Does Presurgical Magnetic Resonance Neurography Predict Surgical Gap Size in Trigeminal Class IV and V Injuries?

PURPOSE: The accuracy of magnetic resonance neurography (MRN) for quantitative assessment of nerve injury gap is unknown. We tested the hypothesis that presurgical MRN predicts the final surgical gap size after neuroma resection at the time of surgery. MATERIALS AND METHODS: This was a retrospective, single-blinded, nonrandomized cohort study on 43 patients with Sunderland Class IV and V injuries of the inferior alveolar (IAN) or the lingual nerve (LN). The MRN maxillofacial protocol was performed on a 3T scanner and was read by 2 musculoskeletal radiologists to determine the maximum size of neuroma and the abnormal nerve segment. Two independent variables were recorded during surgery: 1) the length of neuroma from histologic specimens since only 9 of the 43 neuroma size measurements were accurately measureable at the time of surgery; and 2) the length of nerve gap size after the neuroma was removed and normal fascicles were identified. RESULTS: There were 7 IAN and 36 LN cases analyzed. The mean time in months from injury to MRN was 6.97 ± 9.18 and MRN to surgery was 1.21 ± 1.4. The mean length of the neuroma at surgery was 7.22 ± 2.78 mm and mean nerve gap size was 12.02 ± 4.41 mm. Intraclass coefficient (ICC) agreement was fair for abnormal nerve thickness and neuroma length (ICC = 0.28, 0.39) while it was moderate for neuroma thickness and abnormal nerve length (0.50, 0.59). There was no significant correlation between MRN based measurements and surgical gap size for both readers (P > .05). CONCLUSIONS: Abnormal nerve and neuromas of the peripheral trigeminal nerve as identified on MRN imaging demonstrates no correlation of the assessed MRN findings with the final surgical gap after neuroma removal.

Special Contribution: Third Molar Clinical Trials Annotated Bibliography.

PURPOSE: To provide clinicians with an annotated bibliography of published articles from research funded externally by the Oral and Maxillofacial Surgery Foundation, spanning 1996 to 2015, addressing the topic of third molar management. MATERIALS AND METHODS: A brief summary for each article was generated by the respective authors. RESULTS: The complete annotated bibliography generated by the authors is included in the Appendix. CONCLUSION: The annotated bibliography provides clinicians and other interested individuals with a summary of current literature emanating from clinical studies on third molar topics.

Monitoring for periodontal inflammatory disease in the third molar region.

PURPOSE: To assess changes at 2-year intervals in the periodontal status of the third molar region in participants enrolled with asymptomatic third molars and no clinical evidence of third molar region periodontal pathology. PARTICIPANTS AND METHODS: The included participants who presented with a healthy periodontal status (all probing depths [PDs], <4 mm) in the third molar region, defined as distal of second molars and around adjacent third molars, were from a larger longitudinal study of participants with asymptomatic third molars. Full-mouth periodontal PD data from 6 sites per tooth were obtained clinically at enrollment and at subsequent 2-year intervals. Data were aggregated to the patient level. Outcome variables were the presence or absence of periodontal pathology, defined as at least 1 PD of at least 4 mm in the third molar region. RESULTS: One hundred twenty-nine participants had a third molar region PD shallower than 4 mm at enrollment. Most participants were Caucasian (85%), women (60%), younger than 25 years (62%), educated beyond high school (84%), and with good oral health habits. At 6 years, excluding the 61 participants lost to follow-up, 47% participants had had third molars removed, 21% had developed at least 1 PD of at least 4 mm in the third molar region since enrollment, and 32% retained the periodontal status at enrollment (all PDs in third molar region, <4 mm). Demographic characteristics were not statistically different for participants followed for 6 years compared with those lost to follow-up. CONCLUSIONS: Although not all participants could be followed for 6 years after enrollment or chose to retain third molars, one third of participants maintained the third molar region periodontal status assessed at baseline for 6 years after enrollment; no clinical evidence of pathology developed over time.

