Fracture liaison service model: project design and accreditation.

Frailty fractures place a significant socioeconomic burden on the health care system. The Italian Society of Orthopaedics and Traumatology (SIOT) is proceeding to fracture liaison service (FLS) model accreditation in several Italian Fracture Units (FUs), which provides a multidisciplinary approach for the management of the fragility fracture patient. INTRODUCTION: Osteoporosis and the resulting fragility fractures, particularly femoral fractures, place significant socioeconomic burdens on the health care system globally. In addition, there is a general lack of awareness of osteoporosis, resulting in underestimation of the associated risks and suboptimal treatment of the disease. The fracture liaison service (FLS) represents an exemplary model of post-fracture care that involves a multidisciplinary approach to the frail patient through the collaboration of multiple specialists. The purpose of this article is to highlight the path undertaken by the Italian Society of Orthopaedics and Traumatology (SIOT) for the purpose of certification of numerous FLS centers throughout Italy. METHODS: SIOT is proceeding with international FLS accreditation in several Italian Fracture Units (FUs), following the creation of a model that provides specific operational and procedural steps for the management of fragility fractures throughout the country. FUs that decide to join the project and implement this model within their facility are then audited by an ACCREDIA-accredited medical certification body. RESULTS: The drafted FLS model, thanks to the active involvement of a panel of experts appointed by SIOT, outlines a reference operational model that describes a fluid and articulated process that identifies the procedure of identification, description of diagnostic framing, and subsequent initiation of appropriate secondary prevention programs for fractures of individuals who have presented with a recent fragility fracture of the femur. CONCLUSION: Accreditation of this prevention model will enable many facilities to take advantage of this dedicated diagnostic-therapeutic pathway for the purpose of fracture prevention and reduction of associated health and social costs.

Clusterin silencing restores myoblasts viability and down modulates the inflammatory process in osteoporotic disease.

BACKGROUND: Targeting new molecular pathways leading to Osteoporosis (OP) and Osteoarthritis (OA) is a hot topic for drug discovery. Clusterin (CLU) is a glycoprotein involved in inflammation, proliferation, cell death, neoplastic disease, Alzheimer disease and aging. The present study focuses on the expression and the role of CLU in influencing the decrease of muscle mass and fiber senescence in OP-OA condition. METHODS: Vastus lateralis muscle biopsies were collected from 20 women with OP undergoing surgery for fragility hip fracture and 20 women undergoing arthroplasty for hip osteoarthritis. RESULTS: We found an overexpression of CLU in degenerated fibers in OP closely correlated with interleukin 6 (IL6) and histone H4 acetylation level. Conversely, in OA muscle tissues we observed a weak expression of CLU but no nuclear histone H4 acetylation. Ex vivo studies on isolated human myoblasts confirmed CLU overexpression in OP as compared to OA (p < 0.001). CLU treatment of isolated OP and OA myoblasts showed: modulation of proliferation, morphological changes, increase of histone H4 acetylation and induction of myogenin (MYOG) activation in OP myoblast only. In OP condition, functional knockdown of CLU by siRNA restores proliferative myoblasts capability and tissue damage repair, carried out by an evident upregulation of Transglutaminase 2 (TGM2). We also observed downmodulation of CX3CR1 expression with consequent impairing of the inflammatory infiltrate recruitment. CONCLUSIONS: Results obtained suggest a potential role of CLU in OP by influencing myoblasts terminal differentiation, epigenetic regulation of muscle cell differentiation and senescence. Moreover, CLU silencing points out its role in the modulation of tissue damage repair and inflammation, proposing it as a new diagnostic marker for muscle degeneration and a potential target for specific therapeutic intervention in OP related sarcopenia.

Femoral cortical index: an indicator of poor bone quality in patient with hip fracture.

