We studied the effect of a lipid clearing agent (clinofibrate) on the osteocytes of rabbits treated with corticosteroids. Thirty-one rabbits were divided into four groups: (A) steroid-treated with a normal diet, (B) steroid-treated and one a diet with added clinofibrate, (C) non-steroid-treated, on a diet with clinofibrate; and (D) non-steroid-treated on a normal diet. All the steroid-treated animals demonstrated hyperlipidaemia and fatty degeneration of the liver. Lipid-containing osteocytes were seen in the femoral heads of these animals. However, those which received clinofibrate (group B) had less severe lipidaemia, and less severe degeneration of the liver. In them, only the osteocytes around the haversian canals exhibited lipid inclusions. Clinofibrate appears to modify lipid metabolism, diminishing the steroid induced accumulation of lipids within osteocytes. This effect may protect against steroid-mediated osteonecrosis.
We studied the morphology of the haversian canals in the osteopenic cortical bone of the medial femoral neck from patients with rheumatoid arthritis and compared the findings with those in patients with osteoarthritis and with uncomplicated coxa valga. In the rheumatoid bone, the diameters of the canals were larger and many more contained osteoclasts. Fewer haversian canals showed only lining cells than in the osteoarthritic or coxa valga patients. In bone from rheumatoid patients, especially in canals with osteoclasts, small blood vessels were frequently lined by tall endothelial cells with an infiltration of mononuclear cells. These morphological differences are discussed with reference to the possible mechanisms of loss of cortical bone in rheumatoid arthritis and other conditions.
We have reviewed 41 patients with pustulotic arthro-osteopathy (PAO), all having both the typical skin rash of pustulosis palmaris et plantaris and bone lesions. The most common bones affected were the clavicle, sternum and ribs. Changes in the clavicle started, not as an enthesopathy, but with periosteal bone formation, indicative of a bone marrow disorder. About 30% of the patients also had lesions in the spine, sacroiliac region or the peripheral joints. Bone and joint lesions followed a variable and intermittent clinical course over a long period of time. Biopsies in eight cases showed similar inflammatory changes in skin, bone and synovium, with infiltration of lymphocytes and polymorphonuclear leucocytes. This suggests that there is a common pathogenesis in the three tissues.
In this series, 15 patients with ossification of the posterior longitudinal ligament underwent anterior decompression to relieve moderate or severe myelopathy, which in 11 included urinary disturbance. The operation consisted of partial resection of the vertebrae, release of the ossified plaque from the surrounding tissue and the insertion of an iliac bone graft. The extent of ossification was confirmed by computerised tomography before and after operation. The plaque was completely detached and moved forward in half of the patients, but only partially moved in the remainder. Symptoms improved considerably. Urinary disturbance disappeared in all patients, but sensory disturbance was left in most. Two patients had prolonged symptoms which were not relieved despite the complete release of the ossified defect.