scholarly journals Orthopaedic sequelae of meningococcemia in children: options for the correction of lower and upper limb deformities (preliminary message)

2020 ◽  
Vol 8 (1) ◽  
pp. 63-72
Author(s):  
Yuriy E. Garkavenko ◽  
Alina M. Khodorovskaya ◽  
Bahauddin H. Dolgiev ◽  
Evgeny V. Melchenko
Keyword(s):  
Growth Plate ◽  
Bone Growth ◽  
Deformity Correction ◽  
Long Bone ◽  
Angular Deformity ◽  
Axis Deviation ◽  
Guided Growth ◽  
Limb Deformity ◽  
Distraction Osteosynthesis ◽  
Limb Deformities

Background. Мeningococcal infection with damage to various organs and systems, including the musculoskeletal system, causes growth plate dysfunction, which usually leads to the formation of orthopedic consequences, including axis deviation and/or limb length discrepancy. Aim. This study aimed to analyze the features of limb deformities and methods for their correction in children with consequences of meningococcemia. Materials and methods. The retrospective analysis was performed on patients with consequences of meningococcemia who were examined and surgically treated in the clinic between 2012 and 2018. A total of 12 patients (six boys and six girls) were included, with an age range of 215 years. The examination included clinical, X-ray, and physiological methods. Treatment methods consisted of a combination of angular deformity correction and limb lengthening. Results. In 12 patients, 76 growth plate arrests of long bones were found. Most frequently (17.1%), growth plate arrests of the distal femur and proximal tibia were observed, which resulted in limb shortening and/or axis deviation. For restoration of limb alignment in 10 (83.3%) patients, transosseous compression-distraction osteosynthesis was performed. For limb deformity correction, guided growth technique was applied by using eight-plate for temporary epiphysiodesis of active functioning part of the growth plate in four (33.3%) patients, whereas partial growth plate arrest resection with following epiphysiodesis was achieved in two (16.6%). Conclusions. Meningococcal septicemia leads to long bone growth plate dysfunction. The main complaints in this patient are limb shortening and their deformity. Along with the transosseous compression-distraction osteosynthesis technique, using the guided growth method by carrying out temporary epiphysiodesis of the remaining functioning part of the growth plate of damaged bone was appropriate.

scholarly journals Exposure to the RXR agonist SR11237 in early life causes disturbed skeletal morphogenesis in a rat model

2019 ◽  
Author(s):  
Holly Dupuis ◽  
Michael Andrew Pest ◽  
Ermina Hadzic ◽  
Thin Xuan Vo ◽  
Daniel B. Hardy ◽  
...  
Keyword(s):  
Growth Plate ◽  
Bone Growth ◽  
Long Bone ◽  
Tunel Staining ◽  
Long Bones ◽  
Micro Computed Tomography ◽  
Computed Tomography Scanning ◽  
Calcified Tissue ◽  
Trap Staining ◽  
Tomography Scanning

AbstractLongitudinal bone growth occurs through endochondral ossification (EO), controlled by various signaling molecules. Retinoid X Receptor (RXR) is a nuclear receptor with important roles in cell death, development, and metabolism. However, little is known about its role in EO. In this study, the agonist SR11237 was used to evaluate RXR activation on EO.Rats given SR11237 from post-natal day 5 to 15 were harvested for micro-computed tomography scanning and histology. In parallel, newborn CD1 mouse tibiae were cultured with increasing concentrations of SR11237 for histological and whole mount evaluation.RXR agonist-treated rats were smaller than controls, and developed dysmorphia of the growth plate. Cells invading the calcified and dysmorphic growth plate appeared pre-hypertrophic in size and shape corresponding with P57 immunostaining. Additionally, SOX9 positive cells were found surrounding the calcified tissue. The epiphysis of SR11237 treated bones showed increased TRAP staining, and additional TUNEL staining at the osteo-chondral junction. MicroCT revealed morphological disorganization in the long bones of treated animals. Isolated mouse long bones treated with SR11237 grew significantly less than their DMSO controls.This study demonstrates that stimulation of the RXR receptor causes irregular ossification, premature closure of the growth plate, and disrupted long bone growth in rodent models.

scholarly journals Inner histopathologic changes and disproportionate zone volumes in foetal growth plates following gestational hypoglycaemia in rats

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Vivi F. H. Jensen ◽  
Anne-Marie Mølck ◽  
Ingrid B. Bøgh ◽  
Jette Nowak ◽  
Birgitte M. Viuff ◽  
...  
Keyword(s):  
Growth Plate ◽  
Bone Growth ◽  
Skeletal Development ◽  
Long Bone ◽  
Structural Protein ◽  
Pregnant Rats ◽  
Growth Plates ◽  
Chondrocyte Maturation ◽  
Foetal Growth ◽  
Histopathologic Changes

