PURPOSE 5To examine potential risk factors for development of delayed or nonunion following 6 elective ulnar shortening osteotomy using a dedicated osteotomy plating system. 7 8 METHODS 9We performed a retrospective review of all patients who underwent elective ulnar 10 shortening using the TriMed single osteotomy dynamic compression plating system 11 by one of two fellowship-trained hand surgeons over a five-year period. 12Demographic data and medical, surgical, and social histories were reviewed. Time to 13 bony union was determined radiographically by a blinded reviewer. Bivariate 14 statistical analysis was performed to examine the effect of explanatory variables on 15 the time to union and the incidence of delayed or nonunion. Those variables 16 associated with the development of delayed or nonunion were used in a 17 multivariate logistic regression model. Complications, including the need for 18 additional surgery, were also recorded. 19 20 RESULTS 21Seventy-two ulnar shortening osteotomy procedures were performed in 69 22 patients. Delayed union, defined as ≥ 6 months to union, occurred in 8/72 cases 23 (11%). Four of 72 (6%) surgeries resulted in nonunions, all of which required 24 additional surgery. Hardware removal was performed in 13/72 (18%) of cases. 25Time to union was significantly increased in smokers (6+/-3 months) versus non-26 smokers (3 +/-1 months). On multivariate analysis, diabetics and active smokers 27 demonstrated a significantly higher risk of developing delayed union or nonunion. 28Patient age, sex, body mass index, thyroid disease, workers compensation status, 29 alcohol use, and amount smoked daily did not have an effect on the time to union or 30 the incidence of delayed or nonunion. 31 32 CONCLUSIONS 33Despite the use of an osteotomy-specific plating system, smokers and diabetics were 34 at significantly higher risk for both delayed union and nonunion following elective 35 ulnar shortening osteotomy. Other known risk factors for suboptimal bony healing 36were not found to have a deleterious effect. 37 38 LEVEL OF EVIDENCE 39Prognostic Level III 40
Purpose The trend toward requiring explicit consent from patients participating in observational research introduces the potential for consent bias, either through selection bias or through the Hawthorne effect. In the Hawthorne effect, patients may alter responses based on awareness of participation in a study, thus potentially limiting its applicability to a generalized orthopedic practice. We hypothesized that study subjects’ awareness of participation in an observational study by informed consent would alter responses to a standard upper extremity questionnaire in a statistically and clinically meaningful way compared with patients who filled out the questionnaire as a quality control measure. Methods We retrospectively reviewed data on 39 patients who underwent isolated carpal tunnel release, who had completed preoperative and postoperative Quick Disabilities of the Arm, Shoulder, and Hand (Quick DASH) forms without providing consent for study participation. Next, we approached 35 patients scheduled to undergo isolated carpal tunnel release who completed the intake questionnaire on the day of surgery, for consent to participate in the study. After obtaining consent but before surgery, these patients completed a second questionnaire and then completed a postoperative questionnaire at a mean of 8 weeks postoperatively. Results There were no significant differences in age, sex, insurance status, symptom duration, nerve conduction study and electromyography results, or disease severity between groups. We identified no statistically significant difference in preoperative or postoperative Quick DASH score between the retrospective and prospective cohorts (40 + 23 vs 40 + 19 preoperatively; 27 + 25 vs 19 + 13 postoperatively) or within the prospective cohort before and after obtaining informed consent. Conclusions Informed consent did not significantly alter patients’ responses to the Quick DASH questionnaire. These results suggest that both opt-in and opt-out approaches to observational research in hand surgery provide results that may be applicable to a generalized orthopedic practice. Clinical relevance This study provides evidence that will inform the interpretation of observational research findings in hand surgery.
BackgroundIt has been established that skeletal growth is stunted in lead-exposed children. Because chondrogenesis is a seminal step during skeletal development, elucidating the impact of Pb on this process is the first step toward understanding the mechanism of Pb toxicity in the skeleton.ObjectivesThe aim of this study was to test the hypothesis that Pb alters chondrogenic commitment of mesenchymal cells and to assess the effects of Pb on various signaling pathways.MethodsWe assessed the influence of Pb on chondrogenesis in murine limb bud mesenchymal cells (MSCs) using nodule formation assays and gene analyses. The effects of Pb on transforming growth factor-β (TGF-β) and bone morphogenetic protein (BMP) signaling was studied using luciferase-based reporters and Western analyses, and luciferase-based assays were used to study cyclic adenosine monophosphate response element binding protein (CREB), β-catenin, AP-1, and nuclear factor-kappa B (NF-κB) signaling. We also used an ectopic bone formation assay to determine how Pb affects chondrogenesis in vivo.ResultsPb-exposed MSCs showed enhanced basal and TGF-β/BMP induction of chondrogenesis, evidenced by enhanced nodule formation and up-regulation of Sox-9, type 2 collagen, and aggrecan, all key markers of chondrogenesis. We observed enhanced chondrogenesis during ectopic bone formation in mice preexposed to Pb via drinking water. In MSCs, Pb enhanced TGF-β but inhibited BMP-2 signaling, as measured by luciferase reporter assays and Western analyses of Smad phosphorylation. Although Pb had no effect on basal CREB or Wnt/β-catenin pathway activity, it induced NFκB signaling and inhibited AP-1 signaling.ConclusionsThe in vitro and in vivo induction of chondrogenesis by Pb likely involves modulation and integration of multiple signaling pathways including TGF-β, BMP, AP-1, and NFκB.
There is strong evidence in the clinical literature to suggest that elevated lead (Pb) exposure impairs fracture healing. Since Pb has been demonstrated to inhibit bone formation, and Wnt signaling is an important anabolic pathway in chondrocyte maturation and endochondral ossification, we investigated the impact of Wnt therapy on Pb-exposed mice undergoing bone repair in a mouse tibial fracture model. We established that tibial fracture calluses from Pb-treated mice were smaller and contained less mineralized tissue than vehicle controls. This resulted in the persistence of immature cartilage in the callus and decreased β-catenin levels. Reduction of β-catenin protein was concurrent with systemic elevation of LRP5/6 antagonists DKK1 and sclerostin in Pb-exposed mice throughout fracture healing. β-catenin stimulation by the GSK3 inhibitor BIO reversed these molecular changes and restored the amount of mineralized callus. Overall, Pb is identified as a potent inhibitor of endochondral ossification in vivo with correlated effects on bone healing with noted deficits in β-catenin signaling, suggesting the Wnt/β-catenin as a pivotal pathway in the influence of Pb on fracture repair.
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