Study Design.: A critical review of available and emerging nucleus pulposus replacement implants. Objectives.: To review the biomechanics, design, and clinical data of currently available and developing nucleus pulposus replacement technologies. Summary of Background Data.: The interest in minimally invasive treatment of degenerative disc disease has grown as the technology for intervertebral motion-sparing devices continues to improve. Replacement of nucleus pulposus without anular obliteration represents a tempting alternative to spinal fusion procedures. The aim in nucleus pulposus replacement is to slow adjacent level degeneration, restore normal loads to the diseased level, and restore segmental spinal biomechanics. Methods.: A literature review of currently available biomaterials, biomechanics, and available preclinical and clinical data on nucleus pulposus replacement implants. Results.: New synthetic biomaterials have recently been developed to closely mimic native biomechanics during compressive loading cycles of the intervertebral disc. This, in conjunction with improved understanding of global spine biomechanics, has allowed the development of novel nucleus replacement implants. These implants are currently at different stages of preclinical and clinical investigations. Conclusions.: Although some of the newly designed prosthesis have shown some promising results in preclinical studies, rigorous short- and long-term clinical evaluations will be critical in evaluating their true efficacy.

Purpose.In the last few years, evidence has emerged to support the possible association between increased BMI and susceptibility to some musculoskeletal diseases. We systematically review the literature to clarify whether obesity is a risk factor for the onset of tendinopathy.Methods.We searched PubMed, Cochrane Central, and Embase Biomedical databases using the keywords “obesity,” “overweight,” and “body mass index” linked in different combinations with the terms “tendinopathy,” “tendinitis,” “tendinosis,” “rotator cuff,” “epicondylitis,” “wrist,” “patellar,” “quadriceps,” “Achilles,” “Plantar Fascia,” and “tendon.”Results.Fifteen studies were included. No level I study on this subject was available, and the results provided are ambiguous. However, all the 5 level II studies report the association between obesity measured in terms of BMI and tendon conditions, with OR ranging between 1.9 (95% CI: 1.1–2.2) and 5.6 (1.9–16.6).Conclusions.The best evidence available to date indicates that obesity is a risk factor for tendinopathy. Nevertheless, further studies should be performed to establish the real strength of the association for each type of tendinopathy, especially because the design of the published studies does not allow identifying a precise cause-effect relationship and the specific role of obesity independently of other metabolic conditions.

Ceramic bearing surfaces are increasingly used for total hip replacement, notwithstanding that concern is still related to ceramic brittleness and its possible mechanical failure. The aim of this systematic review is to answer three questions: (1) Are there risk factors for ceramic component fracture following total hip replacement? (2) Is it possible to perform an early diagnosis of ceramic component failure before catastrophic fracture occurs? (3) Is it possible to draw guidelines for revision surgery after ceramic components failure? A PubMed and Google Scholar search was performed and reference citations from publications identified in the literature search were reviewed. The use of 28 mm short-neck femoral head carries an increased risk of fracture. Acetabular component malposition might increase the risk of ceramic liner fractures. Synovial fluid microanalysis and CT scan are promising in early diagnosis of ceramic head and liner failure. Early revision is suggested in case of component failure; no consensus exists about the better coupling for revision surgery. Ceramic brittleness remains a major concern. Due to the increased number of ceramic on ceramic implants, more revision surgeries and reports on ceramic components failure are expected in the future. An algorithm of diagnosis and treatment for ceramic hip failure is proposed.

Rat lumbar discs comprising nucleus pulposus, annulus fibrosus, and cartilaginous endplates were cultured for 1 week in a specialized media containing either TGF-beta1 or TGF-beta3. Role of TGF-beta isoforms on cell function was evaluated. To develop an in vitro organ culture of rat intervertebral disc and evaluate effects of TGF-beta3 on disc cell function. An in vitro model system is of considerable value in understanding the cell biology of the intervertebral disc. Development of a useful organ culture model would enhance understanding of disc function in health and disease. Rat lumbar intervertebral discs were maintained in organ culture in media supplemented with TGF-beta3 or TGF-beta1 for 1 week. Tissue morphology was studied using routine histologic, histochemical and immunohistochemical techniques. Cell function was assessed by gene expression, sulfate incorporation, and Western blot analysis. After 1 week in culture with TGF-beta3 and TGF-beta1, the gross morphology and tissue architecture of the disc were preserved. TUNEL analysis indicated that there was no evidence of cell death in the nucleus pulposus or the anulus fibrosus. The level of Alcian blue staining in the nucleus pulposus was similar to that of the freshly isolated disc. However, when compared with TGF-beta1, TGF-beta3 elevated the expression of critical matrix genes, enhanced [S] incorporation into proteoglycans, preserved the expression of TGF-beta receptors, and decreased aggrecan turnover. There was also increased activation (phosphorylation) of ERK, a critical signaling protein. Moreover, inhibition of ERK activity, in the presence TGF-beta3, resulted in suppression of collagen Type II, aggrecan, TGF-beta-RI, TGF-beta-RII and TGF-beta-RIII mRNA expression. TGF-beta3 maintains the phenotype of disc cells in organ culture. It exerts this effect, in part, by elevating the levels of activated ERK1/2, which in turn regulates the expression of TGF-beta-RI and TGF-beta-RII.