Background:Achilles tendon (AT) ruptures are one of the most common tendon ruptures, but there have been no studies investigating these injuries in the United States (US) using data representative of the entire US population.Purpose/Hypothesis:The purpose of this study was to determine the incidence and risk factors for AT ruptures in the US. We hypothesized that male sex, older age, and sport participation would increase the risk for AT ruptures.Study Design:Descriptive epidemiology study.Methods:All patients presenting to an emergency department with ruptured AT in the US from 2012 through 2016 were selected from the National Electronic Injury Surveillance System (NEISS) database. Incidence was calculated for sex, race, and age. AT ruptures were characterized based on the mechanism of injury, with subanalyses performed on sport-related AT ruptures to examine sex-, race-, and age-related differences.Results:From 2012 to 2016, a significant increase in the incidence of AT ruptures was observed, from 1.8 per 100,000 person-years in 2012 to 2.5 per 100,000 person-years in 2016 (P < .01), for an overall incidence of 2.1 per 100,000 person-years. The majority of AT ruptures occurred in male compared with female patients, with an incidence rate ratio of 3.5 (P < .01). The largest overall incidence of AT ruptures occurred in those aged 20-39 years for male patients (5.6/100,000 person-years) and in those aged 40-59 years for female patients (1.2/100,000 person-years). The largest rise in the incidence of AT ruptures during the study period was observed in patients aged 40-59 years (78% increase). The most common injury mechanism was participation in a sport or recreational activity (81.9% of all injuries), with basketball being the most common overall cause of AT ruptures.Conclusion:While AT ruptures in the US most commonly occur in young male patients (20-39 years old), the largest rise in the incidence was observed in middle-aged patients (40-59 years old), with participation in recreational sports being the most likely mechanism. Recognizing high-risk patients can help physicians counsel them and recommend strategies for injury prevention.
Interactions between tumor cells and cancer-associated fibroblasts (CAFs) in the tumor microenvironment (TMEN) significantly influence cancer growth and metastasis. Transforming growth factor-β (TGF-β) is known to be a critical mediator of the CAF phenotype, and osteopontin (OPN) expression in tumors is associated with more aggressive phenotypes and poor patient outcomes. The potential link between these two pathways has not been previously addressed. Utilizing in vitro studies using human mesenchymal stem cells (MSCs) and MDA-MB231 (OPN+) and MCF7 (OPN−) human breast cancer cell lines, we demonstrate that OPN induces integrin-dependent MSC expression of TGF-β1 to mediate adoption of the CAF phenotype. This OPN-TGF-β1 pathway requires the transcription factor, myeloid zinc finger 1 (MZF1). In vivo studies with xenotransplant models in NOD-scid mice showed that OPN expression increases cancer growth and metastasis by mediating MSC-to-CAF transformation in a process that is MZF1- and TGF-β1-dependent. We conclude that tumor-derived OPN engenders MSC-to-CAF transformation in the microenvironment to promote tumor growth and metastasis via the OPN-MZF1-TGF-β1 pathway.
Epithelial-mesenchymal transition (EMT) is a process essential to wound healing and tissue remodeling after a thermal burn or other injury. EMT is characterized by phenotypic changes in epithelial cells that render them apolar, with decreased cell-cell adhesions, increased motility, and changes in cytoskeletal architecture similar to mesenchymal stem cells. With regard to healing a thermal burn wound, many facets of wound healing necessitate cells to undergo these phenotypic changes; two will be described in the following review. The first is the differentiation of epithelial cells into myofibroblasts that rebuild the extracellular matrix and facilitate wound contraction. The second is reepithelialization by keratinocytes. The primary cytokine signal identified in the literature that triggers EMT is transforming growth factor (TGF)-β. In addition to its vital role in the induction of EMT, TGF-β has many other roles in the wound healing process. The following review will provide evidence that EMT is a central event in wound healing. It will also show the importance of a regulated amount of TGF-β for proper wound healing. Finally, osteopontin will be briefly discussed with its relation to wound healing and its connections to EMT and TGF-β.
Background: There is a paucity of literature regarding risk factors and mechanisms of Achilles tendon (AT) ruptures in the National Basketball Association (NBA). Purpose: To identify the risk factors and outcomes of AT ruptures in NBA athletes. Furthermore, using video analysis, to characterize the mechanisms of rupture by identifying the most common playing situations and lower extremity positions at the time of injury. Study Design: Descriptive epidemiology study. Methods: AT ruptures in the NBA that occurred between the seasons of 1969-1970 and 2017-2018 were identified. Player data collected included age, position, body mass index, total games started before and after injury, and Player Efficiency Rating. Injury-related variables collected included date of injury, laterality, minutes played before injury, operative versus nonoperative treatment, and time to return to play. Available video footage was analyzed for the mechanism and body position at the time of injury. Univariable and multivariable linear regression was used to compare changes in performance before and after AT rupture. Statistical significance was set at P < .05. Results: Forty-four ruptures were identified between 1970 and 2018. The mean age was 28.3 years, with players averaging 6.8 seasons before AT rupture. AT ruptures were most prevalent during early-season game play (27.3%), followed by preseason (18.2%) and late season (18.2%). More than a third (36.8%) of players either did not return to play or started in fewer than 10 games in the remainder of their career, with 21% of ruptures leading to retirement. The mean time to return to play was 10.5 months. The Player Efficiency Rating declined by an average of 2.9 points (range, –11.5 to +2.3) ( P < .001). Analysis of available injury footage (n = 12) demonstrated all ruptures to be noncontact in nature, most commonly occurring just before takeoff as the player began to push off from a stopped position, with the foot in dorsiflexion, the knee in early flexion, and the hip in extension. Conclusion: In the NBA, a majority of AT ruptures occur early in the season, in veteran players, with almost half not returning to play or starting fewer than 10 games in the remainder of their career. The most common mechanism of injury is taking off from a stopped position just before toe-off in a dorsiflexed foot.
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