40 research outputs found
Formation of blood clot on biomaterial implants influences bone healing
No full textThe first step in bone healing is forming a blood clot at injured bones. During bone implantation, biomaterials unavoidably come into direct contact with blood, leading to a blood clot formation on its surface prior to bone regeneration. Despite both situations being similar in forming a blood clot at the defect site, most research in bone tissue engineering virtually ignores the important role of a blood clot in supporting healing. Dental implantology has long demonstrated that the fibrin structure and cellular content of a peri-implant clot can greatly affect osteoconduction and de novo bone formation on implant surfaces. This paper reviews the formation of a blood clot during bone healing in related to the use of platelet-rich plasma (PRP) gels. It is implicated that PRP gels are dramatically altered from a normal clot in healing, resulting conflicting effect on bone regeneration. These results indicate that the effect of clots on bone regeneration depends on how the clots are formed. Factors that influence blood clot structure and properties in related to bone healing are also highlighted. Such knowledge is essential for developing strategies to optimally control blood clot formation, which ultimately alter the healing microenvironment of bone. Of particular interest are modification of surface chemistry of biomaterials, which displays functional groups at varied composition for the purpose of tailoring blood coagulation activation, resultant clot fibrin architecture, rigidity, susceptibility to lysis, and growth factor release. This opens new scope of in situ blood clot modification as a promising approach in accelerating and controlling bone regeneration
Shear properties of bilaminar polymethylmethacrylate cement mantles in revision hip joint arthroplasty.
No full textAlthough cement-within-cement revision arthroplasty minimizes the complications associated with removal of secure PMMA, failure at the interfacial region between new and old cement mantles remains a theoretical concern. This article assesses the variability in shear properties of bilaminar cement mantles related to duration of postcure and the use of antibiotic cements. Bilaminar cement mantles were 15% to 20% weaker than uniform mantles (P < .001) and demonstrated variability in shear strength related to duration of postcure of the freshly applied cement (P < .001). The use of Antibiotic Simplex did not significantly influence interfacial cement adhesion (P = .52). Interfacial adhesion by mechanisms other than mechanical interlock plays a significant role in the bond formed between new and old PMMA cements, with an important contribution by diffusion-based molecular interdigitation. In the presence of a secure cement-bone interface, we recommend cement-within-cement revision techniques in suitable patients.Griffith Health FacultyNo Full Tex
Elution and mechanical properties of antifungal bone cement.
No full textThe effect of the incorporation of amphotericin B into bone cement was examined; as literature suggests, this may be a feasible method for the treatment of periprosthetic fungal infections. Addition of antifungal increased the compressive strength of the bone cement--a statistically significant amount from 107 +/- 2.3 to 121 +/- 1.5 MPa. Elution of tobramycin and amphotericin B was quantified using ultraviolet-visible spectroscopy. Spectroscopy showed that 18% of the antibiotic was released during the first week, with most released in the first 24 hours. The elution of antifungal, however, was unable to be detected after 1 week, with less than 0.03% released. Amphotericin B does not weaken bone cement. Its inability to be delivered at a clinically significant dose gives no clear indication for its incorporation into cement.Griffith Health FacultyNo Full Tex
Pilot study conducted on Exeter PMMA cement reamer
No full textPilot study and critical appraisal of the prototype Exeter PMMA Cement Reamer conducted in order to determine potential applications and improvements to design
Transplanted abdominal granulation tissue induced bone formation - an in vivo study in sheep
No full textCombined VEGF and PDGF Treatment Reduces Secondary Degeneration after Spinal Cord Injury
No full textTrauma to the spinal cord creates an initial physical injury damaging neurons, glia and blood vessels, which then induces a prolonged inflammatory response leading to secondary degeneration of spinal cord tissue and further loss of neurons and glia surrounding the initial site of injury. Angiogenesis is a critical step in tissue repair but in the injured spinal cord angiogenesis fails; blood vessels formed initially, later regress. Stabilizing the angiogenic response is therefore a potential target to improve recovery after for spinal cord injury. Vascular Endothelial Growth Factor (VEGF) can initiate angiogenesis but cannot sustain blood vessel maturation. Platelet Derived Growth Factor (PDGF) can promote blood vessel stability and maturation. We therefore investigated a combined application of VEGF and PDGF as treatment for traumatic spinal cord injury, with the aim to reduce secondary degeneration by promotion