Regulation of osteoblast levels during bone healing

Margaret L. Olmedo, Patricia S. Landry, Kalia K. Sadasivan, James A. Albright, William D. Meek, Robert Routh, Andrew A. Marino

Research output: Contribution to journalArticle

30 Citations (Scopus)

Abstract

Objective: To confirm the occurrence of programmed cell death of osteoblasts during bone healing and to evaluate the role of interleukin-1β (IL-1β) in regulating osteoblast concentration. Study Design: Electron microscopic study of the response of rats to a controlled bone injury, and a randomized controlled study of the effect of IL-1β administered continuously for three days. Methods: A standardized defect (1.1 millimeter in diameter, 0.5 millimeter deep) was created unilaterally on the anteromedial surface of the tibia. In some animals, the injury site was recovered five days after operation and processed for ultrastructural evaluation of osteoblasts in the callus. In another group, IL-1β was delivered to the bone defect using micro-osmotic pumps (0.5 nanograms/hour); control rats received vehicle only. The bones were recovered one to fourteen days after injury, and concentrations of proliferating cells, osteoblasts, and apoptotic bodies were determined. The amount of callus that formed in the defect was measured. Results: Osteoblasts in the callus exhibited ultrastructural changes characteristic of cells undergoing apoptosis, including condensation of chromatin, membrane blebbing, formation of apoptotic bodies, and phagocytosis by nearby osteoblasts. Addition of IL-1β significantly increased the number of osteoblasts at the injury site and significantly decreased the number of apoptotic bodies in relation to the number of osteoblasts. The amount of callus in the bone defect was not affected by IL-1β treatment. Conclusion: The role of programmed cell death of osteoblasts as a normal concomitant of bone healing was confirmed. Evidence was found suggesting that IL-1β mediated the appearance and disappearance of osteoblasts, possibly by affecting the rates of differentiation and apoptosis, respectively. Understanding these mechanisms conceivably could lead to the ability to control osteoblast levels at an injury site.

Original languageEnglish
Pages (from-to)356-362
Number of pages7
JournalJournal of Orthopaedic Trauma
Volume13
Issue number5
DOIs
StatePublished - 1 Jun 1999
Externally publishedYes

Fingerprint

Osteoblasts
Bone and Bones
Interleukin-1
Bony Callus
Wounds and Injuries
Cell Death
Apoptosis
Blister
Tibia
Phagocytosis
Chromatin
Electrons
Membranes

Keywords

  • Apoptosis
  • Bone healing
  • Interleukin-1β
  • Osteoblasts

Cite this

Olmedo, M. L., Landry, P. S., Sadasivan, K. K., Albright, J. A., Meek, W. D., Routh, R., & Marino, A. A. (1999). Regulation of osteoblast levels during bone healing. Journal of Orthopaedic Trauma, 13(5), 356-362. https://doi.org/10.1097/00005131-199906000-00006
Olmedo, Margaret L. ; Landry, Patricia S. ; Sadasivan, Kalia K. ; Albright, James A. ; Meek, William D. ; Routh, Robert ; Marino, Andrew A. / Regulation of osteoblast levels during bone healing. In: Journal of Orthopaedic Trauma. 1999 ; Vol. 13, No. 5. pp. 356-362.
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Olmedo, ML, Landry, PS, Sadasivan, KK, Albright, JA, Meek, WD, Routh, R & Marino, AA 1999, 'Regulation of osteoblast levels during bone healing', Journal of Orthopaedic Trauma, vol. 13, no. 5, pp. 356-362. https://doi.org/10.1097/00005131-199906000-00006

Regulation of osteoblast levels during bone healing. / Olmedo, Margaret L.; Landry, Patricia S.; Sadasivan, Kalia K.; Albright, James A.; Meek, William D.; Routh, Robert; Marino, Andrew A.

In: Journal of Orthopaedic Trauma, Vol. 13, No. 5, 01.06.1999, p. 356-362.

Research output: Contribution to journalArticle

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T1 - Regulation of osteoblast levels during bone healing

AU - Olmedo, Margaret L.

AU - Landry, Patricia S.

AU - Sadasivan, Kalia K.

AU - Albright, James A.

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AU - Routh, Robert

AU - Marino, Andrew A.

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N2 - Objective: To confirm the occurrence of programmed cell death of osteoblasts during bone healing and to evaluate the role of interleukin-1β (IL-1β) in regulating osteoblast concentration. Study Design: Electron microscopic study of the response of rats to a controlled bone injury, and a randomized controlled study of the effect of IL-1β administered continuously for three days. Methods: A standardized defect (1.1 millimeter in diameter, 0.5 millimeter deep) was created unilaterally on the anteromedial surface of the tibia. In some animals, the injury site was recovered five days after operation and processed for ultrastructural evaluation of osteoblasts in the callus. In another group, IL-1β was delivered to the bone defect using micro-osmotic pumps (0.5 nanograms/hour); control rats received vehicle only. The bones were recovered one to fourteen days after injury, and concentrations of proliferating cells, osteoblasts, and apoptotic bodies were determined. The amount of callus that formed in the defect was measured. Results: Osteoblasts in the callus exhibited ultrastructural changes characteristic of cells undergoing apoptosis, including condensation of chromatin, membrane blebbing, formation of apoptotic bodies, and phagocytosis by nearby osteoblasts. Addition of IL-1β significantly increased the number of osteoblasts at the injury site and significantly decreased the number of apoptotic bodies in relation to the number of osteoblasts. The amount of callus in the bone defect was not affected by IL-1β treatment. Conclusion: The role of programmed cell death of osteoblasts as a normal concomitant of bone healing was confirmed. Evidence was found suggesting that IL-1β mediated the appearance and disappearance of osteoblasts, possibly by affecting the rates of differentiation and apoptosis, respectively. Understanding these mechanisms conceivably could lead to the ability to control osteoblast levels at an injury site.

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Olmedo ML, Landry PS, Sadasivan KK, Albright JA, Meek WD, Routh R et al. Regulation of osteoblast levels during bone healing. Journal of Orthopaedic Trauma. 1999 Jun 1;13(5):356-362. https://doi.org/10.1097/00005131-199906000-00006