Risk factors for reoperation following inguinal hernia repair: results from a cohort of patients from an integrated healthcare system.

PURPOSE: Inguinal hernia repair is one of the most common operations performed globally. Identification of risk factors that contribute to hernia recurrence following an index inguinal hernia repair, especially those that are modifiable, is of paramount importance. Therefore, we sought to investigate risk factors for reoperation following index inguinal hernia repair. METHODS: 125,133 patients aged ≥ 18 years who underwent their first inguinal hernia repair with mesh within a large US integrated healthcare system were identified for a cohort study (2010-2020). Laparoscopic, robotic, and open procedures were included. The system's integrated electronic health record was used to obtain data on demographics, patient characteristics, surgical characteristics, and reoperations. The association of these characteristics with ipsilateral reoperation during follow-up was modeled using Cox proportional-hazards regression. Risk factors were selected into the final model by stepwise regression with Akaike Information Criteria, which quantifies the amount of information lost if a factor is left out of the model. Factors associated with reoperation with p < 0.05 were considered statistically significant. RESULTS: The cumulative incidence of reoperation at 5-year follow-up was 2.4% (95% CI 2.3-2.5). Increasing age, female gender, increasing body mass index, White race, chronic pulmonary disease, diabetes, drug abuse, peripheral vascular disease, and bilateral procedures all associated with a higher risk for reoperation during follow-up. CONCLUSION: This study identifies several risk factors associated with reoperation following inguinal hernia repair. These risk factors may serve as targets for optimization protocols prior to elective inguinal hernia repair, with the goal of reducing reoperation risk.

Use of polyvinyl siloxane to maintain peri-implant submucosal contours on removal of screw-retained implant-supported restorations.

When submucosal screw-retained implant-supported restorations are removed for a short period, the soft-tissue contours collapse, which can affect treatment expediency and patient comfort when restorations are reinserted. This technique involves the fabrication of a polyvinyl siloxane submucosal template to help mitigate the soft-tissue collapse and its potential sequelae. This method of maintaining peri-implant soft-tissue contours is achieved through a quick succession of steps: removing the screw-retained implant prosthesis, drying the soft tissue thoroughly, injecting light-bodied fast-set polyvinyl siloxane directly into the implant fixture of the internal connection implants and the screw channel for external connection implants together with the remaining submucosal areas, allowing the polyvinyl siloxane submucosal template to polymerize undisturbed, and removing it when ready to replace the prosthesis.

Evaluation of Fracture Resistance of Zirconia Modification/Polishing Around Implant Abutments.

Subcrestal placement of implants may have interproximal bone proximity issues that interfere with the submucosal contour of implant-supported zirconia restorations during delivery of the restorations. Modification of the mesial distal submucosal areas may be necessary to fully seat the restoration without impingement of the interproximal bone. Our aim was to determine if modification of submucosal cervical contour of implant supported zirconia-titanium base (Zi-Ti base) restorations resulted in a significant change in fracture strength compared with Zi-Ti base restorations without any modification near the cervical submucosal area. Implant Zi-Ti base restorations designed in the form of a maxillary premolar were made for the Straumann implant lab analog. Zirconia samples were cemented onto the Ti-base and the test group (N = 20) underwent recontouring and polishing at the junction of the Zi-Ti base cervical areas. The control group (N = 20) did not undergo any modifications. All 40 samples underwent fracture testing with an Instron machine. We assessed differences between modified and unmodified implants restorations using a 2-tailed t test for independent samples. Fracture strength values (N) ranged from 4354.68 to 6412.49 in the test group (N = 20) and from 5400.31 to 6953.22 in the control group (N = 20). The average fracture strength in the control group (6154.84 ± 320.50) was higher than in the modified group (5593.13 ± 486.51; P < .001). Modification of submucosal contour significantly decreased fracture strength. However, the average fracture strength exceeded the masticatory forces of humans.

Retrospective Comparison of Postinsertion Maintenances Between Conventional and 3D Printed Complete Dentures Fabricated in a Predoctoral Clinic.

