Publications by authors named "Arun Shanbhag"

Aim: This study aimed to evaluate the stress distribution in an endodontically treated tooth restored with two different reinforcing fibers followed by direct composite restoration using a finite element analysis (FEA).

Settings And Design: FEA.

Subjects And Methods: Two three-dimensional models of endodontically treated maxillary central incisors were restored with two reinforcing fibers: the polyethylene fibers (PFs) and the short fiber-reinforced composite (SFRC), respectively.

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Potential systemic markers of implant wear include products of the wear process (particles and ions) and mediators of the inflammatory reaction that can be induced by wear. Ions from polymers used in arthroplasty are not specific, but high metal ion levels may help identify patients with unexpectedly high wear of metal-on-metal implants. The kinetics of ion production, transport, and excretion are complex, however, so it is currently difficult to interpret the significance of mild elevations in metal ions.

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Aseptic loosening of total joint replacements is believed to be initiated by a macrophage response to prosthetic wear debris. To better characterize the early response to clinically relevant wear debris, we challenged primary human macrophages from four donors with ultra high molecular weight polyethylene (UHMWPE), TiAlV, CoCr, and alumina particles. After a 24-h culture, protein arrays were used to quantify the secretion of 30 different cytokines and chemokines.

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The long-term durability of total joint replacements is critically dependent on adequate peri-implant bone stock, which can be compromised by wear debris-mediated osteolysis. This study investigated the effects of bisphosphonates on enhancing peri-implant bone in the presence of clinically relevant ultra-high molecular weight polyethylene (UHMWPE) wear debris. Fiber-mesh coated titanium-alloy plugs were implanted bilaterally in the femoral condyles of 36 New Zealand white rabbits.

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Background: Previous studies of bone resorption around failed joint replacements have focused on a limited number of cytokines, primarily tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1, and IL-6, with use of enzyme-linked immunosorbent assay and immunohistochemistry techniques. In this study, we utilized high-throughput protein chips to profile twenty-nine inflammatory cytokines around failed total joint replacements.

Methods: Peri-implant granulomatous tissues were harvested from around the failed total hip prostheses of thirteen patients.

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Osteolysis remains a common mode of total hip arthroplasty failure. In vitro and animal models have been used to determine the pathophysiology of osteolysis by carefully dissecting the biochemical pathways leading to particulate wear debris and periprosthetic bone loss. Numerous cytokines and inflammatory mediators, including TNF-alpha and IL-1, are critical participants in this cascade and may represent prime targets for pharmacologic intervention.

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Total joint arthroplasty is very effective for improving the quality of life of patients with end-stage arthritis. Despite advances in materials, surgical technique, and rehabilitation regimens, joint replacements are still fraught with complications leading to their premature failure. Aseptic loosening and osteolysis are the primary causes of implant failure.

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A total of 750 images of individual ultra-high molecular weight polyethylene (UHMWPE) particles isolated from periprosthetic failed hip, knee, and shoulder arthroplasties were extracted from archival scanning electron micrographs. Particle size and morphology was subsequently analyzed using computerized image analysis software utilizing five descriptors found in ASTM F1877-98, a standard for quantitative description of wear debris. An online survey application was developed to display particle images, and allowed ten respondents to classify particle morphologies according to commonly used terminology as fibers, flakes, or granules.

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Alendronate and other bisphosphonates are clinically efficacious in treating postmenopausal osteoporosis, Paget's disease and hypercalcemia associated with malignancy. Because bisphosphonates are being considered for use in younger patients with joint replacements to prevent osteolysis, and for stress fracture prophylaxis in military recruits, it is important to know how bisphosphonate therapy affects healthy bone. We sought to determine whether bones from healthy male dogs exhibit alterations in structural or mechanical properties following alendronate treatment for 23 weeks.

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Bisphosphonates are well known potent inhibitors of osteoclast activity and are widely used to treat metabolic bone diseases. Recent evidence from in vitro and in vivo studies indicates that bisphosphonates may additionally promote osteoblastic bone formation. In this study, we evaluated the effects of three FDA-approved and clinically utilized bisphosphonates, on the proliferation and osteogenic differentiation of human bone marrow stromal cells (BMSC).

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The most common cause of total joint replacement failure is peri-implant bone loss causing pain and prosthesis loosening. This process, known as osteolysis or aseptic loosening, is characterized by macrophage phagocytosis of particulate implant wear debris. In an incompletely defined step, particulate biomaterial debris induces macrophages to release a variety of inflammatory mediators and signaling proteins that lead to bone loss.

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Aseptic loosening and osteolysis are currently the most common causes of failure of total joint replacements. Osteolysis is initiated by a macrophage response to wear debris, resulting in localized, osteoclastic peri-implant bone loss. We have previously inhibited osteoclast-mediated bone resorption in a canine total hip arthroplasty model using oral bisphosphonate therapy.

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To prevent wear debris-induced osteolysis and aseptic loosening, cross-linked ultra-high molecular weight polyethylene's (UHMWPE) with improved wear resistance have been developed. Hip simulator studies have demonstrated very low wear rates with these new materials leading to their widespread clinical use. However, the biocompatibility of this material is not known.

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Numerous in vitro models have demonstrated the capacity of wear particles to stimulate the release of soluble pro-inflammatory products with the ability to induce local bone resorption. Recent observations have demonstrated that binding of lipopolysaccharide (LPS) to particulate wear debris can significantly modulate the pattern of cell response in the in vitro models. These findings raise concerns over the possible role of LPS in the pathogenesis of aseptic loosening after total joint replacements, and also indicates the importance of controlling for possible confounding effects of LPS contamination in the in vitro models used to study the reactive nature of wear debris.

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Total hip arthroplasty (THA) has provided dramatic pain relief and improvement in function for millions of patients with end-stage arthritis; however, periprosthetic osteolysis following THA has become increasingly recognized as a major clinical problem in both cemented and cementless reconstructions. An aggressive granulomatous tissue (interfacial membrane) consisting predominantly of fibroblasts, aggregates of macrophages, and foreign body giant cells develops at the interface of bone/prostheses or bone/cement. It is believed that particulate wear debris from prosthetic materials and/or bone cement are phagocytized by histiocytic cells of interfacial membrane and then these cells produce inflammatory mediators and proteolytic enzymes to provoke a cascade of osteolytic events.

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