Helfrich Miep H, Hocking Lynne J
Bone and Musculoskeletal Research Programme, University of Aberdeen, Institute of Medical Sciences, School of Medicine and Dentistry, Foresterhill, Aberdeen AB25 2ZD, UK.
Arch Biochem Biophys. 2008 May 15;473(2):172-82. doi: 10.1016/j.abb.2008.02.045. Epub 2008 Mar 10.
Paget's disease of bone (PDB) is a late-onset disorder characterised by focal areas of increased bone turnover containing enlarged hyperactive osteoclasts. The disease has a strong genetic predisposition and mutations in SQSTM1 have been associated with familial and sporadic disease in up to 40% of cases. Additional genetic loci have been associated in other cases, but genes are yet to be identified. Earlier-onset conditions with similar bone pathology (familial expansile osteolysis, expansile skeletal hyperphosphatasia and early-onset PDB) are caused by mutations in TNFRSF11A (RANK). The syndrome of inclusion body myositis, Paget's disease and frontotemporal dementia is caused by mutations in VCP. Despite the increased knowledge about genes involved in PDB and related disorders, the etiology of the diseases remains puzzling. Presence of inclusion bodies appears to link Pagetic diseases mechanistically to diseases associated with presence of misfolded proteins or abnormalities in the ubiquitin-proteasomal, or autophagy pathways. Juvenile PDB, caused by osteoprotegerin deficiency, appears mechanistically distinct from the other Pagetic diseases. This review will discuss evidence from recent studies, including new animal models for Pagetic diseases.
骨佩吉特病(PDB)是一种迟发性疾病,其特征是骨转换增加的局灶性区域含有增大的高活性破骨细胞。该疾病具有很强的遗传易感性,在高达40%的病例中,SQSTM1基因突变与家族性和散发性疾病有关。在其他病例中还发现了其他相关的基因位点,但相关基因尚未确定。具有相似骨病理的早发性疾病(家族性扩张性骨溶解、扩张性骨胳性高磷酸酶血症和早发性PDB)是由TNFRSF11A(RANK)基因突变引起的。包涵体肌炎、佩吉特病和额颞叶痴呆综合征是由VCP基因突变引起的。尽管对参与PDB及相关疾病的基因的了解有所增加,但这些疾病的病因仍然令人困惑。包涵体的存在似乎在机制上将佩吉特病与与错误折叠蛋白的存在或泛素-蛋白酶体或自噬途径异常相关的疾病联系起来。由骨保护素缺乏引起的青少年PDB在机制上似乎与其他佩吉特病不同。本综述将讨论近期研究的证据,包括佩吉特病的新动物模型。