Limits...
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

Effects of knee loading on osteoclast migration and adhesion.Bone marrow-derived cells (2 × 106/ml) were cultured with M-CSF and RANKL in 6-well plates for 4 days to obtain pre-osteoclasts used for the migration and adhesion assays. (A) Bone marrow-derived cells were treated with M-CSF and RANKL. Then, osteoclast precursors were loaded onto vitronectin-coated polycarbonate membrane of the upper chamber of transwells in 24-well plates at a density of 1 × 105 cells/well at day 4. After 6 h, cells were stained with crystal violet (Bar = 100 μm). (B) Bone marrow-derived cells were treated with M-CSF and RANKL for four days. Then osteoclast precursors were plated onto vitronectin-coated 96-well plates at a density of 1 × 105 cells/well. After incubation for 1 h, adherent cells were stained with crystal violet. The number of cells adherent to the bottom of plates was counted (Bar = 100 μm). (C) Quantitative analysis of number of migration cells. (D) Quantitative analysis of number of adhesion cells. n = 10; ***P < 0.001.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4834538&req=5

f4: Effects of knee loading on osteoclast migration and adhesion.Bone marrow-derived cells (2 × 106/ml) were cultured with M-CSF and RANKL in 6-well plates for 4 days to obtain pre-osteoclasts used for the migration and adhesion assays. (A) Bone marrow-derived cells were treated with M-CSF and RANKL. Then, osteoclast precursors were loaded onto vitronectin-coated polycarbonate membrane of the upper chamber of transwells in 24-well plates at a density of 1 × 105 cells/well at day 4. After 6 h, cells were stained with crystal violet (Bar = 100 μm). (B) Bone marrow-derived cells were treated with M-CSF and RANKL for four days. Then osteoclast precursors were plated onto vitronectin-coated 96-well plates at a density of 1 × 105 cells/well. After incubation for 1 h, adherent cells were stained with crystal violet. The number of cells adherent to the bottom of plates was counted (Bar = 100 μm). (C) Quantitative analysis of number of migration cells. (D) Quantitative analysis of number of adhesion cells. n = 10; ***P < 0.001.

Mentions: The osteoclast migration (Fig. 4A) and adhesion (Fig. 4B) were conducted to evaluate the effect of knee loading in osteoclast function. The OA group elevated migration and adhesion, while alendronate and knee loading significantly attenuated migration (Fig. 4C) and adhesion (Fig. 4D) (all P < 0.001).


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)

Effects of knee loading on osteoclast migration and adhesion.Bone marrow-derived cells (2 × 106/ml) were cultured with M-CSF and RANKL in 6-well plates for 4 days to obtain pre-osteoclasts used for the migration and adhesion assays. (A) Bone marrow-derived cells were treated with M-CSF and RANKL. Then, osteoclast precursors were loaded onto vitronectin-coated polycarbonate membrane of the upper chamber of transwells in 24-well plates at a density of 1 × 105 cells/well at day 4. After 6 h, cells were stained with crystal violet (Bar = 100 μm). (B) Bone marrow-derived cells were treated with M-CSF and RANKL for four days. Then osteoclast precursors were plated onto vitronectin-coated 96-well plates at a density of 1 × 105 cells/well. After incubation for 1 h, adherent cells were stained with crystal violet. The number of cells adherent to the bottom of plates was counted (Bar = 100 μm). (C) Quantitative analysis of number of migration cells. (D) Quantitative analysis of number of adhesion cells. n = 10; ***P < 0.001.
© Copyright Policy - open-access
Related In: Results  -  Collection

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

f4: Effects of knee loading on osteoclast migration and adhesion.Bone marrow-derived cells (2 × 106/ml) were cultured with M-CSF and RANKL in 6-well plates for 4 days to obtain pre-osteoclasts used for the migration and adhesion assays. (A) Bone marrow-derived cells were treated with M-CSF and RANKL. Then, osteoclast precursors were loaded onto vitronectin-coated polycarbonate membrane of the upper chamber of transwells in 24-well plates at a density of 1 × 105 cells/well at day 4. After 6 h, cells were stained with crystal violet (Bar = 100 μm). (B) Bone marrow-derived cells were treated with M-CSF and RANKL for four days. Then osteoclast precursors were plated onto vitronectin-coated 96-well plates at a density of 1 × 105 cells/well. After incubation for 1 h, adherent cells were stained with crystal violet. The number of cells adherent to the bottom of plates was counted (Bar = 100 μm). (C) Quantitative analysis of number of migration cells. (D) Quantitative analysis of number of adhesion cells. n = 10; ***P < 0.001.
Mentions: The osteoclast migration (Fig. 4A) and adhesion (Fig. 4B) were conducted to evaluate the effect of knee loading in osteoclast function. The OA group elevated migration and adhesion, while alendronate and knee loading significantly attenuated migration (Fig. 4C) and adhesion (Fig. 4D) (all P < 0.001).

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