›› 2020, Vol. 40 ›› Issue (5): 404-410.

• Basic Research • Previous Articles     Next Articles

Study of morphological feature and mechanism of maxillofacial bone abnormalities secondary to chronic kidney disease in mice

  

  • Received:2019-12-23 Revised:2020-01-27 Online:2020-05-26 Published:2020-06-08
  • Supported by:
    A Project Funded by the Priority Academic Program Development of Jiangsu Higher Education Institutions;the Jiangsu Provincial Key Medical Discipline

Abstract: Abstract:Objective To investigate the morphological characteristics of maxillofacial bone abnormalities secondary to chronic kidney disease (CKD), meanwhile evaluating the biological function of mesenchymal stem cells (MSCs) and osteoclast precursors from the mouse model in vitro. Methods A mouse model of CKD was established by adenine diet induction. Monitor changes in body weight and serum biochemical indicators of blood urea nitrogen (BUN), creatinine (CREA), calcium (Ca), and phosphorus (P) every 4 weeks, and perform HE staining of kidney tissues at the end of the 12th week. The mandibles were analyzed by Micro-CT and HE staining. Enzyme-linked immunosorbent assay (ELISA) was used to determine the serum level of parathyroid hormone (PTH). MSCs were cultured in vitro to detect their proliferation and osteogenic differentiation ability. Bone marrow macrophage (BMMs) were induced into osteoclasts to observe the osteoclast differentiation. Results Compared with the normal control group, the body weights were decreased and serum levels of BUN, CREA, CA, P were increased in the CKD group(P<0.05). The HE staining of kidney tissues in the CKD group showed the number of glomerulus was decreased, renal interstitial inflammatory cell infiltration and fibrosis. Micro-CT analysis revealed that the bone density and mass of mandible were reduced in the CKD group (P<0.05); The HE staining of the CKD group showed an increase in mandibular osteoid and irregular trabecular shape. ELISA showed serum PTH levels were significantly increased in the CKD group (P<0.05). In vitro experiments showed that the proliferation and early osteogenic differentiation ability of MSCs of the CKD group were increased(P<0.05), but CKD osteoblasts mineralized slowly in the later period(P<0.05). The TRAP staining results showed osteoclast differentiation to be more active in the CKD group(P<0.05). Conclusions Hyperparathyroidism secondary to CKD can lead to osteogenesis and mineralization disorder of high-proliferation MSCs in the late stage,and contribute to the differentiation of osteoclast, and accelerate bone transformation. The maxillofacial bone may show a decrease in bone mass and changes in bone microstructure.

Key words: Chronic kidney disease parathyroid hormone bone microstructure Osteoblast Osteoclast

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