Survival analysis of joint replacement relies on the assumption that surgical procedures in patients lost to follow-up have the same chance of failing as those in patients who continue to be assessed. Our study questions that assumption.

During the 16-year follow-up of 2268 patients who had received total hip replacements 142 (6%) were lost to follow-up. The cumulative loss at 15 years was 20%. At their last assessment, patients who subsequently failed to attend for follow-up had significantly worse pain, range of movement and opinion of their progress (p < 0.001) and significantly worse radiological features than a matched control group (p < 0.01).

Patients lost to follow-up have a worse outcome than those who continue to be assessed. Consequently, a survival analysis that does not take into account such patients is likely to give falsely optimistic results. It is therefore essential that vigorous attempts are made to minimise loss to follow-up, and that the rate of such loss is quoted. The overall loss to follow-up disguises the magnitude of the problem, which is best quantified by a cumulative rate of follow-up.

The reliability of a study can be assessed by a loss-to-follow-up quotient, calculated by the number of failures: the lower the quotient the more reliable the data. Ideally, the quotient should be less than 1.

We have assessed the relative value of various outcome measures after THR, by the analysis of follow-up data from over 2000 patients. They had been reviewed clinically and radiologically six months after operation, at one year, and then every two years, some for 16 years. At each review their pain level, stiffness and opinion of progress were scored and a radiograph taken.

We found that pain level was the most informative outcome as a predictor of revision and correlated well with the patients’ opinions.

We made a comparison between the six types of implant in the series, using survival analysis and log-rank testing with different pain levels as endpoints. This analysis revealed differences which were not detected by survival analysis using the traditional endpoint of revision.

We therefore recommend the use of different levels of pain as the main outcome measures after total hip replacement.

A heavy infiltrate of foreign-body macrophages is commonly seen in the fibrous membrane which surrounds an aseptically loose cemented implant. This is in response to particles of polymethylmethacrylate (PMMA) bone cement and other biomaterials. We have previously shown that monocytes and macrophages responding to particles of bone cement are capable of differentiating into osteoclastic cells which resorb bone.

To determine whether the radio-opaque additives barium sulphate (BaSO₄) and zirconium dioxide (ZrO₂) influence this process, particles of PMMA with and without these agents were added to mouse monocytes and cocultured with osteoblast-like cells on bone slices. Osteoclast differentiation, as shown by the presence of the osteoclast-associated enzyme tartrate-resistant acid phosphatase (TRAP) and lacunar bone resorption, was observed in all cocultures.

The addition of PMMA alone to these cocultures caused no increase in TRAP expression or bone resorption relative to control cocultures. Adding PMMA particles containing BaSO₄ or ZrO₂, however, caused an increase in TRAP expression and a highly significant increase in bone resorption. Particles containing BaSO₄ were associated with 50% more bone resorption than those containing ZrO₂.

Our results suggest that radio-opaque agents in bone cement may contribute to the bone resorption of aseptic loosening by enhancing macrophage-osteoclast differentiation, and that PMMA containing is BaSO₄ likely to be associated with more osteolysis than that containing ZrO₂.

The recommendation that patients having a total hip replacement should receive pharmacological thromboprophylaxis is based on the belief that fatal pulmonary embolism is common, and that prophylaxis will decrease the death rate. To investigate these assumptions we performed a meta-analysis of all studies on hip replacement which included information about death or fatal pulmonary embolism. A total of 130 000 patients was included. The studies were so varied in content and quality that the results of our analysis must be interpreted with some caution.

The fatal pulmonary embolism rate was 0.1% to 0.2% even in patients who received no prophylaxis. This is an order of magnitude lower than that which is generally quoted, and therefore the potential benefit of prophylaxis is small and may not justify the risks. To balance the risks and benefits we must consider the overall death rate. This was 0.3% to 0.4%, and neither heparin nor any other prophylactic agent caused a significant decrease.

Our study demonstrates that there is not enough evidence in the literature to conclude that any form of pharmacological thromboprophylaxis decreases the death rate after total hip replacement. For this reason guidelines which recommend their routine use to prevent death after hip replacement are not justified.

Children who present late with hip dislocation may require femoral osteotomy after reduction, to correct valgus and anteversion deformity of the femoral neck. After these procedures proximal femoral growth is unpredictable. We have studied proximal femoral growth in 40 children who had been treated by femoral osteotomy.

Preoperatively, the mean femoral neck-shaft angle was 5° greater on the affected side than on the contralateral side. Postoperatively, it was 28° less. There was progressive recorrection; after five years the angle was not significantly different from that on the contralateral side. In our series 70% of the capital epiphyses became abnormally shaped, taking the appearance of a ‘jockey’s cap’. All the growth plates became angulated but this corrected with time.

Correction of the neck-shaft angle probably results from the more normal mechanical environment provided by reduction. The abnormal radiographic appearance of the epiphysis and growth plate is probably due to the rotation produced by the osteotomy.

We reviewed the records of the long-term outcome of 208 Charnley and 982 Stanmore total hip replacements (THR) performed by or under the supervision of one surgeon from 1973 to 1987. The Stanmore implant had a better survival rate before revision at 14 years (86% to 79%, p = 0.004), but the difference only became apparent at ten years.

The later Stanmore implants did better than the early ones (97% to 92% at ten years, p = 0.005), the improvement coinciding with the introduction of a new cementing technique using a gun. Most of the Charnley implants were done before most of the Stanmore implants so that the difference between the results may in part be explained by improved methods, but this is not the complete explanation since a difference persisted for implants carried out during the same period of time.

We conclude that improved techniques have reduced failure rates substantially. This improvement was much greater than that observed between these two designs of implant. Proof of the difference would require a very large randomised controlled trial over a ten-year period.

We studied the migration of 58 cemented Hinek femoral components for total hip replacement,using roentgen stereophotogrammetric analysis over four years. The implants migrated faster during the first year than subsequently, and the pattern of migration in the second period was very different. During the first year they subsided, tilted into varus and internally rotated. After this there was slow distal migration with no change in orientation. None of the prostheses has yet failed.

The early migration is probably caused by resorption of bone damaged by surgical trauma or the heat generated by the polymerisation of bone cement. Later migration may be due to creep in the bone cement or the surrounding fibrous membrane.

The prosthesis which we studied allows the preservation of some of the femoral neck, and comparison with published migration studies of the Charnley stem suggests that this decreases rotation and may help to prevent loosening.

We used a rabbit model to investigate the mechanism by which the angulation of fractures is corrected in children. We produced a transverse proximal tibial fracture in one leg of 12 eight-week-old New Zealand white rabbits and measured bone alignment and length and the patterns of bone growth and remodelling.

The angle between the joint surfaces changed rapidly to correct the alignment of the limb as a result of asymmetrical growth of epiphyseal plates. In an adult with closed plates, the angle between the joint surfaces cannot therefore improve. The angle at the fracture itself showed slow improvement because of bone drift and the asymmetrical growth of the epiphyseal plates. Remodelling corrected the shape of the bone in the region of the fracture.

Periosteal division on the convex side increased the growth of the epiphyseal plate on that side, thus slowing the correction. The effect was relatively small, providing an indication that factors other than the periosteum are important in inducing correction.

External torsional deformities developed because of helical growth at the plate. This was probably caused by abnormal posture which induced a torque at the growth plate. Helical growth is the mechanism by which rotational deformities can occur and correct.