Defect repair in the rat mandible with bone morphogenic protein 5 and prostaglandin E1.
OBJECTIVE
To compare the osteogenic abilities of 2 growth factors (bone morphogenic protein 5 [BMP-5] and prostaglandin E1 [PGE1]) and 2 carriers (collagen/polylactic acid [PLA] and collagen/calcium hydroxyapatite cement [HAC]) in the repair of a rat mandibular body defect.


METHODS
Prospective controlled trial. Subjects Twenty-nine Sprague-Dawley rats.


METHODS
Critical size defects were created in the bilateral mandibular bodies of the rats. Each hemimandible was assigned to an experimental group. The defects were filled with PLA (group 1), PLA with BMP-5 (group 2), PLA with PGE1 (group 3), HAC (group 4), HAC with BMP-5 (group 5), or HAC with PGE1 (group 6). The control group (group 7) had unfilled defects. The animals were killed after 12 weeks, and the nondemineralized specimens were processed histologically. Stereologic techniques were used to determine the volume fractions of new bone, osteoid, marrow, remaining implant, and fibrous tissue in each defect.


RESULTS
The HAC/BMP-5 group (group 5) contained significantly more new bone than the PLA/BMP-5 group (group 2) (P =.02), the HAC and HAC/PGE1 groups (groups 4 and 6) (P =.002), and the control group (group 7) (P<.01). The HAC/BMP-5 group also had less fibrous tissue than the HAC group and the HAC/PGE1 group (P<.001). Groups 5 and 6 had less fibrous tissue than group 7 (P<.01). The groups containing PGE1 demonstrated significantly more osteoid development than the other experimental groups (P<.001).


CONCLUSIONS
Inclusion of BMP-5 in an implant with calcium hydroxyapatite cement resulted in the formation of significantly larger fractions of new bone and less fibrous tissue ingrowth than occurred in the other experimental groups. The presence of PGE1 resulted in larger amounts of osteoid deposition, suggesting the potential for delayed bone healing.
Arosarena
Oneida A
OA
Division of Otolaryngology, Department of Surgery, University of Kentucky Medical Center, Lexington 40536, USA. oaaros2@pop.uky.edu
Collins
Wesley L
WL
D000527:Alprostadil / Q000008:administration & dosage*; D000818:Animals; D001672:Biocompatible Materials / Q000008:administration & dosage; D055417:Bone Morphogenetic Protein 5; D019485:Bone Morphogenetic Proteins / Q000008:administration & dosage*; D003094:Collagen / Q000008:administration & dosage; D004195:Disease Models, Animal; D004337:Drug Carriers / Q000008:administration & dosage; D004359:Drug Therapy, Combination; D017886:Durapatite / Q000008:administration & dosage; D006133:Growth Substances / Q000008:administration & dosage*; D019344:Lactic Acid / Q000008:administration & dosage; D008297:Male; D008338:Mandibular Injuries / Q000188:drug therapy* / Q000473:pathology; D010012:Osteogenesis / Q000187:drug effects*; D011091:Polyesters; D011108:Polymers / Q000008:administration & dosage; D011446:Prospective Studies; D051381:Rats; D017207:Rats, Sprague-Dawley
D001672:Biocompatible Materials; D055417:Bone Morphogenetic Protein 5; D019485:Bone Morphogenetic Proteins; D004337:Drug Carriers; D006133:Growth Substances; D011091:Polyesters; D011108:Polymers; D019344:Lactic Acid; C033616:poly(lactide); D003094:Collagen; D017886:Durapatite; D000527:Alprostadil