Orthopaedic surgery

2021 ◽  
pp. 597-698
Keyword(s):  
Fracture Healing ◽  
Bone Healing ◽  
Orthopaedic Surgery ◽  
Fracture Reduction ◽  
Fracture Reduction And Fixation ◽  
Reduction Techniques ◽  
Careful Handling ◽  
Tunnel Syndrome ◽  
Primary Bone ◽  
Secondary Bone Healing

This chapter examines orthopaedic surgery. It begins by detailing the examination of a joint and of the limbs and trunk. The chapter then discusses fracture healing and the reduction and fixation of fractures. Fracture healing occurs as either primary or secondary bone union. Primary bone healing does not produce callus, while secondary bone healing does. Modern fracture reduction and treatment centres around four key principles: fracture reduction and fixation to restore anatomical relationships; stability by fixation or splintage as the personality of the fracture and the injury dictates; preservation of the blood supply to the soft tissue and bone by careful handling and gentle reduction techniques; and early and safe mobilization of the part and patient. Finally, the chapter looks at the skeletal radiograph and considers injuries of the phalanges and metacarpals; wrist injuries; dislocations and fractures of the elbow, shoulders, ribs, pelvis, and neck; spinal injuries; bone tumours; osteoarthrosis (osteoarthritis); Paget’s disease (osteitis deformans); and carpal tunnel syndrome.

Current concepts in bone healing. Review of the literature

1993 ◽  
Vol 83 (3) ◽  
pp. 123-129 ◽  
Author(s):  
MA Greenbaum ◽  
IO Kanat
Keyword(s):  
Internal Fixation ◽  
Bone Healing ◽  
Review Of The Literature ◽  
Rigid Internal Fixation ◽  
Primary Bone ◽  
Secondary Bone Healing

Bone healing is a process of reconstitution of tissue. With the development of rigid internal fixation, primary bone healing has exhibited certain histologic characteristics not previously seen. The authors discuss the histologic, biochemical, and physiologic processes seen in primary and secondary bone healing following fracture or osteotomy.

scholarly journals OP0244 A PRECLINICAL TESTING TOOL: THE IN VITRO 3D FRACTURE GAP MODEL

2020 ◽  
Vol 79 (Suppl 1) ◽  
pp. 154.1-154
Author(s):  
M. Pfeiffenberger ◽  
A. Damerau ◽  
P. Hoff ◽  
A. Lang ◽  
F. Buttgereit ◽  
...  
Keyword(s):  
Fracture Healing ◽  
Bone Healing ◽  
Inflammatory Markers ◽  
Initial Phase ◽  
Gap Model ◽  
Osteogenic Markers ◽  
Immunosuppressed Patients ◽  
The Impact

