Clinical orthopaedics and related research
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Clin. Orthop. Relat. Res. · Apr 2008
Clinical TrialJoint gap changes with patellar tendon strain and patellar position during TKA.
Balancing of the joint gap in extension and flexion is a prerequisite for success of a total knee arthroplasty. The joint gap is influenced by patellar position. We therefore hypothesized the state of the knee extensor mechanism (including the patellar tendon) would influence the joint gap. In 20 knees undergoing posterior-stabilized type total knee arthroplasties, we measured the joint gap and the patellar tendon strain from 0 degrees to 135 degrees flexion with the femoral component in position. When the patella was reduced, the joint gap was decreased at 90 degrees and 135 degrees (by 1.9 mm and 5.5 mm, respectively) compared with the gap with the patella everted. The patellar tendon strain increased with knee flexion. Patellar tendon strain at 90 degrees flexion correlated with the joint gap difference with the patella in everted and reduced positions. This suggests that in addition to the collateral ligaments, the knee extensor mechanism may have an influence on the joint gap. Therefore, accounting for extensor mechanism tightness may be important in achieving the optimal joint gap balance during total knee arthroplasty. ⋯ Level IV, therapeutic study. See the Guidelines for Authors for a complete description of levels of evidence.
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Clin. Orthop. Relat. Res. · Apr 2008
Exclusion of COL2A1 and VDR as developmental dysplasia of the hip genes.
Developmental dysplasia of the hip (DDH) is a spectrum of disorders affecting the proximal femur and/or acetabulum leading to an abnormal formation of the hip. Genetic factors are involved in the etiology of DDH. Early recognition of DDH affords the best results from treatment and a better knowledge of the genetics of DDH could enhance early diagnosis. ⋯ To see whether there was linkage between the COL2A1/VDR locus and nonsyndromic DDH, we conducted a linkage study on 11 families with multiple cases of DDH. We demonstrated no evidence of linkage between the COL2A1/VDR locus and nonsyndromic DDH (LOD score < -2), suggesting, although variants in these genes could play a role in osteoarthritis in patients with DDH, they do not contribute to nonsyndromic DDH. The search for causal gene variants should proceed with other candidates.