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Orthopaedic Proceedings
Vol. 102-B, Issue SUPP_11 | Pages 63 - 63
1 Dec 2020
Debnath A Dalal S Setia P Guro R Kotwal RS Chandratreya AP
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Introduction

Recurrent patellar dislocation is often reported in bilateral knees in young active individuals. The medial patellofemoral ligament (MPFL) tear is the attributable cause behind many of them and warrants reconstruction of the ligament to stabilize the patellofemoral joint. Besides, trochleoplasty and Fulkerson's osteotomy are some other procedures that are performed to treat this problem. This study aimed to compare the clinical and functional outcomes in a cohort of patients with single-stage bilateral realignment procedures vs staged procedures.

Methods

It was a retrospective matched cohort study with prospectively collected data. A total of 36 patients (mean age-26.9 years, range 13 years to 47 years) with recurrent patellar dislocations, who underwent a surgical correction in both the knees, were divided into two matched groups (age, sex, follow-up, and type of procedure). Among them, 18 patients had surgeries in one knee done at least six months later than the other knee. The remaining 18 patients had surgical interventions for both knees done in a single stage. Lysholm, Kujala, Tegner, and subjective knee scores of both groups were compared and analyzed. The rate of complications and return to the theatre were noted in both groups.


Orthopaedic Proceedings
Vol. 94-B, Issue SUPP_XVIII | Pages 37 - 37
1 May 2012
Kotwal RS Brakspear K Roberts H Wilson C Williams R Sultan J Mason DJ
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Glutamate is a neurotransmitter that transmits mechanical signals in bone (1) and activates glutamate receptors and transporters, in bone, cartilage, meniscus and synovium (2). Glutamate receptor activation influences inflammatory, degenerative and nociceptive pathways in arthritic joints (2). Thus glutamate signalling is a mechanism whereby mechanical load can directly influence joint pathology and pain. We have investigated components of glutamate signalling in the subchondral bone of patients with osteoarthritis to determine which are expressed and whether this varies in anatomical regions subject to different loads. Subchondral bone was sampled from tibial cuts derived from total knee arthroplasty (n=2, TKR, Kellgren Lawrence grade 3) and from tibial drill hole sites from high tibial osteotomy (n=5, HTO, KL grades 2 and 3) for osteoarthritis. RNA was extracted, reverse transcribed and RT-PCR performed for a housekeeping gene GAPDH, a glutamate transporters (EAAT-1, EAAT1ex9skip), glutamate receptors (NR2A and KA1), a bone matrix protein, osteocalcin, and signaling molecules (osteoprotegerin [OPG], RANKL). We found differential mRNA expression in different regions of subchondral bone. In one TKR patient, EAAT-1 expression was significantly reduced in the anterior zone versus the middle or posterior zones of the tibial plateau (ANOVA, p<0.001). HTO bone cores were subdivided medial/lateral and anterior/posterior. Good quality RNA was obtained from bone cores removed from drill holes during HTO surgery, with GAPDH, osteocalcin, EAAT-1, EAAT1ex9skip, NR2A, KA1, OPG and RANKL mRNA expression detected. In one patient, comparison of gene expression in bone cores obtained pre and post HTO revealed that EAAT1ex9skip was rarely detected in post-op bone whereas KA1 was rare in pre-op bone. This differential mRNA expression may be due to the altered loading through the joint caused by the osteotomy, although these on/off differences need to be quantified to confirm this.

We have shown that glutamate transporters and receptors are expressed in human subchondral bone. Activation of these receptors and transporters by the increased synovial fluid concentrations of glutamate released in arthritis will influence pathological changes and nociception. In some patients, glutamate transporter mRNA expression appears to vary with anatomical location in bone, or after HTO surgery, consistent with our original discovery of this transporter as mechanically-regulated in bone (1). If glutamatergic signaling is mechanically regulated in the human knee, this will vary during arthritic disease progression and after joint realignment, providing a direct mechanism linking mechanical loading through the joint to pathology and pain in arthritis.