Teriparatide prevented synovial inflammation and cartilage destruction in mice with DMM

Liang, Xu; Li, Sen-Rui; Zhang, Xin-Xin; He, Shi-Hao; Li, Shan-Shan; Li, Tian-Fang

doi:10.1080/03008207.2022.2157723

Cited by 5 publications

(5 citation statements)

References 40 publications

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“…When synovitis and fibrosis occur, proinflammatory mediators (e.g., IL-6, TNF-α, IL-1β) are released into the joint space. These mediators attract immune cells and are a major cause of joint damage and pain ( Liang et al, 2022 ). Therefore, it is important to develop reliable and effective therapies for synovitis and fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Chrysin ameliorates synovitis and fibrosis of osteoarthritic fibroblast-like synoviocytes in rats through PERK/TXNIP/NLRP3 signaling

et al. 2023

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Objective: Synovitis and fibrosis are common pathological features of knee osteoarthritis (KOA). The interaction of synovitis and fibrosis can promote KOA progression. Chrysin (CHR), a natural flavonoid, may treat inflammation and prevent fibrosis. However, the effect and mechanism of CHR in KOA synovitis and fibrosis remains unclear.Methods: The KOA model was established in male SD rats by anterior cruciate ligament transection (ACLT), and histological analysis was used to evaluate synovitis and fibrosis. IL-6, IL-1β and TNF-α mRNA expression in synovial tissue was measured by qRT‒PCR. Immunohistochemistry (IHC) was performed to detect GRP78, ATF-6 and TXNIP expression in vivo. Synovial fibroblasts (SFs) were treated with TGF-β1 to stimulate the inflammatory response and fibrosis. CCK-8 assays were used to detect the viability of CHR-treated SFs. The IL-1β level was detected by immunofluorescence analysis. Coimmunoprecipitation (Co-IP) and double immunofluorescence colocalization were used to detect the physiological interaction between TXNIP and NLRP3. The expression of fibrosis-related mediators and PERK/TXNIP/NLRP3 signaling molecules was detected by western blotting and qRT-PCR.Results: Four weeks after CHR treatment, pathological sections and associated scores showed that CHR improved synovitis and fibrosis in the ACLT model. In vitro, CHR attenuated the TGF-β1-induced inflammatory response and fibrosis in SFs. Moreover, CHR suppressed the expression of synovial fibrosis markers and PERK/TXNIP/NLRP3 signaling molecules in the synovial tissue of rats with ACLT and cultured SFs. More importantly, we found that CHR inhibited TXNIP-NLRP3 interactions in TGF-β-induced SFs.Conclusion: Our findings indicate that CHR can ameliorate synovitis and fibrosis in KOA. The underlying mechanism may be related to the PERK/TXNIP/NLRP3 signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Chrysin ameliorates synovitis and fibrosis of osteoarthritic fibroblast-like synoviocytes in rats through PERK/TXNIP/NLRP3 signaling

et al. 2023

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“…found that teriparatide could potentially inhibit the overexpression of MMP-13 induced by TNF-α. This inhibition might contribute to the prevention of synovitis and cartilage degradation, while simultaneously promoting the regeneration of articular cartilage [ 36 ]. However, teriparatide injections are quite costly and need to be administered daily [ 37 ].…”

Section: Discussionmentioning

confidence: 99%

Denosumab ameliorates osteoarthritis by protecting cartilage against degradation and modulating subchondral bone remodeling

Shangguan,

Ding,

Wang

et al. 2024

Regenerative Therapy

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“…The lack of an effect on articular cartilage may result from biological variables that blunted the effect of GC, as previously mentioned. It is possible that GC and PTH(1-34)-dependent effects on the joint ( 98 – 102 ) would be more apparent with injury, since suppressed PLR exacerbated post-traumatic osteoarthritis in male mice with an osteocyte-intrinsic deletion of transforming growth factor, beta receptor II ( Tgfβr2 ) ( 20 ).…”

Section: Discussionmentioning

confidence: 99%

The osteocytic actions of glucocorticoids on bone mass, mechanical properties, or perilacunar remodeling outcomes are not rescued by PTH(1-34)

Yee,

Meliadis,

Kaya

et al. 2024

Front. Endocrinol.

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Glucocorticoids (GC) and parathyroid hormone (PTH) are widely used therapeutic endocrine hormones where their effects on bone and joint arise from actions on multiple skeletal cell types. In osteocytes, GC and PTH exert opposing effects on perilacunar canalicular remodeling (PLR). Suppressed PLR can impair bone quality and joint homeostasis, including in GC-induced osteonecrosis. However, combined effects of GC and PTH on PLR are unknown. Given the untapped potential to target osteocytes to improve skeletal health, this study sought to test the feasibility of therapeutically mitigating PLR suppression. Focusing on subchondral bone and joint homeostasis, we hypothesize that PTH(1-34), a PLR agonist, could rescue GC-suppressed PLR. The skeletal effects of GC and PTH(1-34), alone or combined, were examined in male and female mice by micro-computed tomography, mechanical testing, histology, and gene expression analysis. For each outcome, females were more responsive to GC and PTH(1-34) than males. GC and PTH(1-34) exerted regional differences, with GC increasing trabecular bone volume but reducing cortical bone thickness, stiffness, and ultimate force. Despite PTH(1-34)’s anabolic effects on trabecular bone, it did not rescue GC’s catabolic effects on cortical bone. Likewise, cartilage integrity and subchondral bone apoptosis, tartrate-resistant acid phosphatase (TRAP) activity, and osteocyte lacunocanalicular networks showed no evidence that PTH(1-34) could offset GC-dependent effects. Rather, GC and PTH(1-34) each increased cortical bone gene expression implicated in bone resorption by osteoclasts and osteocytes, including Acp5, Mmp13, Atp6v0d2, Ctsk, differences maintained when GC and PTH(1-34) were combined. Since PTH(1-34) is insufficient to rescue GC’s effects on young female mouse bone, future studies are needed to determine if osteocyte PLR suppression, due to GC, aging, or other factors, can be offset by a PLR agonist.

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Teriparatide prevented synovial inflammation and cartilage destruction in mice with DMM

Cited by 5 publications

References 40 publications

Chrysin ameliorates synovitis and fibrosis of osteoarthritic fibroblast-like synoviocytes in rats through PERK/TXNIP/NLRP3 signaling

Chrysin ameliorates synovitis and fibrosis of osteoarthritic fibroblast-like synoviocytes in rats through PERK/TXNIP/NLRP3 signaling

Denosumab ameliorates osteoarthritis by protecting cartilage against degradation and modulating subchondral bone remodeling

The osteocytic actions of glucocorticoids on bone mass, mechanical properties, or perilacunar remodeling outcomes are not rescued by PTH(1-34)

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