The cortical structure of human fibula varies widely throughout the bone suggesting a more selective adaptation to different mechanical environments with respect to the adjacent tibia. To test this hypothesis, serial-pQCT scans of the dominant fibulae and tibiae of 15/15 men/women chronically trained in long-distance running were compared with those of 15/15 untrained controls. When compared to controls, the fibulae of trained individuals had similar (distally) or lower (proximally) cortical area, similar moments of inertia (MI) for anterior-posterior bending (xMI) and lower for lateral bending (yMI) with a lower “shape-index” (yMI/xMI ratio) throughout, and higher resistance to buckling distally. These group differences were more evident in men and independent of group differences in bone mass. These results contrast with those observed in the tibia, where, as expected, structural indicators of bone strength were greater in trained than untrained individuals. Proximally, the larger lateral flexibility of runners' fibulae could improve the ability to store energy, and thereby contribute to fast-running optimization. Distally, the greater lateral fibular flexibility could reduce bending strength. The latter appears to have been compensated by a higher buckling strength. Assuming that these differences could be ascribed to training effects, this suggests that usage-derived strains in some bones may modify their relative structural resistance to different kinds of deformation in different regions, not only regarding strength, but also concerning other physiological roles of the skeleton.
The human fibula responds to its mechanical environment differently from the tibia accordingly with foot usage. Fibula structure is unaffected by disuse, and is stronger concerning lateral bending in soccer players (who evert and rotate the foot) and weaker in long-distance runners (who jump while running) with respect to untrained controls, along the insertion region of peroneus muscles. These features, strikingly associated to the abilities of the fibulae of predator and prey quadrupeds to manage uneven surfaces and to store elastic energy to jump, respectively, suggest that bone mechanostat would control bone properties with high selective connotations beyond structural strength.
La OMS distingue osteopenias (simples pérdidas de masa ósea mineralizada) de osteoporosis (pérdidas con tendencia a la fractura) según la simple magnitud densitométrica del déficit mineral. En realidad, la resistencia de un hueso no depende de su masa mineralizada, sino de la combinación de la rigidez (resistencia a deformarse) y la tenacidad (resistencia a resquebrajarse) de su estructura, determinadas, a su vez, por la ‘calidad mecánica’ (rigidez y tenacidad) del tejido mineralizado y la ‘calidad arquitectónica’ de su distribución en cortezas y tramas trabeculares (diseño óseo). La resistencia ósea responde a un mecanismo retroalimentado (‘mecanostato’), que adecua la distribución del tejido a su calidad, en función del sensado de las mini—deformaciones derivadas del uso, a cargo de los osteocitos. Ergo, la resistencia ósea no es una cuestión de masa, sino de ‘estructura’ y ‘organización’ servo—controladas. Entonces, la diferencia entre osteopenias y osteoporosis, independientemente de la masa densitométrica, debe interpretarse evaluando el impacto estructural de la variable interacción de dos determinantes independientes: 1. el entorno mecánico direccional del esqueleto (input del mecanostato), y 2. su entorno sistémico humoral, no direccional, cuyas alteraciones perturban el control biomecánico direccional ‘1’. El componente ‘1’ (desuso) debe tratarse fisiátricamente, mediante estímulos mecánicos específicamente direccionados. El componente ‘2’ (metabólico) requiere drogas específicas, cuyos efectos sistémicos sobre osteocitos, osteoblastos formadores y osteoclastos destructores de hueso están fuertemente condicionados a la normalidad de (1). El éxito terapéutico dependerá de en qué medida se reconsidere a las osteoporosis, no como enfermedades de la masa, sino del diseño óseo.
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