RESUMEN
Protein malnutrition leads to growth retardation that can be reversed through catch-up growth, once normative nutrition is restored. Because growth is a dynamic process, catch-up capacity is likely influenced by the maturity of the animal and/or the duration of the insult, in addition to the type of insult experienced. We compared length of malnutrition, sexual dimorphism, body mass, and skeletal growth. Eighty Rattus norvegicus were divided into 10 treatment groups (five diets; male and female) and followed for more than 1 year. At weaning, animals were placed on either a control or low-protein isocaloric diet. Three experimental groups were switched to the control diet at 40, 60, or 90 days. Beginning with 21 days of age, animals were weighed daily and radiographed throughout the study. To determine the presence of catch-up growth, growth rates (GRs) were calculated (linear regression) for 20-day time spans before and after diet changes and compared among treatment groups. Targeted growth was measured as final size or as the coefficient of variation with age. These results show that 1) protein-restricted animals experience catch-up growth with dietary rehabilitation; 2) for females, catch-up GRs are proportional to GRs in control animals at the same age as the timing of dietary rehabilitation but not for males; and 3) targeted growth was observed in some, but not all, aspects of anatomy. The length of the tibia and humerus was indistinguishable from controls, regardless of length of malnutrition or gender, whereas the ulna and male body mass exceeded control sizes. Although most measures decreased in variation with ontogeny, the tibia failed to do so. These results support a complex biological regulation of catch-up and targeted growth. The implications for selection are that flexible and responsive developmental trajectories may have an advantage over those programed into a single size.
Asunto(s)
Desarrollo Óseo , Deficiencia de Proteína/dietoterapia , Aumento de Peso , Animales , Dieta con Restricción de Proteínas , Femenino , Masculino , Ratas , Caracteres SexualesRESUMEN
Periosteum's role in fracture healing is widely recognized, and its function in bone tissue engineering shows great potential. Here we introduce a novel periosteal free flap to be used as an abundant source of periosteum in the engineering and repair of bone. The descending branch of the lateral femoral circumflex vessels were isolated on 11 fresh human cadavers, preserving perforators to the vastus intermedius muscle. A cuff of vastus intermedius and approximately 75% of the circumference of the femoral periosteum were harvested from 6 cm proximal to the knee to 8 cm distal to the greater trochanter. Flap pedicle length and periosteal dimensions were measured. The pedicle arteries were injected with radiopaque dye, and radiographs were taken. A musculoperiosteal flap was elevated with visible descending perforators in each case. Mean flap surface area was 128 cm(2) (+/-99-143 cm(2)). Average pedicle length was 8 cm (+/-6-11 cm). Dye injection confirmed that the flaps blood supply was the descending branch of the lateral femoral circumflex artery. This anatomical study confirms the vascular supply of this large musculoperiosteal flap. Future work will test its efficacy as an osteoinductive agent in bone repair and tissue engineering in humans.
Asunto(s)
Periostio/irrigación sanguínea , Músculo Cuádriceps/irrigación sanguínea , Músculo Cuádriceps/cirugía , Colgajos Quirúrgicos/irrigación sanguínea , Cadáver , Disección , Femenino , Humanos , Masculino , Periostio/cirugía , Sensibilidad y Especificidad , Traumatismos de los Tejidos Blandos/cirugía , Ingeniería de TejidosRESUMEN
Skeletal anomalies are common in patients with muscular dystrophy, despite an absence of mutations to genes that specifically direct skeletogenesis. In order to understand these anomalies further, we examined two strains of muscular dystrophy (laminin- and merosin-deficient) relative to controls, to determine how the weakened muscle forces affected skull shape in a mouse model. Shape was characterized with geometric morphometric techniques, improving upon the limited analytical power of the standard linear measurements. Through these techniques, we document the specific types of cranial skeletal deformation produced by the two strains, each with individual shape abnormalities. The mice with merosin deficiency (with an earlier age of onset) developed skulls with more deformation, probably related to the earlier ontogenetic timing of disease onset. Future examinations of these mouse models may provide insight regarding the impact of muscular forces and the production and maintenance of craniofacial integration and modularity.