Heterotopic ossification is a condition characterized by the presence of mature lamellar bone and often bone marrow in soft tissues surrounding a major joint. It represents a common complication after total hip arthroplasty (THA). The etiology and predisposing factors are not completely known, but some authors reported that the implant of a non-cemented prosthesis seems to be associated with a greater incidence of HO. Two hundred and two non-cemented total hip arthroplasties were performed between October 1997 and February 2002. The mean age was 70.2 years. The average follow-up for 181 hips included in the study was 96 months (range, 72–120 months). A standard lateral approach (Hardinge) was performed for the implant of a non-cemented femoral component and a non-cemented acetabular component. Radiographs were done before and after surgery, at 1, 4 and 12 months postop, then every year. The incidence of HO was assessed in the antero-posterior view at each interval and graded according to Brooker classification. Out of 181 implants, HO was observed in 52 hips (28,7%). Heterotopic bone was graded as class I in 32 (17.7%) hips, class II in 14 (7.73%) hips, class III in 6 (3,3%) hips and class IV in none (0%). The mean preoperative Harris hip score was 48; at the last follow-up, the mean postoperative score was preoperatively to a mean of 89 points (range, 76–97 points) in HO Hip and of 91 points (range, 78–100 points) in the other Hip. In our experience, non-cemented THA led to a higher incidence of class I and II HO according to Brooker Classification, the incidence of HO is comparable to the rates reported in recent studies about the HO finding after a non-cemented THA, the importance of clinical symptoms in the presence of HO is very low.

Purpose of this study is to conduct a meta-analysis comparing the results of open and arthroscopic Bankart repair using suture anchors in recurrent traumatic anterior shoulder instability. Using Medline Pubmed, Cochrane and Embase databases we performed a search of all published articles. We included only studies that compared open and arthroscopic repair using suture anchors. Statistical analysis was performed using chi-square test. Six studies met the inclusion criteria. The total number of patients was 501, 234 suture anchors and 267 open. The rate of recurrent instability in the arthroscopic group was 6% versus 6.7% in the open group; rate of reoperation was 4.7% in the arthroscopic group vs. 6.6% in open (difference not statistically significant). The difference was statistically significant only in the studies after 2002 (2.9% of recurrence in the arthroscopic group vs. 9.2% in open; 2.2% of reoperation in the arthroscopic group vs. 9.2% in open). Results regarding function couldn't be combined because of non-homogeneous scores reported in the original articles, but the arthroscopic treatment led to better functional results. Arthroscopic repair using suture anchors results in similar redislocation and reoperation rate compared to open Bankart repair; however, we need larger and more homogeneous prospective studies to confirm these findings.

OBJECTIVE:Extra corporeal shock waves (ESW) have been proposed as additional therapy in bone fracture repair and osteoarthrtitis (OA). However, little is known on the effects of ESW on osteoblast metabolism. The aim of this study was to evaluate phenotype changes of healthy and OA human osteoblasts following ESW treatment.METHODS:Osteoblasts were isolated from subchondral bone of 13 OA patients and 7 healthy donors. Osteoblasts were treated or not with ESW at different levels of energy and impulses. IL-10, TNF-alpha, CD29/Beta1 integrin, and CD105/endoglin expression was evaluated by flowcytometry.RESULTS:Intracellular IL-10 significantly increased using 1000 impulses at 0.055 mJ/mm2 in both healthy and OA osteoblasts in comparison with untreated osteoblasts (p<0.01). Only in the OA osteoblasts CD29 and CD105 expression significantly increased at 500 impulses and 0.17 mJ/mm2 ESW treatment (p<0.05).CONCLUSION:ESW are capable of modifying IL-10 expression in osteoblasts. There is evidence that IL-10 can play a role in bone remodelling by inhibiting osteoclast differentiation and this suggests that ESW may favour bone growth and healing. This further supports the use of ESW in treating bone fracture to promote callus formation. However, the possible use of ESW in OA therapy needs further studies since in OA, osteoblast metabolism is already enhanced with bone sclerosis and ESW application may further increase bone deposition and osteophyte formation, leading to a subsequent worsening of the disease.

Activin A is a potent growth and differentiation factor whose synthesis and bioactivity are tightly regulated. Both follistatin binding and inhibin subunit heterodimerization block access to the activin receptor and/or receptor activation. We postulated that the activin-beta(C) subunit provides another mechanism regulating activin bioactivity. To test our hypothesis, we examined the biological effects of activin C and produced mice that overexpress activin-beta(C). Activin C reduced activin A bioactivity in vitro; in LNCaP cells, activin C abrogated both activin A-induced Smad signaling and growth inhibition, and in LbetaT2 cells, activin C antagonized activin A-mediated activity of an follicle-stimulating hormone-beta promoter. Transgenic mice that overexpress activin-betaC exhibited disease in testis, liver, and prostate. Male infertility was caused by both reduced sperm production and impaired sperm motility. The livers of the transgenic mice were enlarged because of an imbalance between hepatocyte proliferation and apoptosis. Transgenic prostates showed evidence of hypertrophy and epithelial cell hyperplasia. Additionally, there was decreased evidence of nuclear Smad-2 localization in the testis, liver, and prostate, indicating that overexpression of activin-beta(C) antagonized Smad signaling in vivo. Underlying the significance of these findings, human testis, liver, and prostate cancers expressed increased activin-betaC immunoreactivity. This study provides evidence that activin-beta(C) is an antagonist of activin A and supplies an impetus to examine its role in development and disease.

