Florina Moldovan

CHU Sainte-Justine, Montréal, Quebec, Canada

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Publications (64)209.14 Total impact

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    ABSTRACT: This in vivo study aimed at investigating the effects of dynamic compression on the growth plate. Rats (28 days old) were divided into three dynamically loaded groups, compared with two groups (control, sham). A device was implanted on the 6th and 8th caudal vertebrae for 15 days. Controls (n = 4) did not undergo surgery. Shams (n = 4) were operated but not loaded. Dynamic groups had sinusoidal compression with a mean value of 0.2 MPa: 1.0 Hz and ±0.06 MPa (group a, n = 4); 0.1 Hz and ±0.2 MPa (group b, n = 4); 1.0 Hz and ±0.14 MPa (group c, n = 3). Growth rates (µm/day) of dynamic groups (a) and (b) were lower than shams (p < 0.01). Growth plate heights, hypertrophic cell heights and proliferative cell counts per column did not change in dynamic (a) and (b) groups compared with shams (p > 0.01). Rats from dynamic group (c) had repeated inflammations damaging tissues; consequently, their analysis was unachievable. Increasing magnitude or frequency leads to growth reduction without histomorphometric changes. However, the combined augmentation of magnitude and frequency alter drastically growth plate integrity. Appropriate loading parameters could be leveraged for developing novel growth modulation implants to treat skeletal deformities. © 2014 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res.
    Journal of Orthopaedic Research 06/2014; · 2.88 Impact Factor
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    ABSTRACT: Objective: To demonstrate the involvement of 4-hydroxynonenal (HNE), a very reactive aldehyde derived from lipid peroxidation, in the pathogenesis of osteoarthritis (OA) in vivo.Methods: (i) OA was induced by anterior cruciate ligament transection (ACLT) of the right knee of crossbred dogs (n=6/group). The animals were treated with placebo and HNE-trapping carnosine (5 and 20 mg/kg/day) orally for 8 weeks. Another group was treated for 4 weeks with 20 mg/kg/day of carnosine, starting 4-weeks after surgery. Sham-operated dogs served as controls. (ii) A pathophysiological dose of HNE (80 nmol/ml) or vehicle was injected weekly into the right knee joint of crossbred dogs (n=6) for 8 weeks. Articular cartilage underwent macroscopic, histomorphological and immunohistochemical analyses. Cartilage-degrading enzymes and oxidative stress-related products were assessed in synovial fluid and cartilage explants. Markers of inflammation were evaluated in synovium and synovial fluid.Results: In dogs with ACLT, carnosine treatment reduced the severity and histopathological score of OA cartilage lesions as well as HNE/protein adducts, pentosidine, nitrosylated proteins, cartilage-degrading enzymes and markers of inflammation. Intra-articular injection of HNE induced cartilage lesions, assessed by macroscopic and microscopic criteria. Cartilage-degrading enzymes and markers of inflammation increased in HNE-treated dogs.Conclusion: This is the first in vivo study to demonstrate the pathophysiological role of HNE in OA. That carnosine abolishes HNE production and a number of factors known to be involved in OA pathogenesis renders it a clinically-valuable agent in prevention of the disease. © 2014 American College of Rheumatology.
    Arthritis & Rheumatology. 05/2014;
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    ABSTRACT: PURPOSE: Adolescent Idiopathic Scoliosis (AIS) is considered a complex genetic disease, in which malfunctioning or dysregulation of one or more genes has been proposed to be responsible for the expressed phenotype. However, to date, no disease causing genes has been identified and the pathogenesis of AIS remains unknown. The aim of this study is, therefore, to identify specific molecules with differing expression patterns in AIS compared to healthy individuals. METHODS: Microarray analysis and quantitative RT-PCR have examined differences in the gene transcription profile between primary osteoblasts derived from spinal vertebrae of AIS patients and those of healthy individuals. RESULTS: There are 145 genes differentially expressed in AIS osteoblasts. A drastic and significant change has been noted particularly in the expression levels of Homeobox genes (HOXB8, HOXB7, HOXA13, HOXA10), ZIC2, FAM101A, COMP and PITX1 in AIS compared to controls. Clustering analysis revealed the interaction of these genes in biological pathways crucial for bone development, in particular in the differentiation of skeletal elements and structural integrity of the vertebrae. CONCLUSIONS: This study reports on the expression of molecules that have not been described previously in AIS. We also provide for the first time gene interaction pathways in AIS pathogenesis. These genes are involved in various bone regulatory and developmental pathways and many of them can be grouped into clusters to participate in a particular biological pathway. Further studies can be built on our findings to further elucidate the association between different biological pathways and the pathogenesis of AIS.