Background:Approximately 10% of fractures lead to significant fracture healing disorders, with a tendency to further increase due to the aging population. Of note, especially immunosuppressed patients with ongoing inflammation show difficulties in the correct course of fracture healing leading to fracture healing disorders. Most notably, invading immune cells and secreted cytokines are considered to provide an inflammatory microenvironment within the fracture gap, primarily during the initial phase of fracture healing. Current research has the focus on small animal models, facing the problem of translation towards the human system. In order to improve the therapy of fracture healing disorders, we have developed a human cell-basedin vitromodel to mimic the initial phase of fracture healing adequately. This model will be used for the development of new therapeutic strategies.Objectives:Our aim is to develop anin vitro3D fracture gap model (FG model) which mimics thein vivosituation in order to provide a reliable preclinical test system for fracture healing disorders.Methods:To assemble our FG model, we co-cultivated coagulated peripheral blood and primary human mesenchymal stromal cells (MSCs) mimicking the fracture hematoma (FH model) together with a scaffold-free bone-like construct mimicking the bony part of the fracture gap for 48 h under hypoxic conditions (n=3), in order to reflect thein vivosituation after fracture most adequately. To analyze the impact of the bone-like construct on thein vitroFH model with regard to its osteogenic induction capacity, we cultivated the fracture gap models in either medium with or without osteogenic supplements. To analyze the impact of Deferoxamine (DFO, known to foster fracture healing) on the FG model, we further treated our FG models with either 250 µmol DFO or left them untreated. After incubation and subsequent preparation of the fracture hematomas, we evaluated gene expression of osteogenic (RUNX2,SPP1), angiogenic (VEGF,IL8), inflammatory markers (IL6,IL8) and markers for the adaptation towards hypoxia (LDHA,PGK1) as well as secretion of cytokines/chemokines using quantitative PCR and multiplex suspension assay, respectively.Results:We found via histology that both the fracture hematoma model and the bone-like construct had close contact during the incubation, allowing the cells to interact with each other through direct cell-cell contact, signal molecules or metabolites. Additionally, we could show that the bone-like constructs induced the upregulation of osteogenic markers (RUNX2, SPP1) within the FH models irrespective of the supplementation of osteogenic supplements. Furthermore, we observed an upregulation of hypoxia-related, angiogenic and osteogenic markers (RUNX2,SPP1) under the influence of DFO, and the downregulation of inflammatory markers (IL6,IL8) as compared to the untreated control. The latter was also confirmed on protein level (e.g. IL-6 and IL-8). Within the bone-like constructs, we observed an upregulation of angiogenic markers (RNA-expression ofVEGF,IL8), even more pronounced under the treatment of DFO.Conclusion:In summary, our findings demonstrate that our establishedin vitroFG model provides all osteogenic cues to induce the initial bone healing process, which could be enhanced by the fracture-healing promoting substance DFO. Therefore, we conclude that our model is indeed able to mimic correctly the human fracture gap situation and is therefore suitable to study the influence and efficacy of potential therapeutics for the treatment of bone healing disorders in immunosuppressed patients with ongoing inflammation.Disclosure of Interests:Moritz Pfeiffenberger: None declared, Alexandra Damerau: None declared, Paula Hoff: None declared, Annemarie Lang: None declared, Frank Buttgereit Grant/research support from: Amgen, BMS, Celgene, Generic Assays, GSK, Hexal, Horizon, Lilly, medac, Mundipharma, Novartis, Pfizer, Roche, and Sanofi., Timo Gaber: None declared

scholarly journals Can Optimizing the Mechanical Environment Deliver a Clinically Significant Reduction in Fracture Healing Time?

Biomedicines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 691
Author(s):  
Jan Barcik ◽  
Devakara R. Epari
Keyword(s):  
Fracture Healing ◽  
Bone Healing ◽  
Mechanical Stimulation ◽  
Callus Formation ◽  
Weight Bearing ◽  
Healing Process ◽  
Healing Time ◽  
Mechanical Environment ◽  
Clinically Significant ◽  
The Impact

The impact of the local mechanical environment in the fracture gap on the bone healing process has been extensively investigated. Whilst it is widely accepted that mechanical stimulation is integral to callus formation and secondary bone healing, treatment strategies that aim to harness that potential are rare. In fact, the current clinical practice with an initially partial or non-weight-bearing approach appears to contradict the findings from animal experiments that early mechanical stimulation is critical. Therefore, we posed the question as to whether optimizing the mechanical environment over the course of healing can deliver a clinically significant reduction in fracture healing time. In reviewing the evidence from pre-clinical studies that investigate the influence of mechanics on bone healing, we formulate a hypothesis for the stimulation protocol which has the potential to shorten healing time. The protocol involves confining stimulation predominantly to the proliferative phase of healing and including adequate rest periods between applications of stimulation.

Osteocytes

2018 ◽  
Vol 157 (02) ◽  
pp. 154-163 ◽  
Author(s):  
Markus Rupp ◽  
Felix Merboth ◽  
Diaa Daghma ◽  
Christoph Biehl ◽  
Thaqif El Khassawna ◽  
...  
Keyword(s):  
Wnt Signaling ◽  
Fracture Healing ◽  
Bone Metabolism ◽  
Bone Remodeling ◽  
Bone Healing ◽  
Wnt Signaling Pathway ◽  
Monoklonaler Antikörper ◽  
Orthopädie Und Unfallchirurgie ◽  
Healing Bone ◽  
Fgf 23

