Discipline of Orthopaedics and Trauma, The University of Adelaide, Adelaide, Australia; Bone and Joint Research Laboratory, SA Pathology, Adelaide, Australia.
Discipline of Orthopaedics and Trauma, The University of Adelaide, Adelaide, Australia.
Bone. 2018 Mar;108:193-201. doi: 10.1016/j.bone.2018.01.012. Epub 2018 Jan 10.
Bone marrow lesions (BMLs) in the subchondral bone in osteoarthritis (OA) are suggested to be multifactorial, although the pathogenic mechanisms are unknown. Bone metabolism and cardiovascular risk factors associate with BML in epidemiologic studies. However, there are no studies at the tissue level investigating the relationship between these processes and BML. The aim of this study was to investigate the relationship between BMLs in the tibial plateau (TP) of knee OA and bone matrix microdamage, osteocyte density and vascular changes.
TP were obtained from 73 patients at total knee replacement surgery and BMLs were identified ex vivo in TP tissue using MRI. Comparator 'No BML' tissue was from matched anatomical sites to the BMLs. Quantitative assessment was made of subchondral bone microdamage, bone resorption indices, osteocyte cellularity, and vascular features.
Several key parameters were different between BML and No BML tissue. These included increased microcrack burden (p = .01, p = .0001), which associated positively with bone resorption and negatively with cartilage volume, and greater osteocyte numerical density (p = .02, p = .01), in the subchondral bone plate and subchondral trabeculae, respectively. The marrow tissue within BML zones contained increased arteriolar density (p = .04, p = .0006), and altered vascular characteristics, in particular increased wall thickness (p = .007) and wall:lumen ratio (wall thickness over internal lumen area) (p = .001), compared with No BML bone.
Increased bone matrix microdamage and altered vasculature in the subchondral bone of BMLs is consistent with overloading and vascular contributions to the formation of these lesions. Given the important role of BMLs in knee OA, these contributing factors offer potential targets for the treatment and prevention of knee OA.
骨关节炎（OA）软骨下骨中的骨髓病变（BML）被认为是多因素的，尽管其发病机制尚不清楚。在流行病学研究中，骨代谢和心血管危险因素与 BML 相关。然而，在组织水平上，尚无研究调查这些过程与 BML 之间的关系。本研究旨在探讨膝骨关节炎胫骨平台（TP）的 BML 与骨基质微损伤、骨细胞密度和血管变化之间的关系。
从 73 例全膝关节置换术患者中获得 TP，并在 TP 组织中使用 MRI 对 BML 进行体外识别。对照“无 BML”组织来自与 BML 相匹配的解剖部位。对软骨下骨微损伤、骨吸收指数、骨细胞密度和血管特征进行定量评估。
BML 和 No BML 组织之间存在几个关键参数差异。这些参数包括微裂纹负荷增加（p = .01，p = .0001），与骨吸收呈正相关，与软骨体积呈负相关，以及骨细胞数量密度增加（p = .02，p = .01），分别在软骨下骨板和软骨下小梁中。BML 区域内的骨髓组织中，动静脉密度增加（p = .04，p = .0006），血管特征发生改变，特别是壁厚度增加（p = .007）和壁腔比（壁厚度与内部管腔面积的比值）（p = .001），与 No BML 骨相比。
BML 软骨下骨中骨基质微损伤和血管改变与这些病变的过度负荷和血管贡献一致。鉴于 BML 在膝骨关节炎中的重要作用，这些致病因素为膝骨关节炎的治疗和预防提供了潜在的靶点。
