Time filter

Source Type

Boston, MA, United States

Kurtz S.M.,Exponent, Inc. | Kurtz S.M.,Drexel University | Ong K.L.,Exponent, Inc. | Lau E.,Exponent, Inc. | And 2 more authors.
ASTM Special Technical Publication

The purpose of this study was to describe actual usage patterns for metal-on-metal (MOM) bearings in the United States using a nationally representative database. The 2005-2009 nationwide inpatient sample (NIS), in combination with the 2009-2010 state inpatient databases (SIDs), was employed to identify primary total hip arthroplasty (THA), revision THA, and resurfacing hip arthroplasty (RHA) patients implanted with a MOM bearing using ICD-9-CM codes. The MOM patient population was characterized by gender, age, race, U.S. Census region, hospital characteristics, and insurance coverage. The prevalence of MOM bearing usage was estimated between 2000 and 2010. Between 2005 and 2010, MOM bearing usage in the United States ranged between from 32 % and 40 % of primary THAs and from 26 % and 32 % of revision THAs. Utilization of MOM bearing types in primary/revision THA and RHA peaked in 2008. By 2010, 755000 patients were estimated to be implanted with MOM bearings in the United States between 2000 and 2010, we estimated that 83.7 % of MOM bearings in the United States were implanted during primary THA procedures, 11.7 % during revision THA, and the remaining 4.6 % during RHA. Our research demonstrates that the prevalence of MOM increased substantially up to a high water mark in 2008. Despite uncertain indications for use, MOM bearings were used extensively in female and elderly patients. Copyright © 2013 by ASTM International. Source

Hoshino Y.,University of Pittsburgh | Wang J.H.,Sungkyunkwan University | Lorenz S.,TU Munich | Fu F.H.,University of Pittsburgh | And 2 more authors.
Knee Surgery, Sports Traumatology, Arthroscopy

Purpose: The variation of distal femur morphology has been often reported, especially in relation to ACL injury. However, it remains unknown how morphological differences affect knee kinematics and ACL function. The location of the transcondylar axis, a common anatomical reference line, may be a significant aspect of morphological variation. It was hypothesized that the location of this axis would be different between genders, and between ACL-injured and non-injured subjects. Methods: 3D CT scans of contralateral healthy femurs in 38 unilateral soft tissue injured patients (20 men/18 women, 26 ACL injury/12 non-ACL injury (7 with PCL injuries and 5 with medial meniscus root tears)) were analyzed three-dimensionally. Condyle offset was calculated as the distance between the transcondylar axis and the anatomical axis of the femur. Condyle offset ratio (COR) was then calculated by dividing the condyle offset by the condyle radius. Gender and ACL-injured and non-injured group differences were assessed. Results: Larger COR was found in women, 1.10 ± 0.14, than men, 0.96 ± 0.08. In women, the ACL-injured group had significantly larger COR than the non-ACL injury group, but no difference was found in men. Conclusion: COR is a unique morphological feature which is measureable from 3D CT. COR is larger in women, and could be a possible risk indicator for ACL injury in the female population. Level of evidence: III. © 2011 Springer-Verlag. Source

Craft A.M.,University of Toronto | Craft A.M.,Princess Margaret Cancer Center | Craft A.M.,Orthopedic Research Laboratories | Rockel J.S.,Hubrecht Institute for Developmental Biology and Stem Cell Research | And 8 more authors.
Nature Biotechnology

The replacement of articular cartilage through transplantation of chondrogenic cells or preformed cartilage tissue represents a potential new avenue for the treatment of degenerative joint diseases. Although many studies have described differentiation of human pluripotent stem cells (hPSCs) to the chondrogenic lineage, the generation of chondrocytes able to produce stable articular cartilage in vivo has not been demonstrated. Here we show that activation of the TGFβ pathway in hPSC-derived chondrogenic progenitors promotes the efficient development of articular chondrocytes that can form stable cartilage tissue in vitro and in vivo. In contrast, chondrocytes specified by BMP4 signaling display characteristics of hypertrophy and give rise to cartilage tissues that initiate the endochondral ossification process in vivo. These findings provide a simple serum-free and efficient approach for the routine generation of hPSC-derived articular chondrocytes for modeling diseases of the joint and developing cell therapy approaches to treat them. © 2015 Nature America, Inc. All rights reserved. Source

Perathoner S.,Max Planck Institute for Developmental Biology | Daane J.M.,Orthopedic Research Laboratories | Daane J.M.,Harvard University | Henrion U.,Universitatsklinikum Munster | And 6 more authors.
PLoS Genetics

The scaling relationship between the size of an appendage or organ and that of the body as a whole is tightly regulated during animal development. If a structure grows at a different rate than the rest of the body, this process is termed allometric growth. The zebrafish another longfin (alf) mutant shows allometric growth resulting in proportionally enlarged fins and barbels. We took advantage of this mutant to study the regulation of size in vertebrates. Here, we show that alf mutants carry gain-of-function mutations in kcnk5b, a gene encoding a two-pore domain potassium (K+) channel. Electrophysiological analysis in Xenopus oocytes reveals that these mutations cause an increase in K+ conductance of the channel and lead to hyperpolarization of the cell. Further, somatic transgenesis experiments indicate that kcnk5b acts locally within the mesenchyme of fins and barbels to specify appendage size. Finally, we show that the channel requires the ability to conduct K+ ions to increase the size of these structures. Our results provide evidence for a role of bioelectric signaling through K+ channels in the regulation of allometric scaling and coordination of growth in the zebrafish. © 2014 Perathoner et al. Source

Smits P.,Orthopedic Research Laboratories | Bolton A.D.,Harvard University | Funari V.,Cedars Sinai Medical Center | Funari V.,University of California at Los Angeles | And 19 more authors.
New England Journal of Medicine

BACKGROUND: Establishing the genetic basis of phenotypes such as skeletal dysplasia in model organisms can provide insights into biologic processes and their role in human disease. METHODS: We screened mutagenized mice and observed a neonatal lethal skeletal dysplasia with an autosomal recessive pattern of inheritance. Through genetic mapping and positional cloning, we identified the causative mutation. RESULTS: Affected mice had a nonsense mutation in the thyroid hormone receptor interactor 11 gene (Trip11), which encodes the Golgi microtubule-associated protein 210 (GMAP-210); the affected mice lacked this protein. Golgi architecture was disturbed in multiple tissues, including cartilage. Skeletal development was severely impaired, with chondrocytes showing swelling and stress in the endoplasmic reticulum, abnormal cellular differentiation, and increased cell death. Golgi-mediated glycosylation events were altered in fibroblasts and chondrocytes lacking GMAP-210, and these chondrocytes had intracellular accumulation of perlecan, an extracellular matrix protein, but not of type II collagen or aggrecan, two other extracellular matrix proteins. The similarities between the skeletal and cellular phenotypes in these mice and those in patients with achondrogenesis type 1A, a neonatal lethal form of skeletal dysplasia in humans, suggested that achondrogenesis type 1A may be caused by GMAP-210 deficiency. Sequence analysis revealed loss-of-function mutations in the 10 unrelated patients with achondrogenesis type 1A whom we studied. CONCLUSIONS: GMAP-210 is required for the efficient glycosylation and cellular transport of multiple proteins. The identification of a mutation affecting GMAP-210 in mice, and then in humans, as the cause of a lethal skeletal dysplasia underscores the value of screening for abnormal phenotypes in model organisms and identifying the causative mutations. Copyright © 2010 Massachusetts Medical Society. Source

Discover hidden collaborations