Gait analysis of foot compensation in symptomatic Hallux Rigidus patients

BACKGROUND: Compensatory motion of foot joints in hallux rigidus (HR) are not fully known. This study aimed to clarify the kinematic compensation within the foot and to detect whether this affects plantar pressure distribution. METHODS: Gait characteristics were assessed in 16 patients (16 feet) with HR and compared with 15 healthy controls (30 feet) with three-dimensional gait analysis by using the multi-segment Oxford Foot Model, measuring spatio-temporal parameters, joint kinematics and plantar pressure. RESULTS: HR subjects showed less hallux plantar flexion during midstance and less hallux dorsiflexion during push-off, while increased forefoot supination was detected during push-off. No significant differences in plantar pressure were detected. Step length was significantly smaller in HR subjects, while gait velocity was comparable between groups. CONCLUSIONS: HR significantly affects sagittal hallux motion, and the forefoot compensates by an increased supination during push-off. Despite this kinematic compensatory mechanism, no significant differences in plantar loading were detected

Metallic hemiarthroplasty or arthrodesis of the first metatarsophalangeal joint as treatment for hallux rigidus:A systematic review and meta-analysis

BACKGROUND: Arthrodesis and metallic hemiarthroplasty are two surgical interventions for the treatment of end-stage osteoarthritis of the first metatarsophalangeal (MTP1) joint. This systematic review and meta-analysis aims to compare the two operations with regards to patient-reported outcomes, pain reduction, complications and revision rates. METHODS: A systematic literature search identified all relevant studies. The methodological quality was assessed using two validated tools. Data of interest were derived and presented. For non-comparative studies, data was assessed for trends, while for comparative studies pooling statistics were performed. RESULTS: A total of 33 studies were included for analysis. The majority of studies (>75%) reported an AOFAS-HMI score greater than 80 points after both metallic hemiarthroplasty and arthrodesis. The lowest VAS pain score was observed after arthrodesis (weighted mean difference -1.58, 95% confidence interval (CI) -2.16 to -1.00 P< 0.00001). Comparable numbers of complications (odds radio 1.48, 95% CI 0.81 to 2.73, P = 0.21, favoring: hemiarthroplasty) and revisions (odds ratio 1.16, 95% CI 0.62 to 2.15 P = 0.64, favoring: hemiarthroplasty) were observed after both interventions. The included non-comparative studies seem to confirm these findings of the comparative studies. CONCLUSION: Metallic hemiarthroplasty and arthrodesis have excellent clinical outcomes and acceptable complication- and revision rates. Arthrodesis seems to be superior in pain reduction, while metallic hemiarthroplasty is a suitable alternative for patients performing activities that requires motion in the first metatarsophalangeal joint

Impairment of Cyclo-oxygenase-2 Function Results in Abnormal Growth Plate Development and Bone Microarchitecture but Does Not Affect Longitudinal Growth of the Long Bones in Skeletally Immature Mice

Objective: Despite the general awareness that cyclo-oxygenase-2 (COX-2) is crucial for endochondral ossification, the role of COX-2 in skeletal development is largely unknown. We hypothesized that inhibition or genetic loss of COX-2 leads to impaired growth plate development and consequently impaired postnatal development of the long bones. Design: Skeletally immature (5 weeks old) B6;129S-Ptgs2 tm1Jed /J wildtype mice were treated for 10 weeks with celecoxib (daily oral administration 10 mg/kg) or placebo and compared with B6;129S-Ptgs2 tm1Jed /J homozygous knockout mice (n = 12 per group). Results: Fifteen weeks postnatally, no significant difference in growth plate (zone) thickness was found between groups. However, significantly higher proteoglycan content and lower expression levels of collagen type II and X staining in the growth plates of celecoxib-treated mice, and to a lesser extent in COX-2 knockout mice. In addition, a significantly decreased cell number and cell size were observed in the hypertrophic zone of the growth plates of both experimental groups. Micro–computed tomography analysis of the subchondral bone region directly beneath the growth plate showed significantly higher bone density and trabecular thickness, following celecoxib treatment. Despite the detected differences in growth plate extracellular matrix composition and subchondral bone morphology, no difference was found in the length of the tibia in celecoxib-treated mice or COX-2 knockout mice. Conclusions: Genetic loss of COX-2 or treatment with celecoxib did not result in detectable differences in gross murine formation of the tibia or femur. However, there were notable phenotypic features detected in the maturation of the growth plate (hypertrophic zone and subchondral bone) as a result of the celecoxib treatment

Evaluation of impaired growth plate development of long bones in skeletally immature mice by antirheumatic agents

Restriction of physical growth and development is a known problem in patients with juvenile idiopathic arthritis (JIA). However, the effect of medical treatment for JIA on skeletal growth in affected children has not been properly investigated. We, therefore, hypothesize that naproxen and methotrexate (MTX) affect endochondral ossification and will lead to reduced skeletal development. Treatment of ATDC5 cells, an in vitro model for endochondral ossification, with naproxen or MTX resulted in increased chondrogenic but decreased hypertrophic differentiation. In vivo, healthy growing C57BL/6 mice were treated with naproxen, MTX, or placebo for 10 weeks. At 15 weeks postnatal, both the length of the tibia and the length of the femur were significantly reduced in the naproxen- and MTX-treated mice compared to their controls. Growth plate analysis revealed a significantly thicker proliferative zone, while the hypertrophic zone was significantly thinner in both experimental groups compared to their controls, comparable to the in vitro results. Micro-computed tomography analysis of the subchondral bone region directly below the growth disc showed significantly altered bone microarchitecture in naproxen and MTX groups. In addition, the involvement of the PTHrP-Ihh loop in naproxen- and MTX-treated cells was shown. Overall, these results demonstrate that naproxen and MTX have a profound effect on endochondral ossification during growth plate development, abnormal subchondral bone morphology, and reduced bone length. A better understanding of how medication influences the development of the growth plate will improve understanding of endochondral ossification and reveal possibilities to improve the treatment of pediatric patients

