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Teoría del Sistema Nervioso Central para la <strong>Osteo</strong>artritis Cambios del sistema simpático Oportunidades más allá de la articulación Inflamación de bajo grado Alteración de la sincronización (excitatoria/inhibitoria) Circuitos de retroalimentación articular propios Tono simpático desbalanceado: • Aumento influjo simpático (luchar, huir) • Disminución parasimpático (reposo) • Altera múltiples funciones corporales • Hábitos de vida • Reduce la reserva fisiológica para responder al estrés Médula ósea (MO): • Aumento de la salida de neutrófilos y monocitos inflamatorios • Tráfico y proliferación de leucocitos • Aumento de la respuesta inmune mediada por células Aumento de la producción de citoquinas MCP-1,TNF α, Il-1β, IL-6 Eje Hipotálamo-Hipófisis-Adrenal (HPA) sobre regulado: CHR,Vasopresina Neuronas del núcleo paraventricular de hipotálamo Metabolismo y regulación Redox Microbioma intestinal Estado catabólico aberrante del Condrocito • Disminución de la producción ATP por mitocondrias • Aumento de producción de productos de glicación avanzados (AGE) Aumento del estrés oxidativo Disfunción endotelial • Aumento de citoquinas inflamatorias inducidas por Condrocitos • Catabolismo de la matriz extracelular (EC), Calcificación de la matriz • Aumento de la apoptosis de condrocitos Componentes bacterianos atraviesan las barreras intestinales Transfieren información entre: Intestina-SNC-células inmunesarticulación Interacción mediada por receptores: • Directa de la carga celular al huésped • Alteración de programa de expresión genética Morris Jl et al. The CNS theory of osteoarthritis: Opportunities beyond the joint. Semin Arthritis Rheum. <strong>20</strong>19 Mar 16.
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