failure as a result of implant fatigue, improving prognosis for equine fracture patients. While autogenous cancellous bone grafting enhances and stimulates bone healing, fatigue failure of implants during the healing process continues to be a major postoperative complication in equine long bone fracture repair [26, 28]. The osteogenic potential of equine autogenous cancellous bone graft from various donor sites including tuber coxae, sternum, proximal tibial metaphysis, and fourth coccygeal vertebrae has been investigated [15]. During the early stages of bone healing, new bone formation at the fracture site may result from viable graft cells or cells from the environment surrounding the graft [6, 28, 29]. Therefore, transplantation of viable osteogenic cells in bone graft or donor tissue is critical to early bone healing [10, 28, 30, 31]. When the host environment is traumatized, as with most adult equine fractures, new bone formation is a product of osteogenic cells from the graft bone that remain viable following transplantation [29].
Prevention
Optimizing transplantation of tissue from a donor site to yield a greater number of viable osteogenic cells should lead to greater new bone formation [15]. Results of comparison of osteogenic potential of donor sites revealed that the tuber coxae most consistently yielded viable osteogenic cells with an acceptable percentage of osteoprogenitor cells, while the sternum and tibia were less reliable in providing osteogenic cells [15]. Two additional donor sites have been examined; the fourth coccygeal vertebra and the tibial periosteum, were tissues with good osteogenic potential, and may be considered when the tuber coxae is not accessible or does not provide an adequate amount quantity of cancellous bone.
Autografts have greater osteogenic capacity in comparison to either allograft or xenograft, and are the most commonly used type of bone graft in equine surgery [1, 32–34]. The use of allografts would eliminate the need for a second surgery to harvest the graft, thereby reducing morbidity postoperatively. However, allogeneic bone demonstrates lower osteogenic capacity and therefore slower new bone formation and may be subject to rejection by the recipient immune system. Bone allografts are subject to the same immunologic factors as other tissue grafts [6]. The rejection of bone allograft is considered to be a primarily cellular immune response, although the humoral component of the immune system may play a role as well. Host response is related to antigen concentration and total dose. Rejection of bone allograft is observed clinically and histologically as an inflammatory process with callus bridging, nonunions, and fatigue fractures [6]. The use of allogeneic bone has declined in human medicine due to concern over the possibility of viral contamination of graft material and possible transmission of disease to graft recipients [35]. Xenogenic bone is not generally considered useful as an alternative to autogenous bone, as the antigenic response elicited upon grafting results in failure of the graft in the majority of cases [32]. Partial deproteination and defatting of xenograft have been shown to decrease the antigenic response, but this process also removes the majority of osteoinductive proteins [36].
Diagnosis
Graft rejection may be recognized clinically as a non‐union fracture, slow‐healing fracture or fatigue fracture. Histologically, evidence of an inflammatory process with callus bridging may be apparent.
Monitoring
Monitoring of graft acceptance in the recipient site may be monitored indirectly with radiographic and clinical signs indicative of fracture healing. Adult horses may require 4 to 6 months for complete fracture healing.
Treatment
In cases where non‐union fracture or graft rejection result in prolonged fracture healing, further surgical intervention may be indicated, depending upon the fracture configuration and intended use of the patient.
Expected outcome
Suboptimal or failure of osteoconduction, osteoinduction, and osteogenesis processes induced by the graft will lead to instability and prolonged fracture healing. Graft rejection resulting in nonunion, fatigue fracture and implant failure has been reported [6].The consequences will depend upon the location and condition that was being treated; unstable long bone fractures will have a poor prognosis associated with increased morbidity and mortality risk, while other locations may be associated with prolonged healing and site infection and/or suboptimal cosmetic outcome but survival of the patient.
References
1 1 Auer, J.A., von Rechenberg, B., Bohner, M. et al. (2012). Auer and Stick Equine Surgery, 4e, 1081–1085. St. Louis: Elsevier Saunders.
2 2 Bramlage, L.R. (1981). Autologous cancellous bone grafting in the horse. Proc. Am. Assoc. Equine Pract. 27: 243–247.
3 3 Harriss, F.K., Galuppo, L.D., Decock, H.E.V. et al. (2004). Evaluation of a technique for collection of cancellous bone graft from the proximal humerus in horses. Vet. Surg. 33: 293.
4 4 Millis, D. and Martinez, S.A. (2003). Bone grafts. In: Textbook of Small Animal Surgery, 3e (ed. D.H. Slatter), 1875. Philadelphia: Saunders.
5 5 Marino, J.T. and Ziran, B.H. (2010). Use of solid and cancellous autologous bone graft for fractures and nonunions. Ortho. Clin. N. Am. 41: 15–26.
6 6 Burchardt, H. (1983). The biology of bone graft repair. Clin. Orthop. 174: 28–42.
7 7 Heppenstall, R.B. (1983). Bone grafting. In: Surgery of the Musculoskeletal System (ed. C. McCollister‐Evarts), 189. New York: Churchill‐Livingston.
8 8 Burchardt, H. (1989). Biology of cortical bone graft incorporation. In: Bone Transplantation (ed. M. Aebi and P. Regazzoni), 23. Berlin, Springer‐Verlag.
9 9 Urist, M.R. (1989). Introduction to update on allograft surgery. In: Bone Transplantation (ed. M. Aebi and P. Regazzoni), 1. Berlin: Springer‐Verlag.
10 10 Bassett, C.A.L. (1972). Clinical implications of cell function in bone grafting. Clin. Orthop. Relat. Res. 87: 49.
11 11 Gray, J.C. and Elves, M.W. (1979). Early osteogenesis in compact bone isografts: a quantitative study of the contributions of different graft cells. Calcif. Tissue Int. 29: 225–237.
12 12 Boero, M.J., Schneider, J.E., Mosier, J.E. et al. (1989). Evaluation of the tibia as a source of autogenous cancellous bone in the horse. Vet. Surg. 18: 323.
13 13 Fackelman, G.E. and Auer, J.A. (2000). Bone graft biology and autogenous grafting. In: Principles of Equine Osteosynthesis, 1e (ed. G.E. Fackelman, J.A. Auer, D.M. Nunamaker, et al.), 323–331. Switzerland, AO Publishing.
14 14 Auer, J.A. (1999). Bone grafting. In: Equine Medicine and Surgery, 5e (ed. P. Colahan, I.G. Mayhew, A.L. Merritt, et al.), 1397. St. Louis, Mosby.
15 15 McDuffee, L.A. and Anderson. G.I. (2003). In vitro comparison of equine cancellous bone graft donor sites and tibial periosteum as sources of viable osteoprogenitors. Vet. Surg. 32: 455.
16 16 Richardson, G.L., Pool, R.R., Pascoe, J.R. et al. (1986). Autogenous cancellous bone grafts from the sternum in horses: comparison with other donor sites and results of use in orthopedic surgery. Vet. Surg. 15: 9.
17 17 Stashak, T.S. and Adams, O.R. (1975). Collection of bone grafts from the tuber coxae of the horse. J. Am. Vet. Med. Assoc. 167: 397.
18 18 Auer, J.A. (1991). Bone grafting. In: Equine Medicine and Surgery, 4e (ed. P. Colahan, I.G. Mayhew, A.L. Merritt, et al.), 1243–1246. Santa Barbara, CA: American Veterinary Publications.
19 19 Turner, A.S. (1982). Bone grafting. In: Equine Medicine and Surgery,
