There is no general consensus on the use of growth factors (GF) in surgery.
IntroductionWe aimed to assess the incidence and hospitalization rate of hip and "minor" fragility fractures in the Italian population.MethodsWe carried out a 3-year survey at 10 major Italian emergency departments to evaluate the hospitalization rate of hip, forearm, humeral, ankle, and vertebral fragility fractures in people 45 years or older between 2004 and 2006, both men and women. These data were compared with those recorded in the national hospitalizations database (SDO) to assess the overall incidence of fragility fractures occurring at hip and other sites, including also those events not resulting in hospital admissions.ResultsWe observed 29,017 fractures across 3 years, with hospitalization rates of 93.0% for hip fractures, 36.3% for humeral fractures, 31.3% for ankle fractures, 22.6% for forearm/wrist fractures, and 27.6% for clinical vertebral fractures. According to the analyses performed with the Italian hospitalization database in year 2006, we estimated an annual incidence of 87,000 hip, 48,000 humeral, 36,000 ankle, 85,000 wrist, and 155,000 vertebral fragility fractures in people aged 45 years or older (thus resulting in almost 410,000 new fractures per year). Clinical vertebral fractures were recorded in 47,000 events per year.ConclusionsThe burden of fragility fractures in the Italian population is very high and calls for effective preventive strategies.
BackgroundBone repair alteration is hypothesized for nonunion fracture pathogenesis. Since it is involved in osteoclast regulation, the RANK/RANKL/OPG system (receptor activator of nuclear factor kB/its ligand/osteoprotegerin) may play a role.Materials and methodsSerum OPG, free RANKL, bone alkaline phosphatase (BAP), osteocalcin (OC), and urinary deoxypyridinoline (DPD) were determined in 16 male patients (20–39 years) with long bone atrophic nonunion fractures. Serum markers were also measured in 18 age-matched male controls who healed from the same type of fractures within six months, and in 14 age-matched male controls who were healing from the same fractures one month after injury. One-way ANOVA and Bonferroni’s test were used for statistical analysis.ResultsOnly OPG was significantly higher (0.56 sd 0.11 ng/ml) in the patients compared to healed (0.26 sd 0.04 ng/ml; P < 0.001) and healing (0.29 sd 0.09 ng/ml; P < 0.001) controls. The patients’ DPD levels were normal. No correlations were found between bone markers and the characteristics of the subjects in all groups.ConclusionsA normal steady state of bone metabolism seems to be present in patients with atrophic nonunion fractures, despite the high serum OPG. The reason for the inability of the patients’ OPG to inhibit osteoclastic activity is unknown. Osteoblast activity also appears normal, so another cellular source of OPG can be hypothesized.
IntroductionOsteoprotegerin (OPG), a glycoprotein prevalently produced by the osteoblast, is involved in osteoclastogenesis regulation with inhibiting action [1]. In the literature, controversial data have appeared regarding levels of OPG in post-menopausal women and about its correlation with bone turnover markers and bone mass [2][3][4][5]. OPG seems to play a role as a possible marker for diagnosing and monitoring post-menopausal osteoporosis [2][3][4].The aim of this study was to evaluate circulating levels of OPG in osteoporotic post-menopausal women, and to determine if OPG correlated with serum bone turnover markers and with bone mineral density of spine and femur. Patients and methodsThe study enrolled 25 women (aged 63+8 years) with a menopause duration of 15±9 years, in whom diseases and other conditions affecting bone metabolism had been already excluded. We measured serum levels of OPG (Bio Vendor; Brno, Czech Republic), total alkaline phosphatase (Roche, Basel, Switzerland), osteocalcin, bone isoenzyme of alkaline phosphatase and urinary deoxypyridinoline (Quidel, San Diego, USA). We also measured bone mineral density (BMD) of the lumbar spine and femur (total, neck and Ward's triangle) by means of a densitometer DXA QDR 4500A (Hologic). All patients presented a T-score <-2.5 SD in all the explored skeletal sites, including femoral subregions. All the patients gave informed consent to inclusion in the study.Student's t test for unpaired data and Pearson's correlation test were used for statistical analysis. O R I G I N A L J Orthopaed Traumatol (2005) 6:88-90Abstract An increase of setum osteoprotegerin has been found in post-menopausal women, that is positively correlated with age and bone markers, negatively with bone mass. In 25 post-menopausal women (mean age, 63±8 years) we measured serum levels of osteoprotegerin, total and bone alkaline phosphatase, osteocalcin, urinary deoxypyridinoline and bone mineral density of the lumbar spine and femur. Osteoprotegerin and bone markers did not differ from range of normal values. Bone mineral density appeared markedly reduced both at the spine and the femur.A significant correlation between osteoprotegerin and age, duration of menopause, osteocalcin and bone alkaline phosphatase was found. No correlation was found between osteoprotegerin and bone mineral density in all measured skeletal sites. In conclusion, osteoprotegerin does not appear to be an interesting parameter for the evaluation of bone turnover in post-menopausal osteoporosis.
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