Study design A literature review was conducted. Objectives To review the discovery of the bone morphogenetic proteins and describe the bone morphogenetic protein products that will or may be available for clinical use. Summary of background data Bone morphogenetic proteins comprise the osteoinductive component of several tissue engineering products in late-stage development as replacements for autogenous bone graft, and for bone augmentation and repair. Methods The literature on bone morphogenetic proteins was reviewed. Results Bone morphogenetic proteins were discovered originally on the basis of their presence in osteoinductive extracts of bone matrix. Molecular cloning of bone morphogenetic proteins demonstrated that they are a family of related differentiation factors, each capable of inducing the formation of new bone tissue when implanted. Two of the molecules in clinical use, recombinant human bone morphogenetic protein-2 and recombinant human bone morphogenetic protein-7 (OP-1) are produced in a biotechnology process using recombinant deoxyribonucleic acid technology that offers unlimited supply and substantial control over purity and reproducible activity. A third material, bovine bone morphogenetic protein extract, is extracted from bone, and contains a mixture of bone morphogenetic protein molecules. Each of these molecules, although osteoinductive in vivo, has different physiologic roles and biologic activities in vivo and in vitro. Successful development of a product for use in spinal fusion involves selecting the osteoinductive molecule, the amount of the bone morphogenetic protein required, and the method of delivery, as well as conducting subsequent preclinical and clinical studies to evaluate its efficacy and safety. Conclusions On the basis of the data provided in this issue of Spine, some of these bone morphogenetic protein-based products provide for revolutionary therapies in orthopedic practice.

/pdf/overview-of-bone-morphogenetic-proteins-2x527er6hu.pdf

Overview of bone morphogenetic proteins.

We studied the precise role of the fracture haematoma in healing by the experimental transplantation of the haematoma at two days and four days after fracture of the rat femur to subperiosteal and intramuscular sites. We used bone marrow and peripheral blood haematomas for control experiments. The transplanted two-day fracture haematoma produced new bone by endochondral ossification at the subperiosteal site, but not at the intramuscular site. Four-day fracture haematoma produced new bone formation at both subperiosteal and intramuscular sites. These results suggest that fracture haematoma has an inherent osteogenetic potential.

/pdf/the-osteogenetic-potential-of-fracture-haematoma-1gnuiaeuaf.pdf

The osteogenetic potential of fracture haematoma. Subperiosteal and intramuscular transplantation of the haematoma.

Dysfunctional teeth, donated by community dental clinics, were recycled for research on bone morphogenetic protein (BMP) in health and disease. The crown remnants were trimmed away, and the roots were washed in 70% alcohol, demineralized, lyophilized, and prepared in one of two forms: (1) human partially demineralized root dentin matrix (PDM) or (2) autolysed, antigen-extracted root matrix (AAAD), including attached cementum. Composites of either PDM or antigen-extracted, autolysed, delipidized allogenic dentin matrix (AAAM) and recombinant human bone morphogenetic protein (rhBMP-2) were implanted in either normal or athymic mice. The percentage of muscle replaced by heterotopic bone was estimated by computer-assisted random point analysis. Implants of PDM and AAAD made from dysfunctional teeth exhibited little or no endogenous BMP activity and failed to induce new bone formation. Composites of 1 microgram of rhBMP-2 per 70 mg of PDM carrier induced 61% replacement of muscle by bone formation; 1 microgram of rhBMP-2 in 70 mg of AAAM matrix induced 78% replacement of muscle mass by bone; 2 or 5 micrograms of rhBMP-2 and 70 mg of AAAM carrier induced 100% replacement of thigh muscle mass by bone. In athymic mice, the areas of new bone were only slightly greater than those in normal mice. These observations suggest that root dentin prepared from extracted teeth may be recycled for use as a carrier of rhBMP-2 because it induces new bone formation in the periodontium.

Recycled Dentin Root Matrix for a Carrier of Recombinant Human Bone Morphogenetic Protein

The osteogenic factor from murine osteosarcoma was soluble in 4M guanidine-HCl. The precipitate that appeared after dialysis of the guanidine solution against deionized water showed a higher osteogenetic activity than did the initial dry powder of tumor tissue. Electron-microscopically, this bone-inducing fraction seems to be homogenous. Neither a fibrous nor collagenous cross-banded structure was observed in the fraction. Since the chemical analysis of the fraction also showed a relatively low content of hydroxyproline, the osteogenic factor is probably not collagen.

Solubilization and concentration of a bone-inducing substance from a murine osteosarcoma.

Purpose
This retrospective study compares the amount of bone resorption around implants between an autogenous tooth bone graft (AutoBT) and a synthetic bone graft after a bone-added crestally approached sinus lift with simultaneous implant placements.

/pdf/comparison-of-autogenous-tooth-bone-graft-and-synthetic-bone-3gx624nfsg.pdf

Comparison of autogenous tooth bone graft and synthetic bone graft materials used for bone resorption around implants after crestal approach sinus lifting: a retrospective study

Histophysiology, ultrastructure, chemical analyses of transplants and implants of Dunn and Ridgway mouse osteosarcomas demonstrate that tumorigenesis is a manifestation of deranged morphogenesis in developing mesenchymal cell populations. The end product of development is defective, incompletely calcified, disorganized bone without any inclusions of bone marrow tissue. When Dunn osteosarcoma is freeze-dried and then implanted, the tumor is resorbed and replaced by deposits of normal cartilage, bone, and bone marrow. Freeze-dried Ridgway osteosarcoma is replaced only by a fibrous connective tissue scar. Disaggregated Dunn tumor osteoblasts synthesize a trypsin-labile collagenase-resistant cell surface localized bone morphogen. Tumor matrix stroma, prepared by sequential chemical extraction of soluble non-collagenous proteins also contains significant quantities of the same bone morphogen. Tumor tissue pulverized to particle size as small as 44 micrometer3 transmitted bone morphogen more rapidly than intact tumor tissue. The total tumor cell and stroma mediated bone morphogen produces three times more normal bone than normal cortical bone matrix. Our working hypothesis is that a normal bone morphogenetic polypeptide (BMP) is synthesized by Dunn osteosarcoma cells and retained by the tumor matrix stroma. Neither the mechanism of transmission nor the mesenchymal cell receptor sites of BMP are known.

An osteosarcoma cell and matrix retained morphogen for normal bone formation.

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An osteosarcoma cell and matrix retained morphogen for normal bone formation.