Tendon adhesion is acknowledged to be a function of both an overwhelming inflammatory response at the surgical site and the loss of physical separation that is normally present between the tendons and the synovial sheath. Adhesions bind the flexor tendons to each other and to surrounding structures, interfering with their normal gliding function. The clinical result of adhesion formation following flexor tendon surgery is poor digital function. This study investigated the effect of intraoperative treatments of high viscosity absorbable gels made of various combinations of hyaluronic acid and nonsteroidal anti-inflammatory drugs, on adhesion formation in a leghorn chicken flexor tendon model. Forty-eight mature, white leghorn chickens were used to verify the surgical model and to test five different gel treatments. The gels were formed from: 2% sodium hyaluronate in phosphate buffered saline alone or combined with 1 mg/mL tolmetin sodium; 1 mg/mL naproxen sodium; 0.216 g/mL calcium acetate; or 0.216 g/mL calcium acetate plus 1 mg/mL naproxen sodium. The gels were applied by injecting 0.2 mL of the specified composition into the intrasheath space near the conclusion of the surgical procedure. Gross and histological evaluations were conducted to analyze the efficacy. All of the treatments significant reduced the extent and severity of postsurgical tendon adhesion in this animal model as compared with the control (no gel treatment) (p < 0.05). The combination of naproxen sodium and calcium acetate in a high viscosity sodium hyaluronate carrier was the most effective composition. The combination of a high viscosity gel and nonsteroidal anti-inflammatory drugs appears to maintain the natural separation between the tendons and their sheaths and decrease the tissue inflammatory response through mediating two of the major stimuli in adhesion formation.
We evaluated the effects of a serum protein coating on prosthetic infection in 29 adult male rabbits divided into three groups: control, albumin-coated and uncoated. We used 34 grit-blasted, commercially pure titanium implants. Eleven were coated with cross-linked albumin. All the implants were exposed to a suspension of Staphylococcus epidermidis before implantation.Our findings showed that albumin-coated implants had a much lower infection rate (27%) than the uncoated implants (62%). This may be a useful method of reducing the infection of prostheses.
The purpose of this study was to investigate the feasibility of fabricating a drug delivery system that serves a dual function, to eradicate infection as well as to provide a scaffold for osseous integration. Two porous composite systems were fabricated using hydroxyapatite (HA) as the carrier for gentamicin sulfate (GS), an aminoglycoside antibiotic. Structural and mechanical properties of porous HA-GS composites were characterized and the in vitro release behavior of GS from fabricated composites was monitored and compared with the well-known polymethylmethacrylate (PMMA)-GS delivery system. Scanning electron microscopy revealed a macropore range of 150 to 200 microm and 100 to 190 microm for the sintered and unsintered HA-GS composites, respectively. The effect of GS inclusion on bone apposition and ingrowth was assessed using a caprine model. Plugs 10 mm x 6 mm of cylindrical tricalcium phosphate, sintered HA, and sintered HA-GS were implanted in the femoral diaphysis for a period of 6 weeks. Data collected during the in vitro study showed that GS can successfully be incorporated into HA and used as a drug delivery system to eradicate Staphylococcus aureus. In vivo data confirmed that the inclusion of GS within a ceramic matrix did not stimulate or inhibit osteointegration or bone apposition. In conclusion, the fabricated sintered HA-GS composite may be beneficial in the treatment of infected osseous sites as a drug delivery system.
Legg-Calvé-Perthes disease (LCPD) results from avascular necrosis of the capital femoral epiphysis in growing children. This disease often yields a significant deformity of the proximal femur, which may result in osteoarthritis. Its cause is unknown, although extensive radiographic, clinical, and histologic evaluations have been performed. Attempts at developing an animal model for LCPD have been unsuccessful. Previous models have been based predominantly on determining the vascular etiology of the disease. There is a need for an animal model that mimics the growth pattern of the proximal femur seen in LCPD. Such a model would allow for the development and testing of new treatments. Thus far, no treatment strategy has been completely successful. A study involving graphic analysis of radiographs found that arrested anterolateral physeal growth with continued or accelerated perichondrial ring and posteromedial epiphyseal growth would account for the most severe morphologic changes observed in the femoral heads of patients with LCPD. A surgical procedure was performed to ablate the capital femoral physis in goat kids in an attempt to mimic the changes noted in this study. The procedure was evaluated with radiographs, gross specimens, and histopathologic slides. Graphic analysis of the radiographs revealed changes in the shape of the operated femoral head compared with the unoperated femoral head. While bone, fibrous, and fibrocartilaginous bridges were histologically observed across the physis, the resultant deformities did not mimic the changes identified in the graphic analysis study, perhaps because of inconsistencies in the surgical ablative techniques, which will require further modification. This study provides the basis for further research to develop a successful model.
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