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RANKL与组织蛋白酶K在下颌骨弥漫性硬化性骨髓炎中的作用

RANKL and cathepsin K in diffuse sclerosing osteomyelitis of the mandible.

作者信息

Montonen M, Li T-F, Lukinmaa P-L, Sakai E, Hukkanen M, Sukura A, Konttinen Y T

机构信息

Department of Oral and Maxillofacial Surgery, Helsinki University Central Hospital, Helsinki, Finland.

出版信息

J Oral Pathol Med. 2006 Nov;35(10):620-5. doi: 10.1111/j.1600-0714.2006.00454.x.

Abstract

BACKGROUND

Diffuse sclerosing osteomyelitis (DSO) of the mandible is characterized by mixed bone resorption and formation.

METHODS

Immunohistopathology of DSO in the clinically acute and subacute phases was compared with healthy bone.

RESULTS

Receptor activator of nuclear factor kappaB ligand (RANKL) was found in DSO lesions. When it was used in vitro to stimulate monocytes, cathepsin K expression was observed in mononuclear prefusion precursors and in multinuclear giant cells. Similarly, exacerbations of DSO were characterized by RANKL and induction of cathepsin K in mononuclear precursor cells, which subsequently seem to differentiate into osteoclasts or foreign body giant cells. The proportion of bone to soft tissue increased with the duration of disease.

CONCLUSIONS

RANKL-driven osteoclastogenesis and acidic cysteine endoproteinase cathepsin K seem to play important roles in DSO as osteoclast-mediated bone resorption may represent the primary disease process later followed by new bone formation.

摘要

背景

下颌骨弥漫性硬化性骨髓炎(DSO)的特征是骨吸收和形成混合存在。

方法

将临床急性和亚急性期DSO的免疫组织病理学与健康骨进行比较。

结果

在DSO病变中发现核因子κB受体活化因子配体(RANKL)。当在体外使用它刺激单核细胞时,在单核前融合前体细胞和多核巨细胞中观察到组织蛋白酶K的表达。同样,DSO的病情加重表现为RANKL以及单核前体细胞中组织蛋白酶K的诱导,这些细胞随后似乎分化为破骨细胞或异物巨细胞。骨与软组织的比例随疾病持续时间增加。

结论

RANKL驱动的破骨细胞生成和酸性半胱氨酸内肽酶组织蛋白酶K似乎在DSO中起重要作用,因为破骨细胞介导的骨吸收可能代表主要的疾病过程,随后是新骨形成。

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