AbstractMaternal hypoglycaemia throughout gestation until gestation day (GD)20 delays foetal growth and skeletal development. While partially prevented by return to normoglycaemia after completed organogenesis (GD17), underlying mechanisms are not fully understood. Here, we investigated the pathogenesis of these changes and significance of maternal hypoglycaemia extending beyond organogenesis in non-diabetic rats. Pregnant rats received insulin-infusion until GD20 or GD17, with sacrifice on GD20. Hypoglycaemia throughout gestation increased maternal corticosterone levels, which correlated with foetal levels. Growth plates displayed central histopathologic changes comprising disrupted cellular organisation, hypertrophic chondrocytes, and decreased cellular density; expression of pro-angiogenic factors, HIF-1α and VEGF-A increased in surrounding areas. Disproportionately decreased growth plate zone volumes and lower expression of the structural protein MATN-3 were seen, while bone ossification parameters were normal. Ending maternal/foetal hypoglycaemia on GD17 reduced incidence and severity of histopathologic changes and with normal growth plate volume. Compromised foetal skeletal development following maternal hypoglycaemia throughout gestation is hypothesised to result from corticosterone-induced hypoxia in growth plates, where hypoxia disrupts chondrocyte maturation and growth plate structure and volume, decreasing long bone growth. Maternal/foetal hypoglycaemia lasting only until GD17 attenuated these changes, suggesting a pivotal role of glucose in growth plate development.

scholarly journals Analysis of short-term treatment with the phosphodiesterase type 5 inhibitor tadalafil on long bone development in young rats

2018 ◽  
Vol 315 (4) ◽  
pp. E446-E453 ◽  
Author(s):  
Luqiang Wang ◽  
Haoruo Jia ◽  
Robert J. Tower ◽  
Michael A. Levine ◽  
Ling Qin
Keyword(s):  
Growth Plate ◽  
Time Course ◽  
Bone Growth ◽  
Bone Structure ◽  
Primary Cultures ◽  
Long Bone ◽  
Short Term ◽  
Short Term Treatment ◽  
Bone Properties ◽  
Phosphodiesterase Type 5 Inhibitor

Cyclic GMP (cGMP) is an important intracellular regulator of endochondral bone growth and skeletal remodeling. Tadalafil, an inhibitor of the phosphodiesterase (PDE) type 5 (PDE5) that specifically hydrolyzes cGMP, is increasingly used to treat children with pulmonary arterial hypertension (PAH), but the effect of tadalafil on bone growth and strength has not been previously investigated. In this study, we first analyzed the expression of transcripts encoding PDEs in primary cultures of chondrocytes from newborn rat epiphyses. We detected robust expression of PDE5 as the major phosphodiesterase hydrolyzing cGMP. Time-course experiments showed that C-type natriuretic peptide increased intracellular levels of cGMP in primary chondrocytes with a peak at 2 min, and in the presence of tadalafil the peak level of intracellular cGMP was 37% greater ( P < 0.01) and the decline was significantly attenuated. Next, we treated 1-mo-old Sprague Dawley rats with vehicle or tadalafil for 3 wk. Although 10 mg·kg−1·day−1 tadalafil led to a significant 52% ( P < 0.01) increase in tissue levels of cGMP and a 9% reduction ( P < 0.01) in bodyweight gain, it did not alter long bone length, cortical or trabecular bone properties, and histological features. In conclusion, our results indicate that PDE5 is highly expressed in growth plate chondrocytes, and short-term tadalafil treatment of growing rats at doses comparable to those used in children with PAH has neither obvious beneficial effect on long bone growth nor any observable adverse effect on growth plate structure and trabecular and cortical bone structure.

scholarly journals Estrogen stimulates leptin receptor expression in ATDC5 cells via the estrogen receptor and extracellular signal-regulated kinase pathways

2012 ◽  
Vol 213 (2) ◽  
pp. 163-172 ◽  
Author(s):  
Shan-Jin Wang ◽  
Xin-Feng Li ◽  
Lei-Sheng Jiang ◽  
Li-Yang Dai
Keyword(s):  
Growth Plate ◽  
Cross Talk ◽  
Bone Growth ◽  
Leptin Receptor ◽  
Receptor Expression ◽  
Long Bone ◽  
Endochondral Bone Formation ◽  
Dependent Manner ◽  
Growth Plate Chondrocytes ◽  
Concentration Dependent Manner

