Parathyroid hormone (1-34) retards the lumbar facet joint degeneration and activates Wnt/ß-catenin signaling pathway in ovariectomized rats.
J Orthop Surg Res
; 19(1): 352, 2024 Jun 14.
Article
en En
| MEDLINE
| ID: mdl-38877549
ABSTRACT
PURPOSE:
Facet joint degeneration (FJD) is a major cause of low back pain. Parathyroid hormone (PTH) (1-34) is commonly used to treat osteoporosis. However, little is known about its effects on FJD induced by estrogen deficiency. This study aims to investigate the effects of PTH (1-34) on FJD induced by estrogen deficiency and the underlying pathogenesis of the disease.METHODS:
Forty 3-month-old female Sprague-Dawley rats were randomly divided into four groups 30 received bilateral ovariectomy (OVX) followed by 12 weeks of treatment with normal saline, PTH (1-34) or 17ß-estradiol (E2), and 10 received sham surgery followed by administration of normal saline. Status and Wnt/ß-catenin signaling activity in the cartilage and subchondral bone of the L4-L5 FJs and serum biomarkers were analyzed.RESULTS:
Administration of PTH (1-34) and E2 ameliorated cartilage lesions, and significantly decreased MMP-13 and caspase-3 levels and chondrocyte apoptosis. PTH (1-34) but not E2 significantly increased cartilage thickness, number of chondrocytes, and the expression of aggrecan. PTH (1-34) significantly improved microarchitecture parameters of subchondral bone, increased the expression of collagen I and osteocalcin, and decreased RANKL/OPG ratio. E2 treatment significantly increased the OPG level and decreased the RANKL/OPG ratio in the subchondral bone of ovariectomized rats, but it did not significantly improve the microarchitecture parameters of subchondral bone. Wnt3a and ß-catenin expression was significantly reduced in the articular cartilage and subchondral bone in OVX rats, but PTH (1-34) could increase the expression of these proteins. E2 significantly increased the activity of Wnt/ß-catenin pathway only in cartilage, but not in subchondral bone. The restoration of Wnt/ß-catenin signaling had an obvious correlation with the improvement of some parameters associated with the FJs status.CONCLUSION:
Wnt/ß-catenin signaling may be a potential therapeutic target for FJD induced by estrogen deficiency. PTH (1-34) is effective in treating this disease with better efficacy than 17ß-estradiol, and the efficacy may be attributed to its restoration of Wnt/ß-catenin signaling.Palabras clave
Texto completo:
1
Colección:
01-internacional
Asunto principal:
Hormona Paratiroidea
/
Ovariectomía
/
Articulación Cigapofisaria
/
Vía de Señalización Wnt
/
Vértebras Lumbares
Límite:
Animals
Idioma:
En
Revista:
J Orthop Surg Res
/
J. orthop. surg. res
/
Journal of orthopaedic surgery and research
Año:
2024
Tipo del documento:
Article
País de afiliación:
China