ZusammenfassungLange Zeit galten Osteozyten als passive Zuschauer der Knochenhomöostase, dem Gleichgewicht zwischen Knochenaufbau durch Osteoblasten und Knochenabbau durch Osteoklasten. Das Dogma der ruhenden, im Knochen eingemauerten funktionslosen Zellen hat sich seit der Jahrtausendwende grundlegend gewandelt. Osteozyten stehen vielmehr im Mittelpunkt des Knochenstoffwechsels und können somit als dessen Dirigent angesehen werden. Auf Grundlage einer Literaturrecherche in PubMed und Google Scholar mit den einzeln oder in Kombination verwendeten Suchbegriffen „osteocyte“, „fracture healing“, „bone healing“, „bone remodeling“, „bone metabolism“, „sclerostin“, „RANKL/OPG“, „Wnt-signaling pathway“, „FGF-23“ wurde die Rolle der Osteozyten im Knochenstoffwechsel anhand von präklinischen und klinischen Studien sowie Übersichtsarbeiten erarbeitet. Einzelne Fallberichte wurden hierfür nicht verwandt. Im Rahmen der Literaturrecherche wurden nur Publikationen in englischer oder deutscher Sprache berücksichtigt. Die sich aus Osteoblasten entwickelnden Osteozyten sind funktionell die zentrale Schaltstelle im Knochenmetabolismus. Morphologisch bildet ein Netzwerk von Osteozyten, die 90 – 95% der Zellen im Knochen ausmachen und im Gegensatz zu Osteoblasten und Osteoklasten das Alter des Gesamtorganismus erreichen können, durch mit Nexus miteinander verbundenen Dendriten innerhalb des Knochens die optimale Grundlage für deren funktionelle Aufgaben. Neben der Aufgabe als Mechanosensor im Knochen wird die Osteoblastenfunktion über Sclerostin, die Osteoklastenfunktion über den RANK/RANKL/OPG-Signalweg gesteuert. Ferner wird die Mineralisierung des Knochens über die lokale Phosphatkonzentration, der systemische Phosphathaushalt in Interaktion mit der Niere über FGF23 hormonell gesteuert. Das Verständnis der Rolle der Osteozyten verspricht eine weitere Verbesserung möglicher Therapiealternativen. Hinsichtlich des Knochenstoffwechsels sind bereits Sclerostinantikörper und Denosumab, ein monoklonaler Antikörper, der als OPG-Agonist fungiert, eingeführt worden. Neben den in der Osteoporosetherapie bereits etablierten Therapieansätzen sind Antikörper gegen FGF23 oder dessen Rezeptoren in der präklinischen und klinischen Erprobung. Auch Bortezomib, ein Proteasomeninhibitor, der die Lebensfähigkeit von Osteozyten verbessert, ist zur Therapie des multiplen Myeloms im klinischen Einsatz. Das zunehmende Verständnis der osteozytären Funktion lässt darüber hinaus weitere Therapiemöglichkeiten erwarten – in Orthopädie und Unfallchirurgie sind dies insbesondere die ossäre Integration von Implantaten und die medikamentöse Beeinflussung der (gestörten) Frakturheilung.

scholarly journals Measuring Intertrochanteric Fracture Stability with a Novel Strain-Sensing Sliding Hip Screw

2020 ◽  
Author(s):  
Nathan T. Carrington ◽  
Paul W. Millhouse ◽  
Caleb J. Behrend ◽  
Thomas B. Pace ◽  
Jeffrey N. Anker ◽  
...  
Keyword(s):  
Finite Element ◽  
Fracture Healing ◽  
Bone Healing ◽  
Revision Surgery ◽  
Intertrochanteric Fracture ◽  
Strain Sensing ◽  
Sliding Hip Screw ◽  
The Status ◽  
Fracture Models ◽  
Hip Screw

