Vidal Bruno, Cascão Rita, Vale Ana Catarina, Cavaleiro Inês, Vaz Maria Fátima, Brito José Américo Almeida, Canhão Helena, Fonseca João Eurico
Instituto de Medicina Molecular, Faculdade de Medicina da Universidade de Lisboa, Lisbon, Portugal.
Instituto de Ciência e Engenharia de Materiais e Superfícies, Instituto Superior Técnico, University of Lisbon, Lisbon, Portugal.
PLoS One. 2015 Jan 24;10(1):e0117100. doi: 10.1371/journal.pone.0117100. eCollection 2015.
We have previously found in the chronic SKG mouse model of arthritis that long standing (5 and 8 months) inflammation directly leads to high collagen bone turnover, disorganization of the collagen network, disturbed bone microstructure and degradation of bone biomechanical properties. The main goal of the present work was to study the effects of the first days of the inflammatory process on the microarchitecture and mechanical properties of bone.
Twenty eight Wistar adjuvant-induced arthritis (AIA) rats were monitored during 22 days after disease induction for the inflammatory score, ankle perimeter and body weight. Healthy non-arthritic rats were used as controls for compar-ison. After 22 days of disease progression rats were sacrificed and bone samples were collected for histomorphometrical, energy dispersive X-ray spectroscopical analysis and 3-point bending. Blood samples were also collected for bone turnover markers.
AIA rats had an increased bone turnover (as inferred from increased P1NP and CTX1, p = 0.0010 and p = 0.0002, respectively) and this was paralleled by a decreased mineral content (calcium p = 0.0046 and phos-phorus p = 0.0046). Histomorphometry showed a lower trabecular thickness (p = 0.0002) and bone volume (p = 0.0003) and higher trabecular sepa-ration (p = 0.0009) in the arthritic group as compared with controls. In addition, bone mechanical tests showed evidence of fragility as depicted by diminished values of yield stress and ultimate fracture point (p = 0.0061 and p = 0.0279, re-spectively) in the arthritic group.
We have shown in an AIA rat model that arthritis induc-es early bone high turnover, structural degradation, mineral loss and mechanical weak-ness.
我们之前在关节炎慢性SKG小鼠模型中发现，长期（5个月和8个月）炎症直接导致高胶原蛋白骨转换、胶原蛋白网络紊乱、骨微结构破坏以及骨生物力学性能退化。本研究的主要目的是探讨炎症过程初期对骨微结构和力学性能的影响。
28只Wistar佐剂诱导性关节炎（AIA）大鼠在疾病诱导后22天内监测炎症评分、踝关节周长和体重。健康非关节炎大鼠作为对照进行比较。疾病进展22天后处死大鼠，收集骨样本进行组织形态计量学、能量色散X射线光谱分析和三点弯曲试验。还收集血样检测骨转换标志物。
AIA大鼠骨转换增加（分别从P1NP和CTX1升高推断，p = 0.0010和p = 0.0002），同时矿物质含量降低（钙p = 0.0046，磷p = 0.0046）。组织形态计量学显示，与对照组相比，关节炎组小梁厚度更低（p = 0.0002）、骨体积更小（p = 0.0003）、小梁间距更大（p = 0.0009）。此外，骨力学测试显示关节炎组屈服应力和极限骨折点值降低，表明存在脆性证据（分别为p = 0.0061和p = 0.0279）。
我们在AIA大鼠模型中表明，关节炎会引发早期骨高转换、结构退化、矿物质流失和力学性能减弱。