BACKGROUND: Osteoporosis is a common disease in elderly, characterized by poor bone quality as a result of alterations affecting trabecular bone. However, recent studies have described also an important role of alterations of cortical bone in the physiopathology of osteoporosis. Although dual-energy X-ray absorptiometry (DXA) is a valid method to assess bone mineral density, in the presence of comorbidities real bone fragility is unable to be evaluated. The number of hip fractures is rising, especially in people over 85 years old. AIMS: The aim is to evaluate an alternative method so that it can indicate fracture risk, independent of bone mineral density (BMD). Femoral cortical index (FCI) assesses cortical bone stock using femur X-ray. METHODS: A retrospective study has been conducted on 152 patients with hip fragility fractures. FCI has been calculated on fractured femur and on the opposite side. The presence of comorbidities, osteoporosis risk factors, vitamin D levels, and BMD have been analyzed for each patient. RESULTS: Average values of FCI have been 0.42 for fractured femurs and 0.48 at the opposite side with a statistically significant difference (p = 0.002). Patients with severe hypovitaminosis D had a minor FCI compared to those with moderate deficiency (0.41 vs. 0.46, p < 0.011). 42 patients (27.6%) with osteopenic or normal BMD have presented low values of FCI. DISCUSSION AND CONCLUSION: A significant correlation among low values of FCI, comorbidities, severe hypovitaminosis D. and BMD in patients with hip fractures has been found. FCI could be a useful tool to evaluate bone fragility and to predict fracture risk even in the normal and osteopenic BMD patients.

Changes in serum levels of TNF-alpha, IL-6, OPG, RANKL and their correlation with radiographic and clinical assessment in fragility fractures and high energy fractures.

Stages of bone turnover during fracture repair can be assessed employing serum markers of osteoblastic and osteoclastic activity, inflammatory cytokines, clinical evaluation and imaging instruments. Our study compare the fracture healing process in fragility fractures and high energy fractures by evaluating serum changes of interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-alpha), osteoprotegerin (OPG) and receptor activator of the nuclear factor-kB ligand (RANKL) in combination with radiographic (Radiographic Union Scale for Tibial fractures, RUST) and clinical (Lower extremity measure, LEM) assessments. We enrolled 56 patients divided into four corresponding groups: group A with high energy trauma fracture (tibial/femoral shaft); group B with low energy trauma fracture (femoral fractures); healthy (control A) and osteoporotic subjects (control B). Blood samples were collected before surgery (T0) and after 10 weeks (T10). Serum concentrations of IL-6, TNF-alpha, RANKL and OPG were quantified using commercial enzyme-linked immunosorbent assay (ELISA) kits. Our results show that RANKL values are significantly higher at T10 than at T0 in low energy trauma fractures (group B). OPG is significantly lower in each control group than that of the respective fractured group and its concentration at T0 and at T10 is significantly lower in high than in low energy fractures. RANKL/OPG ratio is significantly higher in both controls than in fractured groups, and significantly increases after 10 weeks. IL-6 and TNF-alpha concentrations significantly decrease during fracture healing and are higher in high (group A) than in low energy fractures (group B). Significant differences were also found in both RUST score and LEM between groups A and B. Changes in TNF-alpha and IL-6 levels correlate with RUST and LEM in fragility and high energy fractures, while RANKL/OPG ratio is associated with these clinical parameters only in fragility fractures. These findings suggest that serum levels of IL-6, TNF-alpha, RANKL and OPG might be used to monitor the stages of fracture repair. Further studies will be needed to confirm the role of these cytokines in fracture repair.

Open medial dislocation of the ankle without fracture.

A 20-year-old man sustained an open medial dislocation of the ankle without an associated fracture after a low-energy inversion injury. Prompt debridement and reduction with primary wound closure of the skin were performed without suture of the capsule. Immobilisation in a non-weight-bearing cast for 30 days followed by ankle bracing for two weeks and subsequent physiotherapy, produced full functional recovery by three months. At follow-up at one year there was a full range of pain-free movement, although the radiographs and MR scan showed early post-traumatic degenerative change at the medial aspect of the tibiotalar and the calcaneocuboid joints.