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Journal articles on the topic 'Acelerated Bone fracture healing'

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Author: Grafiati

Published: 10 December 2022

Last updated: 28 January 2023

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1

Smith, Robert G. "Fracture Healing." Journal of the American Podiatric Medical Association 105, no. 2 (March 1, 2015): 160–72. http://dx.doi.org/10.7547/0003-0538-105.2.160.

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Background Recognizing the existence of adverse drug effects of frequently prescribed drugs can empower a clinician with knowledge to avoid dangerous adverse effects that may result in hazardous, negative patient outcomes on either fracture healing or bone health. Pharmacovigilance reports have described the influence of medications, allowing for bone health to be quite unpredictable. Methods First, mechanisms found in the medical literature of potential drug adverse effects regarding fracture healing are presented. Second, the 100 most frequently prescribed medications in 2010 are reviewed regarding adverse effects on fracture healing. These reported adverse effects are evaluated for medical causation. Last, a data table describing the 100 reviewed medications and their reported effects on fracture healing is provided. Results The actual number of different medications in the review was 72. Reported drug adverse effects on bone and fracture healing occurred with 59 of the 72 drugs (81.9%). These adverse effects are either described as a definitive statement or represented by postmarketing case reports. Thirteen of the 72 review drugs (18.1%) did not have any description of the possible effects on bone health. A total of 301 cases reports describing delayed union, malunion, and nonunion of fractures represent 31 of the 72 medications reviewed (43.1%). Conclusions This review offers the health-care provider information regarding potential adverse drug effects on bone health. Empowered with this information, clinicians may assist their patients in maximizing pharmacologic outcomes by avoiding these reported harmful adverse effects.

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2

Cornell, Charles, and Gregory S. DiFelice. "Fracture healing in osteoporotic bone." Current Opinion in Orthopaedics 7, no. 5 (October 1996): 12–15. http://dx.doi.org/10.1097/00001433-199610000-00003.

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3

Richards, Mark, James A. Goulet, Jeffrey A. Weiss, Nicholas A. Waanders, Mitchell B. Schaffler, and Steven A. Goldstein. "Bone Regeneration and Fracture Healing." Clinical Orthopaedics and Related Research 355S (October 1998): S191—S204. http://dx.doi.org/10.1097/00003086-199810001-00020.

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4

Cheung, Wing Hoi, Theodore Miclau, Simon Kwoon-Ho Chow, Frank F. Yang, and Volker Alt. "Fracture healing in osteoporotic bone." Injury 47 (June 2016): S21—S26. http://dx.doi.org/10.1016/s0020-1383(16)47004-x.

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5

Ono, Takehito, and Hiroshi Takayanagi. "Osteoimmunology in Bone Fracture Healing." Current Osteoporosis Reports 15, no. 4 (June 24, 2017): 367–75. http://dx.doi.org/10.1007/s11914-017-0381-0.

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6

Giannoudis, Peter V., Elena Jones, and Thomas A. Einhorn. "Fracture healing and bone repair." Injury 42, no. 6 (June 2011): 549–50. http://dx.doi.org/10.1016/j.injury.2011.03.037.

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7

Mick, Paul, and Christian Fischer. "Delayed Fracture Healing." Seminars in Musculoskeletal Radiology 26, no. 03 (June 2022): 329–37. http://dx.doi.org/10.1055/s-0041-1740380.

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AbstractPhysiologic bone healing involves numerous parameters, such as microstability, fracture morphology, or tissue perfusion, to name just a few. Slight imbalances or a severe impairment of even one of these factors may, as the figurative weakest link in the chain, crucially or completely inhibit the regenerative potential of a fractured bone. This review revisits the physiology and pathophysiology of fracture healing and provides an insight into predispositions, subtypes, diagnostic tools, and therapeutic principles involved with delayed fracture healing and nonunions. Depending on the patients individual risk factors, nonunions may develop in a variety of subtypes, each of which may require a slightly or fundamentally different therapeutical approach. After a detailed analysis of these individual factors, additional diagnostic tools, such as magnetic resonance imaging (MRI), dynamic contrast-enhanced MRI, sonography, or contrast-enhanced ultrasonography, may be indicated to narrow down the most likely cause for the development of the nonunion and therefore help find and optimize the ideal treatment strategy.

