Slipped upper femoral epiphysis remains a disease of unknown aetiology. Recent evidence has bolstered speculation that the immune system may play a role in the aetiology or pathogenesis of slipped epiphysis or of one of its complications, chondrolysis. This study reports the finding of immune complexes in the synovial fluid of all but one hip affected with slipped epiphysis in a consecutive series. In seven patients, immune complexes were detected by both the Raji cell assay and C1q-binding assay; in two, by the C1q-assay only; and in one, by the Raji cell assay only. No patients had immune complexes in the serum. Twenty-one patients with synovitis of the knee or hip caused by a variety of disorders served as the control group. Two of these patients had immune complexes in their synovial fluid. It appears that the immune complexes characterise the synovitis found with slipped upper femoral epiphysis as distinct from most other synovitides

The development of lateral tibial torsion in the paralysed lower limb is well documented, but its pathogenesis is poorly understood. This paper attempts to provide an explanation for its development when it is associated with a varus or equinovarus deformity of the hindfoot. Correction of the lateral tibial torsion by supramalleolar derotation tibial osteotomy and reorientation of the ankle mortise appear to unlock the talus from the laterally rotated position, correcting a mobile hindfoot varus deformity and altering soft-tissue tensions about the ankle so that the correction achieved is maintained. In the presence of a fixed hindfoot deformity, supramalleolar derotation tibial osteotomy is useful as a first-stage procedure before corrective osteotomies of the foot. The operation described is technically simple and carries a low morbidity. Twenty supramalleolar derotation tibial osteotomies in 18 patients have been performed with satisfactory results and few complications

Two distinct lesions affect the articular cartilage of the patella. Surface degeneration occurs particularly on the odd facet; it is age dependent, often present in youth and it becomes more frequent with increasing age. It probably does not occasion patello-femoral pain in youth, but may predispose to degenerative arthritis in that joint in later years and is regarded as a consequence of habitual disuse. The term "basal degeneration" is used to describe a lesion in which there is a fasciculation of collagen in the middle and deep zones of cartilage without, at first, affecting the surface. It was found astride the ridge separating the medial from the odd facet in twenty-three adolescents who had complained of prolonged patello-femoral pain. They were treated by excision of the disc of affected cartilage, with relief of pain in most cases. The pathogenesis of basal degeneration is related to the functional anatomy of the patella

1. An unusual congenital anomaly of the cervical spine is described. This lesion caused a localised cervical kyphosis and resulted in the development of a mild tetraparesis. 2. The case reported is believed to be the first on record in the English literature of multiple posterior hemivertebrae in the cervical region. 3. The neck deformity was associated with an unusual combination of developmental anomalies–namely, brachyphalangy and bilateral congenital optic atrophy. 4. The importance of differentiating between congenital and acquired causes of kyphosis is emphasised. 5. The radiographic appearances of posterior hemivertebra are described, and the differential diagnosis is considered. 6. The development of the vertebral body, and the relationship between coronal cleft vertebra and posterior hemivertebra, are discussed. The possible role of a disturbance of vascular supply in pathogenesis is mentioned. 7. This report augments the growing literature on congenital skeletal anomalies occurring in combination with isolated congenital ocular defects

Sterilisation by gamma irradiation in the presence of air causes free radicals generated in polyethylene (PE) to react with oxygen, which could lead to loss of physical properties and reduction in fatigue strength. Tissue retrieved from failed total hip replacements often has large quantities of particulate PE and most particles associated with peri-implant osteolysis are oxidised. Consequently, an understanding of the cellular responses of oxidised PE particles may lead to clarification of the pathogenesis of osteolysis and aseptic loosening. We have used the agarose system to demonstrate the differential effects of oxidised and non-oxidised PE particles on the release of proinflammatory products such as interleukin-1β (IL-1β), IL-6, and tumour necrosis factor-α (TNF-α) from monocytes/ macrophages (M/M). Oxidised PE particles were shown to stimulate human M/M to phagocytose and to release cytokines. Oxidation may alter the surface chemistry of the particles and enhance the response to specific membrane receptors on macrophages, such as scavenger-type receptors

Aims

Despite advances in the treatment of paediatric hip disease, adolescent and young adult patients can develop early onset end-stage osteoarthritis. The aims of this study were to address the indications and medium-term outcomes for total hip arthroplasty (THA) with ceramic bearings for teenage patients.

