Trochleoplasty with a flexible osteochondral flap: results from an 11-year series of 214 cases.

AIMS: The Bereiter trochleoplasty has been used in our unit for 12 years to manage recurrent patellar instability in patients with severe trochlea dysplasia. The aim of this study was to document the outcome of a large consecutive cohort of patients who have undergone this operation. PATIENTS AND METHODS: Between June 2002 and August 2013, 214 consecutive trochleoplasties were carried out in 185 patients. There were 133 women and 52 men with a mean age of 21.3 years (14 to 38). All patients were offered yearly clinical and radiological follow-up. They completed the following patient reported outcome scores (PROMs): International Knee Documentation Committee subjective scale, the Kujala score, the Western Ontario and McMaster Universities Arthritis Index score and the short-form (SF)-12. RESULTS: Outcomes were available for 199 trochleoplasties in 173 patients giving a 93% follow-up rate at a mean of 4.43 years (1 to 12). There were no infections or deep vein thromboses. In total, 16 patients reported further patella dislocation, giving an 8.3% rate of recurrence. There were 27 re-operations, giving a rate of re-operation of 14%. Overall, 88% were satisfied with the operation and 90% felt that their symptoms had been improved. CONCLUSION: All PROMs improved significantly post-operatively except for the mental component score of the SF-12. Trochleoplasty performed using a flexible osteochondral flap is an effective treatment for recurrent patellar instability in patients with severe trochlea dysplasia and gives good results in the medium term. Cite this article: Bone Joint J 2017;99-B:344-50.

Bearing exchange in the management of pseudotumours.

INTRODUCTION: Soft tissue reactions following metal-on-metal (MoM) arthroplasty of the hip have been under considerable discussion. These reactions are seen following both hip resurfacing and MoM total hip arthroplasty (THA). The phenomenon may arise owing to shedding of metal particles in high wear states, hypersensitivity with normal metal wear rates or a combination of the two. METHODS: Three patients were identified who had developed a soft tissue reaction (pseudotumour) following MoM hip resurfacing procedures. The prostheses were revised to ceramic-on-ceramic (CoC) THA with only minimal debridement of the pseudotumour. Pre and postoperative magnetic resonance imaging was performed to assess the size of the lesions. RESULTS: Progressive and satisfactory resolution of the associated pseudotumours was identified following revision of the prostheses to CoC THA. CONCLUSIONS: In the early stages of pseudotumour formation following MoM hip resurfacing, this potentially devastating condition can be managed adequately with revision to a CoC bearing THA with minimal soft tissue excision.

Investigating meniscal symptoms in patients with knee osteoarthritis--is MRI an unnecessary investigation?

The aim of this study was to evaluate the relationship between radiographic knee osteoarthritis and the presence of a relevant meniscal tear detected on MRI in symptomatic patients over the age of 60. Seventy seven patients over the age of 60 who had been investigated with a knee MRI over a 1-year period were identified. Sixty patients had a full set of data available for analysis. Their plain radiographs were blindly graded for osteoarthritis using the Kellgren-Lawrence (K-L) scale. The indications for the MRI were subdivided into: meniscal symptoms, general knee pain and "other". These indications were correlated with the K-L grade and result of the MRI. Overall, 40% of patients with a K-L grade of 0 had a meniscal tear compared to 89% of patients with a K-L score of 3, and 88% with a K-L score of 4. The indications for an MRI were grouped into meniscal symptoms (49), general pain (6) and other (5). In the group investigated for meniscal symptoms, the incidence of meniscal tears was 92% and 100% with a K-L grade of 3 and 4 respectively. This equated to a positive predictive value of 93% for K-L grade 3 and above, and 100% for K-L grade 4 alone. Given the predictability of the MRI findings in patients with significant osteoarthritis as well as meniscal symptoms, we conclude that this is an unnecessary investigation when used for this indication.

Impaired corpus luteum function in ectopic pregnancy cannot be explained by altered human chorionic gonadotropin.

We studied the cause of the low serum progesterone, 17 beta-estradiol, and 17-hydroxyprogesterone levels that occur in women with an ectopic pregnancy. Only women who had been amenorrheic for less than 8 weeks were studied in order to assess corpus luteum rather than placental biosynthesis of these steroids; each woman with an ectopic pregnancy was matched to a woman with a normal intrauterine pregnancy on the basis of serum intact hCG levels within 10% of one another to obviate the influence of different levels of this luteotropic hormone. Every woman with an ectopic pregnancy had lower serum progesterone, estradiol, and 17-hydroxyprogesterone levels than her matched normal pregnant pairmate (median values: progesterone, 27.9 vs. 83.5 mmol/L; estradiol, 0.36 vs. 1.79 nmol/L; 17-hydroxyprogesterone, 4.95 vs. 22.1 nmol/L, respectively; all P less than 0.002). The ratios of intact hCG, measured by immunoradiometric assay, to hCG, measured by a hCG beta-specific RIA, were similar in the two groups. Serum hCG bioactivity was assayed by measuring the ability of serum to stimulate testosterone secretion from mouse Leydig cells. The mean biological to intact immunological hCG ratios were 2.06 +/- 1.39 (+/- SD) for ectopic pregnancy and 1.91 +/- 0.81 for normal pregnancy (P greater than 0.05). The biological hCG to immunoreactive hCG beta ratios were 1.98 +/- 0.75 and 2.02 +/- 0.82, respectively. Serum hCG from both groups of women stimulated cAMP generation by testicular cells similarly. We conclude that the lower serum steroid levels in women with ectopic pregnancy cannot be explained by altered hCG bioactivity. The lower steroid levels may thus reflect a primary defect of the corpus luteum, absence of another stimulator of ovarian steroid biosynthesis, or more subtle alterations in hCG glycosylation which are important in vivo but not assessed by the in vitro bioassay.