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8

Deguine, Christian, and Jack L. Pulec. "Temporal Bone Fracture following Spontaneous Healing." Ear, Nose & Throat Journal 82, no. 6 (June 2003): 414. http://dx.doi.org/10.1177/014556130308200604.

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9

Protopappas, V. C., M. G. Vavva, D. I. Fotiadis, and K. N. Malizos. "Ultrasonic monitoring of bone fracture healing." IEEE Transactions on Ultrasonics, Ferroelectrics and Frequency Control 55, no. 6 (June 2008): 1243–55. http://dx.doi.org/10.1109/tuffc.2008.787.

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10

Johnson, Mark A. "Biochemical bone fracture healing process model." IFAC Proceedings Volumes 36, no. 15 (August 2003): 335–40. http://dx.doi.org/10.1016/s1474-6670(17)33525-5.

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11

Craig, Joseph G., Jon A. Jacobson, and Berton R. Moed. "ULTRASOUND OF FRACTURE AND BONE HEALING." Radiologic Clinics of North America 37, no. 4 (July 1999): 737–51. http://dx.doi.org/10.1016/s0033-8389(05)70126-3.

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12

Ray, Marks. "Vitamin D and bone fracture healing." World Journal of Pharmacology 3, no. 4 (2014): 199. http://dx.doi.org/10.5497/wjp.v3.i4.199.

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13

Takebe, Hiroaki, Nazmus Shalehin, Akihiro Hosoya, Tsuyoshi Shimo, and Kazuharu Irie. "Sonic Hedgehog Regulates Bone Fracture Healing." International Journal of Molecular Sciences 21, no. 2 (January 20, 2020): 677. http://dx.doi.org/10.3390/ijms21020677.

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Bone fracture healing involves the combination of intramembranous and endochondral ossification. It is known that Indian hedgehog (Ihh) promotes chondrogenesis during fracture healing. Meanwhile, Sonic hedgehog (Shh), which is involved in ontogeny, has been reported to be involved in fracture healing, but the details had not been clarified. In this study, we demonstrated that Shh participated in fracture healing. Six-week-old Sprague–Dawley rats and Gli-CreERT2; tdTomato mice were used in this study. The right rib bones of experimental animals were fractured. The localization of Shh and Gli1 during fracture healing was examined. The localization of Gli1 progeny cells and osterix (Osx)-positive cells was similar during fracture healing. Runt-related transcription factor 2 (Runx2) and Osx, both of which are osteoblast markers, were observed on the surface of the new bone matrix and chondrocytes on day seven after fracture. Shh and Gli1 were co-localized with Runx2 and Osx. These findings suggest that Shh is involved in intramembranous and endochondral ossification during fracture healing.

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14

Cox, G., T. A. Einhorn, C. Tzioupis, and P. V. Giannoudis. "Bone-turnover markers in fracture healing." Journal of Bone and Joint Surgery. British volume 92-B, no. 3 (March 2010): 329–34. http://dx.doi.org/10.1302/0301-620x.92b3.22787.

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15

Thompson, David D. "Bone anabolic agents in fracture healing." Bone 47 (October 2010): S347—S348. http://dx.doi.org/10.1016/j.bone.2010.09.087.

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16

Gajdobranski, Djordje, and Dragana Zivkovic. "Impaired fracture healing." Medical review 56, no. 3-4 (2003): 146–51. http://dx.doi.org/10.2298/mpns0304146g.

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Introduction Bone fracture healing is a complex cascade of events at cellular and biochemical levels, that ends by complete structural and functional restoration of a damaged bone. Impaired healing develops in 5-10% of all fractures, and manifests as delayed union or non-union. This paper deals with the problem of impaired healing as well as with methods of fracture healing enhancement. Causes of impaired fracture healing There are many factors causing impaired fracture healing (inadequate vascularization, mechanical causes, infection, etc.), and it is very important to recognize the principle cause of delayed union and non-union, since therapy is based on eliminating the factor that causes it. Fracture healing enhancement Through constant attempts to find adequate solutions and procedures in order to resolve the problem of impaired fracture healing, many alternatives in treatment of impaired healing have been developed. Some of these procedures may also be useful in treatment of fresh fractures, especially when it comes to fractures that are prone to delayed union and non-union more than usual. All currently known methods of healing enhancement may be classified as biological, mechanical and biophysical. Conclusion Certain methods are in clinical use for several decades. The newest methods, such as locally applied growth factors, composite biosynthetic grafts, gene therapy and systemic approaches are studied all around the world, and are on the verge of clinical application. Due to impressive number of therapeutic options, certain therapeutic procedures of choice will be developed for specific impairments.