Macrophages and their fused products are commonly found at the polymethylmethacrylate cement-bone interface, but it is not known if they contribute directly to the osteolysis associated with loosening of the cemented prosthesis. We isolated mononuclear phagocytes from granulomas formed by subcutaneous implantation of polymethylmethacrylate into mice and incubated them on bone slices in which they formed resorption lacunae after co-culture for seven to 14 days with both marrow stromal cells and osteoblast-like cells (in the presence of 1 alpha,25-dihydroxyvitamin D3 and dexamethasone). Increased numbers of tartrate-resistant acid phosphatase-positive mononuclear and multinucleated cells formed in these cultures. Both in the presence and absence of stromal cells, macrophages produced extensive superficial roughening of the bone surface. Polymethylmethacrylate-induced macrophages are thus capable of low-grade surface and high-grade lacunar osteolysis, the latter requiring the presence of specific hormonal and stromal cell elements. These two forms of bone resorption could account for the pathogenesis and clinical patterns associated with loosening of the cemented prosthesis

Radiographs of 155 Indian children were examined to identify the acetabular changes which occur in Perthes' disease. These changes included osteoporosis of the acetabular roof, irregularity of contour, premature fusion of the triradiate cartilage, hypertrophy of articular cartilage and changes in dimensions. These changes tended to be more marked in older children and when more than half of the femoral epiphysis was involved. Comparison with 25 cases of Perthes' disease from Liverpool showed the same picture. Several of the acetabular changes noted during the active stages were also seen in a series of 24 adult hips after Perthes' disease. Radio-isotope scans of the hips of 27 children with Perthes' disease showed a consistently increased uptake in the acetabulum on the affected side, indicative of a local increase in vascularity and metabolic activity. It was possible to postulate a working model for the pathogenesis of all the acetabular changes. A number of statistical correlations suggest that most of the changes have a bearing on the final outcome

1. The pathology and pathogenesis of dislocations and fracture-dislocations of the cervical spine has been reviewed. 2. A method of treatment using skeletal traction and manipulation under relaxant general anaesthesia is described. Results of treatment are given for all patients admitted to the Centre with flexion-rotation dislocations of the cervical spine complicated by neurological lesions, between November 1961 and December 1968. 3. After reviewing the literature and considering the results obtained in seventy-six cases, we advocate a policy of conservative management with gentle manipulation of the cervical spine in selected cases, reduction being maintained thereafter by skeletal traction. We reserve operation for the few cases that demonstrate late instability or for those rarer cases in which manipulation fails and the patient has either an incomplete neurological lesion or a double skeletal injury. 4. The low incidence of late instability after adequate conservative treatment is stressed, and the danger of overdistraction of the cervical spine by heavy traction in patients with severe ligamentous damage is emphasised

Aims

Malignancy and surgery are risk factors for venous thromboembolism (VTE). We undertook a systematic review of the literature concerning the prophylactic management of VTE in orthopaedic oncology patients.

Surgical dislocation of the hip is rarely undertaken. The potential danger to the vascularity of the femoral head has been emphasised, but there is little information as to how this danger can be avoided. We describe a technique for operative dislocation of the hip, based on detailed anatomical studies of the blood supply. It combines aspects of approaches which have been reported previously and consists of an anterior dislocation through a posterior approach with a ‘trochanteric flip’ osteotomy. The external rotator muscles are not divided and the medial femoral circumflex artery is protected by the intact obturator externus. We report our experience using this approach in 213 hips over a period of seven years and include 19 patients who underwent simultaneous intertrochanteric osteotomy. The perfusion of the femoral head was verified intraoperatively and, to date, none has subsequently developed avascular necrosis. There is little morbidity associated with the technique and it allows the treatment of a variety of conditions, which may not respond well to other methods including arthroscopy. Surgical dislocation gives new insight into the pathogenesis of some hip disorders and the possibility of preserving the hip with techniques such as transplantation of cartilage

Aims

Arthrofibrosis is a relatively common complication after joint injuries and surgery, particularly in the knee. The present study used a previously described and validated rabbit model to assess the biomechanical, histopathological, and molecular effects of the mast cell stabilizer ketotifen on surgically induced knee joint contractures in female rabbits.

Aims

Osteoarthritis (OA) is the most prevalent joint disease. However, the specific and definitive genetic mechanisms of OA are still unclear.