of angiogenesis. Immediately after hemi-section of the spinal cord in the rat we delivered VEGF and PDGF and to the injury site. One and three months later the size of the lesion was significantly smaller in the treated group compared to controls and there was significantly reduced gliosis surrounding the lesion. There was no significant effect of the treatment on blood vessel density, although there was a significant reduction in the numbers of macrophages/microglia surrounding the lesion, and a shift in the distribution of morphological and immunological phenotypes of these inflammatory cells. VEGF and PDGF delivered singly exacerbated the secondary degeneration, increasing the size of the lesion cavity. These results demonstrate a novel therapeutic intervention for spinal cord injury and reveal an unanticipated synergy for these growth factors whereby they modulated inflammatory processes and create a microenvironment conducive to axon preservation/sprouting.Full Tex
Low cost polymer intramedullary nails for fracture fixation: a biomechanical study in a porcine femur model
No full textControlling whole blood activation and resultant\ud clot properties by carboxyl and alkyl functional\ud groups on material surfaces : a possible therapeutic\ud approach for enhancing bone healing\ud
No full textMost research virtually ignores the important role of a blood clot in supporting bone healing. In this study,\ud
we investigated the effects of surface functional groups carboxyl and alkyl on whole blood coagulation,\ud
complement activation and blood clot formation. We synthesised and tested a series of materials with\ud
different ratios of carboxyl (–COOH) and alkyl (–CH3, –CH2CH3 and –(CH2)3CH3) groups. We found that\ud
surfaces with –COOH/–(CH2)3CH3 induced a faster coagulation activation than those with –COOH/–\ud
CH3 and –CH2CH3, regardless of the –COOH ratios. An increase in –COOH ratios on –COOH/–CH3\ud
and –CH2CH3 surfaces decreased the rate of coagulation activation. The pattern of complement\ud
activation was entirely similar to that of surface-induced coagulation. All material coated surfaces\ud
resulted in clots with thicker fibrin in a denser network at the clot/material interface and a significantly\ud
slower initial fibrinolysis when compared to uncoated glass surfaces. The amounts of platelet-derived\ud
growth factor-AB (PDGF-AB) and transforming growth factor-b (TGF-b1) released from an intact clot\ud
were higher than a lysed clot. The release of PDGF-AB was found to be correlated with the fibrin density.\ud
This study demonstrated that surface chemistry can significantly influence the activation of blood\ud
coagulation and complement system, resultant clot structure, susceptibility to fibrinolysis as well as\ud
release of growth factors, which are important factors determining the bone healing process
Tailoring hydrogel surface properties to modulate cellular response to shear loading
No full textBiological tissues at articulating surfaces, such as articular cartilage, typically have remarkable low-friction properties that limit tissue shear during movement. However, these frictional properties change with trauma, aging, and disease, resulting in an altered mechanical state within the tissues. Yet, it remains unclear how these surface changes affect the behaviour of embedded cells when the tissue is mechanically loaded. Here, we developed a cytocompatible, bilayered hydrogel system that permits control of surface frictional properties without affecting other bulk physicochemical characteristics such as compressive modulus, mass swelling ratio, and water content. This hydrogel system was applied to investigate the effect of variations in surface friction on the biological response of human articular chondrocytes to shear loading. Shear strain in these hydrogels during dynamic shear loading was significantly higher in high-friction hydrogels than in low-friction hydrogels. Chondrogenesis was promoted following dynamic shear stimulation in chondrocyte-encapsulated low-friction hydrogel constructs, whereas matrix synthesis was impaired in high-friction constructs, which instead exhibited increased catabolism. Our findings demonstrate that the surface friction of tissue-engineered cartilage may act as a potent regulator of cellular homeostasis by governing the magnitude of shear deformation during mechanical loading, suggesting a similar relationship may also exist for native articular cartilage.\ud
\ud
<b>STATEMENT OF SIGNIFICANCE:</b>\ud
\ud
Excessive mechanical loading is believed to be a major risk factor inducing pathogenesis of articular cartilage and other load-bearing tissues. Yet, the mechanisms leading to increased transmission of mechanical stimuli to cells embedded in the tissue remain largely unexplored. Here, we demonstrate that the tribological properties of loadbearing tissues regulate cellular behaviour by governing the magnitude of mechanical deformation arising from physiological tissue function. Based on these findings, we propose that changes to articular surface friction as they occur with trauma, aging, or disease, may initiate tissue pathology by increasing the magnitude of mechanical stress on embedded cells beyond a physiological level
