Modulation of vertebral and tibial growth by compression loading: Diurnal versus full‐time loading

Stokes, Ian A. F.; Gwadera, Jodie; Dimock, A. N.; Farnum, Cornelia E.; Aronsson, David D.

doi:10.1016/j.orthres.2004.06.012

Cited by 54 publications

(53 citation statements)

References 22 publications

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“…Compression (8.2% reduction of cell height at −0.1 MPa loading) is predicted to be slightly less effective than tension (12.2% enhanced growth at +0.1 MPa loading) in modulating hypertrophy with the default parameter set. This concurs with averaged changes in hypertrophic cell size between rat, calve and rabbit versus sham-operated animals, which show lowered final cell size during 0.1 MPa compression by 5% (tibia) or 7% (vertebra) and enlarged sizes during 0.1 MPa tension by 15% (tibia) or 8% (vertebra) (Stokes 2002;Stokes et al 2005). In another study, continuous 0.1 MPa compression reduced final chondrocyte size in rat tibiae 7% and in vertebrae 12% (Stokes 2002;Stokes et al 2005).…”

Section: Resultssupporting

confidence: 85%

“…This concurs with averaged changes in hypertrophic cell size between rat, calve and rabbit versus sham-operated animals, which show lowered final cell size during 0.1 MPa compression by 5% (tibia) or 7% (vertebra) and enlarged sizes during 0.1 MPa tension by 15% (tibia) or 8% (vertebra) (Stokes 2002;Stokes et al 2005). In another study, continuous 0.1 MPa compression reduced final chondrocyte size in rat tibiae 7% and in vertebrae 12% (Stokes 2002;Stokes et al 2005). Upon increasing the turnover rate of collagen, hypertrophy is faster and ultimate chondrocyte height increases.…”

Section: Resultssupporting

confidence: 85%

“…After corroborating model predictions with the literature, we alter selective parameters and compare predictions with effects that are known to occur experimentally. These include extended simulations to accommodate more extreme terminal cell sizes (Hunziker 1994), application of axial tension or compression to corroborate the Hueter-Volkmann principle, which says that bone growth in epiphyseal plates is load-dependently reduced by compression and enhanced by tension and is predominantly the results of changes in the rate of hypertrophy and the ultimate size of hypertrophic cells (Stokes 2002;Stokes et al 2007Stokes et al , 2005, and simulations of hypertrophy in case of partially or fully compromised proteoglycan expression (Vanky et al 2000). Finally, we explore how mechanical conditions may be involved in the aforementioned S1Pcko knock-out mouse model in which cells do not hypertrophy (Patra et al 2006a,b).…”

Section: Introductionmentioning

confidence: 99%

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Mechanics of chondrocyte hypertrophy

Donkelaar

Wilson

2011

Biomech Model Mechanobiol

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Chondrocyte hypertrophy is a characteristic of osteoarthritis and dominates bone growth. Intra-and extracellular changes that are known to be induced by metabolically active hypertrophic chondrocytes are known to contribute to hypertrophy. However, it is unknown to which extent these mechanical conditions together can be held responsible for the total magnitude of hypertrophy. The present paper aims to provide a quantitative, mechanically sound answer to that question. To address this aim requires a quantitative tool that captures the mechanical effects of collagen and proteoglycans, allows temporal changes in tissue composition, and can compute cell and tissue deformations. These requirements are met in our numerical model that is validated for articular cartilage mechanics, which we apply to quantitatively explain a range of experimental observations related to hypertrophy. After validating the numerical approach for studying hypertrophy, the model is applied to evaluate the direct mechanical effects of axial tension and compression on hypertrophy (Hueter-Volkmann principle) and to explore why hypertrophy is reduced in case of partially or fully compromised proteoglycan expression. Finally, a mechanical explanation is provided for the observation that chondrocytes do not hypertrophy when enzymatical collagen degradation is prohibited (S1Pcko knock-out mouse model). This paper shows that matrix turnover by metabolically active chondrocytes, together with externally applied mechanical conditions, can explain quantitatively the volumetric change of chondrocytes during hypertrophy. It provides a mechanistic explanation for the observation that collagen degradation results in chondrocyte hypertrophy, both under physiological and pathological conditions.

