Mechanical, biochemical and morphometric alterations in the femur of mdx mice

Nakagaki, Wilson Romero; Bertran, Celso Aparecido; Matsumura, Cíntia Yuri; Santo-Neto, Humberto; Camilli, José Ângelo

doi:10.1016/j.bone.2010.09.011

Cited by 40 publications

(47 citation statements)

References 56 publications

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“…The authors suggested that dystrophin could play a direct role in metabolism and in the morphology of tendon or, alternatively, the tendon could undergo alterations in its structure due to the influence of muscle damage. According to the literature, at 21 days of age mdx mice do not present intense or significant muscle degeneration (Pastoret and Sebille, 1995;Grounds and Torrisi, 2004;Nakagaki et al, 2011). Our results together propose that the absence of dystrophin can probably alter morphofunctional characteristics of mdx tendons, irrespective of muscle fiber involvement.…”

Section: Discussionsupporting

confidence: 75%

“…The authors observed a reduction in the elasticity of the anterior tibial and long digital extensor tendons in mdx mice at 14-18 weeks of age, as well as higher rate of cell death, when compared to normal animal. Studying 21-day-old mdx mice, Nakagaki et al (2011) demonstrated mechanical, morphological, and biochemical changes in the femur of these animals even without evidence of degenerative process of the quadriceps fiber. The researchers proposed the occurrence of a bone tissue disorder linked to some genetic component perhaps related to the deficiency or absence of dystrophin.…”

mentioning

confidence: 97%

“…Like humans with DMD, mdx mice present a mutation that leads to the absence of dystrophin, with these animals presenting muscle degeneration and intense inflammation (Biggar et al, 2002;Evans et al, 2009). In dystrophic muscles of mdx mice, the episodes of degeneration followed by regeneration come to be most marked at 21 days of age (Pastoret and Sebille, 1995;Grounds and Torrisi, 2004;Nakagaki et al, 2011). However, as opposed to the DMD, there appears to be less fibrosis and preservation of muscle function in young mdx animal compared to older animals, suggesting that muscle fiber degeneration seems to be compensated by regenerative process in this animal model (Evans et al, 2009).…”

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confidence: 99%

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Mechanical and morphological aspects of the calcaneal tendon of mdx mice at 21 days of age

Nakagaki

Tomiosso

Pimentel

et al. 2013

The Anatomical Record

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A relationship between compromised muscles and other tissues has been demonstrated in mdx mouse, an animal model studied for understanding of Duchenne muscular dystrophy. The hypothesis is that changes in the calcaneal tendon of mdx mice occur previous to the onset of rigorous and most marked episodes of muscle degeneration, which start suddenly after 21 days of life. Thus, this study aimed to identify possible alterations in the calcaneal tendon of mdx mouse at 21 days of age. Control and mdx tendons were submitted to mechanical tensile testing, quantification of hydroxyproline, and staining with toluidine blue and picrosirius red. Hydroxyproline content was similar between mdx and control groups. The control tendon presented higher mechanical strength (load, stress, and elastic modulus) and its morphological analysis showed a larger number of round fibroblasts, nuclei with well-decondensed chromatin, and slightly metachromatic well-stained cytoplasmic material, different from that observed in mdx tendons. The results suggest that the absence of dystrophin in mdx mouse can provoke directly or indirectly alterations in the mechanical properties and morphology of the calcaneal tendon. Anat Rec, 296:1546Rec, 296: -1551

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Section: Discussionsupporting

confidence: 75%

mentioning

confidence: 97%

mentioning

confidence: 99%

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Mechanical and morphological aspects of the calcaneal tendon of mdx mice at 21 days of age

Nakagaki

Tomiosso

Pimentel

et al. 2013

The Anatomical Record

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Section: Accepted Manuscriptmentioning

confidence: 95%

“…Significantly lower bone strength and smaller cortical area and thickness along with decreased epiphyseal trabecular bone area were already apparent at 3 weeks of age [25]. At 4 weeks of age, tibias of mdx mice had smaller cross-sectional areas and thinner cortices that withstood lower ultimate loads compared to wild-type mice [25]. At 7 weeks of age trabecular bone was decreased in mdx mice in one study [26] but not in another [27] and at 10 weeks of age trabecular bone in both the distal femur and proximal tibia was also reported to be significantly lower than control [28].…”

Section: Accepted Manuscriptmentioning

confidence: 95%

Prophylactic pamidronate partially protects from glucocorticoid-induced bone loss in the mdx mouse model of Duchenne muscular dystrophy

Yoon

Chen

Grynpas

et al. 2016

Bone

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Spontaneous Healing Capacity of Calvarial Bone Defects inmdxMice

Nakagaki

Camilli

2012

The Anatomical Record

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The mdx mouse is an experimental model widely used for the study of Duchenne muscular dystrophy, which is characterized by the lack of dystrophin and cycles of muscle degeneration/regeneration. Studies demonstrated elevated levels of growth factors and accelerated skin wound repair in these animals. We therefore raised the hypothesis that the bone repair process might also be altered in these animals. Thus, the objective of this study was to evaluate the spontaneous healing of calvarial defects in mdx mice by histomorphometric analysis. Animals (45 days old) were divided into mdx and control groups. A defect measuring 2 mm in diameter was produced surgically in the right parietal bone of each animal. The animals were sacrificed 15, 30, and 60 days after surgery, and the skulls were processed by routine histological procedures. No difference in the volume of new bone inside the defect was observed between the two groups at any of the three postoperative time points. There was also no difference between the different periods of healing when each group was analyzed separately. The lower quality of femoral and calvarial bone in mdx mice reported in previous studies and the similar bone regeneration rates seen in two groups suggest that the healing capacity of calvarial defects was more expressive in mdx mice than in control animals. An increase in the amount of osteogenic factors released by damaged myofibers may have favored osteogenesis during bone defect healing in mdx mice. Anat Rec,

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Mechanical, biochemical and morphometric alterations in the femur of mdx mice

Cited by 40 publications

References 56 publications

Mechanical and morphological aspects of the calcaneal tendon of mdx mice at 21 days of age

Mechanical and morphological aspects of the calcaneal tendon of mdx mice at 21 days of age

Prophylactic pamidronate partially protects from glucocorticoid-induced bone loss in the mdx mouse model of Duchenne muscular dystrophy

Spontaneous Healing Capacity of Calvarial Bone Defects inmdxMice

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