PURPOSE: A retrospective study to analyze the clinical performance of 3D printed complete dentures in edentulous patients compared with conventional complete dentures regarding postinsertion visits and patient reported outcomes. MATERIAL AND METHODS: Electronic charts were reviewed to analyze 420 (maxilla 270, mandible 150) heat-polymerized conventional complete dentures (CCD) inserted between July 1, 2015 and June 30, 2016 and 217 (maxilla 130, mandible 86) 3D printed complete dentures (PCD) inserted between July 1, 2017 and June 30, 2018. Number of remakes, number of postinsertion adjustments, type and number of repairs, and patient reported complications were compared between two types of complete dentures. The frequency of denture repair and patient reported complications were analyzed using chi-square of independence test. RESULTS: The frequency of pain and visible ulcer lesions in the maxilla was determined to be 46.67% with CCD and 36.15% in PCD (p = 0.047). There was no statistical significance in other items. The majority of esthetic concerns was dissatisfaction with the shape of dentures with CCD (4.67%) and they had statistically significant, less frequent, esthetic problems than PCD (11.63%) (p = 0.047). CONCLUSIONS: Similar clinical performance was recorded between the two groups, but the overall pain and visible ulcer lesions were less in the printed complete dentures then the conventionally processed dentures. However, the esthetic aspect was better in conventionally processed complete dentures.

Evaluating the relationship between tooth color and enamel thickness, using twin flash photography, cross-polarization photography, and spectrophotometer.

OBJECTIVES: To understand (a) the effects of labial enamel on tooth color (b) relationship of color data taken by nonpolarized (NP), cross-polarization photography (CP), and spectrophotometry (SP). MATERIALS AND METHODS: Fifty extracted human maxillary incisors were coated with resin on their palatal surfaces. Their color was measured with NP, CP, and SP and their dimensions were scanned by an intraoral scanner. The labial enamel was removed using a modified selective enamel demineralization technique. Tooth dimensions and color were recorded again. The differences in the labial enamel thickness (ΔT) and color (∆E*00 and ∆L*, ∆a*, ∆b*) were statistically analyzed with the Pearson correlation coefficient and simple linear regression. RESULTS: In CP and SP methods, ΔT and ∆E*00 were weakly to moderately positively correlated (r = .38 and .27). In NP, CP, and SP methods, ∆T and ∆b* are weakly positively correlated (r = .27, .27 and .29). The color data of three measuring methods were highly positively correlated (r > .8). A linear relationship between ∆E*00 and ∆T were found (CP and SP groups). CONCLUSIONS: (a) Thicker labial enamel has a greater impact on tooth color. (b) Reducing labial enamel thickness shifts the tooth color toward yellow. (c) Tooth color measured from the three methods were highly correlated. CLINICAL SIGNIFICANCE: Knowing the relationship between enamel thickness and tooth color, a clinician can better predict the stump shade before tooth preparation. Due to the highly correlated measuring outcomes, it is reasonable to combine these three methods during shade matching.

Evaluation of Fracture Resistance of Varying Thicknesses of Zirconia Around Implant Abutment Cylinders.

Zirconia is becoming increasingly used as a restorative material for implant-supported restorations; however, information is lacking with respect to the minimum thickness of zirconia surrounding the implant components. The purpose of this study is to evaluate the resistance to fracture of different thicknesses of zirconia luted to implant components. Thirty cylinders of zirconia (Prettau, Zirkonzahn) with 13-mm height, designed with indented occlusal surface for loading, and varying wall thicknesses (0.5 mm, 1 mm, 1.5 mm; n = 10/group) were milled using a computer-aided design/computer-aided manufacturing system (Modellier, Zirkonzahn), after which they were sintered. Titanium temporary cylinders (ITCS41, Biomet3i) were attached to 30 implant analogs (ILA20, Biomet3i) that were embedded into polymethylmethacrylate blocks (Palapress Vario, Heraeus Kulzer) with dimensions of 4.5 × 1.8 × 2 cm. Zirconia specimens were cemented to the titanium cylinders using a self-adhesive, dual-cure resin cement (Panavia SA, Kuraray). Load to failure test was performed under compression until fracture using a universal testing machine (Instron5965, Instron) at a crosshead speed of 0.5 mm/min and measured in N (Newton). Statistical analysis was performed using 1-way analysis of variance and Tukey B test at α = .05 (SPSS19, IBM). Mean load to failure was 1059.94 N, 2019.46 N, and 4074.79 N for groups 0.5 mm, 1 mm, and 1.5 mm, respectively. Values were significantly different between the groups (P < .05). Study limitations are that it is in vitro, specimens do not replicate tooth dimensions, and forces are static and directed toward the occlusal portion of each specimen. Within these limitations and considering the average human bite force, a thickness of 0.5 mm to 1 mm of this particular type of zirconia around this type of implant component can avoid fracture with these dimensions.

Genetic rescue of nonclassical ERα signaling normalizes energy balance in obese Erα-null mutant mice.

