scholarly journals Erratum: “BMPR1A Antagonist Differentially Affects Cartilage and Bone Formation During Fracture Healing” [J Orthop Res. Vol 34, 2096-2105 (2016)]

Author(s):  
Elise F. Morgan ◽  
Jason Pittman ◽  
Anthony DeGiacomo ◽  
Daniel Cusher ◽  
Chantal M. J. de Bakker ◽  
...  
2015 ◽  
Vol 30 (9) ◽  
pp. 1572-1584 ◽  
Author(s):  
Tao Wang ◽  
Yongmei Wang ◽  
Alicia Menendez ◽  
Chak Fong ◽  
Muriel Babey ◽  
...  

2011 ◽  
Vol 26 (11) ◽  
pp. 2597-2609 ◽  
Author(s):  
Rachel Grimes ◽  
Karl J Jepsen ◽  
Jennifer L Fitch ◽  
Thomas A Einhorn ◽  
Louis C Gerstenfeld

2018 ◽  
Vol 20 (1) ◽  
pp. 83 ◽  
Author(s):  
Gabriele Russow ◽  
Denise Jahn ◽  
Jessika Appelt ◽  
Sven Märdian ◽  
Serafeim Tsitsilonis ◽  
...  

Osteoporosis represents the most common bone disease worldwide and results in a significantly increased fracture risk. Extrinsic and intrinsic factors implicated in the development of osteoporosis are also associated with delayed fracture healing and impaired bone regeneration. Based on a steadily increasing life expectancy in modern societies, the global implications of osteoporosis and impaired bone healing are substantial. Research in the last decades has revealed several molecular pathways that stimulate bone formation and could be targeted to treat both osteoporosis and impaired fracture healing. The identification and development of therapeutic approaches modulating bone formation, rather than bone resorption, fulfils an essential clinical need, as treatment options for reversing bone loss and promoting bone regeneration are limited. This review focuses on currently available and future approaches that may have the potential to achieve these aims.


PLoS ONE ◽  
2013 ◽  
Vol 8 (11) ◽  
pp. e81399 ◽  
Author(s):  
Alayna E. Loiselle ◽  
Shane A. J. Lloyd ◽  
Emmanuel M. Paul ◽  
Gregory S. Lewis ◽  
Henry J. Donahue

2010 ◽  
Vol 20 (2) ◽  
pp. 105-127 ◽  
Author(s):  
Marlon O. Coulibaly ◽  
Debra L. Sietsema ◽  
Travis A. Burgers ◽  
Jim Mason ◽  
Bart Williams ◽  
...  

Bone Research ◽  
2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Gehua Zhen ◽  
Yang Dan ◽  
Ruomei Wang ◽  
Ce Dou ◽  
Qiaoyue Guo ◽  
...  

AbstractOsteoporosis (OP) is a common age-related disease characterized by a deterioration of bone mass and structure that predisposes patients to fragility fractures. Pharmaceutical therapies that promote anabolic bone formation in OP patients and OP-induced fracture are needed. We investigated whether a neutralizing antibody against Siglec-15 can simultaneously inhibit bone resorption and stimulate bone formation. We found that the multinucleation of osteoclasts was inhibited in SIGLEC-15 conditional knockout mice and mice undergoing Siglec-15 neutralizing antibody treatment. The secretion of platelet-derived growth factor-BB (PDGF-BB), the number of tartrate-resistant acid phosphatase-positive (TRAP+) mononuclear cells, and bone formation were significantly increased in the SIGLEC-15 conditional knockout mice and antibody-treated mice. The anabolic effect of the Siglec-15 neutralizing antibody on bone formation was blunted in mice with Pdgfb deleted in TRAP+ cells. These findings showed that the anabolic effect of the Siglec-15 neutralizing antibody was mediated by elevating PDGF-BB production of TRAP+ mononuclear cells. To test the therapeutic potential of the Siglec-15 neutralizing antibody, we injected the antibody in an ovariectomy-induced osteoporotic mouse model, which mimics postmenopausal osteoporosis in women, and in two fracture healing models because fracture is the most serious health consequence of osteoporosis. The Siglec-15 neutralizing antibody effectively reduced bone resorption and stimulated bone formation in estrogen deficiency-induced osteoporosis. Of note, the Siglec-15 neutralizing antibody promoted intramembranous and endochondral ossification at the damaged area of cortical bone in fracture healing mouse models. Thus, the Siglec-15 neutralizing antibody shows significant translational potential as a novel therapy for OP and bone fracture.


