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Knee loading inhibits osteoclast lineage in a mouse model of osteoarthritis.

Li X, Yang J, Liu D, Li J, Niu K, Feng S, Yokota H, Zhang P - Sci Rep (2016)

Bottom Line: Knee loading promotes bone formation, but its effects on OA have not been well investigated.Two weeks application of daily dynamic knee loading significantly reduced OARSI scores and CC/TAC (calcified cartilage to total articular cartilage), but increased SBP (subchondral bone plate) and B.Ar/T.Ar (trabecular bone area to total tissue area).Furthermore, knee loading exerted protective effects by suppressing osteoclastogenesis through Wnt signaling.

View Article: PubMed Central - PubMed

Affiliation: Department of Anatomy and Histology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China.

ABSTRACT
Osteoarthritis (OA) is a whole joint disorder that involves cartilage degradation and periarticular bone response. Changes of cartilage and subchondral bone are associated with development and activity of osteoclasts from subchondral bone. Knee loading promotes bone formation, but its effects on OA have not been well investigated. Here, we hypothesized that knee loading regulates subchondral bone remodeling by suppressing osteoclast development, and prevents degradation of cartilage through crosstalk of bone-cartilage in osteoarthritic mice. Surgery-induced mouse model of OA was used. Two weeks application of daily dynamic knee loading significantly reduced OARSI scores and CC/TAC (calcified cartilage to total articular cartilage), but increased SBP (subchondral bone plate) and B.Ar/T.Ar (trabecular bone area to total tissue area). Bone resorption of osteoclasts from subchondral bone and the differentiation of osteoclasts from bone marrow-derived cells were completely suppressed by knee loading. The osteoclast activity was positively correlated with OARSI scores and negatively correlated with SBP and B.Ar/T.Ar. Furthermore, knee loading exerted protective effects by suppressing osteoclastogenesis through Wnt signaling. Overall, osteoclast lineage is the hyper responsiveness of knee loading in osteoarthritic mice. Mechanical stimulation prevents OA-induced cartilage degeneration through crosstalk with subchondral bone. Knee loading might be a new potential therapy for osteoarthritis patients.

No MeSH data available.


Related in: MedlinePlus

Histological changes of articular cartilage and subchondral bone by Safranin O staining.(A) Safranin O staining of tibial subchondral bone. Scale bar, 200 μm. (B) Safranin O staining of tibial articular cartilage, red indicates proteoglycan. Scale bar, 50 μm. (C) Subchondral bone volume fraction (B.Ar/T.Ar). (D) Osteoarthritis development was evaluated by OARSI scores. n = 10; **P < 0.01, ***P < 0.001.
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f2: Histological changes of articular cartilage and subchondral bone by Safranin O staining.(A) Safranin O staining of tibial subchondral bone. Scale bar, 200 μm. (B) Safranin O staining of tibial articular cartilage, red indicates proteoglycan. Scale bar, 50 μm. (C) Subchondral bone volume fraction (B.Ar/T.Ar). (D) Osteoarthritis development was evaluated by OARSI scores. n = 10; **P < 0.01, ***P < 0.001.

Mentions: The Safranin O staining showed the surface of the cartilage was smooth in the sham control group; however, it had superficial fibrillation, surface discontinuity, and vertical fissure with apparent hypocellularity in OA group. The OA group also showed massive proteoglycan loss. The cartilage in OA group presented denudation and deformation (Fig. 2B). OARSI scores revealed the significant degeneration of articular cartilage in OA group compared to the sham control (P < 0.001). Both knee loading and ALN treatment significantly decreased the OARSI scores (P < 0.001; Fig. 2D).


Knee loading inhibits osteoclast lineage in a mouse model of osteoarthritis.

Li X, Yang J, Liu D, Li J, Niu K, Feng S, Yokota H, Zhang P - Sci Rep (2016)

Histological changes of articular cartilage and subchondral bone by Safranin O staining.(A) Safranin O staining of tibial subchondral bone. Scale bar, 200 μm. (B) Safranin O staining of tibial articular cartilage, red indicates proteoglycan. Scale bar, 50 μm. (C) Subchondral bone volume fraction (B.Ar/T.Ar). (D) Osteoarthritis development was evaluated by OARSI scores. n = 10; **P < 0.01, ***P < 0.001.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4834538&req=5

f2: Histological changes of articular cartilage and subchondral bone by Safranin O staining.(A) Safranin O staining of tibial subchondral bone. Scale bar, 200 μm. (B) Safranin O staining of tibial articular cartilage, red indicates proteoglycan. Scale bar, 50 μm. (C) Subchondral bone volume fraction (B.Ar/T.Ar). (D) Osteoarthritis development was evaluated by OARSI scores. n = 10; **P < 0.01, ***P < 0.001.
Mentions: The Safranin O staining showed the surface of the cartilage was smooth in the sham control group; however, it had superficial fibrillation, surface discontinuity, and vertical fissure with apparent hypocellularity in OA group. The OA group also showed massive proteoglycan loss. The cartilage in OA group presented denudation and deformation (Fig. 2B). OARSI scores revealed the significant degeneration of articular cartilage in OA group compared to the sham control (P < 0.001). Both knee loading and ALN treatment significantly decreased the OARSI scores (P < 0.001; Fig. 2D).

Bottom Line: Knee loading promotes bone formation, but its effects on OA have not been well investigated.Two weeks application of daily dynamic knee loading significantly reduced OARSI scores and CC/TAC (calcified cartilage to total articular cartilage), but increased SBP (subchondral bone plate) and B.Ar/T.Ar (trabecular bone area to total tissue area).Furthermore, knee loading exerted protective effects by suppressing osteoclastogenesis through Wnt signaling.

View Article: PubMed Central - PubMed

Affiliation: Department of Anatomy and Histology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin 300070, China.

ABSTRACT
Osteoarthritis (OA) is a whole joint disorder that involves cartilage degradation and periarticular bone response. Changes of cartilage and subchondral bone are associated with development and activity of osteoclasts from subchondral bone. Knee loading promotes bone formation, but its effects on OA have not been well investigated. Here, we hypothesized that knee loading regulates subchondral bone remodeling by suppressing osteoclast development, and prevents degradation of cartilage through crosstalk of bone-cartilage in osteoarthritic mice. Surgery-induced mouse model of OA was used. Two weeks application of daily dynamic knee loading significantly reduced OARSI scores and CC/TAC (calcified cartilage to total articular cartilage), but increased SBP (subchondral bone plate) and B.Ar/T.Ar (trabecular bone area to total tissue area). Bone resorption of osteoclasts from subchondral bone and the differentiation of osteoclasts from bone marrow-derived cells were completely suppressed by knee loading. The osteoclast activity was positively correlated with OARSI scores and negatively correlated with SBP and B.Ar/T.Ar. Furthermore, knee loading exerted protective effects by suppressing osteoclastogenesis through Wnt signaling. Overall, osteoclast lineage is the hyper responsiveness of knee loading in osteoarthritic mice. Mechanical stimulation prevents OA-induced cartilage degeneration through crosstalk with subchondral bone. Knee loading might be a new potential therapy for osteoarthritis patients.

No MeSH data available.


Related in: MedlinePlus