Abstract
Golden Retriever Muscular Dystrophy (GRMD) is a dystrophin-deficient canine model genetically homologous to Duchenne Muscular Dystrophy (DMD) in humans. Muscular fibrosis secondary to cycles of degeneration/regeneration of dystrophic muscle tissue and muscular weakness leads to biomechanical adaptation that impairs the quality of gait. Physical therapy (PT) is one of the supportive therapies available for DMD, however, motor PT approaches have controversial recommendations and there is no consensus regarding the type and intensity of physical therapy. In this study we investigated the effect of physical therapy on gait biomechanics and muscular collagen deposition types I and III in dystrophin-deficient dogs. Two dystrophic dogs (treated dogs-TD) underwent a PT protocol of active walking exercise, 3×/week, 40 minutes/day, 12 weeks. Two dystrophic control dogs (CD) maintained their routine of activities of daily living. At t0 (pre) and t1 (post-physical therapy), collagen type I and III were assessed by immunohistochemistry and gait biomechanics were analyzed. Angular displacement of shoulder, elbow, carpal, hip, stifle and tarsal joint and vertical (Fy), mediolateral (Fz) and craniocaudal (Fx) ground reaction forces (GRF) were assessed. Wilcoxon test was used to verify the difference of biomechanical variables between t0 and t1, considering p<.05. Type I collagen of endomysium suffered the influence of PT, as well as gait speed that had decreased from t0 to t1 (p<.000). The PT protocol employed accelerates morphological alterations on dystrophic muscle and promotes a slower velocity of gait. Control dogs which maintained their routine of activities of daily living seem to have found a better balance between movement and preservation of motor function.
Highlights
Animal models for Duchenne Muscular Dystrophy (DMD) studies are used to attest the viability of therapies that aims to reduce the progression of this disease in humans
GRMD (Golden Retriever Muscular Dystrophy) is a dystrophin-deficient canine model that has been widely studied [1] since it presents muscle abnormalities that are closest to the ones seen in humans: increased creatine kinase activity, muscle hypotrophy, contractures, degeneration, endomysial and perimysial fibrosis [2,3]
Collagen type III was observed at perymisium and endomysium of TD and control dogs (CD) from t0, and did not change between t0 and t1 (Figure 3)
Summary
Animal models for Duchenne Muscular Dystrophy (DMD) studies are used to attest the viability of therapies that aims to reduce the progression of this disease in humans. GRMD (Golden Retriever Muscular Dystrophy) is a dystrophin-deficient canine model that has been widely studied [1] since it presents muscle abnormalities that are closest to the ones seen in humans: increased creatine kinase activity, muscle hypotrophy, contractures, degeneration, endomysial and perimysial fibrosis [2,3]. This model presents repeated cycles of muscular necrosis and regeneration, muscle wasting, postural abnormalities and respiratory or heart failure, as seen in DMD patients [4]. These therapies cannot cure DMD, they should be well investigated as they intend to lead these patients to a better quality of life and to decrease the complications of DMD [6]
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