A preliminary report on the effects of sustained administration of corticosteroid on traumatized disc using the adult male rat model.
METHODS
A novel degenerative disc disease model and sustained delivery method for corticosteroid in male Sprague-Dawley albino rats.


OBJECTIVE
To develop a model of degenerative disc disease and to determine the effect of continuous sustained release of corticosteroid on the process of degeneration within the traumatized disc.


BACKGROUND
The current modalities of treating symptomatic degenerative disc disease are either conservative or surgical. However, there is no cure for the degenerative process and prevention, therefore, is the ideal treatment. An understanding of the mechanisms involved in disc degeneration is crucial to develop new methods for prevention and treatment, including appropriate delivery systems and dosages of repair factors.


METHODS
The L5-L6 intervertebral disc was pierced with a 23-gauge needle in 18 rats. The animals received either sham or corticosterone-charged tricalcium phosphate ceramic capsules. The rats were euthanized at 4 weeks. Chondrocytes in the transition zone areas were counted and compared statistically.


RESULTS
The surgical technique induced degeneration of the nucleus without evidence of inflammation at adjacent levels when compared with nontraumatized controls. The number of chondrocytes per area was significantly less in the sham group than in the control group. Corticosteroid treatment showed chondrocyte numbers similar to control in 4 of 5 different views of the disc. The anterior region of the disc had 50% less chondrocytes per area than the control; however, the chondrocyte numbers were 50% greater than in the same site from discs of sham animals.


CONCLUSIONS
The results show the development of a degenerative disc animal model that can be used to test the effects of growth enhancing factors in disc repair. Administration of continuous sustained release of corticosterone can slow the process of degeneration within the traumatized disc in the rat model.
Ragab
Ashraf A
AA
Departments of Orthopaedic Surgery and Rehabilitation, University of Mississippi Medical Center, Jackson, 39216, USA.
Woodall
James W
JW
Tucci
Michelle A
MA
Wingerter
Scott A
SA
Fosnaugh
Adam W
AW
Franklin
Laura N
LN
Benghuzzi
Hamed A
HA
D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology* / Q000627:therapeutic use; D001672:Biocompatible Materials / Q000494:pharmacology / Q000627:therapeutic use; D002130:Calcium Phosphates / Q000494:pharmacology / Q000627:therapeutic use; D002452:Cell Count; D019902:Chondrocytes / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D003345:Corticosterone / Q000494:pharmacology* / Q000627:therapeutic use; D004195:Disease Models, Animal; D004334:Drug Administration Schedule; D051445:Fibrocartilage / Q000166:cytology / Q000187:drug effects / Q000502:physiology; D007249:Inflammation / Q000188:drug therapy / Q000473:pathology / Q000503:physiopathology; D007403:Intervertebral Disc / Q000166:cytology / Q000187:drug effects* / Q000502:physiology; D055959:Intervertebral Disc Degeneration / Q000188:drug therapy* / Q000473:pathology / Q000503:physiopathology; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012038:Regeneration / Q000187:drug effects / Q000502:physiology; D016896:Treatment Outcome
D000893:Anti-Inflammatory Agents; D001672:Biocompatible Materials; D002130:Calcium Phosphates; C018392:tricalcium phosphate; D003345:Corticosterone