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Introduction: Greater trochanteric pain syndrome (GTPS) includes patients with symptoms of peritrochanteric pain, gluteus medius/minimus tendinopathy, and external snapping hip. Non-operative treatment includes iliotibial band (ITB) stretching, gluteal exercises and cortisone injections. When surgery is indicated due to the failure of non-operative strategies, open Z-plasty at the level of the greater trochanter has been the traditional procedure. Endoscopic release of the ITB and bursectomy at the level of the greater trochanter has over the last decades evolved and is established as an alternative method of surgery. Case Reports: We here present a case series with 11 consecutive patients who have undergone endoscopic release of the ITB and bursectomy at the level of the greater trochanter due to GTPS. The patients were all Caucasians, 43–years of age, and six were female. The patients retrospectively scored their pre-operative function and pain during follow-up at 28 months (range 15–42). Post-operative pain and function were scored at follow-up. In this paper, we discuss investigation, differential diagnoses, surgical options, and outcomes in the treatment of GTPS. All patients reported significant reduction of pain, and 10 of 11 patients reported an improvement in function. We observed no complications. Conclusions: Endoscopic release of the ITB and bursectomy at the level of the greater trochanter appears to be an effective and safe procedure when conservative treatment options for GTPS have failed.

Summary Determinants of trabecular bone score (TBS) and vertebral fractures assessed semiquantitatively (SQ1–SQ3) were studied in 496 women with fragility fractures. TBS was associated with age, parental hip fracture, alcohol intake and BMD, not SQ1–SQ3 fractures. SQ1–SQ3 fractures were associated with age, prior fractures, and lumbar spine BMD, but not TBS. Introduction Trabecular bone score (TBS) and vertebral fractures assessed by semiquantitative method (SQ1–SQ3) seem to reflect different aspects of bone strength. We therefore sought to explore the determinants of and the associations between TBS and SQ1–SQ3 fractures. Methods This cross-sectional sub-study of the Norwegian Capture the Fracture Initiative included 496 women aged ≥ 50 years with fragility fractures. All responded to a questionnaire about risk factors for fracture, had bone mineral density (BMD) of femoral neck and/or lumbar spine assessed, TBS calculated, and 423 had SQ1–SQ3 fracture assessed. Results Mean (SD) age was 65.6 years (8.6), mean TBS 1.27 (0.10), and 33.3% exhibited SQ1–SQ3 fractures. In multiple variable analysis, higher age (βper SD = − 0.26, 95% CI: − 0.36,− 0.15), parental hip fracture (β = − 0.29, 95% CI: − 0.54,− 0.05), and daily alcohol intake (β = − 0.43, 95% CI − 0.79, − 0.08) were associated with lower TBS. Higher BMD of femoral neck (βper SD = 0.34, 95% CI 0.25–0.43) and lumbar spine (βper SD = 0.40, 95% CI 0.31–0.48) were associated with higher TBS. In multivariable logistic regression analyses, age (ORper SD = 1.94, 95% CI 1.51–2.46) and prior fragility fractures (OR = 1.71, 95% CI 1.09–2.71) were positively associated with SQ1–SQ3 fractures, while lumbar spine BMD (ORper SD = 0.75 95% CI 0.60–0.95) was negatively associated with SQ1–SQ3 fractures. No association between TBS and SQ1–SQ3 fractures was found. Conclusion Since TBS and SQ1–SQ3 fractures were not associated, they may act as independent risk factors, justifying the use of both in post-fracture risk assessment.

Importance Fragility fracture is a major health issue because of the accompanying morbidity, mortality, and financial cost. Despite the high cost to society and personal cost to affected individuals, secondary fracture prevention is suboptimal in Norway, mainly because most patients with osteoporotic fractures do not receive treatment with antiosteoporotic drugs after fracture repair. Objectives To improve secondary fracture prevention by introducing a standardized intervention program and to investigate the effect of the program on the rate of subsequent fractures. Design, Setting, and Participants Trial protocol of the Norwegian Capture the Fracture Initiative (NoFRACT), an ongoing, stepped wedge cluster randomized clinical trial in 7 hospitals in Norway. The participating hospitals were cluster randomized to an intervention starting date: May 1, 2015; September 1, 2015; and January 1, 2016. Follow-up is through December 31, 2019. The outcome data were merged from national registries of women and men 50 years and older with a recent fragility fracture treated at 1 of the 7 hospitals. Discussion The NoFRACT trial is intended to enroll 82 000 patients (intervention period, 26 000 patients; control period, 56 000 patients), of whom 23 578 are currently enrolled by January 2018. Interventions include a standardized program for identification, assessment, and treatment of osteoporosis in patients with a fragility fracture that is led by a trained coordinating nurse. The primary outcome is rate of subsequent fracture (per 10 000 person-years) based on national registry data. Outcomes before (2008-2015; control period) and after (2015-2019; intervention period) the intervention will be compared, and each hospital will act as its own control. Use of outcomes from national registry data means that all patients are included in the analysis regardless of whether they are exposed to the intervention (intention to treat). A sensitivity analysis with a transition window will be performed to mitigate possible within-cluster contamination. Results Results are planned to be disseminated through publications in peer-reviewed journals and presented at local, national, and international conferences. Conclusions By introducing a standardized intervention program for assessment and treatment of osteoporosis in patients with fragility fractures, we expect to document reduced rates of subsequent fractures and fracture-related mortality. This is an open access article distributed under the terms of the CC-BY License.

© Nordic Orthopaedic Federation This is an open-access article distributed under the terms of the CC-BY-NC-ND 3.0 License which permits users to download and share the article for non-commercial purposes, so long as the article is reproduced in the whole without changes, and provided the original source is credited.

Mesenchymal stem cells (MSC), found in the bone-marrow, the blood circulation, adipose tissue and fetal lungs, have recently been subject to great interest from researchers and clinicians worldwide. These cells provide the body with progenitors for mesodermal derived tissues such as bone, cartilage, muscles, fat and haematopoietic stroma. Whether MSCs also give rise to cells from other embryological derms, the ekto- and endoderm, is under investigation. Suggested explanations why MSCs seem to differentiate into cells of non-mesodermal tissues include transdifferentiation, de-and re-differentiation and cell-fusion. The existence of a pluripotent cell like the ones found in early embryological life is another possibility. How the MSCs function in vivo is subject to discussion. The cells have experimentally been shown to incorporate into certain tissues as functional cells. In yet other sites MSCs provide damaged tissues with humoral factors stimulating tissue repair. MSCs used in therapeutic medicine can be autologous cells (from the patient himself) or allogenous (from another individual). They can be mobilized to the circulation from the bone-marrow by colony stimulating factors or be extracted directly from tissues. MSCs harvested from the body can then be subject to manipulation ex vivo or simply undergo expansion. The cells will then, after intravenous infusion, find their way to the harmed tissues probably by different homing mechanisms. MSCs can also be transplanted directly into the tissue of interest. This paper will discuss the above and in addition include several studies on the potential use of MSCs in clinical practise.