    European Spine Journal 03/2013; · 2.47 Impact Factor
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    ABSTRACT: Nitric oxide (NO) and the lipid peroxidation (LPO) product 4-hydroxynonenal (HNE) are considered to be key mediators of cartilage destruction in osteoarthritis (OA). NO is also known to be an important intermediary in LPO initiation through peroxynitrite formation. The aim of the present study was to assess the ability of the inducible NO synthase (iNOS) inhibitor N-iminoethyl-L-lysine (L-NIL) to prevent HNE generation via NO suppression in human OA chondrocytes and cartilage explants. Human OA chondrocytes and cartilage explants were treated with L-NIL and thereafter with or without interleukin-1beta (IL-1β) or HNE at cytotoxic or non-cytotoxic concentrations. Parameters related to oxidative stress, apoptosis, inflammation, and catabolism were investigated. L-NIL stifled IL-1β-induced NO release, iNOS activity, nitrated proteins, and HNE generation in a dose-dependent manner. It also blocked IL-1β-induced inactivation of the HNE-metabolizing glutathione-s-transferase (GST). L-NIL restored both HNE and GSTA4-4 levels in OA cartilage explants. Interestingly, it also abolished IL-1β-evoked reactive oxygen species (ROS) generation and p47 NADPH oxidase activation. Furthermore, L-NIL significantly attenuated cell death and markers of apoptosis elicited by exposure to a cytotoxic dose of HNE as well as the release of prostaglandin E(2) and metalloproteinase-13 induced by a non-cytotoxic dose of HNE. Altogether, our findings support a beneficial effect of L-NIL in OA by (i) preventing the LPO process and ROS production via NO-dependent and/or independent mechanisms and (ii) attenuating HNE-induced cell death and different mediators of cartilage damage.
    Journal of Cellular Biochemistry 07/2012; 113(7):2256-67. · 3.06 Impact Factor
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    ABSTRACT: The purpose of this review is to elucidate the metabolic processes involved in the pathogenesis of adolescent idiopathic scoliosis (AIS) in light of research by the present authors as well as current literature. Pathogenetic mechanisms involved in AIS were modeled as (a) a form of neuromuscular scoliosis (in conjunction with an adverse mechanical environment such as bipedality), in which hormonal and other chemical factors act as regulators of skeletal muscle tone and function; (b) as a consequence of an abnormality in growth of the spinal column (in conjunction with an adverse mechanical environment such as bipedality), in which hormones and other chemical factors act as regulators of growth; and (c) as a mechanical failure of one side of the vertebral column due to a defect in trabecular formation or mineralization (in conjunction with an adverse mechanical environment such as bipedality); in which hormonal and other chemical factors act as regulators of bone formation, mineralization and/or resorption. Current evidence supporting these models individually or in combination is discussed.
    European Spine Journal 03/2012; 21(6):1033-42. · 2.47 Impact Factor
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    ABSTRACT: Aim: The objectives of this study were to investigate various factors involved in AIS and specifically to highlight the possible effect of biomechanical stress and estrogen on human osteoblasts derived from AIS patients and healthy subjects. Methods: Human osteoblasts were derived from tissues obtained at surgery, and cultured in presence or absence of estradiol. We used microarray analysis to examine differences in the gene transcription profile between primary human osteoblasts RNA extracted from AIS patients was compared to the RNA of healthy patients. In addition, osteoblasts were exposed to biomechanical stress (0-2 g/cm<sup>2</sup>) and then examined for changes in their cell proliferation and the level of biochemical factors produced by cultured cells such as NO, COX-2, OPN and ATP. Results: Biomechanical stress differentially influenced cell proliferation of the control osteoblasts to AIS cells. Following the biomechanical stress, we found that NO, COX-2, OPN and ATP levels were increased in both control cells and AIS cells, but a significantly higher levels of NO and COX-2 were observed in AIS cells. Using microarray analysis, we found that 86 genes were expressed at relatively higher levels in AIS osteoblasts compared to controls, while 59 genes were expressed at lower levels. These genes are involved in various bone regulatory and developmental pathways. Conclusion and significance: We demonstrated that biomechanical stress and hormonal factor are involved expression of certain genes. These factors could be associated to the spinal curve progression and consequently they could impact AIS progression. Our study provided a previously unrecognized list of AIS candidate genes. These genes are mainly involved in bone metabolism and embryonic development. Thus, our study suggests various gene interaction and pathways in AIS pathogenesis. Supported by Yves Cotrel Foudation.