The Achilles tendon rupture (ATR) is a severe injury and requires a surgical treatment which can result in functional impairment, limiting unprofessional sports activities. In order to evaluate this potential impairment 20 subjects (SG) who had received surgical treatment for ATR and 20 healthy subjects (CG) were required to execute vertical jump according to counter movement jump and squat jump protocol. For both groups the flying time (Tv) of each foot has been acquired, adopting accelerometric transducers positioned posteriorly at the level of malleolar axis. The SG's Tv is significantly lesser than the CG's one, demonstrating an inferior global performance respect to healthy people and the operated leg has a Tv 6% higher than the contralateral, while in the CG there are no statistical difference between the Tv of the limbs. For seven operated subjects Tv values are lesser than threshold values obtained from CG. For them sports activity which implies high and cyclic stress on the lower limbs could be dangerous. Functional evaluation, consequently, allow to assess impairments not differently estimable.

Activin A is a member of the transforming growth factor-β superfamily, which we have identified as having a role in inflammatory responses. We show that circulating levels of activin increase rapidly after LPS-induced challenge through activation of Toll-like receptor 4 and the key adaptor protein, MyD88. Treatment with the activin-binding protein, follistatin, alters the profiles of TNF, IL-1β, and IL-6 after LPS stimulation, indicating that activin modulates the release of several key proinflammatory cytokines. Further, mice administered one 10-μg dose of follistatin to block activin effects have increased survival after a lethal dose of LPS, and the circulating levels of activin correlate with survival outcome. These findings demonstrate activin A's crucial role in the inflammatory response and show that blocking its actions by the use of follistatin has significant therapeutic potential to reduce the severity of inflammatory diseases.

Activin A, a member of the transforming growth factor-beta superfamily, is constitutively expressed in hepatocytes and regulates liver mass through tonic inhibition of hepatocyte DNA synthesis. Follistatin is the main biological inhibitor of activin bioactivity. These molecules may be involved in hepatic fibrogenesis, although defined roles remain unclear. We studied activin and follistatin gene and protein expression in cultured rat hepatic stellate cells (HSCs) and in rats given CCl4 for 8 wk and examined the effect of follistatin administration on the development of hepatic fibrosis. In activated HSCs, activin mRNA was upregulated with high expression levels, whereas follistatin mRNA expression was unchanged from baseline. Activin A expression in normal lobular hepatocytes redistributed to periseptal hepatocytes and smooth muscle actin-positive HSCs in the fibrotic liver. A 32% reduction in fibrosis, maximal at week 4, occurred in CCl4-exposed rats treated with follistatin. Hepatocyte apoptosis decreased by 87% and was maximal at week 4 during follistatin treatment. In conclusion, activin is produced by activated HSCs in vitro and in vivo. Absence of simultaneous upregulation of follistatin gene expression in HSCs suggests that HSC-derived activin is biologically active and unopposed by follistatin. Our in vivo and in vitro results demonstrate that activin-mediated events contribute to hepatic fibrogenesis and that follistatin attenuates early events in fibrogenesis by constraining HSC proliferation and inhibiting hepatocyte apoptosis.

We estimate the effectiveness of the manual lymphodrainage in the patients with post-mastectomy lymphedema of the upper limb associated to axillary lymphnodes dissection of the ipsilateral arm. The best results were found in the patients with soft and recent lymphedema (which means that was seen within one year); the worst were found in the chronic hard lymphedema. An important psychological assistance and physiotherapy were required to complete the rehabilitation. However, the physiotherapy was very effective when associated to pressed bandage of the arm, at the end of the LDM therapy. Furthermore, the muscle contraction in the bandage had reinforced the lymphoematic pump effect.

www.gimle.fsm.it We estimate the effectiveness of the manual lymphodrainage in the patients with post-mastectomy lymphedema of the upper limb associated to axillary lymphnodes dissection of the ipsilateral arm. The best results were found in the patients with soft and recent lymphedema (which means that was seen within one year); the worst were found in the chronic hard lymphedema. An important psychological assistance and physiotherapy were required to complete the rehabilitation. However, the physiotherapy was very effective when associated to pressed bandage of the arm, at the end of the LDM therapy. Furthermore, the muscle contraction in the bandage had reinforced the lymphoematic pump effect.