Background: Bone healing after internal fixation of intertrochanteric hip fractures is difficult to monitor with radiography, particularly with internal fixation implants such as the sliding hip screw (SHS). In this study, we evaluate a robust, user-friendly device to non-invasively determine the loading on the screw implant. This will allow clinicians to better monitor the status of bone healing and take preventative steps if complications occur. Methods: A novel strain-sensing sliding hip screw (SS-SHS) was designed and refined using a finite element model of a simple intertrochanteric fracture and a standard SHS implant. The SS-SHS houses an internally fixed indicator rod, whose position relative to the screw body can be viewed on plain film radiographs to measure screw bending. Screw bending was assessed in an intact femur and an unstable A1 intertrochanteric fracture using a finite element computational model and compared with experimental axial loading of a femoral Sawbones composite and human cadaveric femur specimens. Indicator rod position relative to the screw was visually tracked using plain radiographs at each load state. Results: The indicator rod was found to displace linearly in response to implant strain in the unstable fracture. This movement was consistently visible and measurable using radiography throughout loading cycles across the mechanical and cadaveric fracture models. Sensor movement was not detected in healed fracture models. The slope of the curve was approximately equal in the computations, composite and cadaveric models (0.08 μm/N, 1.0 μm/N, 0.08 μm/N, respectively). The noise level was approximately 25 N in the composite model and 63 N in the cadaveric specimen and this was sufficient to see 1/10th of body weight or more for an 80 kg patient which is likely good enough to track fracture healing. Conclusions: In current practice, clinicians must carefully monitor their patients for signs of implant failure after surgery. However, by the time signs of failure are apparent, it is often too late to avoid revision surgery. This device enables clinicians to quantitatively track fracture healing, and better communicate the process to the patient. Clinicians can also take preventive measures with at-risk patients before revision surgery is needed, thus reducing mortality risks. Clinical Relevance: By augmenting an existing SHS system with an indicator rod, crucial information on the status of fracture healing can be ascertained from follow-up radiographs already taken with no additional risk to the patient.

Repurposing denosumab for recalcitrant bone healing

2021 ◽  
Vol 14 (2) ◽  
pp. e238460
Author(s):  
Sanjay Agarwala ◽  
Mayank Vijayvargiya
Keyword(s):  
Adverse Effect ◽  
Fracture Healing ◽  
Bone Healing ◽  
Surgical Intervention ◽  
Volume Density ◽  
Bone Union ◽  
Callus Volume ◽  
Haematoma Formation

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.

Orthopaedic surgery

2014 ◽  
Author(s):  
Sebastian Dawson-Bowling
Keyword(s):  
Fracture Healing ◽  
Orthopaedic Surgery ◽  
Soft Tissues ◽  
Orthopaedic Practice ◽  
Non Union ◽  
Valuable Adjunct ◽  
The Common ◽  
Musculoskeletal Function ◽  
Comprehensive History ◽  
Primary Modality

Sound knowledge of anatomy and understanding of musculoskeletal function underpins good orthopaedic practice. Bones and joints may be affected by genetic and degenerative conditions, by infection, primary and secondary neoplasia, by endocrine and metabolic anomalies, and by trauma. As in other areas of surgery, a comprehensive history and thorough examination are essential in leading the clinician to a correct diagno­sis. Appropriate imaging complements clinical acuity. The plain X-ray remains the primary modality of investigation for visualizing bony injuries and pathology, but MRI is a valuable adjunct for investigating soft tissues and joints. Principles of fracture healing, reduction and fixation, and knowledge of consequences of complications which delay healing, or cause non-union, are integral to the practice of orthopaedic surgery. This chapter will help you to revise basic tenets of orthopaedic prac­tice and the common injuries and conditions encountered by the ortho­paedic surgeon.

scholarly journals Effects of Local Opioid Antagonist on Diabetic Fracture Rat Model

2018 ◽  
Vol 3 (3) ◽  
pp. 2473011418S0017
Author(s):  
Jarrett D. Cain ◽  
Michelle Titunick ◽  
Patricia McLaughlin ◽  
Ian Zagon
Keyword(s):  
Growth Factor ◽  
Fracture Healing ◽  
Bone Healing ◽  
Calcium Sulfate ◽  
Bone Fractures ◽  
Diabetic Rats ◽  
Receptor Expression ◽  
Opioid Antagonist ◽  
Diabetic Patients ◽  
Opioid Growth Factor

