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. 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. Descriptive epidemiology study. 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. 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. 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.

Objective: The incidence of boxing-related upper-extremity (UE) injuries in the United States has not been well characterized. Recent rule changes have been made to make participation safer for athletes, although the consequences of such rule changes on injury rates is unclear. Therefore, we sought to determine the incidence, characteristics, and trends of boxing-related UE injuries. Methods: The National Electronic Injury Surveillance System (NEISS) was queried for the years 2012–2016. All UE injuries related to boxing from 2012 to 2016 that occurred during organized boxing participation were selected. Examined variables included injured body party, injury diagnosis, patient age, and sex. Annual injury incidence rates by body part and diagnosis were calculated. Results: The mean incidence of boxing-related UE injuries from 2012 to 2016 was 673 injuries (95% CI 537–809) per 100,000 person-years, with hand fractures being the most common injury (132 (95% CI 130–135) per 100,000 person-years). The incidence of UE injury significantly declined from 865 (95% CI 846–884) per 100,000 person-years in 2012 to 656 (95% CI 642–671) per 100,000 person-years in 2016 (p < 0.01). Injuries to the hand exhibited the largest decrease, declining by 33%. The majority of boxers sustaining UE injuries were male (84.4%) and between the ages of 20–39 (59.9%). Conclusions: Injuries to the UE due to participation in boxing accounted for thousands of emergency department visits in the United States annually, with males younger than 20 years of age, most susceptible to injury. Injuries to the hand, wrist and shoulder occurred at the highest rate. Finally, following rule changes made by sanctioning organizations in 2013, a significant decline in boxing-related UE injuries were observed.

Comminuted inferior pole patellar fractures can be treated in numerous ways. To date, there have been no studies comparing the biomechanical properties of transosseous tunnels versus suture anchor fixation for partial patellectomy and tendon advancement of inferior pole patellar fractures. Suture anchor repair will result in less gapping at the repair site. We also hypothesize no difference in load to failure between the groups. Controlled laboratory study. Ten cadaveric knee extensor mechanisms (5 matched pairs; patella and patellar tendon) were used to simulate a fracture of the extra-articular distal pole of the patella. The distal simulated fracture fragment was excised, and the patellar tendon was advanced and repaired with either transosseous bone tunnels through the patella or 2 single-loaded suture anchors preloaded with 1 suture per anchor. Load to failure and elongation from cycles 1 to 250 between 20 and 100 N of force were measured, and modes of failure were recorded. Statistical analysis was performed using a paired 2-tailed Student t test. The suture anchor group had less gapping during cyclic loading as compared with the transosseous tunnel group (mean ± SD, 6.83 ± 2.23 vs 13.30 ± 5.74 mm; P = .047). There was no statistical difference in the load to failure between the groups. The most common mode of failure was at the suture-anchor interface in the suture anchor group (4 of 5) and at the knot proximally on the patella in the transosseous tunnel group (4 of 5). Suture anchors yielded similar strength profiles and less tendon gapping with cyclic loading when compared with transosseous tunnels in the treatment of comminuted distal pole of the patellar fractures managed with partial patellectomy and patellar tendon advancement. Suture anchors may offer robust repair and earlier range of motion in the treatment of fractures of the distal pole of the patella. Clinical randomized controlled trials would help clinicians better understand the difference in repair techniques and confirm the translational efficacy in clinical practice.

Studies have shown that mutations in the matrilin-3 gene (MATN3) are associated with multiple epiphyseal dysplasia (MED) and spondyloepimetaphyseal dysplasia (SEMD). We tested whether MATN3 mutations affect the differentiation of chondroprogenitor and/or mesenchymal stem cells, which are precursors to chondrocytes. ATDC5 chondroprogenitors stably expressing wild-type (WT) MATN3 underwent spontaneous chondrogenesis. Expression of chondrogenic markers collagen II and aggrecan was inhibited in chondroprogenitors carrying the MED or SEMD MATN3 mutations. Hypertrophic marker collagen X remained attenuated in WT MATN3 chondroprogenitors, whereas its expression was elevated in chondroprogenitors expressing the MED or SEMD mutant MATN3 gene suggesting that these mutations inhibit chondrogenesis but promote hypertrophy. TGF-β treatment failed to rescue chondrogenesis markers but dramatically increased collagen X mRNA expression in mutant MATN3 expressing chondroprogenitors. Synovium derived mesenchymal stem cells harboring the SEMD mutation exhibited lower glycosaminoglycan content than those of WT MATN3 in response to TGF-β. Our results suggest that the properties of progenitor cells harboring MATN3 chondrodysplasia mutations were altered, as evidenced by attenuated chondrogenesis and premature hypertrophy. TGF-β treatment failed to completely rescue chondrogenesis but instead induced hypertrophy in mutant MATN3 chondroprogenitors. Our data suggest that chondroprogenitor cells should be considered as a potential target of chondrodysplasia therapy.