Masa, calidad, direccionalidad. ¿Cuál es la verdadera diferencia entre ‘osteopenias’ y ‘osteoporosis’?
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Revista de la Facultad de Ciencias Médicas. Universidad Nacional de Rosario.
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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.
The WHO differentiates between osteopenias (simple losses of mineralized bone mass) and osteoporoses (losses with increased fracture risk) based on just the amount of the remaining, densitometrically—assessed bone mineral mass. To note, the strength of a bone does not depend on its mineralized mass but on the combination of its stiffness (resistance to deformation) and toughness (resistance to split). These ‘structural’ properties result from the quality (stiffness, toughness) and spatial distribution (cortical/trabecular design) of bone tissue. The whole—bone strength is controlled by a feedback mechanism (‘mechanostat’) that adapts tissue distribution to tissue quality as a function of the usage—derived bone strains sensed by osteocytes. Therefore, bone strength does not reflect a metabolically accumulated mass but a biomechanically servo—controlled structure oriented by a well—established organization. Thus, the difference between osteopenias and osteoporoses, regardless of bone mineral data, must be interpreted by assessing the structural impact of the variable interaction of two independent determinants, namely, 1. The directional (‘vectorial’) mechanical environment of the skeleton (mechanostat input), and 2. The non—directional (‘systemic’) endocrine—metabolic environment, which privileges the mineral homeostasis control (essential to bone health) over bone structural integrity, thus tending rather to disturb than co—adjuvate the directional control of bone strength by changing the mechanostat setpoint. The mechanical component (1) must be treated by a directionally specific mechanical stimulation of bones. The metabolic component (2) requires drugs whose systemic effects are strongly conditioned to (1). Treatment success will depend largely on reconsidering osteoporoses as diseases of bone design rather than bone mass.
The WHO differentiates between osteopenias (simple losses of mineralized bone mass) and osteoporoses (losses with increased fracture risk) based on just the amount of the remaining, densitometrically—assessed bone mineral mass. To note, the strength of a bone does not depend on its mineralized mass but on the combination of its stiffness (resistance to deformation) and toughness (resistance to split). These ‘structural’ properties result from the quality (stiffness, toughness) and spatial distribution (cortical/trabecular design) of bone tissue. The whole—bone strength is controlled by a feedback mechanism (‘mechanostat’) that adapts tissue distribution to tissue quality as a function of the usage—derived bone strains sensed by osteocytes. Therefore, bone strength does not reflect a metabolically accumulated mass but a biomechanically servo—controlled structure oriented by a well—established organization. Thus, the difference between osteopenias and osteoporoses, regardless of bone mineral data, must be interpreted by assessing the structural impact of the variable interaction of two independent determinants, namely, 1. The directional (‘vectorial’) mechanical environment of the skeleton (mechanostat input), and 2. The non—directional (‘systemic’) endocrine—metabolic environment, which privileges the mineral homeostasis control (essential to bone health) over bone structural integrity, thus tending rather to disturb than co—adjuvate the directional control of bone strength by changing the mechanostat setpoint. The mechanical component (1) must be treated by a directionally specific mechanical stimulation of bones. The metabolic component (2) requires drugs whose systemic effects are strongly conditioned to (1). Treatment success will depend largely on reconsidering osteoporoses as diseases of bone design rather than bone mass.
Palabras clave
Osteopenia, Osteoporosis, Estructura ósea, Resistencia ósea, Biomecánica ósea, Mecanostato, Osteopenia, Osteoporosis, Bone structure, Bone strength, Bone biomechanics, Mechanostat