Diagnosis:
Delayed union of metacarpus (mid-diaphyseal) fracture, complicated by secondary 
osteomyelitis.

The radiographs provide evidence of a delayed union, with significant radiopacity on all sides of the mid-diaphyseal metacarpus.  Upon fracture of the metacarpus, improper stabilization of the fracture did not provide adequate support for proper union.  This was complicated by the presence of an open wound (resulting from the the delivery process - chains partially degloving the metacarpus).  Culture of the soft tissue lesions included growth of S. aureus, a normal flora of human skin, and E. coli, suggsting fecal contamination as well. A fracture with a superficial tissue wound (exposed blood vessels) should be considered to be an open fracture, even if the bone is not directly exposed to air, because of the exposed blood vessels.

Inflammation at the site of a fracture is a necessary first step towards bone reformation.  However, when this inflammation does not subside and allow for the cells responsible for laying down new cartilage and bone to take over, the healing process is severely complicated.  In other words, involvement of inflammatory cells, infectious organisms and the resultant purulent exudate impedes with the normal vascular and tissue responses of bone remodeling.  

With osteomyelitis, replicating gram-negative bacteria may be present around the periphery of the bone, or may enter the bone, via hematogenous spread.  The bacteria may release lipopolysachharide (LPS) as they replicate and die.  This LPS, or endotoxin, may have direct effects on the integrity of the surrounding soft tissues.  For example, smooth muscle and endothelial cells of blood vessels respond to LPS by relaxing, affording vasodilation and possible decreased perfusion of some parts of the bone.  In other words, dilation of blood vessels may impede bone reformation as the process is highly dependent upon proper supportive blood flow for delivery of nutrients (most notably oxygen). 

Neutrophils are also capable of responding to the LPS.  As the PMNs follow the LPS concentration gradient and ultimately come across the bacteria, they are upregulated and secrete destructive enzymes and oxygen species free radicals, in an attempt to remove the organism from the body.  Although quite effective at destroying the bacteria, damage to the surrounding tissue further impedes support of the bone restoration. Indeed, necrosis of cortical bone may be common when inflammation is present during osteosynthesis, and is due to the combined effect of ischemia, bacterial endotoxin, and host inflammation. As a section of the bone becomes necrotic, this avascular zone may allow further bacterial proliferation.  As this occurs, the likelihood that a more severe and chronic inflammation will develop increases.


Because of the physical limitations of being within the bone cavity, inflammation may also create a significant physical pressure, further decreasing the ability of the fibroblasts, chondroblasts, and osteoblasts to successfully remodel the bone tissue.

In summary, this animal had a delayed union, which was complicated by infection with bacteria, and the ensuing osteomyelitis severely limited the bone repair process.