Using an osteotomy of the olecranon as a model of a transverse fracture in 22 cadaver elbows we determined the ability of three different types of suture and stainless steel wire to maintain reduction when using a tension-band technique to stabilise the bone. Physiological cyclical loading simulating passive elbow movement (15 N) and using the arms to push up from a chair (450 N) were applied using an Instron materials testing machine whilst monitoring the osteotomy site with a video extensometer. Each osteotomy was repaired by one of four materials, namely, Stainless Steel Wire (7), No 2 Ethibond (3), No 5 Ethibond (5), or No 2 FiberWire (7). There were no failures (movement of >
2 mm) with stainless steel wire or FiberWire and no significant difference in the movements measured across the site of the osteotomy (p = 0.99). The No. 2 Ethibond failed at 450 N and two of the five of No. 5 Ethibond sutures had a separation of >
2 mm at 450 N. FiberWire as the tension band in this model held the reduction as effectively as stainless steel wire and may reduce the incidence of discomfort from the hardware. On the basis of our findings we suggest that a clinical trial should be undertaken
We evaluated the histological changes before and after fixation in ten knees of ten patients with osteochondritis dissecans who had undergone fixation of the unstable lesions. There were seven males and three females with a mean age of 15 years (11 to 22). The procedure was performed either using bio-absorbable pins only or in combination with an autologous osteochondral plug. A needle biopsy was done at the time of fixation and at the time of a second-look arthroscopy at a mean of 7.8 months (6 to 9) after surgery. The biopsy specimens at the second-look arthroscopy showed significant improvement in the histological grading score compared with the pre-fixation scores (p <
0.01). In the specimens at the second-look arthroscopy, the extracellular matrix was stained more densely than at the time of fixation, especially in the middle to deep layers of the articular cartilage. Our findings show that articular cartilage regenerates after fixation of an unstable lesion in osteochondritis dissecans.
We isolated multilineage mesenchymal progenitor cells from haematomas collected from fracture sites. After the haematoma was manually removed from the fracture site it was cut into strips and cultured. Homogenous fibroblastic adherent cells were obtained. Flow cytometry revealed that the adherent cells were consistently positive for mesenchymal stem-cell-related markers CD29, CD44, CD105 and CD166, and were negative for the haemopoietic markers CD14, CD34, CD45 and CD133 similar to bone-marrow-derived mesenchymal stem cells. In the presence of lineage-specific induction factors the adherent cells could differentiate Our results indicate that haematomas found at a fracture site contain multilineage mesenchymal progenitor cells and play an important role in bone healing. Our findings imply that to enhance healing the haematoma should not be removed from the fracture site during osteosynthesis.
Post-traumatic arthritis is a frequent consequence of articular fracture. The mechanisms leading to its development after such injuries have not been clearly delineated. A potential contributing factor is decreased viability of the articular chondrocytes. The object of this study was to characterise the regional variation in the viability of chondrocytes following joint trauma. A total of 29 osteochondral fragments from traumatic injuries to joints that could not be used in articular reconstruction were analysed for cell viability using the fluorescence live/dead assay and for apoptosis employing the TUNEL assay, and compared with cadaver control fragments. Chondrocyte death and apoptosis were significantly greater along the edge of the fracture and in the superficial zone of the osteochondral fragments. The middle and deep zones demonstrated significantly higher viability of the chondrocytes. These findings indicate the presence of both necrotic and apoptotic chondrocytes after joint injury and may provide further insight into the role of chondrocyte death in post-traumatic arthritis.