Aims

To investigate factors that contribute to patient decisions regarding attendance for arthroplasty during the COVID-19 pandemic.

Noise generation has been reported with ceramic-on-ceramic articulations in total hip replacement (THR). This study evaluated 208 consecutive Delta Motion THRs at a mean follow-up of 21 months (12 to 35). There were 141 women and 67 men with a mean age of 59 years (22 to 84). Patients were reviewed clinically and radiologically, and the incidence of noise was determined using a newly described assessment method. Noise production was examined against range of movement, ligamentous laxity, patient-reported outcome scores, activity level and orientation of the acetabular component. There were 143 silent hips (69%), 22 (11%) with noises other than squeaking, 17 (8%) with unreproducible squeaking and 26 (13%) with reproducible squeaking. Hips with reproducible squeaking had a greater mean range of movement (p < 0.001) and mean ligament laxity (p = 0.004), smaller median head size (p = 0.01) and decreased mean acetabular component inclination (p = 0.02) and anteversion angle (p = 0.02) compared with the other groups. There was no relationship between squeaking and age (p = 0.13), height (p = 0.263), weight (p = 0.333), body mass index (p = 0.643), gender (p = 0.07) or patient outcome score (p = 0.422). There were no revisions during follow-up. Despite the surprisingly high incidence of squeaking, all patients remain satisfied with their hip replacement.

Cite this article: Bone Joint J 2013;95-B:160–5.

Aim

This aim of this study was to investigate apoptosis, reactive oxygen species (ROS), and their upstream markers in Anteromedial Gonarthrosis (AMG).

Anteromedial Osteoarthritis of the Knee (AMOA) is a distinct phenotype of OA. Within this pattern of disease, the anterior third of the medial tibial plateau exhibits full thickness cartilage loss. The middle third has damaged partial thickness cartilage, and the posterior third has retained cartilage, which is seen on macroscopic visual assessment to be normal. This study investigates the molecular features of progressive severities of cartilage damage within this phenotype.

Ten medial tibial plateau specimens were collected from patients undergoing unicompartmental knee replacements. The cartilage within the area of macroscopic damage was divided into equal thirds: T1(most damaged), to T3 (least damaged). The area of macroscopically undamaged cartilage was taken as a 4th sample, N. The specimens were prepared for histological (Safranin-O) and immunohistochemical analysis (Type I and II Collagen, proliferation and apoptosis). Immunoassays were undertaken for Collagens I and II and GAG content. Real time PCR compared gene expression between areas T and N.

There was a decrease in OARSI grade across the four areas, with progressively less fibrillation between areas T1, T2 and T3. Area N had a grade of 0 (normal). The GAG immunoassay showed decreased levels with increasing severity of cartilage damage (p< 0.0001). Proliferation and apoptosis, as expected, were increased in the more damaged areas. There was no significant difference in the Collagen II content or gene expression between areas. The Collagen I immunohistochemistry showed increased staining within chondrocyte pericellular areas in the undamaged region (N) and immunoassays showed that the Collagen I content of this macroscopically and histologically normal cartilage, was significantly higher than the damaged areas (p< 0.0001). Furthermore, real time PCR showed a significant increase in Collagen I expression in the macroscopically normal areas compared to the damaged areas (p=0.04).

We conclude that in this phenotype the Collagen I increase, in areas of macroscopically and histologically normal cartilage, may represent very early changes of the cartilage matrix within the osteoarthritic disease process. This may be able to be used as an assay of early disease and as a therapeutic target for disease modification or treatment.

The aim of this study was to investigate the occurrence of tissue hypoxia and apoptosis at different stages of tendinopathy and tears of the rotator cuff.

We studied tissue from 24 patients with eight graded stages of either impingement (mild, moderate and severe) or tears of the rotator cuff (partial, small, medium, large and massive) and three controls. Biopsies were analysed using three immunohistochemical techniques, namely antibodies against HIF-1α (a transcription factor produced in a hypoxic environment), BNip3 (a HIF-1α regulated pro-apoptotic protein) and TUNEL (detecting DNA fragmentation in apoptosis).