Category: Diabetes Introduction/Purpose: Complications associated with the diabetes include increased incidence of fracture healing, delayed fracture healing, delayed osteoblasts cell replication, decreased angiogenesis, migration and/or osteoblast cell differentiation. The cellular events involved in bone healing are adversely affected by diabetes; however, can be modulated by the Opioid Growth Factor (OGF)–OGF receptor (OGFr) is an inhibitory peptide that downregulates DNA synthesis in a tissue nonspecific manner. Diabetes is associated with elevated serum levels of OGF and dysregulation of the OGFr leading to multiple complications related to healing, sensitivity, and regeneration. This study explores the presence and function of the OGF-OGFr axis in bone tissue from type 1 diabetic rats examining intact and fractured femurs during early phases of the repair process Methods: Seven-week-old Sprague Dawley rats were injected with streptozotocin (40mg/kg i.p.) to induce T1D; other rats received buffer only and served as controls. After one month, hyperglycemia rats underwent surgery to produce a fracture at the distal third of the femur. Four diabetic rats received opioid antagoinist (naltrexone) and calcium sulfate and all remaining rats received calcium sulfate with water only. X-rays were taken immediately after surgery and after rats were euthanized on post-surgery; femur and tibia were collected for protein isolation, western blot analysis along with frozen or paraffin-embedded for histological analysis Results: Immunofluorescence indicated approximately 90% increase in opioid growth factor receptor expression in diabetic femurs compared to age-matched normal femurs. Western Blotting also suggested an increase in the receptor protein in diabetic bones relative to normal bone. TRAP staining for osteoclasts was greater in control and opioid antagonist-treated diabetic fractures when compared to the number of osteoclasts in vehicle-treated diabetic fractured femurs. Safranin O stained sections revealed approximately more bone in opioid growth receptor antagonist-treated diabetic bone fractures than in vehicle-treated bone fractures Conclusion: These data support our hypothesis that expression levels of OGFr are dysregulated in the bone of diabetic patients leading to complications in bone healing. Moreover, modulation of the OGF-OGFr pathway with receptor antagonists restored some aspects of bone healing. With further study, these preliminary results support the role of the OGF-OGFr axis in treatment of diabetic bone healing. New therapies to target dysregulation of the OGF-OGFr regulatory pathway in diabetes would provide a safe and effective disease-modifying treatment for delayed bone healing.

scholarly journals An Improved Methodology to Evaluate Cell and Molecular Signals in the Reparative Callus During Fracture Healing

2020 ◽  
Vol 68 (3) ◽  
pp. 199-208
Author(s):  
Anuradha Valiya Kambrath ◽  
Justin N. Williams ◽  
Uma Sankar
Keyword(s):  
Fracture Healing ◽  
Bone Healing ◽  
High Throughput Screening ◽  
Molecular Mechanisms ◽  
Structural Integrity ◽  
Bone Fractures ◽  
Early Stage ◽  
Antigen Retrieval ◽  
Sample Collection ◽  
Immunofluorescence Labeling

Approximately 5% to 10% of all bone fractures do not heal completely, contributing to significant patient suffering and medical costs. Even in healthy individuals, fracture healing is associated with significant downtime and loss of productivity. However, no pharmacological treatments are currently available to promote efficient bone healing. A better understanding of the underlying molecular mechanisms is crucial for developing novel therapies to hasten healing. The early reparative callus that forms around the site of bone injury is a fragile tissue consisting of shifting cell populations held together by loose connective tissue. The delicate callus is challenging to section and is vulnerable to disintegration during the harsh steps of immunostaining, namely, decalcification, deparaffinization, and antigen retrieval. Here, we describe an improved methodology for processing early-stage fracture calluses and immunofluorescence labeling of the sections to visualize the temporal (timing) and spatial (location) patterns of cellular and molecular events that regulate bone healing. This method has a short turnaround time from sample collection to microscopy as it does not require lengthy decalcification. It preserves the structural integrity of the fragile callus as the method does not entail deparaffinization or harsh methods of antigen retrieval. Our method can be adapted for high-throughput screening of drugs that promote efficacious bone healing:

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