J-y Yan1, F-m Tian2, W-Y Wang3, Y Cheng4, H-P Song5, Y-Z Zhang6, L Zhang7. 1. Department of Orthopedic Surgery, Hebei Medical University, Shijiazhuang, China. Electronic address: tsyjydoctor55@163.com. 2. Medical Research Center, Hebei United University, Tangshan, China. Electronic address: tfm9911316@163.com. 3. Department of Pathology, School of Basic Medical Sciences, Hebei United University, Tangshan, China. Electronic address: wangwenya-3@126.com. 4. Department of Orthopedic Surgery, The Affiliated Hospital of Hebei United University, Tangshan, China. Electronic address: chengying2010@yeah.net. 5. Department of Orthopedic Surgery, The Affiliated Hospital of Hebei United University, Tangshan, China. Electronic address: songhuiping@163.com. 6. Department of Orthopedic Surgery, Hebei Medical University, Shijiazhuang, China. Electronic address: yingze1953@163.com. 7. Department of Orthopedic Surgery, Hebei Medical University, Shijiazhuang, China; Department of Orthopedic Surgery, The Affiliated Hospital of Hebei United University, Tangshan, China. Electronic address: zhliu130@sohu.com.
Abstract
OBJECTIVE: To assess whether parathyroid hormone (PTH) (1-34) could improve the micro-structure of subchondral bone, and retard cartilage degradation in a naturally occurring Osteoarthritis (OA) model. DESIGN: Forty-eight 1-month-old guinea pigs were divided into two groups: 32 were treated by normal saline (NS) and sacrificed at 1, 3, 6 and 9 months of age; the other 16 received PTH (1-34) from 3 months, and were sacrificed at 6 and 9 months. Masson staining and the Osteoarthritis Research Society International (OARSI) grade scores were used to assess cartilage degradation. Immunohistochemistry analyses of type-II collagen, matrix metalloproteinases-13 (MMP-13) and sclerostin (SOST) in the cartilage, osteoprotegerin (OPG) and receptor activator of nuclear factor-kB ligand (RANKL) and PTH receptor (PTH1R) in the cartilage and subchondral bone were performed. Subchondral bone micro-architecture was assessed by micro-computed tomography (micro-CT). RESULTS: Histological analyses revealed OA occurred at 3 months of age and was more severe with increasing age, and PTH (1-34) reduced the OARSI scores at 6 and 9 months of age. Micro-CT analysis indicated that PTH (1-34) treatment increased the bone volume ratio and bone mineral density (BMD), while retarding the subchondral trabecular bone micro-architectural changes from rod-like to plate-like. Immunohistochemical staining demonstrated that PTH (1-34) treatment increased type-II collagen expression and decreased SOST and MMP-13 expression in the cartilage, while elevating the PTH1R, OPG/RANKL expression ratio in the cartilage and subchondral trabecular bone when compared with the control groups. CONCLUSIONS: PTH (1-34) can prevent cartilage damage progression and retard the deterioration of subchondral trabecular bone in guinea pigs.
OBJECTIVE: To assess whether parathyroid hormone (PTH) (1-34) could improve the micro-structure of subchondral bone, and retard cartilage degradation in a naturally occurring Osteoarthritis (OA) model. DESIGN: Forty-eight 1-month-old guinea pigs were divided into two groups: 32 were treated by normal saline (NS) and sacrificed at 1, 3, 6 and 9 months of age; the other 16 received PTH (1-34) from 3 months, and were sacrificed at 6 and 9 months. Masson staining and the Osteoarthritis Research Society International (OARSI) grade scores were used to assess cartilage degradation. Immunohistochemistry analyses of type-II collagen, matrix metalloproteinases-13 (MMP-13) and sclerostin (SOST) in the cartilage, osteoprotegerin (OPG) and receptor activator of nuclear factor-kB ligand (RANKL) and PTH receptor (PTH1R) in the cartilage and subchondral bone were performed. Subchondral bone micro-architecture was assessed by micro-computed tomography (micro-CT). RESULTS: Histological analyses revealed OA occurred at 3 months of age and was more severe with increasing age, and PTH (1-34) reduced the OARSI scores at 6 and 9 months of age. Micro-CT analysis indicated that PTH (1-34) treatment increased the bone volume ratio and bone mineral density (BMD), while retarding the subchondral trabecular bone micro-architectural changes from rod-like to plate-like. Immunohistochemical staining demonstrated that PTH (1-34) treatment increased type-II collagen expression and decreased SOST and MMP-13 expression in the cartilage, while elevating the PTH1R, OPG/RANKL expression ratio in the cartilage and subchondral trabecular bone when compared with the control groups. CONCLUSIONS:PTH (1-34) can prevent cartilage damage progression and retard the deterioration of subchondral trabecular bone in guinea pigs.
Authors: B A Lakin; D J Ellis; J S Shelofsky; J D Freedman; M W Grinstaff; B D Snyder Journal: Osteoarthritis Cartilage Date: 2015-06-09 Impact factor: 6.576
Authors: Lauren B Radakovich; Angela J Marolf; John P Shannon; Stephen C Pannone; Vanessa D Sherk; Kelly S Santangelo Journal: Connect Tissue Res Date: 2017-12-11 Impact factor: 3.417