P > or = .05). CONCLUSIONS: The interim treatment of eugenol pulpotomy using either restorative material reliably prevented pain for six months. For longer periods, both restorations may require repair. CLINICAL IMPLICATIONS: This option should preserve the integrity of the arch and extend the use of the tooth while the patient finds the means to finance complete endodontic treatment.