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Agarwala, Sanjay, and Mayank Vijayvargiya. "Repurposing denosumab for recalcitrant bone healing." BMJ Case Reports 14, no. 2 (February 2021): e238460. http://dx.doi.org/10.1136/bcr-2020-238460.

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Fracture healing has four phases: haematoma formation, soft callus, hard callus and remodelling. Often, non-healing fractures have an arrest of one of these phases, which need resurgery. We have repurposed denosumab for impaired fracture healing cases to avoid surgical intervention. Here, we report a series of three cases of impaired fracture healing where denosumab was given 120 mg subcutaneous dosages for 3 months to enhance healing. All the three cases have shown complete bone union at a mean follow-up of 6.7 months (5–9 months) as assessed clinically and radiologically, and have observed no adverse effect of the therapy. Denosumab given in this dose aids fracture healing by increasing callus volume, density and bridges the fracture gap in recalcitrant fracture healing cases where the callus fails to consolidate.

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18

LaStayo, Paul C., Kerri M. Winters, and Maureen Hardy. "Fracture healing: Bone healing, fracture management, and current concepts related to the hand." Journal of Hand Therapy 16, no. 2 (April 2003): 81–93. http://dx.doi.org/10.1016/s0894-1130(03)80003-0.

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19

Gajdobranski, Djordje, Ivan Micic, Milorad Mitkovic, Desimir Mladenovic, and Miroslav Milankov. "Management of impaired fracture healing: Historical aspects." Medical review 58, no. 9-10 (2005): 507–12. http://dx.doi.org/10.2298/mpns0510507g.

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Introduction Establishing continuity of long bones in cases of impaired bone healing and pseudo-arthrosis is one of the most complex problems in orthopedics. Impaired bone healing The problem of impaired fracture healing is not new. As in other areas of human life, the roots of modern treatment of impaired bone healing lie in ancient medicine. A relatively high percentage of impaired bone healing, as well as unsatisfactory results of standard therapies of impaired bone healing and pseudoarthrosis demonstrate the actuality of this problem. This paper represents an attempt to pay respect to some of those who have dedicated their work to this problem in orthopedic surgery, and it is a historical review on impaired bone fracture healing. At the same time it should be an additional stimulus and challenge for orthopedic surgeons to further study impaired bone fracture healing, improve the existing and find new methods for their adequate treatment. Conclusion The authors are certain that the number of researchers throughout the world who have contributed to treatment modalities of impaired bone healing, is much higher, but not all are mentioned in this paper. However, it does not lessen their contributions to orthopedics.

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Balu, Abhinav, Rong Huang, Kristin Molitoris, and Gurpreet Baht. "Apolipoprotein E impairs aged bone fracture healing." Innovation in Aging 5, Supplement_1 (December 1, 2021): 662. http://dx.doi.org/10.1093/geroni/igab046.2499.

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Abstract Bone fracture healing and osteoblast differentiation are impaired with advanced age. Using a combination of parabiosis and proteomic models, we identified apolipoprotein E (ApoE) to be an aging factor in bone regeneration. Circulating levels of ApoE increased with age in patients and in mice. ApoE impaired bone fracture healing by decreasing bone deposition in the fracture callus which subsequently decreased the mechanical strength of healed tissue. Osteoblasts serve as the sole bone forming cells within the body. In tissue culture models, ApoE treatment decreased osteoblast differentiation and activity which led to decreased matrix formation and mineralization. This inhibition of osteoblast differentiation relied on down-regulation of the Wnt/β-catenin pathway. In mouse models, aged bone repair was rejuvenated when we lowered circulating ApoE levels using a hepatotropic AAV-siRNA model – serving as a proof of concept that ApoE can be targeted to improve bone repair in an older population. While promising, knockdown of circulating ApoE in such a fashion is likely not translatable to patient care. Thus, current work in our laboratory is focused on developing treatment strategies that temporally decrease circulating ApoE levels and consequently improve bone healing after acute injury and/or surgical orthopedic procedure in the geriatric population.