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Section: Resultssupporting

confidence: 85%

Section: Resultssupporting

confidence: 85%

Section: Introductionmentioning

confidence: 99%

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Mechanics of chondrocyte hypertrophy

Donkelaar

Wilson

2011

Biomech Model Mechanobiol

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“…The chosen animal model was the rat tail because of the accessibility to the caudal vertebrae and the numerous growth modulation studies done on this model [14,15]. Caudal rat vertebrae have a second ossification center and therefore the device was adapted to fit the physiology and size of this subject.…”

Section: Methodsmentioning

confidence: 99%

A novel fusionless vertebral physeal device inducing spinal growth modulation for the correction of spinal deformities

et al. 2008

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Current fusionless scoliosis surgical techniques span the intervertebral disc. This alters the spine stiffness, disc pressure equilibrium and possibly may lead to disc degeneration. A new fusionless physeal device was developed that locally modulates vertebral growth by compressing the physeal ring, while maintaining maximum segmental spinal mobility without spanning the intervertebral disc. This study's objective was to test the feasibility of the device on a small animal model by inducing a scoliotic deformity (inverse approach) while analyzing the growth modifications. This study was conducted on caudal vertebrae of 21 rats (26-day-old) divided into 3 groups: (1) ''experimental'' (n = 11) with 4 instrumented vertebrae, (2) sham (n = 5) and (3) control (n = 5). Radiographs were taken at regular intervals during the 7-week experimental period. Tissues were embedded in methyl metacrylate (MMA), prepared by the cutting/grinding method, and then stained (Toluidine blue). The discs physiological alterations were qualitatively assessed and classified by inspection of the histological sections. A mean maximum Cobb angle of 308 (±68) and a mean maximum vertebral wedge angle of 108 (±38) were obtained between the 23rd and 35th day postoperative in the subgroup that underwent a long-term response from the device. The sham group underwent no growth alterations when compared to the control group. Descriptive histological analyses of the operated segments showed that 69% had no alterations to the intervertebral disc. This study presents experimental evidence that the device induces a significant and controlled wedging of the vertebrae while maintaining regular flexibility. In most discs, there were no visible morphological alterations induced. Further analysis of the discs and testing of this device on a larger animal is recommended with the long-term objective of developing an early treatment of progressive idiopathic scoliosis.

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“…No staple back-out was reported [42]. Asymmetrical static loading rat tail was shown to create vertebral wedging [29]. Subsequently, a new technique was established that produced dynamic loading on the rat tail vertebrae and studies revealed that dynamic loading induced a more potent growth modulation compared to static loading [43].…”

Section: Experimental Research On Spinal Growth Modulationmentioning

confidence: 99%

Growth modulation in the management of growing spine deformities

Akel

Yazıcı

2009

Journal of Children's Orthopaedics

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The Hueter-Volkmann law explains the physiological response of the growth plate under mechanical loading. This law mainly explains the pathological mechanism for growing long-bone deformities. Vertebral endplates also show a similar response under mechanical loading. Experimental studies have provided information about spinal growth modulation and, now, it is possible to explain the mechanism of the curvature progression. Convex growth arrest is shown to successfully treat deformities of the growing spine and unnecessary growth arrest of the whole spine is prevented. Both anterior and posterior parts of the convexity should be addressed to achieve a satisfactory improvement in the deformity, albeit epiphysiodesis effect cannot be stipulated at all times. Anterior vertebral body stapling without fusion yielded better results with new shape memory alloys and techniques. This method can be used with minimally invasive techniques and has the potential advantage of producing reversible physeal arrest. Instrumented posterior hemiepiphysiodesis seems to be as effective as classical combined anterior and posterior arthrodesis, where it is less invasive and morbid. Convex hemiepiphysiodesis with concave-side distraction through growing rod techniques provide a better control of the curve immediately after surgery. This method has the advantages of posterior instrumented hemiepiphysiodesis, but necessitates additional surgeries. Concave-side rib shortening and/ or convex-side lengthening is an experimental method with an indirect effect on spinal growth. To conclude, whatever the cause of the spinal deformity, growth modulation can be used to manage the growing spine deformities with no or shorter segment fusions.

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Modulation of vertebral and tibial growth by compression loading: Diurnal versus full‐time loading

Cited by 54 publications

References 22 publications

Mechanics of chondrocyte hypertrophy

Mechanics of chondrocyte hypertrophy

A novel fusionless vertebral physeal device inducing spinal growth modulation for the correction of spinal deformities

Growth modulation in the management of growing spine deformities

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