2020 ◽  
Vol 3 ◽  
Author(s):  
Margaret Bello ◽  
Adam Warrick ◽  
Brett Mattingly ◽  
Justin Williams ◽  
Uma Sankar

Background and Hypothesis: Ca2+/calmo-dulin-dependent protein kinase kinase 2 (CaMKK2) is a serine-threonine protein kinase that plays a significant role in both anabolic and catabolic pathways of bone remodeling. Mechanical loading of bone translates an external force into both biochemical and structural changes. It has been shown that deletion or inhibition of CaMKK2 results in increased bone density in male and female mice. We hypothesize that the lack of CaMKK2 in bone cells will result in loading-induced bone mass accrual with no difference between male and female mice.  Experimental Design or Project Methods: The right tibia of anesthetized 16-week-old wild-type (WT) and CaMKK2 knockout (KO) mice were loaded at 2 Hz for 220 cycles and with peak forces specific to both sex and genotype. Loading was accomplished using an electro actuator (Bose ElectroForce 3200; EnduraTEC, Minnetonka, MN, USA). This was repeated 3, 5, 8 and 10 days after initial loading. The non-loaded left tibia served as an internal control. Calcein and alizarin red were administered intraperitoneally on days 9 and 16, respectively to metabolically label newly formed bone. Nineteen days after initial loading, mice were sacrificed. Blood and long bones of the lower limbs were collected for analysis.  Results: Using microcomputer tomography; dynamic histomorphometry; histology, immunohistochemistry, enzyme-linked immunosorbent assay and real-time reverse transcription-polymerase chain reaction, we will assess bone volume, bone formation rate, and underlying mechanisms at the cellular and molecular level. These data are forthcoming.  Conclusion and Potential Impact: With expanded knowledge on how bone growth is augmented, clinical outcomes related to osteoporosis and fracture healing, for example, may be improved. This may be accomplished through novel therapy related to these pathways that increases bone density or decreases fracture healing time. 


2017 ◽  
Vol 25 (3) ◽  
pp. 95-98 ◽  
Author(s):  
Nizamettin Guzel ◽  
Emrah Sayit ◽  
Osman Aynaci ◽  
Servet Kerimoglu ◽  
Esin Yulug ◽  
...  

ABSTRACT OBJECTIVES: Ginkgo biloba extract (EGb 761) is a plant extract obtained from the leaves of the G. biloba tree. The aim of this study was to assess the histological and radiological effects of G. biloba extract on fracture healing in an experimental fracture model using rat femurs. METHODS: Forty-eight female Sprague-Dawley rats (weight: 195-252 g; age: 20 weeks) were used in the study. The rats were randomly divided into six groups (n=8). A transverse fracture was made in the middle of the right femur of each rat and fixed with a Kirschner wire. The G. biloba groups received 60 mg/kg oral G. biloba extract once daily. No medication was given to the control groups. On days 7, 21 and 35, both sets of femurs were evaluated radiologically and histopathologically. RESULTS: Histological evaluation revealed that the G. biloba groups had significant differences at 21 and 35 days (p<0.05). The G. biloba group showed a significant difference in terms of bone formation on day 21 when compared to the control group (p<0.05). CONCLUSIONS: This study indicated that the use of G. biloba extract accelerated fracture healing. Both radiological and histological differences were detected, but the histological differences were more remarkable. Level of Evidence I, High Quality Randomized Trial.


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