The pathogenesis of aseptic loosening of total joint prostheses is not clearly understood. Two features are associated with loosened prostheses, namely, particulate debris and movement of the implant. While numerous studies have evaluated the cellular response to particulate biomaterials, few have investigated the influence of movement of the implant on the biological response to particles. Our aim was therefore to test the hypothesis that excessive mechanical stimulation of the periprosthetic tissues induces an inflammatory response and that the addition of particulate biomaterials intensifies this. We allocated 66 adult Beagle dogs to four groups as follows: stable implants with (I) and without (II) particulate polymethylmethacrylate (PMMA) and moving implants with (III) and without (IV) particulate PMMA. They were then evaluated at 2, 4, 6, 12 and 24 weeks. The stable implants were well tolerated and a thin, fibrous membrane of connective tissue was observed. There was evidence of positive staining in some cells for interleukin-6 (IL-6). Addition of particulate PMMA around the stable implants resulted in an increase in the fibroblastic response and positive staining for IL-6 and tumour necrosis factor-alpha (TNF-α). By contrast, movement of the implant resulted in an immediate inflammatory response characterised by large numbers of histiocytes and cytokine staining for IL-1ß, TNF-α and IL-6. Introduction of particulate PMMA aggravated this response. Animals with particulate PMMA and movement of the implant have an intense inflammatory response associated with accelerated bone loss. Our results indicate that the initiation of the inflammatory response to biomaterial particles was much slower than that to gross mechanical instability. Furthermore, when there was both particulate debris and movement, there was an amplification of the adverse tissue response as evidenced by the presence of osteolysis and increases in the presence of inflammatory cells and their associated cytokines.
Caveolae, specialised regions of the cell membrane which have been detected in a wide range of mammalian cells, have not been described in bone cells. They are plasmalemmal invaginations, 50 to 100 nm in size, characterised by the presence of the structural protein, caveolin, which exists as three subtypes. Caveolin-1 and caveolin-2 are expressed in a wide range of cell types whereas caveolin-3 is thought to be a muscle-specific subtype. There is little information on the precise function of caveolae, but it has been proposed that they play an important role in signal transduction. As the principal bone-producing cell, the osteoblast has been widely studied in an effort to understand the signalling pathways by which it responds to extracellular stimuli. Our aim in this study was to identify caveolae and their structural protein caveolin in normal human osteoblasts, and to determine which subtypes of caveolin were present. Confocal microscopy showed staining which was associated with the plasma membrane. Transmission electron microscopy revealed the presence of membrane invaginations of 50 to 100 nm, consistent with the appearance of caveolae. Finally, we isolated protein from these osteoblasts, and performed Western blotting using anti-caveolin primary antibodies. This revealed the presence of caveolin-1 and -2, while caveolin-3 was absent. The identification of these structures and their associated protein may provide a significant contribution to our further understanding of signal transduction pathways in osteoblasts.
Dental procedures may lead to a transient bacteraemia lasting for up to 30 minutes. Of the numerous cases of total hip arthroplasty (THA) reported which have been infected from haematogenous sources, dental procedures have been involved only infrequently. We reviewed the records of 2973 patients after THA. Of the late infections identified in 52 patients, three (6%) were strongly associated with a dental procedure. Infection was diagnosed by culture from the affected joint; Infection of a THA after dental procedures is more common than has been previously suspected. Patients with systemic disease, or who are undergoing extensive procedures, should be considered for prophylactic antibiotic treatment.
We have reviewed the results of 30 operations performed on 23 patients with Ficat stage-III or stage-IV osteonecrosis of the femoral head in which autogenous cortical and cancellous bone grafting had been performed through a so-called trapdoor made in the femoral head. At a mean of 56 months (30 to 60) after operation 20 of 24 stage-III hips (83%) had a good or excellent result as determined by the Harris hip-scoring system. Two of six stage-IV hips (33%) had good or excellent results. Eighteen of 21 hips (86%) with a combined necrotic angle of 200° had good or excellent clinical results compared with only four of nine hips (44%) with a combined necrotic angle of more than 200°. Six of the eight hips which had fair or poor results were in patients who had received corticosteroids; five of these six hips had lesions with a combined necrotic angle of greater than 200° or were in a late stage (stage IV). There were no perioperative complications. Our results suggest that the trapdoor procedure with autogenous cancellous and cortical bone grafting can be successful in Ficat and Arlet stage-III osteonecrosis of the hip in patients with small- to medium-sized lesions.
We reviewed 11 patients (17 ankles) who had had core decompression for symptomatic avascular necrosis of the talus before collapse. The Mazur grading system was used to assess function preoperatively and at final follow-up, and radiographs were graded according to the Ficat and Arlet (1980) classification modified for the ankle. At a mean follow-up of seven years (2 to 14) 14 ankles (82%) had an excellent or good outcome (Mazur scores >
80 points; pain scores >
40 points (41 to 50)). The other three ankles required tibiotalar fusion at a mean of 13 months (5 to 20) after core decompression. We conclude that core decompression is a viable method of treatment for symptomatic avascular necrosis of the talus before collapse.
