Introduction: Congenital flexural deformities are an important problem in foals, but no detailed information is available on the architectural parameters and intrinsic proportions of forelimb muscle-tendon units and skeletal geometry. Materials and methods: Sixteen fixed forelimbs of newborns (4 normal and 6 with pathology - grade mild, moderate and severe) were included in the study and 10 muscle-tendon unit lengths (l MT), muscle and free tendon lengths, volumes and pennation angles were measured. After nitric acid digestion fiber bundle and sarcomere lengths were recorded. Optimal fascicle lengths, muscle physiologic cross-sectional areas (PCSA), tendon cross sectional areas (CSAs) and other ratios were calculated. Length and weight of bone segments were recorded and l MT/bone length (l B) and muscle and tendon/skeletal length ratios (%) calculated. Somer’s D statistics was used (p<0.05). Results: Proximal and distal sesamoids were smaller in affected vs normal neonates. In foals with flexural deformity the ratio l MT/ l B was decreased in the FCR, FCU, UL, DDF (hhA, hhB, hhC, RH, UH) and SDF while it was increased in the ECR (p< 0,05). In the DDF (hhB, hhC, RH, UH) and SDF the % of tendon length over l B were also decreased compared to normal foals, while in DDF-hhA % of muscle length over l B was smaller. CSA of tendons was significantly decreased in FCR and UL and in ECR, CDE, UL, DDF, and SDF with moderate and severe flexural limb deformity. AL-SDF was significantly shorter in affected foals and in those with more severe deformity suspensory ligament showed decreased length/ l B ratio, weight, volume and CSA (p<0,05). In moderate to severely affected neonates marked muscle atrophy was found in ECR, CDE, FCU, UL, DDF-hh and SDF. In normal forelimbs, the 4 strongest muscles were DDF, UL, SDF and FCU. In foals with flexural deformities PCSA and therefore estimated maximal isometric forces decreased predominantly in DDF, SDF and UL (24 to 63 % based on severity of deformity). Conclusions: Our study shows distinct involvement of several MT units in the development of congenital flexural deformities. Bone growth (except for sesamoid) did not differ between normal and affected foals but tendon length and muscle development were the primary pathological components suggesting a mechanism of muscle-tendon growth impairment.
Idiopathic flexural limb deformities: muscle architecture and skeletal geometry in normal and affected newborn foals.
ZARUCCO, Laura;
2010-01-01
Abstract
Introduction: Congenital flexural deformities are an important problem in foals, but no detailed information is available on the architectural parameters and intrinsic proportions of forelimb muscle-tendon units and skeletal geometry. Materials and methods: Sixteen fixed forelimbs of newborns (4 normal and 6 with pathology - grade mild, moderate and severe) were included in the study and 10 muscle-tendon unit lengths (l MT), muscle and free tendon lengths, volumes and pennation angles were measured. After nitric acid digestion fiber bundle and sarcomere lengths were recorded. Optimal fascicle lengths, muscle physiologic cross-sectional areas (PCSA), tendon cross sectional areas (CSAs) and other ratios were calculated. Length and weight of bone segments were recorded and l MT/bone length (l B) and muscle and tendon/skeletal length ratios (%) calculated. Somer’s D statistics was used (p<0.05). Results: Proximal and distal sesamoids were smaller in affected vs normal neonates. In foals with flexural deformity the ratio l MT/ l B was decreased in the FCR, FCU, UL, DDF (hhA, hhB, hhC, RH, UH) and SDF while it was increased in the ECR (p< 0,05). In the DDF (hhB, hhC, RH, UH) and SDF the % of tendon length over l B were also decreased compared to normal foals, while in DDF-hhA % of muscle length over l B was smaller. CSA of tendons was significantly decreased in FCR and UL and in ECR, CDE, UL, DDF, and SDF with moderate and severe flexural limb deformity. AL-SDF was significantly shorter in affected foals and in those with more severe deformity suspensory ligament showed decreased length/ l B ratio, weight, volume and CSA (p<0,05). In moderate to severely affected neonates marked muscle atrophy was found in ECR, CDE, FCU, UL, DDF-hh and SDF. In normal forelimbs, the 4 strongest muscles were DDF, UL, SDF and FCU. In foals with flexural deformities PCSA and therefore estimated maximal isometric forces decreased predominantly in DDF, SDF and UL (24 to 63 % based on severity of deformity). Conclusions: Our study shows distinct involvement of several MT units in the development of congenital flexural deformities. Bone growth (except for sesamoid) did not differ between normal and affected foals but tendon length and muscle development were the primary pathological components suggesting a mechanism of muscle-tendon growth impairment.
I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
