Real time monitoring of screw insertion using acoustic emission can predict screw stripping in human cancellous bone.

BACKGROUND: To develop experience, orthopaedic surgeons train their own proprioception to detect torque during screw insertion. This experience is acquired over time and when implanting conventional/non-locked screws in osteopenic cancellous bone the experienced surgeon still strips between 38 and 45%. Technology needs to be investigated to reduce stripping rates. Acoustic-Emission technology has the ability to detect stress wave energy transmitted through a screw during insertion into synthetic bone. Our hypothesis is Acoustic-Emission waves can be detected through standard orthopaedic screwdrivers while advancing screws through purchase and overtightening in cancellous human bone with different bone mineral densities replicating the clinical state. METHODS: 77 non-locking 4 mm and 6.5 mm diameter cancellous bone screws were inserted through to stripping into the lateral condylar area of 6 pairs of embalmed distal femurs. Specimens had varying degrees of bone mineral density determined by quantitative CT. Acoustic-Emission energy and axial force were detected for each test. RESULTS: The tests showed a significant high correlation between bone mineral density and Acoustic-Emission energy with R = 0.74. A linear regression model with the mean stripping load as the dependent variable and mean Acoustic-Emission energy, bone mineral densities and screw size as the independent variables resulted in r2 = 0.94. INTERPRETATION: This experiment succeeded in testing real time Acoustic-Emission monitoring of screw purchase and overtightening in human bone. Acoustic-Emission energy and axial compressive force have positive high correlation to bone mineral density. The purpose is to develop a known technology and apply it to improve the bone-metal construct strength by reducing human error of screw overtightening.

Blood platelets activate the classical pathway of human complement.

OBJECTIVE: Activation of the complement system plays a key role in inflammation associated with vascular injury. Recently, platelet P-selectin was shown to activate C3 via the alternative pathway of human complement. As platelets also posses binding sites for C1q, the recognition unit of the classical complement pathway, the present study examined classical pathway activation on platelets. METHODS: Complement activation was assessed by either a solid phase enzyme-linked immunosorbent assay (ELISA) or flow cytometry. RESULTS: Using the ELISA approach, 2- to 10-fold increases (P < 0.001) in C1q and C4d deposition were demonstrated on adherent platelets following exposure (60 min 37 degrees C) to diluted (1/10) human plasma or serum. Similar results were obtained by flow cytometry using activated platelets in suspension. C1q and C4d deposition on platelets was accompanied by an approximately 4-fold increase in fluid phase C4d and C3a generation. Consistent with activation of the classical complement pathway, C4 cleavage failed to occur in serum depleted of C1q but was unchanged in factor B deficient serum. C4 activation was enhanced by platelet stimulation using chemical (SFLLRN peptide) or mechanical (shear) means, and decreased following platelet exposure to plasmin. These treatments were accompanied by changes in platelet surface gC1qR/p33 expression, a cellular C1q binding protein. In purified systems, recombinant gC1qR/p33 supported C4 activation, in a C1q dependent manner. CONCLUSION: These data provide the first evidence for C1q dependent classical complement pathway activation on platelets, and support a role for gC1qR/p33 in this process. However, monoclonal antibodies (mAb) to gC1qR/p33 produced only modest (20% +/- 8%, mean +/- SD, n = 5) reductions in C4 activation on platelets. Thus, further studies are required to investigate the involvement of additional platelet membrane constituents in classical complement pathway activation.