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强直性脊柱炎中关节突关节重塑的组织形态学和组织形态计量学特征。

Histomorphologic and histomorphometric characteristics of zygapophyseal joint remodeling in ankylosing spondylitis.

机构信息

Charité Universitätsmedizin Berlin, Campus Benjamin Franklin, Berlin, Germany.

出版信息

Arthritis Rheumatol. 2014 Jul;66(7):1745-54. doi: 10.1002/art.38404.

Abstract

OBJECTIVE

To unravel the mechanisms that control bony ankylosis in ankylosing spondylitis (AS).

METHODS

Histomorphologic and histomorphometric analyses were performed on zygapophyseal joints obtained from 18 patients with AS, 9 patients with osteoarthritis (OA), and 10 cadaver donors without a rheumatic disease (controls). The proteoglycan content of the cartilage was determined by Safranin O staining and the chondrocyte apoptosis according to caspase 3 expression.

RESULTS

AS joints were categorized into 3 groups according to the morphology of the joint surfaces and joint space: group 1 were joints with an open joint space, group 2 were joints with cartilaginous fusion, and group 3 were joints with bony fusion of the joint surfaces. Progressive loss of the joint space from group 1 joints to group 3 joints suggests that this grouping corresponds to sequential stages of joint remodeling. Cartilage thickness and subchondral bone plate thickness declined from group 1 to group 3 (P < 0.01). Increased chondrocyte apoptosis rates were found in groups 1 and 2 (P < 0.05), while in group 3, a reduction in the proteoglycan content was found (P < 0.001). Bone marrow replacement and invasion of the subchondral bone plate by fibrous tissue was found predominantly in AS joints in group 2.

CONCLUSION

Cartilage degeneration, indicated by cartilage thinning, enhanced chondrocyte apoptosis, and proteoglycan loss, and subchondral bone thinning, promoted by invasion of the subchondral bone plate by a fibrous tissue originating from the bone marrow, are hallmarks of joint remodeling in AS.

摘要

目的

揭示控制强直性脊柱炎(AS)骨强直形成的机制。

方法

对 18 例 AS 患者、9 例骨关节炎(OA)患者和 10 例无风湿性疾病的尸体供体(对照组)的椎间关节进行组织形态学和组织形态计量学分析。通过番红 O 染色测定软骨的蛋白聚糖含量,并根据 caspase 3 表达测定软骨细胞凋亡。

结果

根据关节表面和关节间隙的形态,AS 关节分为 3 组:第 1 组为关节间隙开放,第 2 组为软骨融合,第 3 组为关节表面骨性融合。从第 1 组关节到第 3 组关节,关节间隙逐渐变窄,提示这种分组对应于关节重塑的连续阶段。软骨厚度和软骨下骨板厚度从第 1 组到第 3 组下降(P < 0.01)。第 1 组和第 2 组发现软骨细胞凋亡率增加(P < 0.05),而第 3 组则发现蛋白聚糖含量减少(P < 0.001)。第 2 组 AS 关节中主要发现骨髓替代和纤维组织侵入软骨下骨板。

结论

由骨髓起源的纤维组织侵入软骨下骨板,导致软骨变薄、增强的软骨细胞凋亡和蛋白聚糖丧失,以及软骨下骨变薄,是 AS 关节重塑的特征。

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