A comparative analysis of bone formation induced by human demineralized freeze-dried bone and enamel matrix derivative in rat calvaria critical-size bone defects.
BACKGROUND
Human demineralized freeze-dried bone allograft (DFDBA) and enamel matrix derivative (EMD) have been used with varying success for the treatment of bone and periodontal defects. The purpose of this study was to compare qualitatively and quantitatively the bone formation induced by DFDBA and EMD to that of a positive control, recombinant human bone morphogenetic protein 2 (rhBMP-2), in the 8-mm rat calvaria critical-size bone defect.


METHODS
Five groups of five rats each were used. The two test groups were DFDBA and EMD. A negative control consisted of a defect without any biomaterial implanted, a positive control consisted of a defect filled with collagen carrying rhBMP-2, and a non-surgical control consisted of the intact rat calvaria. Eight weeks after implantation of the biomaterials, histologic analysis was used for qualitative assessments and microcomputed tomography was used for quantitative assessments of bone formation. Statistical evaluation was performed by analysis of variance followed by the Fisher's least significant difference multiple-comparison test.


RESULTS
In the negative control and EMD groups, the histologic analysis showed no bone formation within the center of the defect and limited bone repair at its margins. In the DFDBA group, granules of DFDBA were still present 8 weeks after implantation, and a limited degree of osteoinduction was seen at the center of the defect. The microcomputed tomography quantitative analysis showed a limited capacity of DFDBA and EMD to induce bone formation, and no statistically significant difference was detected among DFDBA, EMD, and the negative control. On the contrary, the positive control (rhBMP-2) consistently showed regeneration of bone throughout the critical-size defects.


CONCLUSIONS
Unlike rhBMP-2, DFDBA and EMD had limited ability to induce bone formation in the rat calvaria critical-size bone defect; therefore, they may not be effective as bone-regenerative therapy for critical-size defects.
Intini
Giuseppe
G
Department of Oral Biology, University at Buffalo, Buffalo, NY, USA. giuseppe_intini@hsdm.harvard.edu
Andreana
Sebastiano
S
Buhite
Robert J
RJ
Bobek
Libuse A
LA
D000818:Animals; D018775:Bone Demineralization Technique; D001847:Bone Diseases / Q000473:pathology / Q000601:surgery*; D001857:Bone Matrix / Q000473:pathology; D055396:Bone Morphogenetic Protein 2; D019485:Bone Morphogenetic Proteins / Q000627:therapeutic use*; D001861:Bone Regeneration / Q000502:physiology; D016025:Bone Transplantation / Q000379:methods* / Q000473:pathology; D003094:Collagen; D003746:Dental Enamel Proteins / Q000627:therapeutic use*; D004337:Drug Carriers; D005260:Female; D005612:Freeze Drying; D006801:Humans; D010011:Osteocytes / Q000473:pathology; D010012:Osteogenesis / Q000502:physiology*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D011994:Recombinant Proteins; D012886:Skull / Q000473:pathology / Q000601:surgery*; D014021:Tissue Preservation; D014057:Tomography, X-Ray Computed / Q000379:methods; D016212:Transforming Growth Factor beta / Q000627:therapeutic use*
C525718:BMP2 protein, human; C525720:Bmp2 protein, rat; D055396:Bone Morphogenetic Protein 2; D019485:Bone Morphogenetic Proteins; D003746:Dental Enamel Proteins; D004337:Drug Carriers; D011994:Recombinant Proteins; D016212:Transforming Growth Factor beta; C109069:enamel matrix proteins; D003094:Collagen