Salmon Calcitonin Attenuates Degenerative Changes in Cartilage and Subchondral Bone in Lumbar Facet Joint in an Experimental Rat Model

Abstract

BackgroundFacet joint degeneration (FJD) is one of the common causes of low back pain (LBP), and estrogen deficiency is one of the triggers for FJD. Calcitonin may possess the potential for treating osteoarthritis, but to date the hormone has not been studied in the treatment of FJD. Therefore, the aim of this study was to investigate the effects of salmon calcitonin (sCT) on FJD induced by estrogen deficiency after ovariectomy (OVX).Material/MethodsThirty female Sprague-Dawley rats were randomly assigned to 3 groups: the OVX group received bilateral OVX, the OVX + sCT group received subcutaneous administration of sCT (16 IU/kg/2 days) following bilateral OVX, and the Sham group received sham surgery. All rats were euthanized at 12 weeks post-OVX. Serum COMP level, cartilage degradation, and subchondral bone micro-architecture were evaluated.ResultssCT relieved cartilage surface lesions, reduced histological score, and significantly increased cartilage thickness. The OVX + sCT group exhibited significantly increased expression of aggrecan, as well as significantly decreased levels of ADAMTS-4, MMP-13, and caspase-3. The results of micro-computed tomography analysis revealed that the OVX + sCT group exhibited higher BMD, BV/TV, and Tb.Th values but a lower Tb.Sp value than that of the OVX group. Serum COMP concentrations were significantly correlated with histological score and cartilage thickness.ConclusionssCT can inhibit the progression of FJD in OVX rats, which is attributed to its inhibitory effects on cartilage metabolism imbalance, chondrocyte apoptosis, and subchondral bone remodeling. Serum COMP has diagnostic potential for FJD.

Protective Effect of Alendronate on Lumbar Facet Degeneration in Ovariectomized Rats

“…However, it is interesting that the degenerative cartilage changes in OVX rats were mainly manifested as small fissures confined to the surface, and did not extend to the deeper cartilage, indicating relatively modest cartilage lesions compared with those secondary to mechanical instability or chemical stimulation [37–39]. Our findings are consistent with previous studies, in which the main feature of FJ cartilage degeneration was loss of thickness, but not damage to superficial cartilage [40,41], thereby supporting the hypothesis that estrogen can prevent cartilage loss. Based on the present findings and those from previous studies, we conclude that estrogen deficiency stimulated subchondral bone remodeling with resultant deterioration of the subchondral bone microarchitecture and thus impaired the biomechanical properties, and also led to high cartilage turnover with increased chondrocyte apoptosis and catabolic metabolism, which finally caused the cartilage degeneration in this model.…”

“…Our previous study demonstrated that COMP is also a biomarker for FJ degeneration in OVX rats [41]. The present study confirmed that the serum COMP concentration was negatively correlated with cartilage thickness.…”

The Effects of Salmon Calcitonin on the Concentrations of Periaqueductal Gray Monoamines in the Formalin Test

“…sCT can inhibit the progression of facet joint syndrome in ovariectomized rats. This potential is ascribed to the inhibitory impacts of sCT on apoptosis, cartilage metabolism imbalance, and bone remodeling (24). PCR analysis shows that the chronic constriction injury causes the upregulation of tetrodotoxin-sensitive Nav.1.3 mRNA.…”

A Novel Rat Model of Patellofemoral Osteoarthritis Due to Patella Baja, or Low-Lying Patella

“…Finally, the slides were counterstained with hematoxylin. The results were expressed as an average intensity of optical density (IOD/mm 2 ), according to the method previously described [20,21].…”