Regulation of the physiological processes of endochondral bone formation during long bone growth is controlled by various factors including the hormones estrogen and leptin. The effects of estrogen are mediated not only through the direct activity of estrogen receptors (ERs) but also through cross talk with other signaling systems implicated in chondrogenesis. The receptors of both estrogen and leptin (OBR (LEPR)) are detectable in growth plate chondrocytes of all zones. In this study, the expression of mRNA and protein of OBR in chondrogenic ATDC5 cells and the effect of 17β-estradiol (E2) stimulation were assessed using quantitative PCR and western blotting. We have found that the mRNA of Obr was dynamically expressed during the differentiation of ATDC5 cells over 21 days. Application of E2 (10−7 M) at day 14 for 48 h significantly upregulated OBR mRNA and protein levels (P<0.05). The upregulation of Obr mRNA by E2 was shown to take place in a concentration-dependent manner, with a concentration of 10−7 M E2 having the greatest effect. Furthermore, we have confirmed that E2 affected the phosphorylation of ERK1/2 (MAPK1/MAPK3) in a time-dependent manner where a maximal fourfold change was observed at 10 min following application of E2. Finally, pretreatment of the cells with either U0126 (ERK1/2 inhibitor) or ICI 182 780 (ER antagonist) blocked the upregulation of OBR by E2 and prevented the E2-induced phosphorylation of ERK. These data demonstrate, for the first time, the existence of cross talk between estrogen and OBR in the regulation of bone growth whereby estrogen regulates the expression of Obr in growth plate chondrocytes via ERs and the activation of ERK1/2 signaling pathways.

scholarly journals Crecimiento guiado con placas en 8 para la corrección de deformidades angulares en pacientes esqueléticamente inmaduros. [Eight plate guided growth for angular deformity correction in skeletally immature patients.]

10.15417/448 ◽  
2015 ◽  
Vol 80 (4) ◽  
pp. 254 ◽  
Author(s):  
Diego Tourn ◽  
Victoria Allende ◽  
Julio Javier Masquijo
Keyword(s):  
Deformity Correction ◽  
Angular Deformity ◽  
Skeletally Immature ◽  
Guided Growth

<p><strong>Introducción</strong></p><p><strong></strong><em> </em>La manipulación de la fisis permite la corrección de deformidades <em>ón</em>en pacientes esqueléticamente inmaduros. Recientemente, se ha propuesto el empleo de un nuevo implante (placas en 8) que presentaría algunas ventajas con sus antecesores. El objetivo de este estudio es evaluar los resultados radiográficos y las complicaciones de una serie consecutiva de pacientes tratados con este método.</p><p><strong>Material y Métodos</strong></p><p><strong></strong>Se revisaron retrospectivamente las historias clínicas de todos los pacientes esqueléticamente inmaduros con deformidades angulares que se sometieron a cirugía de realineación de miembros inferiores (Rodilla o tobillo) mediante crecimiento guiado con placas en 8 entre Enero de 2009 y Julio del 2013. Se evaluaron los datos demográficos, evolución radiográfica  y la tasa de complicaciones. Todos los niños fueron intervenidos en la misma institución, por tres ortopedistas infantiles.</p><p><strong>Resultado<em>s</em></strong></p><p>Se evaluaron 27 pacientes (47 fisis), 12 de sexo masculino, 15 sexo femenino. 38 fueron tratados por deformidades en valgo y 9 por varo. De las 47 fisis tratadas, 33 fueron en el fémur distal, 12 en la tibia proximal y 2 en la tibia distal.  La edad promedio en la que se realizó el procedimiento fue de 11.8±1.36 años (rango de edad de 8 años – 14 años). El tiempo promedio entre la colocación y el retiro fue de 10.6±3 meses (rango 7 – 26 meses). Todos los pacientes menos uno, presentaron corrección completa de la deformidad. Se presentaron 6 complicaciones postoperatorias y 2 de ellas requirieron una nueva intervención (1 efecto rebote y 1 migración del implante).</p><p><strong>Conclusión</strong></p><p>La utilización de placas en 8 para la corrección de deformidades angulares en pacientes esqueléticamente inmaduros es un método efectivo con una baja tasa de complicaciones.</p>

scholarly journals Guided growth for correction of axial deformities of the knee in children: a literature review

2016 ◽  
Vol 4 (1) ◽  
pp. 57-62 ◽  
Author(s):  
Ekaterina S Morenko ◽  
Vladimir M Kenis
Keyword(s):  
Literature Review ◽  
Growth Plate ◽  
Bone Growth ◽  
Metal Plate ◽  
Lower Limbs ◽  
Guided Growth ◽  
Minimal Invasiveness ◽  
Orthopedic Surgeons ◽  
The Everyday ◽  
Pediatric Orthopedic

