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Orthopaedic Proceedings
Vol. 103-B, Issue SUPP_13 | Pages 111 - 111
1 Nov 2021
Mulder F Senden R Staal H de Bot R van Douveren F Tolk J Meijer K Witlox A
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Introduction and Objective

Slipped Capital Femoral Epiphysis (SCFE) is one of the most common hip disorders in children and is characterized by a proximal femoral deformity, resulting in early osteoarthritis. Several studies have suggested that SCFE patients after in situ fixation show an altered gait pattern. Early identification of gait alterations might lead to earlier intervention programs to prevent osteoarthritis. The aim of this study is to analyse gait alterations in SCFE patients after in situ fixation compared to typically developed children, using the Computer Assisted Rehabilitation Environment (CAREN) system.

Materials and Methods

This is a cross-sectional, multi-center case-control study in the Netherlands. Eight SCFE patients and eight age- and sex-matched typically developed were included from two hospitals. Primary outcomes were kinematic parameters (absolute joint angles), studied with gait analysis using statistical parametric mapping (SPM). Secondary outcomes were spatiotemporal parameters, the Notzli alpha angle, muscle activation patterns (EMG), and clinical questionnaires (VAS, Borg CR10, SF-36, and HOOS), analyzed using non-parametric statistical methods.


Orthopaedic Proceedings
Vol. 100-B, Issue SUPP_3 | Pages 21 - 21
1 Apr 2018
Caron M Castermans T van Rietbergen B Haartmans M van Rhijn L Witlox A Welting T
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INTRODUCTION

Endochondral ossification in the growth plate is directly responsible for skeletal growth and its de novo bone-generating activity. Growth plates are vulnerable to disturbances that may lead to abnormal skeletal development. Non-steroidal anti-inflammatory drugs (NSAIDs) are widely used analgesics but have been reported to impair endochondral ossification-driven fracture healing. Despite the general awareness that NSAIDs affect endochondral ossification, the consequences of NSAIDs on skeletal development are unknown. We hypothesise that the NSAID celecoxib leads to impaired growth plate development and consequently impairs skeletal development.

METHODS

Healthy skeletally immature (5 weeks old) C57BL/6 mice were treated for ten weeks with celecoxib (daily oral administration 10 mg/kg) or placebo (water) (institutional approval 2013–094) (n=12 per group). At 15 weeks postnatally, total growth plate thickness, the thickness of specific growth plate zones, (immuno)histological analysis of extracellular matrix composition in the growth plate, cell number and cell size, longitudinal bone growth and bone micro-architecture by micro-CT were analysed. Inhibition of COX-2 activity was confirmed by determining PGE2 levels in plasma using an ELISA.


Orthopaedic Proceedings
Vol. 100-B, Issue SUPP_4 | Pages 25 - 25
1 Apr 2018
de Bot R Stevens J Hermus J Staal H van Rhijn L Witlox A
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Purpose

Flat feet are an important cause of foot problems in children. The flexible flat foot is the most common form and is normally physiological and asymptomatic. Further assessment is necessary when a symptomatic flat foot persists. Surgical interventions are indicated when conservative therapies have failed. The Kalix arthroereisis is a surgical option and is placed in the subtalar joint of the foot, thereby preventing hyperpronation, and stabilizes the foot against excessive movements. The purpose of this study was to evaluate the functional and radiological outcomes of pediatric patients who had undergone a Kalix implantation for the treatment of a symptomatic flexible flat foot.

Methods

Patient files of our institution were searched for patients who underwent a Kalix implantation between 2009 and 2014. Sixteen patients (26 feet) with symptomatic flexible flat feet were clinically and radiographically evaluated in this retrospective study. The calcaneal pitch and Meary”s angle were measured on the pre-, and postoperative follow-up radiographs and patient satisfaction survey was performed at follow-up to gain insight into functional outcome and satisfaction after the intervention.


Orthopaedic Proceedings
Vol. 99-B, Issue SUPP_2 | Pages 108 - 108
1 Jan 2017
Stevens J Welting T Witlox A van Rhijn L Staal H
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Dysplasia Epiphysealis Hemimelica (DEH) also known as Trevor's Disease is a rare developmental disorder resulting in cartilaginous overgrowth of the epiphysis of long bones. DEH is usually diagnosed in children between two and eight years old and it is three times more often diagnosed in boys. The most reported complaints are pain, limitation in range of motion, and deformity or swelling of the affected joint. Treatment of symptomatic lesions consists of surgical resection of the lesion, resulting in good long-term results.

Based on histological evaluation, DEH is often described as an osteochondroma or an osteochondroma-like lesion, although there are clinical, radiological and genetic differences between DEH and osteochondromas. To investigate the hypothesis that DEH and osteochondromas are histologically identical, two cases of DEH and two cases of osteochondromas in patients with Hereditary Multiple Osteochondroma (HMO) are compared at histological level.

Tissue samples from patients with a histopathologically confirmed diagnosis of DEH were compared with two age and gender matched patients diagnosed with HMO. After tissue sampling and processing, (immuno)histological stainings were performed for Collagen type II, Collagen type X, Sox-9 and Safranin-O.

Histologically, clumping of chondrocytes in a fibrillar matrix, a thick disorganized cartilage cap and ossification centres with small amounts of unresorbed cartilage were observed in DEH. In contrast, chondrocyte organisation in cartilage of osteochondromas displays characteristics of the normal growth plate. In addition, differences in expression of collagen type II, collagen type X and Sox9 were observed. Collagen type II was expressed in the extracellular matrix surrounding proliferative and hypertrophic chondrocytes in osteochondromas, while weak expression was observed in the entire cartilage cap in DEH. Collagen type X was not expressed in DEH, while expressed in the pericellular matrix surrounding hypertrophic chondrocytes in osteochondromas. Staining for Sox9 was positive in the hypertrophic chondrocytes in osteochondromas, while expressed in the nuclei of all chondrocyte clusters in DEH.

Both morphological and immunohistological differences were observed in histological sections of DEH and osteochondromas. These findings reject our hypothesis, and supports the earlier observed clinical, radiological and genetic differences and implies a different aetiology between DEH and osteochondroma formation in HMO.


Orthopaedic Proceedings
Vol. 96-B, Issue SUPP_11 | Pages 168 - 168
1 Jul 2014
Oosterwaal M Telfer S Woodburn J Witlox A Hermus J van Rhijn L Meijer K
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Summary Statement

An alternative way to assess three dimensional skin motion artefacts of kinematic models is presented and applied to a novel kinematic foot model. Largest skin motion is measured in the tarsal region.

Introduction

Motion capture systems are being used in daily clinical practise for gait analysis. Last decade several kinematic foot models have been presented to gain more insight in joint movement in various foot pathologies. No method is known to directly measure bone movement in a clinical setting. Current golden standard is based on measurement of motion of skin markers and translation to joint kinematics. Rigid body assumptions and skin motion artefacts can seriously influence the outcome of this approach and rigorous validation is required before clinical application is feasible. Validation of kinematic models is currently done via comparison with bone pin studies. However, these studies can only assess major bones in a highly invasive way; another problem is the non-synchronous measurement of skin markers and bone pins. Recently the Glasgow Maastricht kinematic foot model, which comprises all 26 foot segments, has been presented. To validate the model we propose a novel non-invasive method for the assessment of skin motion artefact, involving loaded CT data.