A quantitative analysis of the effect of insulin-like growth factor-1 infusion during mandibular distraction osteogenesis in rabbits

Citation
Kj. Stewart et al., A quantitative analysis of the effect of insulin-like growth factor-1 infusion during mandibular distraction osteogenesis in rabbits, BR J PL SUR, 52(5), 1999, pp. 343-350
Citations number
27
Categorie Soggetti
Surgery
Journal title
BRITISH JOURNAL OF PLASTIC SURGERY
ISSN journal
00071226 → ACNP
Volume
52
Issue
5
Year of publication
1999
Pages
343 - 350
Database
ISI
SICI code
0007-1226(199907)52:5<343:AQAOTE>2.0.ZU;2-V
Abstract
Aim. To quantify, by histomorphometry, the effects of local insulin-like gr owth factor-1 (IGF-1) during mandibular distraction at various rates. Methodology. Mature rabbits underwent bilateral mandibular corticotomy and distraction lengthening. Recombinant IGF-1 was administered to two groups o f rabbits via osmotic infusion pumps. Distraction regimes were as follows: Group A, 1 mm/day for 15 days; Group B, as for A plus IGF-I; Group C, 3 mm/ day for 5 days; Group D, as for C plus IGF-1; and Group E, sham-operated co ntrols. After a 28-day consolidation period, rabbits were sacrificed and bo ne deposition quantified using DEXA scanning, three-point bending, histolog ical examination and sampled for histomorphometric analysis. Results. DEXA scanning and three-point bending failed to detect any effect of distraction rate or of IGF-1 infusion. Histological and histomorphometri c analysis suggested 1 mm/day to be the ideal distraction rate, as this was associated with greater osteoblastic activity and consistent bony union. H owever, IGF-1 infusion significantly enhanced osteoblastic activity at both distraction rates and resulted in bony union when distraction was performe d at 3 mm/day. Conclusions. Distraction osteogenesis at a rate of 1 mm/day provides greate r osteogenic stimulus than 3 mm/day Exogenous IGF-1 has a positive influenc e on osteoblastic activity during distraction. Its effect is probably minim ised by high levels of endogenous IGF-1.