Quantitative analysis of quadriceps muscle biopsy in systemic sclerosis

Scarpelli, Marina; Montironi, Rodolfo; Tulli, D; Sisti, S.; Matera, Giovanni; Galluzzi, Cristina Magi; Collan, Yrjö

doi:10.1016/s0344-0338(11)80064-6

Cited by 12 publications

(6 citation statements)

References 4 publications

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“…Because muscle disuse affects mainly type I fiber diameters [46,47], the type II fiber atrophy in our model suggests a mechanism related to mitochondrial dysfunction. This hypothesis is further supported by the predominant type II fiber atrophy in other conditions associated with muscle hypoxia, such as COPD [41], systemic sclerosis [2-4,48], and inflammatory myopathies [5]. Age-related sarcopenia is also associated with a predominant atrophy of type II fibers and an increased abundance of fast myosin heavy-chain isoforms in soleus muscle [49].…”

Section: Discussionmentioning

confidence: 97%

Muscle-fiber transdifferentiation in an experimental model of respiratory chain myopathy

et al. 2012

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IntroductionSkeletal muscle fiber composition and muscle energetics are not static and change in muscle disease. This study was performed to determine whether a mitochondrial myopathy is associated with adjustments in skeletal muscle fiber-type composition.MethodsTen rats were treated with zidovudine, an antiretroviral nucleoside reverse transcriptase inhibitor that induces a myopathy by interfering with mitochondrial functions. Soleus muscles were examined after 21 weeks of treatment. Ten untreated rats served as controls.ResultsZidovudine induced a myopathy with mitochondrial DNA depletion, abnormalities in mitochondrial ultrastructure, and reduced cytochrome c oxidase activity. Mitochondrial DNA was disproportionally more diminished in type I compared with type II fibers, whereas atrophy predominated in type II fibers. Compared with those of controls, zidovudine-exposed soleus muscles contained an increased proportion (256%) of type II fibers, whereas neonatal myosin heavy chains remained repressed, indicating fiber-type transformation in the absence of regeneration. Microarray gene-expression analysis confirmed enhanced fast-fiber isoforms, repressed slow-fiber transcripts, and reduced neonatal fiber transcripts in the mitochondrial myopathy. Respiratory chain transcripts were diminished, whereas the enzymes of glycolysis and glycogenolysis were enhanced, indicating a metabolic adjustment from oxidative to glycolytic capacities. A coordinated regulation was found of transcription factors known to orchestrate type II fiber formation (upregulation of MyoD, Six1, Six2, Eya1, and Sox6, and downregulation of myogenin and ERRγ).ConclusionsThe type I to type II fiber transformation in mitochondrial myopathy implicates mitochondrial function as a new regulator of skeletal muscle fiber type.

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Section: Discussionmentioning

confidence: 97%

Muscle-fiber transdifferentiation in an experimental model of respiratory chain myopathy

et al. 2012

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“…Muscle histological findings are heterogeneous in SSc‐associated myopathy and include typical features of inflammatory myopathy, together with SSc‐specific features, in various proportions. Most of pathological studies available in the literature included SSc patients who underwent quadriceps or deltoid biopsies, which were performed either in consecutive patients, whatever the muscular clinical or biological findings, 11,43,44 or only in SSc patients who presented muscle weakness 15,24 . Muscle tissue injuries in SSc mainly include ( a ) endomysial microangiopathy, ( b ) interstitial fibrosis, and ( c ) inflammation.…”

Section: Myopathological Characteristicsmentioning

confidence: 99%

“…The specific histopathological features mainly consist in microangiopathy, which may be observed in 0 44 to 57% of the cases, 10,24 that is, rarefaction of capillaries, capillary wall thickening, endothelial proliferation, and thickening and lamination of the basement membrane upon electron microscopic examination 11,24 . These muscle microvascular abnormalities, particularly the increased capillary diameter and basal membrane thickness 15 and the decreased number of capillary per muscle fiber 43 have been shown to be significantly more frequent in SSc patients as compared to patients with other rheumatic diseases (polymyositis, rheumatoid arthritis). An increased fibrosis can also be observed in the perimysium and epimysium, which appears to be much more frequently identified in autopsy series (93% in Medgser et al 10 ) than in living patients (25–50% 11,24 ).…”

