In recent years, the use of arthroscopy for meniscal repair has increased remarkably, but complications have been reported frequently.' In our series of 106 meniscal repairs, no serious complications, such as popliteal vascular damage, have occurred. We have experienced saphenous nerve neurapraxia (5.7%), which proved to be temporary, but in 1 case the removal of sutures and a neurolysis of the saphenous nerve were needed at 9 months postoperatively. We report a case of a meniscal cyst originating from a repaired meniscus that was torn in the avascular region. The case illustrates some of the pitfalls of meniscal repair in this region.5 5 CASE REPORT A 14-year-old boy visited our hospital in December 1987. This junior high school soccer player complained of locking Figure 1. A tear can be seen in the avascular zone of the meniscus.Figure 2. Arthroscopic findings during meniscal suture (seven sutures).and pain in the medial aspect of the right knee joint that had been troubling him since a soccer match 1 year previously. Physical examination showed a full range of motion of the right knee, normal ligamentous stability, and pain on pressure over the medial joint line. The radiographic appearance was normal, but arthrography demonstrated a longitudinal tear of the medial meniscus. He subsequently had partial excision or repair of the medial meniscus.Arthroscopy revealed a bucket-handle tear of the meniscus at approximately 4 to 5 mm from the periphery of the body, in an area that has proved to be in the avascular zone for most subjects, with no associated degeneration (Fig. 1)). Meniscal repair was performed by the arthroscopic doubleneedle cannula method using nonabsorbable 2-0 nylon sutures (Fig. 2). Because the tear affected the bloodless area of the meniscus, the repair was covered with a synovial pedicle flap. Figure 3 is a diagram of the operative procedure. Postoperatively, the patient's right knee was immobilized in
Fluorescence resonance energy transfer spectroscopy has been used to study the spatial relationships between probes attached to actin and troponin in the reconstituted skeletal muscle thin filament in the presence and absence of Ca2+ ions. Gln-41 and the nucleotide-binding site of actin were selectively labeled with the acceptor probe: fluorescein cadaverine and 2'(or 3')-O-(2,4,6-trinitrophenyl)adenosine 5'-diphosphate (TNP-ADP), respectively. Troponin was selectively labeled at positions 9 or 133 of troponin-I and 98 of troponin-C with a donor probe; 5-(2-iodoacetylaminoethyl)aminonaphthalene 1-sulfonic acid (IAEDANS). The distances between probes attached to position 133 of TnI and Gln-41 or the nucleotide site of actin were determined to be 51.6+/-1.2 and 42.7+/-0.9 A respectively in the presence of Ca2+, and these distances decreased by 11.5 and 9.3 A respectively in the absence of Ca2+ ions. The distances between the probes attached to position 9 of TnI and Gln-41 or the nucleotide site of actin were determined to be 59.1+/-2.0 or 49.3+/-1.5 A respectively in the presence of Ca2+, and the distances decreased by 5.3 or 3.7 A in the absence of Ca2+. The distances between probes attached to position 98 of TnC and Gln-41 or the nucleotide site of actin were determined to be 55.1+/-1.7 and 57+/-5 A in the presence of Ca2+ and the distances increased slightly by approximately 1 A in the absence of Ca2+. The results suggest that the C-terminal domain of troponin I moves to the outer domain of actin during inhibition, while the C-terminal domain of TnC does not move much.
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