Literature review was performed for axial deformities of the knee in children and possible correction by guided growth, which aims to restore the mechanical axis of the lower limbs by targeting the growth plate. In 2004, P. Stevens proposed temporarily blocking the bone growth plate with metal plate and two screws. The method includes the extraperiosteal placement of the metal plate at a certain segment of the growth plate (i.e., at the top of or in plane with the deformity). Its advantages are minimal invasiveness, higher accuracy and reliability, and ease and efficiency of use. In addition, there is a negligible risk of possible complications. The method of guided growth is a preferable alternative to osteotomy for the correction of the axial deformity of the knee joint in children and should be more widely used in the everyday practice of pediatric orthopedic surgeons.

scholarly journals Correction of Complex Lower Limb Deformities by the Ilizarov Technique: An Audit of Complications

2000 ◽  
Vol 8 (1) ◽  
pp. 67-71 ◽  
Author(s):  
Jean-Claude Theis ◽  
H Simpson ◽  
J Kenwright
Keyword(s):  
Lower Limb ◽  
Deformity Correction ◽  
Limb Lengthening ◽  
Bone Transport ◽  
Angular Deformity ◽  
Ilizarov Technique ◽  
Leg Lengthening ◽  
Limb Deformities ◽  
Lower Limb Reconstruction ◽  
Tract Infections

This is an audit of complications resulting from correction of complex lower limb deformities by the Ilizarov technique. 33 patients (40 bone segments) were reviewed and divided into 4 groups according to the type of surgery carried out: limb lengthening and/or correction of deformity, bone or joint stabilisation, treatment of nonunion or bone defect, angular and/or rotation correction. Most minor complications were fixator specific. Pin tract infections were almost universal but responded well to oral antibiotics and rarely resulted in osteomyelitis. Major complications were procedure specific and more common in those patients who underwent leg lengthening, treatment for nonunion and bone transport. There was also a high incidence of nerve injury as a result of acute angular deformity correction. Despite the high complication rate the Ilizarov technique remains an effective tool for complex lower limb reconstruction surgery.

scholarly journals Exposure to the RXR Agonist SR11237 in Early Life Causes Disturbed Skeletal Morphogenesis in a Rat Model

2019 ◽  
Vol 20 (20) ◽  
pp. 5198
Author(s):  
Holly Dupuis ◽  
Michael Andrew Pest ◽  
Ermina Hadzic ◽  
Thin Xuan Vo ◽  
Daniel B. Hardy ◽  
...  
Keyword(s):  
Growth Plate ◽  
Endochondral Ossification ◽  
Bone Growth ◽  
Long Bone ◽  
Tunel Staining ◽  
Long Bones ◽  
Micro Computed Tomography ◽  
Calcified Tissue ◽  
Trap Staining ◽  
Stimulation Of

Longitudinal bone growth occurs through endochondral ossification (EO), controlled by various signaling molecules. Retinoid X Receptor (RXR) is a nuclear receptor with important roles in cell death, development, and metabolism. However, little is known about its role in EO. In this study, the agonist SR11237 was used to evaluate RXR activation in EO. Rats given SR11237 from post-natal day 5 to post-natal day 15 were harvested for micro-computed tomography (microCT) scanning and histology. In parallel, newborn CD1 mouse tibiae were cultured with increasing concentrations of SR11237 for histological and whole-mount evaluation. RXR agonist-treated rats had shorter long bones than the controls and developed dysmorphia of the growth plate. Cells invading the calcified and dysmorphic growth plate appeared pre-hypertrophic in size and shape, in correspondence with p57 immunostaining. Additionally, SOX9-positive cells were found surrounding the calcified tissue. The epiphysis of SR11237-treated bones showed increased TRAP staining and additional TUNEL staining at the osteo-chondral junction. MicroCT revealed morphological disorganization in the long bones of the treated animals. This study suggests that stimulation of RXR causes irregular ossification, premature closure of the growth plate, and disrupted long bone growth in rodent models

Angular deformity correction by guided growth in growing children: Eight-plate versus 3.5-mm reconstruction plate

2017 ◽  
Vol 22 (5) ◽  
pp. 919-923
Author(s):  
Kyeong-Hyeon Park ◽  
Chang-Wug Oh ◽  
Joon-Woo Kim ◽  
Il-Hyung Park ◽  
Hee-June Kim ◽  
...  
Keyword(s):  
Deformity Correction ◽  
Plate Versus ◽  
Angular Deformity ◽  
Reconstruction Plate ◽  
Guided Growth
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