Compromised bone healing following spacer removal in a rat femoral defect model

G. Skaliczki, M. Weszl, K. Schandl, T. Major, M. Kovács, J. Skaliczki, H. Redl, M. Szendrői, K. Szigeti, D. Máté, C. S. Dobó-Nagy, Z. Lacza

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Purpose: The clinical demand for bone grafting materials necessitated the development of animal models. Critical size defect model has been criticized recently, mainly for its inaccuracy. Our objective was to develop a dependable animal model that would provide compromised bone healing, and would allow the investigation of bone substitutes. Methods: In the first group a critical size defect was created in the femur of adult male Wistar rats, and a non-critical defect in the remaining animals (Groups II, III and IV). The defect was left empty in group II, while in groups III and IV a spacer was interposed into the gap. Osteoblast activity was evaluated by NanoSPECT/CT imaging system. New bone formation and assessment of a union or non-union was observed by μCT and histology. Results: The interposition model proved to be highly reproducible and provided a bone defect with compromised bone healing. Significant bone regeneration processes were observed four weeks after removal of the spacer. Conclusion: Our results have shown that when early bone healing is inhibited by the physical interposition of a spacer, the regeneration process is compromised for a further 4 weeks and results in a bone defect during the time-course of the study.

Original languageEnglish
Pages (from-to)223-232
Number of pages10
JournalActa Physiologica Hungarica
Volume99
Issue number2
DOIs
Publication statusPublished - Jun 1 2012

Fingerprint

Thigh
Bone and Bones
Animal Models
Bone Substitutes
Bone Regeneration
Bone Transplantation
Osteoblasts
Osteogenesis
Femur
Wistar Rats
Regeneration
Histology

Keywords

  • Critical size bone defect
  • Delayed healing
  • Fracture
  • Non-union

ASJC Scopus subject areas

  • Physiology (medical)

Cite this

Compromised bone healing following spacer removal in a rat femoral defect model. / Skaliczki, G.; Weszl, M.; Schandl, K.; Major, T.; Kovács, M.; Skaliczki, J.; Redl, H.; Szendrői, M.; Szigeti, K.; Máté, D.; Dobó-Nagy, C. S.; Lacza, Z.

In: Acta Physiologica Hungarica, Vol. 99, No. 2, 01.06.2012, p. 223-232.

Research output: Contribution to journalArticle

Skaliczki, G, Weszl, M, Schandl, K, Major, T, Kovács, M, Skaliczki, J, Redl, H, Szendrői, M, Szigeti, K, Máté, D, Dobó-Nagy, CS & Lacza, Z 2012, 'Compromised bone healing following spacer removal in a rat femoral defect model', Acta Physiologica Hungarica, vol. 99, no. 2, pp. 223-232. https://doi.org/10.1556/APhysiol.99.2012.2.16
Skaliczki, G. ; Weszl, M. ; Schandl, K. ; Major, T. ; Kovács, M. ; Skaliczki, J. ; Redl, H. ; Szendrői, M. ; Szigeti, K. ; Máté, D. ; Dobó-Nagy, C. S. ; Lacza, Z. / Compromised bone healing following spacer removal in a rat femoral defect model. In: Acta Physiologica Hungarica. 2012 ; Vol. 99, No. 2. pp. 223-232.
@article{d40774b8873f4d529d62d09d02e1fa1c,
title = "Compromised bone healing following spacer removal in a rat femoral defect model",
abstract = "Purpose: The clinical demand for bone grafting materials necessitated the development of animal models. Critical size defect model has been criticized recently, mainly for its inaccuracy. Our objective was to develop a dependable animal model that would provide compromised bone healing, and would allow the investigation of bone substitutes. Methods: In the first group a critical size defect was created in the femur of adult male Wistar rats, and a non-critical defect in the remaining animals (Groups II, III and IV). The defect was left empty in group II, while in groups III and IV a spacer was interposed into the gap. Osteoblast activity was evaluated by NanoSPECT/CT imaging system. New bone formation and assessment of a union or non-union was observed by μCT and histology. Results: The interposition model proved to be highly reproducible and provided a bone defect with compromised bone healing. Significant bone regeneration processes were observed four weeks after removal of the spacer. Conclusion: Our results have shown that when early bone healing is inhibited by the physical interposition of a spacer, the regeneration process is compromised for a further 4 weeks and results in a bone defect during the time-course of the study.",
keywords = "Critical size bone defect, Delayed healing, Fracture, Non-union",
author = "G. Skaliczki and M. Weszl and K. Schandl and T. Major and M. Kov{\'a}cs and J. Skaliczki and H. Redl and M. Szendrői and K. Szigeti and D. M{\'a}t{\'e} and Dob{\'o}-Nagy, {C. S.} and Z. Lacza",
year = "2012",
month = "6",
day = "1",
doi = "10.1556/APhysiol.99.2012.2.16",
language = "English",
volume = "99",
pages = "223--232",
journal = "Physiology International",
issn = "2498-602X",
publisher = "Akademiai Kiado",
number = "2",

