In relation to the conduct of this study, one or more of the authors is in receipt of a research grant from a non-commercial source.
Successful reconstructive surgery with allografts is severely limited by a failure rate of 30 – 40%. Allograft failure is due to nonunion of the graft-host junction. The molecular mechanism by which this occurs is not yet fully elucidated. Using a sheep femoral allograft model, we have investigated the cellular and molecular mechanisms associated with nonunion of bone allografts. Five, from a total of twelve operations, resulted in the development of graft-host nonunion, reflecting a failure rate of 42%. Histological assessment revealed that allograft failure was due to the excessive accumulation of and resorption by, osteoclasts (Ocs) on the surface of the bone allograft. Three distinct layers, lying adjacent to the allograft bone surface, in the nonunion groups, were identified. The outer fibroblastic layer contained abundant fibroblasts and connective tissue. Underlying this layer were synovial-like cells and some multinuclear giant cells. The third layer, opposing the bone surface, consisted of Ocs and round mononuclear cells. Histomorphometric analysis showed that allograft unions, featured a large amount of newly formed bone on the surface, (OS/BS = 47.81%) with a small proportion of eroded surface (ES/BS = 20.59%). The number of osteoclasts associated with the allograft bone surface were few (Oc/B.Pm = 1.7190/mm) and activity (ES/BS = 46.68%) of Ocs with a reduced amount of new bone formation (OS = 6.35%). Both calcitonin receptor and H+ATPase mRNA, characteristically expressed by Ocs, were localised to the multinuclear giant cells, indicating that they were Ocs. Synovial-like cells in the histological layer above the Ocs, expressed gene transcript for the Osteoprotegrin Ligand (OPGL), a membrane bound factor that is critical for the induction of Oc activity and osteoclastogenesis. In conclusion, these findings suggest that failure of bone allografts is partially due to excessive resorption by host Ocs, accompanied by reduced bone formation. The production of OPGL by synovial-like cells, may be responsible for the recruitment and generation of Ocs.
A paper was presented two years ago reviewing evidence of absorption of the Bio Interference screw and tunnel widening at three, six and 12 months following anterior cruciate ligament reconstruction using double-stranded hamstrings. The femoral fixation was with an Endobutton with a double loop of Mercylene tape with a Bio Interference screw and an extra small staple for the distal fixation. This paper presents further magnet resonance imaging (MRI) studies at least two years after surgery on 10 of those patients to assess if there was any MRI evidence of absorption of the Bio Interference screw or tunnel widening (in particular ganglion formation) in the femoral or tibial tunnels. The results showed that at least two years after surgery there was little evidence of Bio Interference screw absorption. There was no evidence of tunnel widening.
Articular cartilage defects of the knee occur commonly in sports injuries and trauma. Increasing evidence suggests that the only technique that enables the regeneration of articular hyaline cartilage in chondral defects is autologous chondrocyte implantation (ACI). Here we have reported our clinical experience of autologous chondrocyte implantation using biodegradable type I/III collagen membrane (CACI). A total of 26 patients (age range from 19 to 60 years, average 37 years) was conducted with CACI. Pre-operative magnetic resonance imaging (MRI) scans were performed on all patients. Post-operative MRI scans were planned for approximately three and 12 months after the surgery to determine the success of integration of implanted chondrocytes. The results demonstrated that the initial post-operative MRI scans at three months showed the presence of oedematous tissue at the defect sites in 23 patients, contrasting with the fluid filled defects seen preoperatively and with and MRI signal differing from that of the surrounding normal hyaline articular cartilage. MRI scans in nine patients at 12 months after their operations showed maturation of cartilage graft in all patients. Apopototic testing of the chondrocytes using Annexin IV before implantation showed that the viability of the chondrocytes was over 85% where the apopototic rate of chondrocytes was less than 2%. One patient with an apopototic rate of over 10% has a delayed repair in cartilage defects as shown by MRI. In conclusion, early phase clinical studies showed that autologous chondrocyte implantation remains promising for the treatment of chondral defects with restoration of hyaline cartilage. Longer clinical follow-up of the patients and better assessment of cellular phenotype of chondrocytes before implantation are required.
We report a prospective study of the influence of various factors on the six-month mortality of 531 patients with subcapital hip fractures. We performed univariate and multivariate analyses on the 403 patients treated surgically. The most significant predictors of the six-month mortality were dementia, postoperative chest infection, malignant neoplasia, old age and deep-wound infection, in that order. A simple test of mental ability was the most significant prognostic indicator and this test should be included in future studies of the management of hip fractures in the elderly.
The early results of revision osteoarticular allografts in weight-bearing joints are reported. Sixteen consecutive patients underwent surgery over a six-year period between 1982 and 1988. At the time of review eight patients (50%) had surviving second allografts with an average follow-up time of 48 months (range 12 to 87). Five patients were graded excellent according to the Mankin scale, one good and two fair. Eight patients (50%) required further surgery, but only two patients came to amputation.