Population-specific coding variant underlies genome-wide association with adiponectin level.

Adiponectin is a protein hormone that can affect major metabolic processes including glucose regulation and fat metabolism. Our previous genome-wide association (GWA) study of circulating plasma adiponectin levels in Filipino women from the Cebu Longitudinal Health and Nutrition Survey (CLHNS) detected a 100 kb two-SNP haplotype at KNG1-ADIPOQ associated with reduced adiponectin (frequency = 0.050, P = 1.8 × 10(-25)). Subsequent genotyping of CLHNS young adult offspring detected an uncommon variant [minor allele frequency (MAF) = 0.025] located ~800 kb from ADIPOQ that showed strong association with lower adiponectin levels (P = 2.7 × 10(-15), n = 1695) and tagged a subset of KNG1-ADIPOQ haplotype carriers with even lower adiponectin levels. Sequencing of the ADIPOQ-coding region detected variant R221S (MAF = 0.015, P = 2.9 × 10(-69)), which explained 17.1% of the variance in adiponectin levels and largely accounted for the initial GWA signal in Filipinos. R221S was not present in 12 514 Europeans with previously sequenced exons. To explore the mechanism of this substitution, we re-measured adiponectin level in 20 R221S offspring carriers and 20 non-carriers using two alternative antibodies and determined that the presence of R221S resulted in artificially low quantification of adiponectin level using the original immunoassay. These data provide an example of an uncommon variant responsible for a GWA signal and demonstrate that genetic associations with phenotypes measured by antibody-based quantification methods can be affected by uncommon coding SNPs residing in the antibody target region.

Adiponectin-SOGA Dissociation in Type 1 Diabetes.

CONTEXT: Circulating adiponectin is elevated in human type 1 diabetes (T1D) and nonobese diabetic (NOD) mice without the expected indications of adiponectin action, consistent with tissue resistance. OBJECTIVE: Adiponectin stimulates hepatocyte production of the suppressor of glucose from autophagy (SOGA), a protein that inhibits glucose production. We postulated that due to tissue resistance, the elevation of adiponectin in T1D should fail to increase the levels of a surrogate marker for liver SOGA, the circulating C-terminal SOGA fragment. MAIN OUTCOME MEASURES: Liver and plasma SOGA were measured in NOD mice (n = 12) by Western blot. Serum adiponectin and SOGA were measured in T1D and control (Ctrl) participants undergoing a three-stage insulin clamp for the Coronary Artery Calcification in T1D study (n = 20). Glucose turnover was measured using 6,6[(2)H2]glucose (n = 12). RESULTS: In diabetic NOD mice, the 13%-29% decrease of liver SOGA (P = .003) and the 30%-37% reduction of circulating SOGA (P < .001) were correlated (r = 0.826; P = .001). In T1D serum, adiponectin was 50%-60% higher than Ctrl, SOGA was 30%-50% lower and insulin was 3-fold higher (P < .05). At the low insulin infusion rate (4 mU/m(2)·min), the resulting glucose appearance correlated negatively with adiponectin in T1D (r = -0.985, P = .002) and SOGA in Ctrl and T1D (r = -0.837, P = .001). Glucose disappearance correlated with adiponectin in Ctrl (r = -0.757, P = .049) and SOGA in Ctrl and T1D (r = -0.709, P = .010). At 40 mU/m(2)·min, the lowered glucose appearance was similar in Ctrl and T1D. Glucose disappearance increased only in Ctrl (P = .005), requiring greater glucose infusion to maintain euglycemia (8.58 ± 1.29 vs 3.09 ± 0.87 mg/kg·min; P = .009). CONCLUSIONS: The correlation between liver and plasma SOGA in NOD mice supports the use of the latter as surrogate marker for liver concentration. Reduced SOGA in diabetic NOD mice suggests resistance to adiponectin. The dissociation between adiponectin and SOGA in T1D raises the possibility that restoring adiponectin signaling and SOGA might improve the metabolic response to insulin therapy.