}

TY - JOUR

T1 - Compromised bone healing following spacer removal in a rat femoral defect model

AU - Skaliczki, G.

AU - Weszl, M.

AU - Schandl, K.

AU - Major, T.

AU - Kovács, M.

AU - Skaliczki, J.

AU - Redl, H.

AU - Szendrői, M.

AU - Szigeti, K.

AU - Máté, D.

AU - Dobó-Nagy, C. S.

AU - Lacza, Z.

PY - 2012/6/1

Y1 - 2012/6/1

N2 - Purpose: The clinical demand for bone grafting materials necessitated the development of animal models. Critical size defect model has been criticized recently, mainly for its inaccuracy. Our objective was to develop a dependable animal model that would provide compromised bone healing, and would allow the investigation of bone substitutes. Methods: In the first group a critical size defect was created in the femur of adult male Wistar rats, and a non-critical defect in the remaining animals (Groups II, III and IV). The defect was left empty in group II, while in groups III and IV a spacer was interposed into the gap. Osteoblast activity was evaluated by NanoSPECT/CT imaging system. New bone formation and assessment of a union or non-union was observed by μCT and histology. Results: The interposition model proved to be highly reproducible and provided a bone defect with compromised bone healing. Significant bone regeneration processes were observed four weeks after removal of the spacer. Conclusion: Our results have shown that when early bone healing is inhibited by the physical interposition of a spacer, the regeneration process is compromised for a further 4 weeks and results in a bone defect during the time-course of the study.

AB - Purpose: The clinical demand for bone grafting materials necessitated the development of animal models. Critical size defect model has been criticized recently, mainly for its inaccuracy. Our objective was to develop a dependable animal model that would provide compromised bone healing, and would allow the investigation of bone substitutes. Methods: In the first group a critical size defect was created in the femur of adult male Wistar rats, and a non-critical defect in the remaining animals (Groups II, III and IV). The defect was left empty in group II, while in groups III and IV a spacer was interposed into the gap. Osteoblast activity was evaluated by NanoSPECT/CT imaging system. New bone formation and assessment of a union or non-union was observed by μCT and histology. Results: The interposition model proved to be highly reproducible and provided a bone defect with compromised bone healing. Significant bone regeneration processes were observed four weeks after removal of the spacer. Conclusion: Our results have shown that when early bone healing is inhibited by the physical interposition of a spacer, the regeneration process is compromised for a further 4 weeks and results in a bone defect during the time-course of the study.

KW - Critical size bone defect

KW - Delayed healing

KW - Fracture

KW - Non-union

UR - http://www.scopus.com/inward/record.url?scp=84864707516&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=84864707516&partnerID=8YFLogxK

U2 - 10.1556/APhysiol.99.2012.2.16

DO - 10.1556/APhysiol.99.2012.2.16

M3 - Article

VL - 99

SP - 223

EP - 232

JO - Physiology International

JF - Physiology International

SN - 2498-602X

IS - 2

ER -