We used standard radiographs to evaluate the foot and ankle: AP and lateral views of the foot and the ankle, obtained with the patient standing. We include the same views of the opposite foot and ankle for comparison.Loss of the medial longitudinal arch occurs with pes planus. This can be seen on the lateral radiograph of the foot with the patient standing and can be quantified as the distance from the base of the medial cuneiform to the base of the fifth metatarsal (Fig. 1).1 As the arch collapses, this distance will decrease or actually become negative. In severe cases, the base of the medial cuneiform is actually below the level of the base of the fifth metatarsal (Fig. 2).Uncovering of the head of the talus occurs as the forefoot and hindfoot shift laterally. The exposure of the talar head is evident on the AP view of the foot and
The in vitro response of peripheral blood mononuclear cells (MNC) from patients with cemented total hip or knee arthroplasties, and control individuals, to polymethylmethacrylate (PMMA) was assessed by cell proliferation, cytokine production, and molecular techniques. After seven days in culture, a dose-dependent proliferative response to PMMA stimulation was observed in MNC from fifteen normal individuals. A concomitant dose-dependent production of both IL-1 beta and IL-2 in response to PMMA stimulation was detected. Reverse transcription-polymerase chain reactions (RT-PCR) indicated that both IL-1 beta and IL-2 mRNA was present after 48 hours in culture with PMMA. Cellular proliferation and cytokine production (both IL-1 beta and IL-2) in 10 patients with stable, painless, well-functioning, cemented arthroplasties was significantly lower (p < 0.025) than normal controls and patients with aseptically loosened, painful, arthroplasties. The findings suggest that patients with stable cemented total joint arthroplasties are either inherently or adaptively less responsive to PMMA at a cellular level.
This study investigated immunological responses to Staphylococcus aureus bone infection. Because considerable immunological information is available on the mouse, a murine model of acute hematogenous osteomyelitis was established. Osteomyelitis was created in the proximal tibia of C3H/HeJ mice by a tibial epiphyseal fracture followed by intravenous bacterial inoculation with Staphylococcus aureus (strain LS-1). Swelling and warmth of the limb was found, and following limb exposure, abscess formation was evident in the proximal tibia. Histological examination revealed distortion primarily at the hypertrophic zone of the physis and polymorphonuclear leukocyte infiltration throughout the damaged area of the proximal tibia. Local infection was demonstrated at the fracture site, evidenced by the recovery of Staphylococcus aureus following microbiological analysis of tissue specimens. Polymerase chain reaction was utilized to detect 16S ribosomal prokaryotic nucleic acid to demonstrate that the diagnosis of osteomyelitis could be established in the absence of conventional microbiological techniques. The infected mice had an increase of circulating large leukocytes (granulocytes) and an elevation of total serum immunoglobulin. Flow cytometry revealed significant increases in splenic B lymphocytes and in lymph-node CD4+ T lymphocytes. These results indicate that an experimental model of acute hematogenous osteomyelitis that closely resembles the pathology of the disease in humans may be consistently induced in mice. Furthermore, marked immunological changes may be observed in response to the Staphylococcus aureus bone infection.
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