External fixation: how to make it work.
Humans; Magnetic Resonance Imaging; Equipment Design; Prosthesis Design; Fracture Healing; *External Fixators; Fracture Fixation/*methods; *Orthopedic Fixation Devices; Fracture Fixation/*instrumentation; Minimally Invasive Surgical Procedures/instrumentation; Fractures; Bone/*surgery; Orthopedic Fixation Devices; Fracture Fixation – Methods
The external fixator has been in use for more than a century. Wutzer (1789-1863) used pins and an interconnecting rod-and-clamp system. Parkhill (1897) and Lambotte (1900) used devices that were unilateral with four pins and a bar-clamp system. By 1960, Vidal and Hoffmann had popularized the use of an external fixator to treat open fractures and infected pseudarthroses. The complications associated with the use of external fixation in the late 20th century were predominantly caused by a lack of understanding of the principles of application, the principles of fracture healing with external fixation, and old technology. Its use was reserved for the most severe injuries and for cases complicated by infection. Thus, pin problems, nonunions, and malunions were common. Better technology and understanding have since allowed for greater versatility and better outcomes. Simultaneous with developments in the Western world, Ilizarov developed the principles of external fixation with use of ring and wire fixation. It was not until the late 1980s and early 1990s, when more interaction and exchange between the West and East (Russia) became possible, and with the help of Italians who embraced the philosophy of external fixation, that the use of external fixation was proven to be successful. Several variations of external fixation have been developed, and its use is now widespread. However, in the United States, all but a minority of surgeons still have substantial apprehension about the use of external fixation.
Ziran Bruce H; Smith Wade R; Anglen Jeffrey O; Tornetta Iii Paul
Instructional course lectures
2008
1905-06
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.2106/00004623-200707000-00028" target="_blank" rel="noreferrer noopener">10.2106/00004623-200707000-00028</a>
The associations of 25-hydroxyvitamin D levels, vitamin D binding protein gene polymorphisms, and race with risk of incident fracture-related hospitalization: Twenty-year follow-up in a bi-ethnic cohort (the ARIC Study).
*Polymorphism; African Continental Ancestry Group; Aged; Alleles; Epidemiology; Ethnic Groups; European Continental Ancestry Group; Female; Follow-Up Studies; Fracture; Fracture Healing; Genetic Variation; Genotype; Hip Fractures/blood/*ethnology/*genetics; Hospitalization; Humans; Incidence; Male; Middle Aged; Proportional Hazards Models; Prospective Studies; Race; Risk Factors; Single Nucleotide; Vitamin D; Vitamin D binding protein polymorphisms; Vitamin D-Binding Protein/*genetics; Vitamin D/*analogs & derivatives/blood
BACKGROUND: Deficient levels of 25-hydroxyvitamin D [25(OH)D] have been associated with increased fracture risk. Racial differences in fracture risk may be related to differences in bioavailable vitamin D due to single nucleotide polymorphism (SNP) variations in the vitamin D binding protein (DBP). METHODS: We measured 25(OH)D levels in 12,781 middle-aged White and Black participants [mean age 57 years (SD 5.7), 25% Black] in the ARIC Study who attended the second examination from 1990-1992. Participants were genotyped for two DBP SNPs (rs4588 and rs7041). Incident hospitalized fractures were measured by abstracting hospital records for ICD-9 codes. We used Cox proportional hazards models to evaluate the association between 25(OH)D levels and risk of fracture with adjustment for possible confounders. Interactions were tested by race and DBP genotype. RESULTS: There were 1122 incident fracture-related hospitalizations including 267 hip fractures over a median of 19.6 years of follow-up. Participants with deficient 25(OH)D (\textless20 ng/mL) had a higher risk of any fracture hospitalization [HR=1.21 (95% CI 1.05-1.39)] and hospitalization for hip fracture [HR=1.35 (1.02-1.79)]. No significant racial interaction was noted (p-interaction=0.20 for any fracture; 0.74 for hip fracture). There was no independent association of rs4588 and rs7041 with fracture. However, there was a marginal interaction for 25(OH)D deficiency with rs7041 among Whites (p-interaction=0.065). Whites with both 25(OH)D deficiency and the GG genotype [i.e., with predicted higher levels of DBP and lower bioavailable vitamin D] were at the greatest risk for any fracture [HR=1.48 (1.10-2.00)] compared to Whites with the TT genotype and replete 25(OH)D (reference group). CONCLUSIONS: Deficient 25(OH)D levels are associated with higher incidence of hospitalized fractures. Marginal effects were seen in Whites for the DBP genotype associated with lower bioavailable vitamin D, but result inconclusive. Further investigation is needed to more directly evaluate the association between bioavailable vitamin D and fracture risk.
Takiar Radhika; Lutsey Pamela L; Zhao Di; Guallar Eliseo; Schneider Andrea L C; Grams Morgan E; Appel Lawrence J; Selvin Elizabeth; Michos Erin D
Bone
2015
2015-09
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1016/j.bone.2015.04.029" target="_blank" rel="noreferrer noopener">10.1016/j.bone.2015.04.029</a>