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Zhang, Mingran, Jiaxue Liu, Tongtong Zhu, Hanxiang Le, Xukai Wang, Jinshan Guo, Guangyao Liu, and Jianxun Ding. "Functional Macromolecular Adhesives for Bone Fracture Healing." ACS Applied Materials & Interfaces 14, no. 1 (December 23, 2021): 1–19. http://dx.doi.org/10.1021/acsami.1c17434.

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22

Tosounidis, Theodoros, George Kontakis, Vassilis Nikolaou, Argiris Papathanassopoulos, and Peter V. Giannoudis. "Fracture healing and bone repair: an update." Trauma 11, no. 3 (June 24, 2009): 145–56. http://dx.doi.org/10.1177/1460408609335922.

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23

Gerner, Peter, and J. Patrick O’Connor. "Impact of Analgesia on Bone Fracture Healing." Anesthesiology 108, no. 3 (March 1, 2008): 349–50. http://dx.doi.org/10.1097/aln.0b013e318164938c.

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24

Simon, U., S. J. Shefelbine, P. Augat, and L. Claes. "Simulation of fracture healing in metaphyseal bone." Journal of Biomechanics 39 (January 2006): S456. http://dx.doi.org/10.1016/s0021-9290(06)84866-9.

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25

Cattermole, H. C., J. E. Cook, J. N. Fordham, D. S. Muckle, and J. L. Cunningham. "Bone Mineral Changes During Tibial Fracture Healing." Clinical Orthopaedics and Related Research 339 (June 1997): 190–96. http://dx.doi.org/10.1097/00003086-199706000-00026.

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26

Roberts, Scott J., and Hua Zhu Ke. "Anabolic Strategies to Augment Bone Fracture Healing." Current Osteoporosis Reports 16, no. 3 (May 3, 2018): 289–98. http://dx.doi.org/10.1007/s11914-018-0440-1.

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27

Anglen, Jeff. "Enhancement of Fracture Healing With Bone Stimulators." Techniques in Orthopaedics 17, no. 4 (December 2002): 506–14. http://dx.doi.org/10.1097/00013611-200212000-00014.

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28

Graham, Dustin M. "A leg up on bone-fracture healing." Lab Animal 45, no. 10 (September 21, 2016): 347. http://dx.doi.org/10.1038/laban.1124.

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29

Tajima, Kosuke, Hironari Takaishi, Jiro Takito, Takahide Tohmonda, Masaki Yoda, Norikazu Ota, Naoto Kosaki, et al. "Inhibition of STAT1 accelerates bone fracture healing." Journal of Orthopaedic Research 28, no. 7 (January 8, 2010): 937–41. http://dx.doi.org/10.1002/jor.21086.

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30

Haffner-Luntzer, Melanie, Anna Kovtun, Anna E. Rapp, and Anita Ignatius. "Mouse Models in Bone Fracture Healing Research." Current Molecular Biology Reports 2, no. 2 (April 4, 2016): 101–11. http://dx.doi.org/10.1007/s40610-016-0037-3.

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31

Wähnert, Dirk, Johannes Greiner, Stefano Brianza, Christian Kaltschmidt, Thomas Vordemvenne, and Barbara Kaltschmidt. "Strategies to Improve Bone Healing: Innovative Surgical Implants Meet Nano-/Micro-Topography of Bone Scaffolds." Biomedicines 9, no. 7 (June 28, 2021): 746. http://dx.doi.org/10.3390/biomedicines9070746.

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Successful fracture healing is dependent on an optimal mechanical and biological environment at the fracture site. Disturbances in fracture healing (non-union) or even critical size bone defects, where void volume is larger than the self-healing capacity of bone tissue, are great challenges for orthopedic surgeons. To address these challenges, new surgical implant concepts have been recently developed to optimize mechanical conditions. First, this review article discusses the mechanical environment on bone and fracture healing. In this context, a new implant concept, variable fixation technology, is introduced. This implant has the unique ability to change its mechanical properties from “rigid” to “dynamic” over the time of fracture healing. This leads to increased callus formation, a more homogeneous callus distribution and thus improved fracture healing. Second, recent advances in the nano- and micro-topography of bone scaffolds for guiding osteoinduction will be reviewed, particularly emphasizing the mimicry of natural bone. We summarize that an optimal scaffold should comprise micropores of 50–150 µm diameter allowing vascularization and migration of stem cells as well as nanotopographical osteoinductive cues, preferably pores of 30 nm diameter. Next to osteoinduction, such nano- and micro-topographical cues may also reduce inflammation and possess an antibacterial activity to further promote bone regeneration.

