The use of porous ceramics as bone graft substitutes (BGS) has been under consideration for over 30 years [ It is well established that both pore size [ Phase pure porous HA implants were manufactured using a novel technique [ After 4 weeks new bone had penetrated deep within the macro-pore structure and at high magnification osteocyte-like cells were observed occupying micro-pores within the ceramic struts. Furthermore, there was a significant increase in the MAR of bone formed within and surrounding the PHA (5.21 ìm.day-1, 4.42 ìm.day-1) as compared to the normal turnover rate of control bone (2.07 ìm.day-1, 2.09 ìm.day-1) during weeks 1-2 and 2–3, respectively. The micro-porous network within the scaffold struts clearly influenced the host response. This could be linked to an associated increase in roughness or surface area, or it may reflect the greater level of strut permeability underlining the importance of nutrient transfer and the promotion of angiogenesis in scaffolds for bone repair.
To investigate the underlying mechanism of osteocyte death in osteonecrosis of the femoral head (ONFH). Although there are a plethora of conditions that predispose to ONFH the underlying mechanism that results in the death of osteocytes is poorly understood. Consequently, treatment for early disease has a variable outcome. Recent investigation has focussed on the role of nitric oxide (NO) in the local control of bone turnover. NO is central to bone cell metabolism and has been implicated in the development of apoptosis. Bone samples were harvested from the femoral heads of 40 patients undergoing total hip arthroplasty – 20 for advanced ONFH and 20 for osteoarthritis (control group). Immunocytochemical techniques were used to demonstrate evidence of NO synthase (iNOS and eNOS) as a marker of NO production and for evidence of apoptosis. There was a marked increase in the expression of both eNOS and iNOS in the bone marrow and osteocytes from patients with ONFH secondary to steroids and alcohol with a correspondingly high proportion of apoptotic cells. Very little evidence of either eNOS or iNOS could be demonstrated in the control group and no significant apoptosis could be demonstrated. Samples from patients with ONFH secondary to sickle cell disease likewise had little evidence of apoptosis and a less marked increase iNOS production. Our findings suggest that sickle cell disease may cause infarction of bone which subsequently leads to osteonecrosis. However, steroids and alcohol, or their metabolites, may have a direct cytotoxic effect upon bone leading to an increased NO production and NO-mediated apoptosis rather than necrosis. Our findings may provide important clues as to the underlying pathway leading osteocyte death. Therapeutic measures aimed at preventing production of toxic levels of NO or by blocking specific pathways in apoptosis may provide effective an treatment during the early stages of ONFH by halting disease progression.
Tissues from five patients who underwent revision operations for failed total hip replacements were found to contain large quantities of particulate titanium. In four cases this metal must have come from titanium alloy screws used to fix the acetabular component; in the fifth case it may also have originated from a titanium alloy femoral head. Monoclonal antibody labelling showed abundant macrophages and T-lymphocytes, in the absence of B-lymphocytes, suggesting sensitisation to titanium. Skin patch testing with dilute solutions of titanium salts gave negative results in all five patients. However, two of them had a positive skin test to a titanium-containing ointment.
Thirty-seven patients with extensive acetabular defects due to loose implants had revisions with uncemented components, the acetabulum being augmented with homograft bone. In six of these, a histological study of graft incorporation was made. At a mean follow-up of 1.5 years 34 patients were free of pain and 35 could walk for 30 minutes or longer. No graft had obviously sequestrated. Two components had radiological evidence of migration but remain asymptomatic. We conclude that cementless revision surgery with homograft supplementation of the acetabulum is clinically successful in the short-term. The long-term outcome is unknown.
Mechanical and biomechanical testing of a new bone cement suggests that improved load transfer to the proximal femur could be achieved with the combination of a cement having a lower modulus, a greater ductility and a lower creep resistance than polymethylmethacrylate and a suitably shaped femoral component.
A case of bilateral avascular necrosis of the capitate is presented. A review of the literature has identified a clear-cut clinical syndrome. The aetiology and pathology of this syndrome is discussed and a new method of treatment is proposed.
The occurrence of a radiolucent line at the interface of bone and cement in total joint prostheses is a frequently observed, although little understood, phenomenon. Because of an operative technique utilised in instances of bone loss, we have, within a single implant mass used in each of a series of 18 total knee replacements, been able to observe two separate interfaces, one between bone and cement and the other between bone and cobalt chrome. The average period of observation was 32 months. All of the knees except one demonstrated a lucency at the bone-cement interface; only one of the knees had a similar lucency at the bone-CoCr interface. One of the knees was studied histologically. In the light of the universal observation of macrophages at bone-cement interfaces and the recent finding that osteoclasts are derived from macrophages, these observations are significant in relation to the aetiology of bone-cement lucencies.