Evaluation of impaired growth plate development of long bones in skeletally immature mice by antirheumatic agents

Restriction of physical growth and development is a known problem in patients with juvenile idiopathic arthritis (JIA). However, the effect of medical treatment for JIA on skeletal growth in affected children has not been properly investigated. We, therefore, hypothesize that naproxen and methotrexate (MTX) affect endochondral ossification and will lead to reduced skeletal development. Treatment of ATDC5 cells, an in vitro model for endochondral ossification, with naproxen or MTX resulted in increased chondrogenic but decreased hypertrophic differentiation. In vivo, healthy growing C57BL/6 mice were treated with naproxen, MTX, or placebo for 10 weeks. At 15 weeks postnatal, both the length of the tibia and the length of the femur were significantly reduced in the naproxen- and MTX-treated mice compared to their controls. Growth plate analysis revealed a significantly thicker proliferative zone, while the hypertrophic zone was significantly thinner in both experimental groups compared to their controls, comparable to the in vitro results. Micro-computed tomography analysis of the subchondral bone region directly below the growth disc showed significantly altered bone microarchitecture in naproxen and MTX groups. In addition, the involvement of the PTHrP-Ihh loop in naproxen- and MTX-treated cells was shown. Overall, these results demonstrate that naproxen and MTX have a profound effect on endochondral ossification during growth plate development, abnormal subchondral bone morphology, and reduced bone length. A better understanding of how medication influences the development of the growth plate will improve understanding of endochondral ossification and reveal possibilities to improve the treatment of pediatric patients

Adaptation of the protein translational apparatus during ATDC5 chondrogenic differentiation

Introduction: Ribosome biogenesis is integrated with many cellular processes including proliferation, differentiation and oncogenic events. Chondrogenic proliferation and differentiation require a high cellular translational capacity to facilitate cartilaginous extracellular matrix production. We here investigated the expression dynamics of factors involved in ribosome biogenesis during in vitro chondrogenic differentiation and determined whether protein translation capacity adapts to different phases of chondrogenic differentiation. Materials: SnoRNA expression during ATDC5 differentiation was analyzed by RNA sequencing of samples acquired from day 0 (progenitor stage), 7 (chondrogenic stage) and day 14 (hypertrophic stage). RT-qPCR was used to determine expression of fibrillarin, dyskerin, UBF-1, Sox9, Col2a1, Runx2, Col10a1 mRNAs and 18S, 5.8S and 28S rRNAs. Protein expression of fibrillarin, dyskerin and UBF-1 was determined by immunoblotting. Ribosomal RNA content per cell was determined by calculating rRNA RT-qPCR signals relative to DNA content (SYBR Green assay). Total protein translational activity was evaluated with a puromycilation assay and polysome profiling. Results: As a result of initiation of chondrogenic differentiation (Δt0-t7), 21 snoRNAs were differentially expressed (DE). Hypertrophic differentiation caused DE of 23 snoRNAs (Δt7-t14) and 43 when t0 was compared to t14. DE snoRNAs, amongst others, target nucleotide modifications in the 28S rRNA peptidyl transferase center and the 18S rRNA decoding center. UBF-1, fibrillarin and dyskerin expression increased as function of differentiation and displayed highest fold induction at day 5-6 in differentiation. Ribosomal RNA content per cell was significantly increased at day 7, but not at day 14 in differentiation. Similar dynamics in translational capacity and monosomal ribosome fraction were observed during differentiation. Conclusion: The expression of a great number of ribosome biogenesis factors is altered during chondrogenic differentiation of ATDC5 cells, which is accompanied by significant changes in cellular translational activity. This elucidation of ribosome biogenesis dynamics in chondrogenic differentiation models enables the further understanding of the role of ribosome biogenesis and activity during chondrocyte cell commitment and their roles in human skeletal development diseases

Treatment of centered developmental dysplasia of the hip under the age of 1 year: an evidence-based clinical practice guideline - Part 1

• Despite the high incidence of developmental dysplasia of the hip (DDH), treatment is very diverse. Therefore, the Dutch Orthopedic Society developed a clinical practice guideline with recommendations for optimal and uniform treatment of DDH. This article summarizes the guideline on centered DDH (i.e. Graf types 2A–C). • The guideline development followed the criteria of Appraisal of Guidelines for Research and Evaluation II. A systematic literature review was performed to identify randomized controlled trials and comparative cohort studies including children 6 months; (3) assess patients every 6 weeks; and (4) discontinue the abduction device when the hip has normalized or when the child is 12 months. • This paper presents a summary of part 1 of the first evidence-based guideline for treatment of centered DDH in children <1 year. Part 2 presents the guideline on decentered DDH in a separate article