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32

Song, Lidan. "Effects of Exercise or Mechanical Stimulation on Bone Development and Bone Repair." Stem Cells International 2022 (September 28, 2022): 1–10. http://dx.doi.org/10.1155/2022/5372229.

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The development and regeneration of the bone are tightly regulated by mechanical cues. Multiple cell types, including osteoblasts, osteocytes, osteoclasts, mesenchymal stem cells (MSCs), and recently found skeletal stem cells (SSCs), are responsible for efficient bone development and injury repair. The immune cells in the environment interact with bone cells to maintain homeostasis and facilitate bone regeneration. Investigation of the mechanism by which these cells sense and respond to mechanical signals in bone is fundamental for optimal clinical intervention in bone injury healing. We discuss the effects of exercise programs on fracture healing in animal models and human patients, which encouragingly suggest that carefully designed exercise prescriptions can improve the result of fracture healing during the remodeling phase. However, additional clinical tracing and date accumulation are still required for the pervasive application of exercise prescriptions to improve fracture healing.

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33

Haffner-Luntzer, M., and A. Ignatius. "Animal models for studying metaphyseal bone fracture healing." European Cells and Materials 40 (October 29, 2020): 172–88. http://dx.doi.org/10.22203/ecm.v040a11.

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An estimated 2 million osteoporotic fractures occur annually in the US, resulting in a dramatic reduction in quality of life for affected patients and a high economic burden for society. Osteoporotic fractures are frequently located in metaphyseal bone regions. They are often associated with healing complications, because of the reduced healing capacity of the diseased bone tissue, the poor primary stability of the fracture fixation in the fragile bone, and the high frequency of comorbidities in these patients. Therefore, osteoporotic fractures require optimised treatment strategies to ensure proper bone healing. Preclinical animal models can help understanding of the underlying mechanisms and development of new therapies. However, whereas diaphyseal fracture models are widely available, appropriate animal models for metaphyseal fracture healing are scarce, although essential for translational research. This review covers large and small animal models for metaphyseal fracture healing. General requirements for suitable animal models are presented, as well as advantages and disadvantages of the current models. Furthermore, differences and similarities between metaphyseal and diaphyseal bone fracture healing are discussed. Both large- and small-animal models are available for studying metaphyseal fracture healing, which mainly differ in fracture location and geometry as well as stabilisation techniques. Most common used fracture sites are distal femur and proximal tibia. Each model found in the literature has certain advantages and disadvantages; however, many lack standardisation resulting in a high variability or poor mimicking of the clinical situation. Therefore, further refinement ofanimal models is needed especially to study osteoporotic metaphyseal fracture healing.

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34

Giannoudis, Peter V. "Fracture healing and bone regeneration: Autologous bone grafting or BMPs?" Injury 40, no. 12 (December 2009): 1243–44. http://dx.doi.org/10.1016/j.injury.2009.10.004.

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35

ElHawary, Hassan, Aslan Baradaran, Jad Abi-Rafeh, Joshua Vorstenbosch, Liqin Xu, and Johnny Ionut Efanov. "Bone Healing and Inflammation: Principles of Fracture and Repair." Seminars in Plastic Surgery 35, no. 03 (August 2021): 198–203. http://dx.doi.org/10.1055/s-0041-1732334.

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AbstractBones comprise a significant percentage of human weight and have important physiologic and structural roles. Bone remodeling occurs when healthy bone is renewed to maintain bone strength and maintain calcium and phosphate homeostasis. It proceeds through four phases: (1) cell activation, (2) resorption, (3) reversal, and (4) bone formation. Bone healing, on the other hand, involves rebuilding bone following a fracture. There are two main types of bone healing, primary and secondary. Inflammation plays an integral role in both bone remodeling and healing. Therefore, a tightly regulated inflammatory response helps achieve these two processes, and levels of inflammation can have detrimental effects on bone healing. Other factors that significantly affect bone healing are inadequate blood supply, biomechanical instability, immunosuppression, and smoking. By understanding the different mechanisms of bone healing and the factors that affect them, we may have a better understanding of the underlying principles of bony fixation and thereby improve patient care.