    Studies in health technology and informatics 01/2012; 176:452.
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    ABSTRACT: CHARGE syndrome is caused by mutations in the CHD7 gene. Several organ systems including the retina, cranial nerves, inner ear and heart are affected in CHARGE syndrome. However, the mechanistic link between mutations in CHD7 and many of the organ systems dysfunction remains elusive. Here, we show that Chd7 is required for the organization of the neural retina in zebrafish. We observe an abnormal expression or a complete absence of molecular markers for the retinal ganglion cells and photoreceptors, indicating that Chd7 regulates the differentiation of retinal cells and plays an essential role in retinal cell development. In addition, zebrafish with reduced Chd7 display an abnormal organization and clustering of cranial motor neurons. We also note a pronounced reduction in the facial branchiomotor neurons and the vagal motor neurons display aberrant positioning. Further, these fish exhibit a severe loss of the facial nerves. Knock-down of Chd7 results in a curvature of the long body axis and these fish develop irregular shaped vertebrae and have a reduction in bone mineralization. Chd7 knockdown also results in a loss of proper segment polarity illustrated by flawed efnb2a and ttna expression, which is associated with later vascular segmentation defects. These critical roles for Chd7 in retinal and vertebral development were previously unrecognized and our results provide new insights into the role of Chd7 during development and in CHARGE syndrome pathogenesis.
    PLoS ONE 01/2012; 7(2):e31650. · 3.53 Impact Factor
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    ABSTRACT: Aims: Idiopathic Scoliosis (IS) is a spinal deformity whose etiology remains unknown. Although the role of genetic factors in the development of IS is widely accepted, the causative gene of this disease is still unidentified. Methods: A large multiplex IS French family was chosen for this study on the basis of clinical and radiological data. Whole genome genotyping of the 20 members of this family led to the mapping of a dominant disease-causing gene to two critical genomic intervals. We then performed a whole-exome capture on 4 affected members of the family to try and identify the gene mutation that is linked to IS. All the novel variants from the exome analysis were assessed for co-segregation with IS within the family. Results: In the IS family, a maximum LOD score of 3·01 was reached on two specific chromosomal regions. The interval lengths of these regions were 7 cM and 12 cM. These two regions contain several genes that might be responsible for AIS. The sequencing of the candidate genes' coding sequences was done on the family members. Sequence analysis showed two rare SNPs located on the coding regions of a gene, we named CH5G1 but these SNPs did not co-segregrate with IS in the family. Whole-exome capture resulted in 6501 genetic variants common between the 4 patients, among which 7 were novel variants. Co-segregration analysis of these variants with the disease in the family was performed using the classical Sanger sequencing. Conclusions: Within the two chromosomic loci linked to IS susceptibility (Edery et al 2011), we found seven novel variants and two of these variants co-segregate perfectly with the disease. Significance: Identification of susceptibility genes for IS will help to better understand the pathogenesis of this disease. Supported by the Yves Cotrel Foundation, Institut de France.
    Studies in health technology and informatics 01/2012; 176:453.
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    ABSTRACT: Introduction: Mechanical modulation of bone growth plays a key role in progressive musculoskeletal deformities and in the development of new minimally invasive (MI) treatments for moderate scoliosis. Objective: This in vivo study focuses on determining the influence of dynamic compression parameters on the mechanical modulation of bone growth. Method: Thirty-two rats (28 d.o.) were divided into four groups: control (n=6), sham (n=6), static (n=6), dynamic (n=14). A 0.2 MPa compression was applied for 15 days on the 7th caudal vertebra. Sustained loading was used in the static group and sinusoidal loading in the dynamic groups: (a) 0.1Hz and 30%; (b) 0.1Hz and 100%; (c) 1.0Hz and 30%. Growth rates and histomorphometry of the growth plate were compared. Results: Growth rates (μm/day) of the static (30.5) and dynamic (a:30.4; b:29.2; c:29.4) groups showed no significant difference but were reduced compared with shams (37.8). Growth plate height (μm) decreased for both static (150.9) and dynamic (a: 168.9; c: 167.5) groups but increased significantly (185.5) in dynamic group (b) compared with shams (175.5). Hypertrophic cell heights (μm) decreased similarly and significantly in the static group (23.1) and in all dynamic groups (a: 25.9; b: 25.2; c: 24.4) compared with shams (28.6). Proliferative cell densities decreased in the static group, was similar in the dynamic group (a) but increased in dynamic groups (b) and (c), compared with shams; none of the changes were significant. Conclusion: Static and dynamic loadings, with the same average compression, resulted in similar growth reductions. However, dynamic loadings modulated growth with less damage to the growth plate. Among dynamic loading parameters, increasing magnitude was less detrimental than increasing frequency. Relevance: A comprehensive understanding of growth plate mechanobiology is essential for developing new MI treatments based on bone growth modulation for scoliosis correction.
