No abstract

There is evidence that ethanol inhibits osteoblast function and that chronic ethanol consumption induces systemic bone loss and increases the risk of fracture in humans. The purpose of the present study was to determine whether chronic ethanol consumption also compromises the healing of injured bone. Male Sprague-Dawley rats, 8-10 weeks old, were placed into four feeding groups: group A received ethanol (36% of calories) as part of a liquid diet; group B was pair-fed to group A and received an isocaloric control diet containing maltodextrin; group C was fed the AIN-93M standard semi-purified liquid diet ad libitum; group D was fed the same ethanol diet as group A before bone injury, but after surgery (see below) these rats were given isocaloric control diet ad libitum. After 6 weeks on their respective diets, a bone repair model was surgically created at the midshaft in both fibulae of each rat. Seven weeks after injury the animals were euthanized and bone healing was evaluated by determining rigidity of the fibula by three-point bending, flexural modulus of the repair tissue and mineral content of the repair tissue. Rigidity of fibula in ethanol-fed rats and their pair-fed controls (groups A and B) were respectively 48 and 47% lower than in group C. Flexural modulus of the repair tissue in ethanol-fed rats had a 55% (P = 0.046) deficiency compared with their pair-fed controls. The mineral contents in groups A and B were respectively 16 and 13% lower than in group C. There were no significant differences in the results between groups C and D. Thus, the outcome of bone repair in ethanol-fed rats was deficient compared with rats receiving a standard maintenance diet. The repair tissue in ethanol-fed rats was mechanically inferior to that in pair-fed controls. This deficiency could not be attributed to the reduced food consumption of these animals. On the other hand, the restoration of normal bone healing in group D cannot be attributed solely to the cessation of ethanol feeding after bone injury because of the increased food consumption during this period.

Experimental models were created in rat fibula to represent impaired bone healing 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 segmental 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 the fibula. The experiments in this study involved various modifications of the DBM scaffold designed to reduce its osteoinductive activity: steam sterilization (sDBM), ethylene oxide sterilization (eoDBM), trypsin digestion (tDBM), and guanidine hydrochloride extraction (gDBM). Bone healing was evaluated by bending rigidity of the fibula and mineral content of the repair site at 7 weeks post-surgery. The sDBM scaffolds resorbed completely by 7 weeks and hence this model was a nonhealing negative control. Rigidities in the unmodified DBM and tDBM groups were comparable, whereas in the gDBM and eoDBM groups it was significantly reduced. Histologically, in the 4-mm defects repaired with unmodified DBM, direct and endochondral bone formation in the scaffold and the defect resulted in a neocortex consisting of woven and lamellar bone uniting the broken bone by 7 weeks post-surgery. We conclude that the eoDBM and gDBM groups represent failure or delay of the bone repair process when compared with the unmodified DBM group in which the process is analogous to normal bone healing.

No abstract