The HIF-1α expression was greatest in mild impingement and in partial, small, medium and large tears. BNip3 expression increased significantly in partial, small, medium and large tears but was reduced in massive tears. Apoptosis was increased in small, medium, large and massive tears but not in partial tears.

These findings reveal evidence of hypoxic damage throughout the spectrum of pathology of the rotator cuff which may contribute to loss of cells by apoptosis. This provides a novel insight into the causes of degeneration of the rotator cuff and highlights possible options for treatment.

Aim: To investigate the molecular features of progressive severities of cartilage damage, within the phenotype of Anteromedial Osteoarthritis of the Knee (AMOA).

Methods: Ten medial tibial plateau specimens were collected from patients undergoing unicompartmental knee replacements.

The cartilage within the area of macroscopic damage was divided into equal thirds: T1(most damaged), to T3 (least damaged). The area of macroscopically undamaged cartilage was taken as a 4th sample, N. The specimens were prepared for histological (Safranin-O and H& E staining) and immunohistochemical analysis (Type I and II Collagen, proliferation and apoptosis).

Immunoassays were undertaken for Collagens I and II and GAG content. Real time PCR compared gene expression between areas T and N.

Results: There was a decrease in OARSI grade across the four areas, with progressively less fibrillation between areas T1, T2 and T3. Area N had an OARSI grade of 0 (normal).

The GAG immunoassay showed decreased levels with increasing severity of cartilage damage (ANOVA P< 0.0001).

There was no significant difference in the Collagen II content or gene expression between areas.

The Collagen I immunohistochemistry showed increased staining within chondrocyte pericellular areas in the undamaged region (N) and immunoassays showed that the Collagen I content of this macroscopically and histologically normal cartilage, was significantly higher than the damaged areas (ANOVA P< 0.0001). Furthermore, real time PCR showed that there was a significant difference in Collagen I expression between the damaged and macroscopically normal areas (p=0.04).

Conclusion: In AMOA there are distinct areas, demonstrating progressive cartilage loss. We conclude that in this phenotype the Collagen I increase, in areas of macroscopically and histologically normal cartilage, may represent very early changes of the cartilage matrix within the osteoarthritic disease process. This may be able to be used as an assay of early disease and as a therapeutic target for disease modification or treatment.

We assessed the predictive value of the macroscopic and detailed microscopic appearance of the coracoacromial ligament, subacromial bursa and rotator-cuff tendon in 20 patients undergoing subacromial decompression for impingement in the absence of full-thickness tears of the rotator cuff. Histologically, all specimens had features of degenerative change and oedema in the extracellular matrix. Inflammatory cells were seen, but there was no evidence of chronic inflammation. However, the outcome was not related to cell counts.

At three months the mean Oxford shoulder score had improved from 29.2 (20 to 40) to 39.4 (28 to 48) (p < 0.0001) and at six months to 45.5 (36 to 48) (p < 0.0001). At six months, although all patients had improved, the seven patients with a hooked acromion had done so to a less extent than those with a flat or curved acromion judged by their mean Oxford shoulder scores of 43.5 and 46.5 respectively (p = 0.046). All five patients with partial-thickness tears were within this group and demonstrated less improvement than the patients with no tear (mean Oxford shoulder scores 43.2 and 46.4, respectively, p = 0.04). These findings imply that in the presence of a partial-thickness tear subacromial decompression may require additional specific treatment to the rotator cuff if the outcome is to be improved further.

We report a study of 112 patients with primary anteromedial osteoarthritis of the knee and their families. Sibling risk was determined using randomly selected single siblings. Spouses were used as controls. The presence of symptomatic osteoarthritis was determined using an Oxford knee score of ≥ 29 supported by a Kellgren and Lawrence radiological score of II or greater.

Using Fisher’s exact test we found that there was a significant increased risk of anteromedial osteoarthritis (OA) relative to the control group (p = 0.031). The recurrence risk of anteromedial OA to siblings was 3.21 (95% confidence interval 1.12 to 9.27).

These findings imply that genetic factors may play a major role in the development of anteromedial OA of the knee.