Experimental models were created in rat fibula to represent impaired bone h
ealing so that biological deficiencies that cause bone repair to fail or to
be delayed may be investigated, These models consist of a 4-mm-long segmen
tal defect, created in rat fibula by osteotomy, and fitted with a 7-mm-long
tubular specimen of demineralized bone matrix (DBM) over the cut ends of t
he fibula, The experiments in this study involved various modifications of
the DBM scaffold designed to reduce its osteoinductive activity: steam ster
ilization (sDBM), ethylene oxide sterilization (eoDBM), trypsin digestion (
tDBM), and guanidine hydrochloride extraction (gDBM), Bone healing was eval
uated by bending rigidity of the fibula and mineral content of the repair s
ite at 7 weeks post-surgery. The sDBM scaffolds resorbed completely by 7 we
eks and hence this model was a nonhealing negative control. Rigidities in t
he unmodified DBM and tDBM groups were comparable, whereas in the gDBM and
eoDBM groups it was significantly reduced. Histologically, in the 4-mm defe
cts repaired with unmodified DBM, direct and endochondral bone formation in
the scaffold and the defect resulted in a neocortex consisting of woven an
d lamellar bone uniting the broken bone by 7 weeks post-surgery, We conclud
e that the eoDBM and gDBM groups represent failure or delay of the bone rep
air process when compared with the unmodified DBM group in which the proces
s is analogous to normal bone healing.