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36

Low, Adrian K., Y. Yu, K. J. Gifford, and W. R. Walsh. "Molecular Aspect of Osteoporotic Fracture Healing." Key Engineering Materials 353-358 (September 2007): 2159–62. http://dx.doi.org/10.4028/www.scientific.net/kem.353-358.2159.

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Protein expression of growth factors involved in fracture healing and osteoporosis were investigated in ovariectomised (OVX) rat fracture model using histological and immunohistochemical analysis. The OVX model was confirmed by a significantly increased body weight and reduced bone density of the non-fracture hind limbs. The tissue morphology and the protein expression were assessed on the paraffin sections of the fracture callus at day 7, 14, 28 and 42 after fracture. Histology revealed a significantly higher ratio of fibrous tissue over bone or cartilage over bone in the fracture callus at day 28 and 42 in the OVX rats than in the normal rats. Immunohistochemical staining of IGF-I, IGF-IRα, MMP-1, TIMP-1 and 2 showed a different pattern between the OVX and the control groups. A down-regulation of IGF-I and TIMP-1 and an up-regulation of MMP-1 were observed in OVX rats, which may account in part for the delayed healing of the osteoporotic fracture and may affect extracellular matrix composition, an important determinant of callus strength.

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Behari, J., V. P. Arya, and Z. C. Alex. "Bone Fracture Healing using a Capacitatively Coupled Rffield." Journal of Bioelectricity 10, no. 1-2 (January 1991): 231–39. http://dx.doi.org/10.3109/15368379109031409.

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38

Padmavathi, I. "Musculoskeletal system for healing of a bone fracture." Archives of Anatomy and Physiology 4, no. 1 (December 28, 2019): 001. http://dx.doi.org/10.17352/aap.000012.

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39

Severns, Anne E., Yu-Po Lee, Scott D. Nelson, Eric E. Johnson, and J. Michael Kabo. "Metabolic Measurement Techniques to Assess Bone Fracture Healing." Clinical Orthopaedics and Related Research 424 (July 2004): 231–38. http://dx.doi.org/10.1097/01.blo.0000128286.98083.2a.

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40

Brandi, Maria Luisa. "Healing of the bone with anti-fracture drugs." Expert Opinion on Pharmacotherapy 14, no. 11 (June 17, 2013): 1441–47. http://dx.doi.org/10.1517/14656566.2013.801959.

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41

Morcos, M. W., H. Al-Jallad, J. Li, C. Farquharson, J. L. Millán, R. C. Hamdy, and M. Murshed. "PHOSPHO1 is essential for normal bone fracture healing." Bone & Joint Research 7, no. 6 (June 2018): 397–405. http://dx.doi.org/10.1302/2046-3758.76.bjr-2017-0140.r2.

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Objectives Bone fracture healing is regulated by a series of complex physicochemical and biochemical processes. One of these processes is bone mineralization, which is vital for normal bone development. Phosphatase, orphan 1 (PHOSPHO1), a skeletal tissue-specific phosphatase, has been shown to be involved in the mineralization of the extracellular matrix and to maintain the structural integrity of bone. In this study, we examined how PHOSPHO1 deficiency might affect the healing and quality of fracture callus in mice. Methods Tibial fractures were created and then stabilized in control wild-type (WT) and Phospho1-/- mice (n = 16 for each group; mixed gender, each group carrying equal number of male and female mice) at eight weeks of age. Fractures were allowed to heal for four weeks and then the mice were euthanized and their tibias analyzed using radiographs, micro-CT (μCT), histology, histomorphometry and three-point bending tests. Results The μCT and radiographic analyses revealed a mild reduction of bone volume in Phospho1-/- callus, although it was not statistically significant. An increase in trabecular number and a decrease in trabecular thickness and separation were observed in Phospho1-/- callus in comparison with the WT callus. Histomorphometric analyses showed that there was a marked increase of osteoid volume over bone volume in the Phospho1-/- callus. The three-point bending test showed that Phospho1-/- fractured bone had more of an elastic characteristic than the WT bone. Conclusion Our work suggests that PHOSPHO1 plays an integral role during bone fracture repair and may be a therapeutic target to improve the fracture healing process. Cite this article: M. W. Morcos, H. Al-Jallad, J. Li, C. Farquharson, J. L. Millán, R. C. Hamdy, M. Murshed. PHOSPHO1 is essential for normal bone fracture healing: An Animal Study. Bone Joint Res 2018;7:397–405. DOI: 10.1302/2046-3758.76.BJR-2017-0140.R2.

