IntroductionTransforming growth factor-beta 1(TGF-β1) is a regulatory protein, involved in bone fracture healing. Circulating TGF-β1 levels have been reported to be a predictor of delayed bone healing and non-union, suggesting active relationship between tissue and circulating TGF-β1 in fracture healing. The purpose of this study was to analyse TGF-β1 local and serum concentrations in fracture healing to further contribute to the understanding of molecular regulation of fracture healing.Patients and methodsSerum samples of 113 patients with long bone fractures were collected over a period of 6 months following a standardised time schedule. TGF-β1 serum concentrations were measured using ELISA. Patients were assigned to 2 groups: Group 1 contained 103 patients with physiological healing. Group 2 contained 10 patients with impaired healing. Patients in both groups were matched. One patient of the group 2 had to be excluded because of missing match partner. In addition, fracture haematoma from 11 patients of group 1 was obtained to analyse local TGF-β1 concentrations. 33 volunteers donated serum which served as control.ResultsTGF-β1 serum concentrations increased during the early healing period and were significantly higher in patients with physiological healing compared to controls (P = 0.04). Thereafter, it decreased continuously between weeks 2 and 8 and fell again after week 8. TGF-β1 serum concentrations in patients with physiological healing were significantly higher at week 24 compared to controls (P = 0.05). In non-unions, serum concentrations differed significantly from those of controls at week 6 (P = 0.01). No significant difference in between patients with physiological and impaired fracture healing was observed. Fracture haematoma contained significantly higher TGF-β1 concentrations than peripheral serum of the patients (P = 0.017).ConclusionElevated levels of TGF-β1 in haematoma and in serum after bone fracture especially during the entire healing process indicate its importance for fracture healing.

Purpose Electric scooters (e-scooters) are an emerging way of mobility in cities around the world. Despite quickly rising numbers of e-scooters, limited studies report on incidence and severity of e-scooter-associated injuries. The aim of our study was to report on these injuries and identify potential protective measures to ultimately decrease e-scooter-associated morbidity. Methods We performed a retrospective multicentre study including all patients, who were admitted to three major trauma departments in Vienna from May 2018 to September 2019. We analysed patients' data, including demographics, injury pattern, types of injury and subsequent treatment. Results A total number of 175 patients (115 males, 60 females) sustained e-scooter-associated injuries. Patients' mean age was 34.4 years [4-74]. While the mean Injury Severity Score (ISS) was 3.4, 11 patients presented with an ISS ≥ 9 and 2 patients with an ISS ≥ 16. ISS increased with age. Older patients (≥ 40 years) presented a significantly higher ISS than younger patients (< 40 years) (P = 0.011). Seventy-one patients (40.6%) sustained major injuries affecting head (35.2%) and upper extremities (36.6%). Twenty-three patients (13.1%) required surgery leading to hospitalization of 11 days on average [1-115]. E-scooter-associated injuries increased during late afternoon plateauing at 8.00 pm. However, the largest share of patients (39.2%) sustained their injuries during early night (8.00 pm to 1.59 am) with especially young adults (19-39 years) being at risk. Conclusion The popularity of rideshare e-scooters across cities worldwide seems to be on the rise, so are e-scooter-associated injuries. These injuries should be considered high-energy trauma affecting primarily head and upper extremity; indeed, 17.7% sustained major head injuries. Therefore, the mandatory use of a helmet seems to be adequate to decrease head injuryassociated morbidity. Ultimately, given the remarkably high rates of nighttime injuries, an e-scooter ban during night could further cut injury numbers in half.

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Macrophage colony-stimulating factor (M-CSF) plays a unique role in bone remodeling. However, to our knowledge, no data on the role of M-CSF in fracture healing in humans have been published so far. This study addressed this issue. One hundred and thirteen patients with long-bone fractures were included in the study and divided into two groups, according to their course of fracture healing. The first group contained 103 patients with normal fracture healing. Ten patients with impaired fracture healing formed the second group of the study. Volunteers donated blood samples as control. Serum samples were collected over a period of 6 months, following a standardized time schedule. In addition, M-CSF levels were measured in fracture hematoma and serum of 11 patients with bone fractures. M-CSF concentrations were measured by enzyme-linked immunosorbent assay (ELISA). Fracture hematoma contained significantly higher M-CSF concentrations compared to M-CSF concentrations in patient's serum. M-CSF levels in fracture hematoma and in patient's serum were both significantly higher than M-CSF concentrations measured in serum of healthy controls. Highly elevated M-CSF serum concentrations were found in patients with physiological fracture healing over the entire observation period. Significant differences in the M-CSF serum concentration between patients with normal fracture healing and patients with impaired fracture healing were not observed. This study indicates, for the first time, to our knowledge, a possible local and systemic involvement of M-CSF in humans during fracture healing. Fracture healing is a unique process that leads to bone regeneration. Many studies have focused on the role of cytokines and growth factors in fracture healing; and more than 50 cytokines, angiogenic factors, proteases, and morphogens have been described. 1-4 However, despite intensive research, most of the regulation mechanisms are not well understood. 5 Evidence exists that the local and systemic concentrations of certain cytokines are increased during fracture healing. 2,3,[6][7][8] Among these cytokines, macrophage colony-stimulating factor-1 (M-CSF) plays an important role as it regulates the proliferation and differentiation of mononuclear cells, 9 is crucial in bone remodeling and development of tissue-specific macrophages, 10 and promotes angiogenesis in the bone. 11,12 Various experimental studies to date have focused on the regulatory role of M-CSF in bone remodeling. 12,13-17 M-CSF regulates osteoclast activity, either by stimulating hemopoietic progenitor cells to differentiate along an osteoclastic lineage and fuse to form more osteoclasts, or by directly stimulating existing osteoclasts, thus enhancing their resorptive capacity. 10,18-20 M-CSF and receptor activator of NF-kB ligand (RANKL) are necessary for the development of mature osteoclasts. 13 Moreover, M-CSF seems to be pivotal for the osteoblast-mediated osteoclast production in bone. 16 Our earlier studies in rats with a natural mutation of M-CSF gene, tl-tl mut...