Section: Myopathological Characteristicsmentioning

confidence: 99%

Systemic Sclerosis‐Associated Myopathy

Ranque

Authier

Bérezné

et al. 2007

Annals of the New York Academy of Sciences

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Skeletal muscle involvement is a common feature in systemic sclerosis (SSc) because muscle weakness is found in up to 90% SSc patients when systematically assessed. Muscle clinical, biological, and electromyographic features are similar to those of polymyositis or dermatomyositis, except for a higher proportion of mild symptoms. SSc-associated myopathy is more prevalent in diffuse SSc and is also associated with cardiomyopathy. The pathophysiological process leading to SSc-associated myopathy is likely to be complex, given the heterogeneity of pathological muscle findings, including stigma of microangiopathy, and also inflammatory infiltrate in about half of the cases and interstitial fibrosis. Conflicting results have been reported regarding the correlation between clinicobiological presentation and pathological muscle features, nevertheless there is a general agreement that histologically proven inflammatory myopathies usually regress under high-dose corticosteroid therapy, or even low dose in case of positive anti-PM/Scl antibody. In contrast, noninflammatory myopathies often result in milder clinical expression but do not respond to immunosuppressive treatment.

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“…A number of parameters of fiber size have been used by various investigators in their morphometric studies of muscle, particularly the cross-sectional area [1][2][3][4] and the lesser diameter [5][6][7][8] , or a combination of both 9,10 . It was also observed that most of the investigations on cross-sections of human skeletal muscle were made on the vastus lateralis and the available quantitative data were based on it [11][12][13] .…”

mentioning

confidence: 99%

The effects of aging on biceps brachii muscle fibers: a morphometrical study from biopsies and autopsies

Mattiello-Sverzut

Chimelli

Moura

et al. 2003

Arq. Neuro-Psiquiatr.

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-Objectives: In order to study the morphology and size of muscle fibers, cross sections of biceps brachii samples from autopsies, up to 9 hours after death, and biopsies of 72 subjects were compared. The subjects aged 13 to 84 years in both sexes. Methods: The samples obtained from autopsies (n=47) were from subjects with sudden death, or who died after acute disease without evidence of neuromuscular involvement. The biopsies (n=25) were from patients with symptoms suggestive of inflammatory or metabolic myopathy, not confirmed morphologically. The lesser diameter of muscle fibers was measured using the ATPase reaction. Results: Morphological analysis showed that aging changes were present from the sixth decade in autopsies, and consisted of atrophy and/or type-grouping. The statistical models adjusted for females in both autopsies and biopsies were linear straight with no variation in fiber size with increasing age. The models adjusted for males in both groups were quadratic, indicating that age influenced the size of different type fibers. In males type 2 were larger than type 1 fibers, and than fibers in females. Conclusions: These values might be useful as controls, helping interpretation of changes in fiber size in samples obtained from biopsies and autopsies.KEY WORDS: biceps brachii, morphometry, aging, autopsy, muscle biopsy.Efeitos do envelhecimento sobre as fibras do músculo biceps braquial: estudo morfométrico em biópsias e autópsias RESUMO -Objetivos: Para estudar a morfologia e o tamanho das fibras musculares, foram comparadas cortes transversos do bíceps braquial autopsiados, até 9 horas após o óbito, com biopsias musculares, em 72 indivíduos de ambos os sexos e idades entre 13 e 84 anos. Método: As amostras das autópsias (n=47) foram obtidas de indivíduos que morreram subitamente, ou após uma doença aguda sem evidência de comprometimento neuromuscular. As biópsias (n=25) foram obtidas de pacientes com sintomas sugestivos de miopatias inflamatória ou metabólica, não confirmadas morfologicamente. O diâmetro menor das fibras foi obtido usando a reação de ATPase. Resultados: A análise morfológica mostrou que as mudanças induzidas pelo envelhecimento estiveram presentes a partir da sexta década para autópsias e consistiu de atrofia e grupamento de tipo. O modelo estatístico ajustado para mulheres, para autópsias e biópsias, foi linear e não indicou variação do tamanho das fibras com o aumento da idade. O modelo ajustado para homens, para ambos os casos, foi quadrático, indicando que a idade influenciou o tamanho dos diferentes tipos de fibras. Para homens, as fibras tipo 2 apresentaram-se maiores que as de tipo 1, e maiores que as das mulheres. Conclusão: Os valores encontrados podem ser úteis como controles, auxiliando na interpretação de modificações no tamanho das fibras para amostras provindas de biópsia e autópsia.

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Quantitative analysis of quadriceps muscle biopsy in systemic sclerosis

Cited by 12 publications

References 4 publications

Muscle-fiber transdifferentiation in an experimental model of respiratory chain myopathy

Muscle-fiber transdifferentiation in an experimental model of respiratory chain myopathy

Systemic Sclerosis‐Associated Myopathy

The effects of aging on biceps brachii muscle fibers: a morphometrical study from biopsies and autopsies

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