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42

Bostrom, Mathias P. G. "Expression of Bone Morphogenetic Proteins in Fracture Healing." Clinical Orthopaedics and Related Research 355S (October 1998): S116—S123. http://dx.doi.org/10.1097/00003086-199810001-00013.

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43

Geris, Liesbet, Alf Gerisch, Jos Vander Sloten, Rüdiger Weiner, and Hans Van Oosterwyck. "Angiogenesis in bone fracture healing: A bioregulatory model." Journal of Theoretical Biology 251, no. 1 (March 2008): 137–58. http://dx.doi.org/10.1016/j.jtbi.2007.11.008.

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44

Doblaré, M., J. M. Garcı́a, and M. J. Gómez. "Modelling bone tissue fracture and healing: a review." Engineering Fracture Mechanics 71, no. 13-14 (September 2004): 1809–40. http://dx.doi.org/10.1016/j.engfracmech.2003.08.003.

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45

Xiao, Wan'an, Zhenyu Hu, Tianwei Li, and Jianjun Li. "Bone fracture healing is delayed in splenectomic rats." Life Sciences 173 (March 2017): 55–61. http://dx.doi.org/10.1016/j.lfs.2016.12.005.

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Grgurevic, L., D. Durdevic, I. Erjavec, B. Sanader, S. Prgomet, G. Sarajlic, L. Pintaric, and S. Vukicevic. "BMP-1-3 antibody delayed bone fracture healing." Bone 44 (June 2009): S309. http://dx.doi.org/10.1016/j.bone.2009.03.574.

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Moukoko, Didier, Didier Pourquier, Cécile Genovesio, Simon Thezenas, Patrick Chabrand, Sandrine Roffino, and Martine Pithioux. "Granulocyte-colony stimulating factor enhances bone fracture healing." Clinical Biomechanics 58 (October 2018): 62–68. http://dx.doi.org/10.1016/j.clinbiomech.2018.07.010.

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Vannucci, Letizia, and Maria Luisa Brandi. "Healing of the bone with anti-fracture drugs." Expert Opinion on Pharmacotherapy 17, no. 17 (October 11, 2016): 2267–72. http://dx.doi.org/10.1080/14656566.2016.1241765.

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Chhabra, Anikar, David Zijerdi, Jianxin Zhang, Alex Kline, Gary Balian, and Shephard Hurwitz. "BMP-14 Deficiency Inhibits Long Bone Fracture Healing." Journal of Orthopaedic Trauma 19, no. 9 (October 2005): 629–34. http://dx.doi.org/10.1097/01.bot.0000177108.38461.9c.

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Karpouzos, Athanasios, Evangelos Diamantis, Paraskevi Farmaki, Spyridon Savvanis, and Theodore Troupis. "Nutritional Aspects of Bone Health and Fracture Healing." Journal of Osteoporosis 2017 (2017): 1–10. http://dx.doi.org/10.1155/2017/4218472.

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Abstract:

Introduction. Fractures are quite common, especially among the elderly. However, they can increase in prevalence in younger ages too if the bone health is not good. This may happen as a result of bad nutrition.Methods. A customized, retrospective review of available literature was performed using the following keywords: bone health, nutrition, and fractures.Results. Insufficient intake of certain vitamins, particularly A and D, and other nutrients, such as calcium, may affect bone health or even the time and degree of bone healing in case of fracture. The importance of different nutrients, both dietary and found in food supplements, is discussed concerning bone health and fracture healing.Conclusion. A healthy diet with adequate amounts of both macro- and micronutrients is essential, for both decreasing fracture risk and enhancing the healing process after fracture.

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