    Studies in health technology and informatics 01/2012; 176:469.
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    ABSTRACT: Longitudinal bone growth, which occurs in growth plates, has important implications in pediatric orthopedics. Mechanical loads are essential to normal bone growth, but excessive loads can lead to progressive deformities. In order to compare the effects of in vivo static and dynamic loading on bone growth rate and growth plate histomorphometry, a finely controlled, normalized and equivalent compression was applied for a period of two weeks on the seventh caudal vertebra (Cd7) of rats during their pubertal growth spurt. The load was sustained (0.2MPa, 0.0Hz) in the static group and sinusoidally oscillating (0.2MPa±30%, 0.1Hz) in the dynamic group. Control and sham (operated but no load applied) groups were also studied. Cd7 growth rate was statistically reduced by 19% (p<0.001) for both static and dynamic groups when compared to the sham group. Loading effects on growth plate histomorphometry were greater in the static than dynamic groups with significant reductions (p<0.001) observed for growth plate thickness, proliferative chondrocyte number per column and hypertrophic chondrocyte height in the static group when compared to the sham group. Significant differences (p<0.01) were also found between static and dynamic groups for growth plate thickness and proliferative chondrocyte number per column while the difference nearly reached significance (p=0.014) for hypertrophic chondrocyte height. This in vivo study shows that static and dynamic loading are equally effective in modulating bone growth of rat caudal vertebrae. However, dynamic loading causes less detrimental effects on growth plate histomorphometry compared to static loading. This knowledge is greatly relevant for the improvement and/or development of new minimally invasive approaches, which are based on the local modulation of bone growth, to correct several progressive musculoskeletal deformities.
    Bone 07/2011; 49(5):996-1004. · 4.46 Impact Factor
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    ABSTRACT: Endothelin-1, a vasoconstrictor peptide, influences cartilage metabolism mainly via endothelin receptor type A (ETA). Along with the inflammatory nonapeptide vasodilator bradykinin (BK), which acts via bradykinin receptor B1 (BKB1) in chronic inflammatory conditions, these vasoactive factors potentiate joint pain and inflammation. We describe a preclinical study of the efficacy of treatment of surgically induced osteoarthritis with ETA and/or BKB1 specific peptide antagonists. We hypothesize that antagonism of both receptors will diminish osteoarthritis progress and articular nociception in a synergistic manner. Osteoarthritis was surgically induced in male rats by transection of the right anterior cruciate ligament. Animals were subsequently treated with weekly intra-articular injections of specific peptide antagonists of ETA and/or BKB1. Hind limb nociception was measured by static weight bearing biweekly for two months post-operatively. Post-mortem, right knee joints were analyzed radiologically by X-ray and magnetic resonance, and histologically by the OARSI histopathology assessment system. Single local BKB1 antagonist treatment diminished overall hind limb nociception, and accelerated post-operative recovery after disease induction. Both ETA and/or BKB1 antagonist treatments protected joint radiomorphology and histomorphology. Dual ETA/BKB1 antagonism was slightly more protective, as measured by radiology and histology. BKB1 antagonism improves nociceptive tolerance, and both ETA and/or BKB1 antagonism prevents joint cartilage degradation in a surgical model of osteoarthritis. Therefore, they represent a novel therapeutic strategy: specific receptor antagonism may prove beneficial in disease management.
