Correction: Chondrocytic ephrin B2 promotes cartilage destruction by osteoclasts in endochondral ossification

Tonna, Stephen; Poulton, Ingrid J; Taykar, Farzin; Ho, Patricia W. M.; Tonkin, Brett A.; Crimeen‐Irwin, Blessing; Tatarczuch, Liliana; McGregor, Narelle E; Mackie, Eleanor J.; Martin, T.J.; Sims, Natalie A

doi:10.1242/dev.148460

Cited by 10 publications

(10 citation statements)

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“…Rodeo et al 30 and Ma et al 25 also found that the higher osteoclastic activity at early healing stage of 1 or 3 weeks influenced the new bone formation and bony architecture at the tendon-tobone interface. Furthermore, osteoclast recruitment is likely to cause the newly formed cartilage destruction, degradation, and matrix resorption, 2,18,23,41 which might be related to the minimal cartilage formation at the interface in the OP group. Therefore, considering the possibly negative effects associated with osteoclasts, it might be helpful to control the higher osteoclastic activity at the repaired site in osteoporotic status, thus facilitating bone quality and cartilage formation for better tendon-to-bone healing.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Antiosteoporosis Therapy With Risedronate on Rotator Cuff Healing in an Osteoporotic Rat Model

Chen

et al. 2021

Am J Sports Med

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Background: Osteoporosis increases the revision rate of rotator cuff repair (RCR). Weak fixation might not be the only cause of high RCR failure rates. The biological mechanism associated with tendon-to-bone healing after RCR in osteoporosis should be investigated. Hypothesis: (1) Osteoporosis would impair rotator cuff healing through the high osteoclastic activity at the repaired interface. (2) Risedronate would promote rotator cuff healing by reducing osteoclastic activity at the repaired interface. Study Design: Controlled laboratory study. Methods: A total of 84 female Sprague Dawley rats were randomly treated using ovariectomy or sham surgeries to establish osteoporotic and nonosteoporotic rat models. After confirming osteoporosis, a chronic rotator cuff tear model was created and RCR was performed. Postoperatively, osteoporotic rats were randomly divided into osteoporosis (OP) and osteoporosis with risedronate administration (OP+RIS) groups. Nonosteoporotic rats were used as the control (CON) group. Osteoclastic activity was measured at 1 and 3 weeks after RCR, and histologic analysis of the tendon-to-bone interface, bone morphometric evaluation, and biomechanical tests were performed at 4 and 8 weeks. Results: At the early healing stages of 1 and 3 weeks after RCR, the OP group showed the highest osteoclast density at the repaired interface. Compared with the OP group, risedronate administration significantly decreased osteoclast density in the OP+RIS group. At 8 weeks, histologic scores were greater in the OP+RIS group than in the OP group but still lower than in the CON group. Histologic scores at 8 weeks were negatively correlated with osteoclast density at the early healing stage. Additionally, the OP+RIS group showed better bone morphometric parameters and biomechanical properties than did the OP group. Conclusion: Osteoporosis impaired rotator cuff healing, which might be related to the high osteoclast density at the repaired interface at the early healing stage. Postoperative risedronate administration decreased osteoclast density and enhanced rotator cuff healing in osteoporotic rats, although the effect was inferior to that in nonosteoporotic rats. Clinical Relevance: Postoperative risedronate administration can be considered a potential therapy to enhance rotator cuff healing in patients with postmenopausal osteoporosis. However, this needs to be verified in a clinical setting.

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Section: Discussionmentioning

confidence: 99%

The Effect of Antiosteoporosis Therapy With Risedronate on Rotator Cuff Healing in an Osteoporotic Rat Model

Chen

et al. 2021

Am J Sports Med

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“…In joints with OA, some blood vessels of the subchondral bone can penetrate calcified cartilage and even invade non-calcified cartilage ( Chen et al, 2015 ). Osteoclast precursors invade the area of hypertrophic cartilage and interact with its cells to reshape the cartilage matrix and form an ossification center ( Tonna et al, 2016 ). In addition, mature osteoclasts could regulate nearby chondrocytes, which destroys the connection between the bone and cartilage and degrade articular cartilage via cysteine proteases and matrix metalloproteinases ( Löfvall et al, 2018 ).…”

Section: Various Mechanisms Of Cellular Crosstalk In Oa Pathogenesismentioning

confidence: 99%

Cell Interplay in Osteoarthritis

Huang

Bai

2021

Front. Cell Dev. Biol.

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Osteoarthritis (OA) is a common chronic disease and a significant health concern that needs to be urgently solved. OA affects the cartilage and entire joint tissues, including the subchondral bone, synovium, and infrapatellar fat pads. The physiological and pathological changes in these tissues affect the occurrence and development of OA. Understanding complex crosstalk among different joint tissues and their roles in OA initiation and progression is critical in elucidating the pathogenic mechanism of OA. In this review, we begin with an overview of the role of chondrocytes, synovial cells (synovial fibroblasts and macrophages), mast cells, osteoblasts, osteoclasts, various stem cells, and engineered cells (induced pluripotent stem cells) in OA pathogenesis. Then, we discuss the various mechanisms by which these cells communicate, including paracrine signaling, local microenvironment, co-culture, extracellular vesicles (exosomes), and cell tissue engineering. We particularly focus on the therapeutic potential and clinical applications of stem cell-derived extracellular vesicles, which serve as modulators of cell-to-cell communication, in the field of regenerative medicine, such as cartilage repair. Finally, the challenges and limitations related to exosome-based treatment for OA are discussed. This article provides a comprehensive summary of key cells that might be targets of future therapies for OA.

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“…In bone tissue, ephrins and Ephs are widely expressed in various cells ( differentiation (109). On the contrary, ephrinB2 enhanced osteogenic differentiation through EphB4 of osteoblasts, which is a forward signaling (108,110).…”

Section: Ec-contact Regulation In Bone Biology Is Also An Important Mmentioning

confidence: 99%

Insights into the mechanism of vascular endothelial cells on bone biology

et al. 2021

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In the skeletal system, blood vessels not only function as a conduit system for transporting gases, nutrients, metabolic waste, or cells but also provide multifunctional signal molecules regulating bone development, regeneration, and remodeling. Endothelial cells (ECs) in bone tissues, unlike in other organ tissues, are in direct contact with the pericytes of blood vessels, resulting in a closer connection with peripheral connective tissues. Close-contact ECs contribute to osteogenesis and osteoclastogenesis by secreting various cytokines in the paracrine or juxtacrine pathways. An increasing number of studies have revealed that extracellular vesicles (EVs) derived from ECs can directly regulate maturation process of osteoblasts and osteoclasts. The different pathways focus on targets at different distances, forming the basis of the intimate spatial and temporal link between bone tissue and blood vessels. Here, we provide a systematic review to elaborate on the function of ECs in bone biology and its underlying mechanisms based on three aspects: paracrine, EVs, and juxtacrine. This review proposes the possibility of a therapeutic strategy targeting blood vessels, as an adjuvant treatment for bone disorders.

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Correction: Chondrocytic ephrin B2 promotes cartilage destruction by osteoclasts in endochondral ossification

Cited by 10 publications

References 0 publications

The Effect of Antiosteoporosis Therapy With Risedronate on Rotator Cuff Healing in an Osteoporotic Rat Model

The Effect of Antiosteoporosis Therapy With Risedronate on Rotator Cuff Healing in an Osteoporotic Rat Model

Cell Interplay in Osteoarthritis

Insights into the mechanism of vascular endothelial cells on bone biology

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