The fate of augments to treat type-2 bone defects in revision knee arthroplasty.

We report the five- to-ten year results of Anderson Orthopaedic Research Institute type-2 bone defects treated with modular metal augments in revision knee surgery. A total of 102 revision knee arthroplasties in patients with type-2 defects treated with augments and stems were prospectively studied. Seven patients (seven knees) had incomplete follow-up and 15 patients (16 knees) died with the arthroplasty in situ. The mean follow-up of the 79 remaining knees was 7 +/- 2 years (5 to 11). The presence of non-progressive radiolucent lines around the augment in 14% of knees was not associated with poorer knee scores, the range of movement, survival of the component or the type of insert which was used (p > 0.05). The survival of the components was 92 +/- 0.03% at 11 years (95% CI, 10.3 to 11.2). We recommend the use of modular augmentation devices to treat type-2 defects in revision knee surgery.

The fate of cementless jumbo cups in revision hip arthroplasty.

We report 5-year minimum results of cementless over-sized cups used in revision hip arthroplasty, with significant associated bone defects. Forty-three porous-coated jumbo cups were used to treat acetabular defects in revision hip arthroplasty in 42 patients with a mean age of 63 (range, 25-86). Morsellized allograft only was used in 27 hips, and bulk allograft was used in 8 cases. Two patients were lost to follow-up, and 5 died after a mean 7 years' follow-up, with retention of their prostheses. In the remaining 36 cases, the mean follow-up was 10 years (range, 6-14 years). Two acetabular components were revised for aseptic loosening and graft resorption. Two cases were complicated by dislocation. A satisfactory 92% Kaplan Meier shell survival rate was seen at 14 years.

Radiographic cost reduction strategy in total joint arthroplasty. A prospective analysis.

A consecutive series of 222 patients who underwent cemented total knee arthroplasty (124) and uncemented total hip arthroplasty (98) were evaluated prospectively. The purpose of this study was to determine if routine radiologic interpretation of postoperative total hip and total knee radiographs is cost effective. Also, the study was designed to determine if routine predischarge radiographs, in conjunction with recovery room radiographs, are worthwhile. There were no changes in postoperative patient management based on orthopaedic or radiologic review of either radiograph. No additional information was gained from review of the radiologic evaluations. Therefore, obtaining one series of routine inpatient postoperative total joint radiographs and eliminating postoperative radiologic consultation will significantly reduce costs without compromising patient care.

Long term herpes simplex virus type 1 infection of nerve growth factor-treated PC12 cells.

The behaviour of herpes simplex virus type 1 (HSV-1) strain 17 in tissue cultures of PC12 cells treated with nerve growth factor (NGF) was studied. PC12 cells respond to NGF by ceasing to proliferate and extending long neurites. After differentiation with NGF, cultures were infected with HSV-1 and maintained in the presence of the hormone for several weeks. These long-term infected cultures were tested for HSV DNA, transcripts and the ability to produce virus, before and after NGF removal. Before NGF removal, the cultures were characterized by little or no virus production and the presence of HSV-1 DNA in a predominantly endless form. In situ analysis of long-term infected cultures revealed latency-associated transcript expression in only a portion of the cells. However, as shown by an infectious centre assay, virus was present in almost all cells in the population. Moreover, removal of NGF from long-term cultures resulted in the appearance of significantly increased amounts of virus in the media. The degree to which this system resembles HSV latency in vivo is discussed.

An HSV LAT null mutant reactivates slowly from latent infection and makes small plaques on CV-1 monolayers.

A Herpes simplex virus type I (HSV-I) strain 17 mutant deleted between the NotI and HpaI restriction sites of the latency associated transcript (LAT) region has been constructed. The mutant, therefore, contains a deletion of the putative LAT promoter and is called 17N/H. The 17N/H isolate established latent infections in mice nearly as efficiently as its wildtype parent. However, like other LAT null mutants, 17N/H reactivates from explanted ganglia with much slower kinetics than its LAT competent parent. In tissue culture, although 17N/H produces as much virus per cell as its strain 17 parent, it produces small plaques. The small plaque phenotype appears to be due to the inability of the virus to be released from the infected cell into the medium, following low but not high multiplicities of infection (m.o.i.). The mutant was also shown to produce an aberrant LAT homologous transcript of 1.1 kb as well as overproduce an approximately 29,000-Da HSV-specific polypeptide, which is barely detectable in wildtype infected cells. Rescuants of the 17N/H defect were constructed using a 10-kb restriction fragment containing viral sequences spanning the deletion, make large plaques, and have reactivation patterns and infected cell gene product profiles indistinguishable from the 17 parent. This shows that the phenotypes observed in 17N/H are reversed when the deletion, or at most sequences within 5 kb of each side of the deletion, is corrected. The possibilities that the defect in viral egress from infected cell, the small LAT homologous transcript, and the accumulation of the 29,000 Da polypeptide are related to the delayed reactivation kinetics are discussed.