    Arthritis research & therapy 05/2011; 13(3):R76. · 4.27 Impact Factor
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    ABSTRACT: This study aimed at investigating the effects of static and dynamic compression applied on growth plate explants using matched compressive strains. Growth plate explants from 4-week-old swine ulnae were submitted to in vitro static (10% strain) or dynamic (oscillating between 7% and 13% at 0.1 Hz) unconfined compression for 48 h. The total growth plate height, the combined proliferative and hypertrophic thickness and the resulting ratio between these two thicknesses were evaluated. Standard immunohistochemistry was used to analyze the protein expression of key components of the extracellular matrix: aggrecan, type II collagen, type X collagen, and MMP13. In the statically loaded samples, the columnar organization of the cells was preserved but with slight columns deviation from the growth axis. Decreases in all histomorphological parameters were important and a notable loss of aggrecan, type II and type X collagens expressions was denoted. In the dynamically loaded samples, a severe loss of columnar arrangement was observed in the proliferative and hypertrophic zones. However, dynamic compressive loads preserved the proliferative and hypertrophic zones ratio and contributed to the synthesis of aggrecan and type II collagen in the extracellular matrix. The exact response of the growth plate to mechanical stresses along with optimal loading parameters could help improve the current treatment approaches or develop new treatment approaches for the underlying progressive musculoskeletal deformities.
    Journal of Orthopaedic Research 04/2011; 29(4):473-80. · 2.88 Impact Factor
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    ABSTRACT: Idiopathic scoliosis (IS) is a spine disorder of unknown origin with 1.5-3% prevalence in the general population. Besides the large multifactorial-form sample of IS, there is a good evidence for the existence of a monogenic subgroup in which the disease is inherited in a dominant manner. However, results from literature suggest a strong heterogeneity in the locations of the mutated genes. Using a high-resolution genome-wide scan, we performed linkage analyses in three large multigenerational IS families compatible with dominant inheritance including 9-12 affected members or obligate carriers. In two of these families, our results suggested intra-familial genetic heterogeneity, whereas, in the other, we observed a perfect marker disease co-segregation in two regions at 3q12.1 and 5q13.3. We can state that one of these two locations is a novel IS disease gene locus, as the probability of having this perfect co-segregation twice by chance in the genome is very low (P=0.001). Lastly, in all three families studied, linkage to the previously mapped dominant IS loci on chromosomes 19p13.3, 17p11.2, 9q34, 17q25 and 18q is unlikely, confirming that there is a high genetic heterogeneity within the subgroup of dominant forms of IS.
    European journal of human genetics: EJHG 03/2011; 19(8):865-9. · 3.56 Impact Factor
  • Shunmoogum A Patten, Florina Moldovan
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    ABSTRACT: Adolescent idiopathic scoliosis (AIS) is a condition characterized by a three-dimensional structural deformity of the spine. It is the most common type of spine deformity occurring in children aged 10 to maturity. Although the etiology of AIS still remains unknown, the role of genetic factors in the development of idiopathic scoliosis is widely accepted. However, to date no causative genes of AIS have been identified. Recently, the semicircular canals, which are part of the inner ear, were found to be morphologically abnormal in idiopathic scoliosis patients. Here we hypothesized that genetic predisposition to inner ear anomalies in AIS patients may be a strong factor in the generation of idiopathic scoliosis. The proposed idea is that gene defects could impair the development of the semicircular canals. A malformation of semicircular canals might affect the transmission of sensory signal about rotational movement of the body to the central nervous system; leading to an alteration in the neuronal circuit of balance. This will in turn affect body posture and results in the initiation of the curvature of the spine. This hypothesis may provide new insights in the understanding of the pathophysiologic mechanisms of idiopathic scoliosis. It can also offer hopes for potential early prediction of scoliosis.
    Medical Hypotheses 03/2011; 76(3):438-40. · 1.18 Impact Factor
  • K Fendri, F Moldovan
    Medical Hypotheses 02/2011; 76(5):762-3. · 1.18 Impact Factor
  • Osteoarthritis and Cartilage 01/2011; 19. · 4.26 Impact Factor
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    ABSTRACT: Oxygen is a critical parameter proposed to modulate the functions of chondrocytes ex-vivo as well as in damaged joints. This article investigates the effect of low (more physiological) oxygen percentage on the biosynthetic and catabolic activity of human articular chondrocytes (HAC) at different phases of in vitro culture. HAC expanded in monolayer were cultured in pellets for two weeks (Phase I) or up to an additional two weeks (Phase II). In each Phase, cells were exposed to 19% or 5% oxygen. Resulting tissues and culture media were assessed to determine amounts of produced/released proteoglycans and collagens, metalloproteinases (MMPs), collagen degradation products and collagen fibril organization using biochemical, (immuno)-histochemical, gene expression and scanning electron microscopy analyses. In specific experiments, the hypoxia-inducible factor-1alpha (HIF-1alpha) inhibitor cadmium chloride was supplemented in the culture medium to assess the involvement of this pathway. Independent from the oxygen percentage during expansion, HAC cultured at 5% O(2) (vs 19% O(2)) during Phase I accumulated higher amounts of glycosaminoglycans and type II collagen and expressed reduced levels of MMP-1 and MMP-13 mRNA and protein. Switching to 19% oxygen during Phase II resulted in reduced synthesis of proteoglycan and collagen, increased release of MMPs, accumulation of type II collagen fragments and higher branching of collagen fibrils. In contrast, reducing O(2) during Phase II resulted in increased proteoglycan and type II collagen synthesis and reduced expression and release of MMP-13 mRNA and protein. Supplementation of cadmium chloride during differentiation culture at 5% O(2) drastically reduced the up-regulation of type II collagen and the down-regulation of MMP-1 mRNA. The application of more physiologic oxygen percentage during specific phases of differentiation culture enhanced the biosynthetic activity and reduced the activity of catabolic enzymes implicated in cartilage breakdown. Modulation of the oxygen percentage during HAC culture may be used to study pathophysiological events occurring in osteoarthritis and to enhance properties of in vitro engineered cartilaginous tissues.