Aims

Inflammatory response plays a pivotal role in the pathophysiological process of intervertebral disc degeneration (IDD). A20 (also known as tumour necrosis factor alpha-induced protein 3 (TNFAIP3)) is a ubiquitin-editing enzyme that restricts nuclear factor-kappa B (NF-κB) signalling. A20 prevents the occurrence of multiple inflammatory diseases. However, the role of A20 in the initiation of IDD has not been elucidated. The aim of the study was to investigate the effect of A20 in senescence of TNF alpha (TNF-α)-induced nucleus pulposus cells (NPCs).

Particulate wear debris can induce the release of bone-resorbing cytokines from cultured macrophages and fibroblasts in vitro, and these mediators are believed to be the cause of the periprosthetic bone resorption which leads to aseptic loosening in vivo. Much less is known about the effects of particulate debris on the growth and metabolism of osteoblastic cells. We exposed two human osteoblast-like cell lines (SaOS-2 and MG-63) to particulate cobalt, chromium and cobalt-chromium alloy at concentrations of 0, 0.01, 0.1 and 1.0 mg/ml. Cobalt was toxic to both cell lines and inhibited the production of type-I collagen, osteocalcin and alkaline phosphatase. Chromium and cobalt-chromium were well tolerated by both cell lines, producing no cytotoxicity and no inhibition of type-I collagen synthesis. At the highest concentration tested (1.0 mg/ml), however, chromium inhibited alkaline phosphatase activity, and both chromium and cobalt-chromium alloy inhibited osteocalcin expression. Our results clearly show that particulate metal debris can modulate the growth and metabolism of osteoblastic cells in vitro. Reduced osteoblastic activity at the bone-implant interface may be an important mechanism by which particulate wear debris influences the pathogenesis of aseptic loosening in vivo

We have used dual-energy X-ray absorptiometry to measure bone mineral density (BMD) in patients with ankylosing spondylitis comparing 41 healthy control subjects and 33 patients with either mild or advanced ankylosing spondylitis. A Norland XR-28 bone densitometer was used to measure the BMD of the lumbar spine and that of the head, trunk, arms, femoral neck, Ward's triangle, legs, pelvis, and total body. Mild ankylosing spondylitis was defined as that showing no or incipient syndesmophytes between L1 and L5 vertebrae: we studied 16 men of mean age 37 years and six women of mean age 37 years. Advanced ankylosing spondylitis, in 11 men of mean age 42 years, showed a bamboo spine with bridging syndesmophytes across all disc spaces between L1 and L5. The mean BMD of the lumbar spine was significantly different in the patients and control subjects of the same sex (0.01 < p < 0.05, analysis of variance), being significantly reduced compared with control subjects in mild disease (0.001 < p < 0.01, t-test) and significantly increased in advanced disease over control subjects (0.01 < p < 0.05; t-test) and over patients with mild disease (0.001 < p < 0.01; t-test). The relevance of these findings to the aetiology and pathogenesis of spinal deformities and other complications in ankylosing spondylitis is discussed

Aims

Methicillin-resistant Staphylococcus aureus (MRSA) can cause wound infections via a ‘Trojan Horse’ mechanism, in which neutrophils engulf intestinal MRSA and travel to the wound, releasing MRSA after apoptosis. The possible role of intestinal MRSA in prosthetic joint infection (PJI) is unknown.

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

Chondrocyte hypertrophy represents a crucial turning point during endochondral bone development. This process is tightly regulated by various factors, constituting a regulatory network that maintains normal bone development. Histone deacetylase 4 (HDAC4) is the most well-characterized member of the HDAC class IIa family and participates in different signalling networks during development in various tissues by promoting chromatin condensation and transcriptional repression. Studies have reported that HDAC4-null mice display premature ossification of developing bones due to ectopic and early-onset chondrocyte hypertrophy. Overexpression of HDAC4 in proliferating chondrocytes inhibits hypertrophy and ossification of developing bones, which suggests that HDAC4, as a negative regulator, is involved in the network regulating chondrocyte hypertrophy. Overall, HDAC4 plays a key role during bone development and disease. Thus, understanding the role of HDAC4 during chondrocyte hypertrophy and endochondral bone formation and its features regarding the structure, function, and regulation of this process will not only provide new insight into the mechanisms by which HDAC4 is involved in chondrocyte hypertrophy and endochondral bone development, but will also create a platform for developing a therapeutic strategy for related diseases.

Cite this article: Bone Joint Res. 2020;9(2):82–89.