In addition to its role in reproduction, estradiol-17ß is critical to the regulation of energy balance and body weight. Estrogen receptor α-null (Erα-/-) mutant mice develop an obese state characterized by decreased energy expenditure, decreased locomotion, increased adiposity, altered glucose homeostasis, and hyperleptinemia. Such features are reminiscent of the propensity of postmenopausal women to develop obesity and type 2 diabetes. The mechanisms by which ERα signaling maintains normal energy balance, however, have remained unclear. Here we used knockin mice that express mutant ERα that can only signal through the noncanonical pathway to assess the role of nonclassical ERα signaling in energy homeostasis. In these mice, we found that nonclassical ERα signaling restored metabolic parameters dysregulated in Erα-/- mutant mice to normal or near-normal values. The rescue of body weight and metabolic function by nonclassical ERα signaling was mediated by normalization of energy expenditure, including voluntary locomotor activity. These findings indicate that nonclassical ERα signaling mediates major effects of estradiol-17ß on energy balance, raising the possibility that selective ERα agonists may be developed to reduce the risks of obesity and metabolic disturbances in postmenopausal women.

Progesterone receptor A (PRA) and PRB-independent effects of progesterone on gonadotropin-releasing hormone release.

Progesterone's (P4) negative feedback actions in the female reproductive axis are exerted in part by suppression of hypothalamic GnRH release. Here we show that P4 can inhibit GnRH release by a mechanism independent of a nuclear P4 receptor (PR(A/B)). Injections of P4, but not vehicle, allopregnanolone, or dexamethasone, acutely suppressed LH levels in both wild-type and P4 receptor knockout ovariectomized mice; pituitary responsiveness to GnRH was retained during P4 treatment, indicating a hypothalamic action. Superfusion of GnRH-producing GT1-7 cells with medium containing 10(-7) m P4 produced a rapid reduction in GnRH release. Incubation with P4 (10(-9) to 10(-7) M) inhibited forskolin-stimulated cAMP accumulation; cotreatment with pertussis toxin prevented this effect. Treatment of GT1-7 cell membranes with P4 caused activation of an inhibitory G protein (G(i)), as shown by immunoprecipitation with a G(i) antibody of most of the increase in membrane-bound [(35)S]GTPgamma-S. Saturation binding analyses demonstrated the presence of a high affinity (K(d) 5.85 nM), limited capacity (Bmax 62.2 nM) binding site for P4. RT-PCR analysis revealed the presence of mRNAs encoding both isoforms of the membrane P4 receptors, mPRalpha and mPRbeta. Western blotting, immunocytochemistry, and flow cytometry experiments similarly revealed expression of mPR proteins in the plasma membranes of GT1-7 cells. Treatment with mPRalpha siRNA attenuated specific P4 binding to GT1-7 cell membranes and reversed the P4 inhibition of cAMP accumulation. Taken together, our results suggest that negative feedback actions of P4 include rapid PR(A/B)-independent effects on GnRH release that may in part be mediated by mPRs.

p21-Activated kinase mediates rapid estradiol-negative feedback actions in the reproductive axis.

Nonclassical estrogen receptor alpha (ERalpha) signaling can mediate E(2) negative feedback actions in the reproductive axis; however, downstream pathways conveying these effects remain unclear. These studies tested the hypothesis that p21-activated kinase 1 (PAK1), a serine/threonine kinase rapidly activated by E(2) in nonneural cells, functions as a downstream node for E(2) signaling pathways in cells of the preoptic area, and it may thereby mediate E(2) negative feedback effects. Treatment of ovariectomized (OVX) rats with estradiol benzoate (EB) caused rapid and transient induction of phosphorylated PAK1 immunoreactivity in the medial preoptic nucleus (MPN) but not the arcuate nucleus. To determine whether rapid induction of PAK phosphorylation by E(2) is mediated by nonclassical [estrogen response element (ERE)-independent] ERalpha signaling, we used female ERalpha null (ERalpha(-/-)) mice possessing an ER knock-in mutation (E207A/G208A; AA), in which the mutant ERalpha is incapable of binding DNA and can signal only through membrane-initiated or ERE-independent genotropic pathways (ERalpha(-/AA) mice). After 1-h EB treatment, the number of pPAK1-immunoreactive cells in the MPN was increased in both wild-type (ERalpha(+/+)) and ERalpha(-/AA) mice but was unchanged in ERalpha(-/-) mice. Serum luteinizing hormone (LH) was likewise suppressed within 1 h after EB treatment in ERalpha(+/+) and ERalpha(-/AA) but not ERalpha(-/ -) mice. In OVX rats, 5-min intracerebroventricular infusion of a PAK inhibitor peptide but not control peptide blocked rapid EB suppression of LH secretion. Taken together, our findings implicate PAK1 activation subsequent to nonclassical ERalpha signaling as an important component of the negative feedback actions of E(2) in the brain.