Treatment of infected total knee arthroplasty using an articulating spacer.

Twenty-six patients with late infected total knee arthroplasties were treated by debridement and removal of components and all cement, preserving collateral ligaments. At time of debridement, an articulating spacer was fashioned to allow partial weightbearing and knee range of motion (ROM) during rehabilitation. This spacer was implanted using antibiotic-impregnated bone cement. For this purpose, 4.8 g of powdered tobramycin was mixed with each 40-g batch of Simplex cement. Cement was applied early to the components, but applied late to the femur, tibia, and patella to allow molding to the defects and bone without adherence to bone. Patients received tailored intravenous antibiotic therapy for 6 weeks in addition to this antibiotic-impregnated cement for treatment of a variety of gram positive and gram negative organisms. All patients had cemented revision total knee arthroplasty using antibiotic-impregnated cement with standard cementing techniques used. All patients but 1 had reimplantation; this patient died of unrelated causes before revision. Range of motion before revision was 10 degrees to 95 degrees. Followup averaged 30 months (range, 13-70 months). The average Modified Hospital for Special Surgery Knee Score after revision was 87 points (range, 53-100 points), with 92% good to excellent results. Range of motion after reimplantation was 5 degrees to 106 degrees. There have been no recurrences of infection. Use of an articulating spacer to treat infected total knee arthroplasty improves ultimate ROM and soft tissue health and significantly decreases the risk of reinfection.

An osteolytic lesion associated with polyethylene wear debris adjacent to a stable total knee prosthesis.

Seven years after total knee arthroplasty, a patient with a well-fixed, uncemented femoral component (cobalt-chromium-molybdenum alloy) developed a large cystic lesion in the distal femur adjacent to the femoral component. This lesion contained fibrotic soft tissue, evidence of a foreign-body giant cell reaction, and a large number of polyethylene particles, but no metal wear debris, infection, or malignancy.

Adsorption of collagenase to particulate titanium: a possible mechanism for collagenase localization in periprosthetic tissue.

Osteolysis is a central feature of aseptic loosening of orthopaedic joint prostheses. This destructive process is believed to result from phagocytosis of implant wear debris by periprosthetic and synovial macrophages and the subsequent release of proinflammatory mediators, including collagenase. Isolated murine macrophages were cultured in vitro with particulate titanium in order to explore the mechanism of macrophage activation by particulate wear debris. The results, in which the amount of secreted, soluble collagenase in culture supernatants was inversely proportional to titanium concentration, suggested that titanium strongly adsorbed secreted collagenase. This inference was confirmed by direct binding assays in which particulate titanium coated with adsorbed collagenase bound an alkaline phosphatase conjugated anti-collagenase antibody, but not a conjugated anti-IgG antibody. Adsorption of collagenase was not influenced by preincubation of titanium particles with albumin. The adsorbed collagenase remained enzymatically active as indicated by its ability to hydrolyze a synthetic peptide substrate. These results demonstrate that particulate titanium stimulates collagenase production by macrophages and then strongly adsorbs the secreted proinflammatory enzyme. The process of macrophage stimulation, collagenase secretion, and adsorption may represent an important mechanism for localization and concentration of collagenase in periprosthetic and synovial tissue, a mechanism that ultimately triggers bone resorption through osteoclast activation.

Primary hyperparathyroidism and monoclonal gammopathy.

Coexistent primary hyperparathyroidism and monoclonal gammopathy, although rare, has been reported previously by a number of investigators. We report four patients with such an occurrence who were seen between 1976 and 1988. Another patient with primary hyperparathyroidism also had multiple myeloma and was in remission for 12 years. These patients represent approximately 1% of the 386 patients with primary hyperparathyroidism seen during the same 12-year period. Although several mechanisms have been proposed to explain this concurrence, we believe it is the result of a chance occurrence. A review of the literature, an estimate of the chance occurrence of coincidental monoclonal gammopathy, benign or malignant, in patients with primary hyperparathyroidism, and some practical implications of this interesting coexistence are presented.