    Arthritis research & therapy 03/2010; 12(2):R34. · 4.27 Impact Factor
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    ABSTRACT: We used a microarray approach to evaluate gene expression profiles in human AIS osteoblasts, and to identify genes that are differentially expressed following estrogen exposure in non-AIS and AIS human osteoblasts. We found that more than one gene is likely responsible for AIS. Furthermore, some of these genes are estrogen-regulated, suggesting a possible role of estrogens in the etiology of scoliosis.
    Studies in health technology and informatics 01/2010; 158:3-7.
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    ABSTRACT: Recent discoveries in the pathogenesis of adolescent idiopathic scoliosis (AIS) indicate that various hormones, especially estrogens, have a role in its onset and development. This role for estrogen seems possible because of its interaction with factors that influence the development and progression of this spinal deformity. Additionally, estrogens impact bone remodeling and growth, as well as bone acquisition, all of which are affected in AIS. Despite the fact that estrogens are not causative factors of AIS, they could impact the progression of spinal deformity by interacting with factors that modulate bone growth, biomechanics and structure. Thus, clarifying the role of estrogens is essential for understanding how AIS evolves during skeletal growth and for the development of new therapeutic interventions.
    Trends in Endocrinology and Metabolism 05/2009; 20(4):147-52. · 8.90 Impact Factor
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    ABSTRACT: Spinal deformities, and particularly scoliosis, are the most frequent forms of orthopedic deformities in children and adolescents. About 1-6% of the population has scoliosis. This disorder leads to severe spinal deformities and predominantly affects adolescent girls.Although the multifactorial origin of adolescent idiopathic scoliosis (AIS) is broadly recognized, the genetic causes of AIS are still largely unknown. Our previous studies suggested a generalized dysfunction of melatonin transduction (the hormone that is primarily produced in the brain and epiphysis). In the meantime we have demonstrated that such a defect of signal transduction is caused by chemical alterations, which inactivate the function of the inhibitory G protein-coupled melatonin receptors. This discovery has led to the development of the first blood test to detect children without symptoms who are at risk of developing scoliosis. Since a single function (cellular reaction to melatonin) is determined, the unique advantage of this test is that it can be performed without knowledge of mutations in defective genes that could provoke the onset of AIS.
    Der Orthopäde 03/2009; 38(2):114-6, 118-21. · 0.51 Impact Factor

Publication Stats

785 Citations
209.14 Total Impact Points


  • 2004–2012
    • CHU Sainte-Justine
      Montréal, Quebec, Canada
  • 2009–2011
    • Université du Québec à Montréal
      Montréal, Quebec, Canada
  • 2008–2011
    • Montreal Polytechnic
      • Département de génie mécanique
      Montréal, Quebec, Canada
  • 1997–2011
    • Université de Montréal
      • • Faculty of Dentistry
      • • Osteoarthritis Research Unit
      • • Department of Medicine
      Montréal, Quebec, Canada
  • 2007
    • Unité Inserm U1077
      Caen, Lower Normandy, France
  • 1999–2003
    • Centre hospitalier de l'Université de Montréal (CHUM)
      Montréal, Quebec, Canada
  • 1998
    • Institut de Génétique et de Biologie Moléculaire et Cellulaire
      Strasburg, Alsace, France
  • 1996
    • Université René Descartes - Paris 5
      Lutetia Parisorum, Île-de-France, France